A new study by the University of Colorado Anschutz Medical Campus demonstrates viruses can inflame and disrupt connections between the olfactory system, and the part of the brain associated with memory and learning, which may accelerate the onset of Alzheimer’s disease (AD).
“We know that one of the early signs of Alzheimer’s disease is losing the sense of smell,” explained the study’s lead author Andrew Bubak, PhD, assistant research professor in the division of neurology at the University of Colorado School of Medicine.
The researchers focused on the olfactory tract, olfactory bulb, and the hippocampus. They examined messenger RNA in the brain tissue of six individuals from Colombia who had familial Alzheimer’s disease (FAD) and tissue from a control group without AD. They found signatures of viral infection in the olfactory bulbs of the FAD group and inflammation in the olfactory tract which carries information to the hippocampus. They also discovered altered myelination in the olfactory tract. Myelin is a protective fatty layer around nerves that allows electrical impulses to move quickly and smoothly. If it’s damaged, signaling stalls.
“These findings raise the possibility that viral infection and associated inflammation and dysregulation of myelination of the olfactory system may disrupt hippocampal function, contributing to the acceleration of FAD progression,” the study said.
The study’s senior author, Diego Restrepo, PhD, professor of cell and developmental biology at the University of Colorado School of Medicine, said viruses have long been suspected of playing a role in cognition problems. “Our hypothesis is that some viruses accelerate Alzheimer’s disease,” Restrepo said. “Does the loss of smell specifically accelerate Alzheimer’s? That’s the question.”
“The whole olfactory pathway goes to the hippocampus. If you decrease the signaling along that pathway then you get less signaling to the hippocampus,” Bubak said. “If you don’t use it, you lose it.”
The researchers hope to next focus on better understanding the relationship between the olfactory system and the hippocampus in the context of viral susceptibility and neurodegeneration.
The new study may pave the way for the development of new therapies that detect Alzheimer’s disease earlier and helps illuminate the role that viruses and the olfactory system play in driving the illness.
Cannabis-oriented companies are bringing rigor to medical marijuana through genetic testing, formulation assistance, and drug development
The appellation “medical marijuana” can be understood as a legal category, one distinct from adult-use or recreational marijuana. However, medical marijuana and adult-use marijuana are sometimes used to refer to the same substances and products—pills, liquids, oils, powders, and dried leaves. Medical marijuana can also be understood as something that meets rigorous standards with respect to matters such as composition and potency. Other refinements include alternative formulations and personalized dosages. Finally, medical marijuana can be understood to refer to drug products derived from (or inspired by) cannabis compounds.
As far as scientists are concerned, medical marijuana is exciting because it contains compounds that stimulate the endocannabinoid system, an intricate cell-signaling network that regulates many physiological processes, including those involved in pain, memory, mood, appetite, stress, sleep, metabolism, immune function, and reproductive function. To help medical marijuana realize its many potentialities, scientists are working to better characterize medical marijuana products and how they may exert different effects in different people.
In many instances, medical marijuana—that is, the marijuana that is taken for medical purposes—is basically the same as the marijuana that is taken recreationally. This kind of medical marijuana, then, shares recreational marijuana’s variability. The concentrations of the “active ingredients” can vary, complicating essential considerations such as dosing and whether a given formulation is suitable for a given condition. Also, it can be unclear how a formulation may perform differently in different people. Medical marijuana can also be understood to include drug products that are derived from (or inspired by) cannabis compounds. This kind of medical marijuana is typically better characterized and more consistent. Still, its effects can be variable.
These subtleties escape most cannabis retailers, and they can give medical professionals pause. Fortunately, help is on the way. Cannabis-oriented companies are bringing rigor to medical marijuana through genetic testing, formulation assistance, and drug development. Besides informing the cannabis industry and its consumers, these companies are supporting the work of the medical and pharmaceutical establishments.
Navigating the endocannabinoid system
Medical marijuana contains various compounds that can act on the endocannabinoid system in various ways in various circumstances, leading to various outcomes. All the possibilities can be overwhelming, especially since the endocannabinoid system is still, in many ways, terra incognita.
The endocannabinoid system was discovered in the 1990s by researchers studying the effects of tetrahydrocannabinol, or THC. Since then, studies have found that endocannabinoid receptors are located throughout the body. The primary receptor types are CB1 and CB2. CB1 receptors, which are located mostly in the central nervous system and brain, appear to serve as neuromodulators. CB2 receptors, which are expressed mainly in immune tissues, have been linked to immune system regulation.
These receptors are activated by naturally occurring endogenous cannabinoids, or endocannabinoids, made in the body. They can also be activated by compounds such as the cannabinoids, flavonoids, and terpenes made in plants.
Product matching based on genetics
Medical marijuana’s inconsistency is partly due to the variable nature of the cannabis plant and a lack of standards in processing and production. There are also many product types and consumption methods. In addition, medical marijuana consumers have different genetics and medical histories and take different medications.
As a result, first-time consumers often have no idea what effects, if any, they’re going to experience. They’re left trying multiple products or giving up on cannabis completely after going without the desired result or, worse yet, experiencing an adverse effect.
Endocanna Health offers a solution. The company provides a genetic test and cannabinoid formulation matching system to determine the product that will work best for each person and condition.
“In a nutshell, it looks at your 675,000 single nucleotide polymorphisms that are directly or indirectly associated with your endocannabinoid system,” says Len May, founder and CEO of Endocanna Health. “It gives you a full HIPAA-compliant portal report that is dynamic and is always updated based on new research.”
The system, which is called Endo-DNA, identifies an effective ratio of cannabinoids, the appropriate dose, and any potential drug interactions. “We line all that information up with our marketplace,” May adds. “We give you what the percentage of match is for that specific product based on your genetic predispositions.”
Finding an effective cannabinoid ratio
Some companies making cannabis products reduce the guesswork themselves. One such company is Zelira Therapeutics. It systematically evaluates how well its formulations perform for consumers, and it determines the optimal cannabinoid ratio. The company’s pipeline includes products for autism spectrum disorder.
The endocannabinoid system is responsible for the regulation of emotional responses, behavioral reactivity, and social interactions. And research has found that a deficiency of the endocannabinoid anandamide, which is related to the body’s stress response, is often seen in individuals with autism spectrum disorder.
Endocanna Health’s Endo-DNA is a DNA test that maps each user’s endocannabinoid system and matches the results with a specific cannabinoid ratio and terpene profile aligned with their genotype. This sample dosing report was based on a user’s metabolic properties and provides dose suggestions for tetrahydrocannabinol (THC) and cannabidiol (CBD).
Recognizing the connection, researchers have sought to treat the symptoms of autism spectrum disorder with cannabinoids and have reported some progress, especially in cases where THC was used in addition to cannabidiol, or CBD. Previously, when THC was used, it was present only in small amounts.
Zelira asserts that its research has demonstrated that a CBD:THC ratio of 1:1 has the most remarkable results in patients. Although the use of a psychoactive compound may give some parents pause, the Zelira CEO, Oludare Odumosu, PhD, suggests that they might be impressed by the encouraging results that Zelira has gathered for one of its products, HOPE 1.
Acording to Odumosu, an analysis of the first 45 patients in the study who used HOPE 1 for an average of 68 days showed a 68% reduction in irritability, a 55% reduction in aggression, and an almost 50% reduction in anxiety, while 60% of the participants reported a reduction in their meltdowns and almost 40% had an increase in focus.
“But even better, 69% of the parents believed that the quality of life for the child was improved,” Odumosu adds. “And 58% of the participants said they feel that they can report an improvement in the quality of life for their entire family.”
In addition to treatments for autism spectrum disorder, Zelira has developed treatments for insomnia and chronic pain. The company is also investigating cannabinoid-based treatments for a variety of cancers.
This bar chart summarizes patient responses to Zelira Therapeutics’ HOPE 1, a tincture that contains THC:CBD in a 1:1 ratio and is intended to ameliorate the symptoms of autism spectrum disorder. The results shown here are from a study that was conducted in Australia and that included the first 45 patients who used the treatment. The patients had their responses rated by clinicians, who observed that the longer HOPE 1 was taken, the more the clinical global impression (CGI) scores rose.
Chemical formulation using AI
Cannabis compounds have been shown to induce cancer cell death through many pathways, including apoptosis pathways. These compounds are not necessarily limited to the familiar THC and CBD. To systematically determine which chemical compounds (and which combinations of compounds) would be effective in different circumstances would take a lot of resources.
Which is why Apollon Formularies used AI techniques to comb through a large database of cannabis strains to determine which specific combinations might best target cancer cells. Using this information, Apollon created a line of formulations specifically designed to kill cancer cells. The formulations were tested in preclinical studies in an independent, third-party laboratory using 3D tumor cultures of 10 different cancer cell lines. The results showed the concentration of each formulation needed to kill a large percentage of cancer cells for each cancer type.
Apollon is now combining cannabinoid-based cancer treatments with functional mushrooms, which have been shown to kill cancer through immune-stimulated cytotoxicity.
“Since Apollon’s AI platform can handle infinite dimensional space, we can analyze all of the compounds in cannabis and mushrooms together and take advantage of a ‘super entourage effect,’” says Stephen Barnhill, MD, chairman and CEO of Apollon. “We can create a cannabis-mushroom combination that is more effective than cannabis or mushrooms individually.”
Apollon Formularies develops cannabinoid-based formulations that are designed to kill cancer cells. One of these formulations was assessed by an indendent third-party laboratory, which produced the fluorescence microscopy images shown here. These images show that the formulation effectively killed HER2-positive breast cancer cells in 3D tumor cultures.
An even more effective treatment can be identified when a patient’s genetic biomarkers are taken into consideration.
“Human genome sequencing data can also be analyzed through the same Apollon AI process,” Barnhill explains. “Doing so determines which biomarkers are important for triaging patients into the correct medical cannabis/functional mushroom treatment formulation for true personalized medicine, just as is currently done for traditional chemotherapy triage.”
Apollon’s cannabis formulations are available by prescription in Jamaica, where the company has a federally licensed production facility and a cancer institute for treating patients and performing clinical trials.
Mechanistic studies
Taking a closer look at the mechanisms behind cannabinoid-based cancer treatments is NKore BioTherapeutics. In a recent study, NKore co-founder Anahid Jewett, PhD, and colleagues studied the effects of a synthetic cannabinoid on cancer cells. The scientists compared the effects on cancer cells in well-differentiated tumors to those on cancer cells in poorly differentiated cancer cells.
NKore Biotherapeutics hopes to develop improved versions of WIN 55,212–2, a synthetic cannabinoid that can kill cancer cells. In a recent study led by Anahid Jewett, PhD, NKore’s chief scientific advisor, WIN 55,212–2 was shown to induce a higher rate of cell death in stem-like/poorly differentiated tumor cells (MP2) than in well-differentiated tumor cells (PL-12).
Since well-differentiated cancer cells have increased numbers of CB2 receptors, and since poorly differentiated cancer cells don’t have any on the surface, Jewett expected the cannabinoid to have much more of an effect on the well-differentiated tumors. What she found was just the opposite.
“My prediction did not come true,” said Jewett, who is also professor and director of the Tumor Immunology Laboratory at the University of California, Los Angeles. “We saw that these compounds were targeting more of the cancer stem-like/poorly differentiated tumors. That was very striking to us and a very important observation.”
Poorly differentiated tumors are more aggressive and harder to treat with existing chemotherapeutic or radiotherapeutic drugs. Currently, the most targeted and efficient way to kill these tumors is by the use of natural killer (NK) cells. Having another treatment option would be “very exciting,” Jewett insists.
There are still many questions that need to be addressed. One of the key questions concerns the targeting of cancer cells by cannabinoids. Jewett believes there may be a novel receptor that has yet to be identified on these tumors. Or they’re working through another mechanism entirely.
These unknowns highlight the current scarcity of cannabis research due to its classification as a Schedule I drug by the Drug Enforcement Agency and the resultant lack of federal funding.
“Schedule I means that cannabis is thought to have no therapeutic value and to have high abuse potential, says Swathi Varanasi, PharmD, co-founder and chief scientific officer for the CBD botanical wellness brand Element Apothec. “We now know that’s not true on either account. And so, there’s a huge movement now to get cannabis out of Schedule I.”
Other ways of targeting the endocannabinoid system
There are ways to activate the endocannabinoid system without relying on compounds found in cannabis. Many of the useful compounds found in cannabis plants are also found in other plants. And there are other plants have useful compounds that cannabis plants lack.
A useful compound that is present in cannabis and other plants is b-caryophyllene. This compound, which happens to be one of the most abundant terpenes found in black pepper, has been shown to activate the CB2 receptor, and studies have found that it could have a positive impact on the immune system.
Besides being stimulated by compounds found in plants, the endocannabinoid system may be stimulated by the endocannabinoids that are produced during activities such as exercise and meditation.
“One of the first biochemical processes that occur after you exercise is a rush of endocannabinoids and, in particular, anandamide,” Varanasi notes. “The feeling of the ‘runner’s high’ is caused by anandamide binding with the CB1 receptor, the same cannabinoid receptor for which THC has affinity.”
Compounds that behave like classical cannabinoids are known as cannabimimetics. According to Varanasi, they don’t receive enough attention.
“It’s bizarre that no one really talks about them,” she complains. “There’s not enough education out there, and the average healthcare professional doesn’t know about them because they’re not discussed in school. I think it’s really important to make them a part of the conversation.”
A study led by researchers at the University of Pennsylvania Perelman School of Medicine has found that some species of gut-dwelling bacteria activate nerves in the gut to promote the desire to exercise. The research found that differences in running performance within a large group of lab mice were largely attributable to the presence of certain gut bacterial species in the higher-performing animals. The team then traced this effect to bacterially produced metabolites activating sensory nerves in the gut to stimulate a motivation-controlling brain region, which then promotes the desire to exercise.
“If we can confirm the presence of a similar pathway in humans, it could offer an effective way to boost people’s levels of exercise to improve public health generally,” said Christoph Thaiss, PhD, an assistant professor of Microbiology at Penn Medicine. Apart from the potential to develop inexpensive, safe, diet-based ways of getting ordinary people out running, and possibly even optimizing elite athletes’ performance, the newly discovered pathway offer up insights that point to new strategies for modifying motivation and mood in settings such as addiction and depression.
Thaiss is senior author of the team’s published paper in Nature, which is titled “A microbiome-dependent gut-brain pathway regulates motivation for exercise,” in which the researchers say that their findings suggest “… a possible mechanistic basis for understanding interindividual variability to exercise motivation and performance.”
Exercise is possibly the single most important and accessible lifestyle component that offers protection from a large range of diseases, the authors wrote. “But exercise is strenuous and requires, in addition to cardiovascular and respiratory fitness, a strong motivational state in professional, recreational or therapeutic settings alike.” One important factor in stimulating engagement—whether for competitive or recreational exercise—is the motivating pleasure that is derived from prolonged physical activity, and which is triggered by exercise-induced neurochemical changes in the brain. But as the team also noted, “… the mechanisms regulating an individual’s motivation to engage in physical activity remain incompletely understood.”
Thaiss and colleagues set up their study to search broadly for factors that might determine exercise performance. They recorded the genome sequences, gut bacterial species, bloodstream metabolites, and other data for a cohort of 199 genetically diverse mice. “We deeply profiled this cohort by single nucleotide polymorphism genotyping, serum metabolomics, 16S ribosomal DNA (rDNA) sequencing of stool samples and multiparameter metabolic analysis,” they wrote. The analysis resulted in more than 10,500 collected data points per mouse, and close to 2.1 million data points in total. The investigators then measured the amount of daily voluntary wheel running the animals did, as well as their endurance.
The researchers analyzed these data using machine learning, to look for attributes of the mice that could best explain the animals’ sizeable inter-individual differences in running performance. They were surprised to find that genetics seemed to account for only a small portion of these performance differences—“the genetic contribution to interindividual variability in exercise capacity was minor” they noted in their report—whereas differences in gut bacterial populations appeared to be substantially more important. In fact, the scientists found that giving mice broad-spectrum antibiotics to deplete their gut bacteria reduced the animals’ running performance by about half. “Microbiome ablation by broad-spectrum antibiotics reduced both treadmill and running wheel performance by about 50%,” the scientists wrote.
Following continued detective research involving more than a dozen separate laboratories at Penn and elsewhere, over a number of years, the team found two bacterial species closely tied to better performance, Eubacterium rectale and Coprococcus eutactus, produce fatty acid amides (FAAs), which stimulate receptors called CB1 endocannabinoid receptors on gut-embedded sensory nerves that connect to the brain via the spine. The research indicated that stimulation of these CB1 receptor-studded nerves causes an increase in levels of the neurotransmitter dopamine during exercise, in a brain region called the ventral striatum.
The striatum is, the team pointed out, “a brain region critically involved in motivated behavior and the initiation of physical activity …” They concluded that the extra dopamine in this region during exercise boosts performance by reinforcing the desire to exercise. “In this study, we demonstrate that the brain circuitry involved in regulating the motivation for physical activity is not strictly central nervous system autonomous but is shaped by peripheral influences that originate in the intestinal microbial community, suggesting a possible mechanistic basis for understanding interindividual variability in exercise motivation and performance,” they stated.
“This gut-to-brain motivation pathway might have evolved to connect nutrient availability and the state of the gut bacterial population to the readiness to engage in prolonged physical activity,” said study co-author, J. Nicholas Betley, PhD, an associate professor of Biology at the University of Pennsylvania’s School of Arts and Sciences. “This line of research could develop into a whole new branch of exercise physiology.”
The findings open up many new avenues of scientific investigation. For example, there was evidence from the experiments that the better-performing mice experienced a more intense “runner’s high”—measured in this case by a reduction in pain sensitivity—hinting that this well-known phenomenon is also at least partly controlled by gut bacteria. The results, they noted, “… suggest that the neurochemical effects underlying the ‘runner’s high’, the phenomenon of pleasure, reward, anxiolysis and analgesia that is driven by endocannabinoid release after prolonged physical activity, might be influenced by the gastrointestinal tract.”
Also, the team pointed out, the findings may suggest that other behaviors that are dependent on striatal dopamine signaling could potentially be modifiable through lifestyle interventions, diet or through metabolite supplementation. This they added, could open up the more general concept of “interoceptomimetics,” or molecules that stimulate these sensory pathways and influence brain activity through peripheral intervention. The team now plans further studies to confirm the existence of this gut-to-brain pathway in humans. “If applicable to humans, our findings imply that interoceptomimetics that stimulate the motivation for exercise might present a powerful opportunity to counteract the detrimental health impact of a sedentary lifestyle,” they concluded.
A study led by researchers at the University of Pennsylvania Perelman School of Medicine has found that some species of gut-dwelling bacteria activate nerves in the gut to promote the desire to exercise. The research found that differences in running performance within a large group of lab mice were largely attributable to the presence of certain gut bacterial species in the higher-performing animals. The team then traced this effect to bacterially produced metabolites activating sensory nerves in the gut to stimulate a motivation-controlling brain region, which then promotes the desire to exercise.
“If we can confirm the presence of a similar pathway in humans, it could offer an effective way to boost people’s levels of exercise to improve public health generally,” said Christoph Thaiss, PhD, an assistant professor of Microbiology at Penn Medicine. Apart from the potential to develop inexpensive, safe, diet-based ways of getting ordinary people out running, and possibly even optimizing elite athletes’ performance, the newly discovered pathway offer up insights that point to new strategies for modifying motivation and mood in settings such as addiction and depression.
Thaiss is senior author of the team’s published paper in Nature, which is titled “A microbiome-dependent gut-brain pathway regulates motivation for exercise,” in which the researchers say that their findings suggest “… a possible mechanistic basis for understanding interindividual variability to exercise motivation and performance.”
Exercise is possibly the single most important and accessible lifestyle component that offers protection from a large range of diseases, the authors wrote. “But exercise is strenuous and requires, in addition to cardiovascular and respiratory fitness, a strong motivational state in professional, recreational or therapeutic settings alike.” One important factor in stimulating engagement—whether for competitive or recreational exercise—is the motivating pleasure that is derived from prolonged physical activity, and which is triggered by exercise-induced neurochemical changes in the brain. But as the team also noted, “… the mechanisms regulating an individual’s motivation to engage in physical activity remain incompletely understood.”
Thaiss and colleagues set up their study to search broadly for factors that might determine exercise performance. They recorded the genome sequences, gut bacterial species, bloodstream metabolites, and other data for a cohort of 199 genetically diverse mice. “We deeply profiled this cohort by single nucleotide polymorphism genotyping, serum metabolomics, 16S ribosomal DNA (rDNA) sequencing of stool samples and multiparameter metabolic analysis,” they wrote. The analysis resulted in more than 10,500 collected data points per mouse, and close to 2.1 million data points in total. The investigators then measured the amount of daily voluntary wheel running the animals did, as well as their endurance.
The researchers analyzed these data using machine learning, to look for attributes of the mice that could best explain the animals’ sizeable inter-individual differences in running performance. They were surprised to find that genetics seemed to account for only a small portion of these performance differences—“the genetic contribution to interindividual variability in exercise capacity was minor” they noted in their report—whereas differences in gut bacterial populations appeared to be substantially more important. In fact, the scientists found that giving mice broad-spectrum antibiotics to deplete their gut bacteria reduced the animals’ running performance by about half. “Microbiome ablation by broad-spectrum antibiotics reduced both treadmill and running wheel performance by about 50%,” the scientists wrote.
Following continued detective research involving more than a dozen separate laboratories at Penn and elsewhere, over a number of years, the team found two bacterial species closely tied to better performance, Eubacterium rectale and Coprococcus eutactus, produce fatty acid amides (FAAs), which stimulate receptors called CB1 endocannabinoid receptors on gut-embedded sensory nerves that connect to the brain via the spine. The research indicated that stimulation of these CB1 receptor-studded nerves causes an increase in levels of the neurotransmitter dopamine during exercise, in a brain region called the ventral striatum.
The striatum is, the team pointed out, “a brain region critically involved in motivated behavior and the initiation of physical activity …” They concluded that the extra dopamine in this region during exercise boosts performance by reinforcing the desire to exercise. “In this study, we demonstrate that the brain circuitry involved in regulating the motivation for physical activity is not strictly central nervous system autonomous but is shaped by peripheral influences that originate in the intestinal microbial community, suggesting a possible mechanistic basis for understanding interindividual variability in exercise motivation and performance,” they stated.
“This gut-to-brain motivation pathway might have evolved to connect nutrient availability and the state of the gut bacterial population to the readiness to engage in prolonged physical activity,” said study co-author, J. Nicholas Betley, PhD, an associate professor of Biology at the University of Pennsylvania’s School of Arts and Sciences. “This line of research could develop into a whole new branch of exercise physiology.”
The findings open up many new avenues of scientific investigation. For example, there was evidence from the experiments that the better-performing mice experienced a more intense “runner’s high”—measured in this case by a reduction in pain sensitivity—hinting that this well-known phenomenon is also at least partly controlled by gut bacteria. The results, they noted, “… suggest that the neurochemical effects underlying the ‘runner’s high’, the phenomenon of pleasure, reward, anxiolysis and analgesia that is driven by endocannabinoid release after prolonged physical activity, might be influenced by the gastrointestinal tract.”
Also, the team pointed out, the findings may suggest that other behaviors that are dependent on striatal dopamine signaling could potentially be modifiable through lifestyle interventions, diet or through metabolite supplementation. This they added, could open up the more general concept of “interoceptomimetics,” or molecules that stimulate these sensory pathways and influence brain activity through peripheral intervention. The team now plans further studies to confirm the existence of this gut-to-brain pathway in humans. “If applicable to humans, our findings imply that interoceptomimetics that stimulate the motivation for exercise might present a powerful opportunity to counteract the detrimental health impact of a sedentary lifestyle,” they concluded.
As of 8 December 2022, at least five Member States in the European Region, reported to WHO an increase in cases of invasive group A streptococcus (iGAS) disease and in some cases also scarlet fever. An increase in iGAS-related deaths has also been reported in some of these countries. Children under 10 years of age represent the most affected age group.
Group A Streptococcal (GAS) infection commonly causes mild illnesses such as tonsillitis, pharyngitis, impetigo, cellulitis and scarlet fever. However, in rare instances, GAS infection can lead to invasive iGAS, which can cause life-threatening conditions.
The observed increase may reflect an early start to the GAS infection season coinciding with an increase in the circulation of respiratory viruses and possible viral coinfection which may increase the risk of invasive GAS disease. This is in the context of increased population mixing following a period of reduced circulation of GAS during the COVID-19 pandemic.
In light of the moderate increase in cases of iGAS, GAS endemicity, no new emm gene sequence type identified and no reports of increased antibiotic resistance, WHO assesses that the risk for the general population posed by iGAS infections is low at present.
Description of the situation
During 2022, France, Ireland, the Netherlands, Sweden, and the United Kingdom of Great Britain and Northern Ireland, have been observing an increase in cases of invasive group A streptococcus disease and scarlet fever, mostly affecting children under 10 years of age. The increase has been particularly marked during the second half of the year.
In France, since mid-November 2022, clinicians have reported to Santé Publique France (SpF) and the Regional Health Agencies (ARS), an unusual increase in the number of iGAS cases and the detection of iGAS clusters. Some pediatric cases have been fatal. On 8 December, SpF published a status update reporting an increase in the number of iGAS infections in France since the beginning of 2022 in different regions (Occitanie, Auvergne-Rhône-Alpes, Nouvelle-Aquitaine), mainly in children under 10 years of age. SpF also detected an increase in cases of scarlet fever reported in outpatient clinics in the country since September 2022.
On 6 December, the Irish Health Protection Surveillance Centre (HPSC) reported an increase in iGAS cases in Ireland since the beginning of October. In 2022, as of 8 December, 57 iGAS cases have been notified to HPSC, of which 15 were in children less than 10 years of age. Twenty-three of the 57 iGAS cases have been reported since October 2022, compared to the 11 cases reported for the same period of 2019 (pre-COVID-19 pandemic).
The Public Health Agency of the Netherlands (RIVM) observed an increase in iGAS infections among children from March 2022 onward. Data between March and July 2022 indicates increased numbers of iGAS cases caused by different known emm gene sequence types (the gene encoding the M virulence protein responsible for many Streptococcus pyogenes serotypes). This increase has thus far not subsided. Coinfections with varicella zoster and respiratory viruses were noted.
In Sweden, since October 2022, an increase in iGAS in children under 10 years of age has been noted as compared to COVID-19 pre-pandemic levels for the equivalent period. Out of the 93 cases reported from October to 7 December, 16 (17.2%) occurred among children under 10 years of age. Between October and December 2018, seven iGAS cases were reported in this age group and 10 cases in 2019. According to the Public Health Agency of Sweden, during the season 1 July 2021 through 30 June 2022, 220 cases of iGAS were reported, compared to 173 cases reported in the previous season 2020/21. The highest numbers of iGAS cases, since iGAS became notifiable in Sweden in 2004, were reported before the pandemic in 2018/19 with 794 cases (incidence 7.8 per 100 000) and in 2017/18 with 800 cases (incidence 7.9 per 100 000).
According to the UK Health Security Agency, following a higher-than-expected scarlet fever activity in the summer in England, with a decrease during August 2022, notifications from mid-September to early December have increased again, remaining above what is normally seen at this time of year. A total of 4622 notifications of scarlet fever were reported from weeks 37 to 46 of the current season (2022/23), with 851 notifications received in week 46. This compares with an average of 1294 (range 258 to 2008) for this same period (weeks 37 to 46) in the previous five years. As expected, several scarlet fever outbreaks in nurseries and schools are being reported, of which a number involve the co-circulation of respiratory viruses. Likewise, in the summer of 2022, the levels of iGAS notifications were higher than expected, and iGAS notifications are currently higher than have been recorded over the last five seasons in all age groups (average 248, range 142 to 357 notifications). As of 8 December, 509 notifications of iGAS disease were reported through laboratory surveillance in England, with a weekly high of 73 notifications in week 46 (week commencing on 14 November). So far this season and as of 8 December 2022, the United Kingdom reported 13 deaths within seven days of an iGAS diagnosis in children under 15 years in England. This compares with four deaths in the same period in the 2017 to 2018 (pre-COVID-19 pandemic) season. Antimicrobial susceptibility results from routine laboratory surveillance in the United Kingdom indicated no increased antibiotic resistance. Additionally, laboratory surveillance has not revealed newly emerging emm gene sequence types.
Epidemiology of Group A Streptococcus
Streptococcus pyogenes, also known as Group A Streptococcus, is a group of Gram-positive bacteria which can be carried in human throats or skin; it is responsible for more than 500 000 deaths annually worldwide.
Transmission occurs by close contact with an infected person and can be passed on through coughs, sneezes, or contact with a wound.
GAS infection commonly causes mild illnesses such as tonsillitis, pharyngitis, impetigo, cellulitis and scarlet fever. GAS infections are easily treated with antibiotics, and a person with a mild illness stops being contagious after 24 hours of treatment.
GAS is considered a common cause of bacterial pharyngitis in school-aged children and may also affect younger children. The incidence of GAS pharyngitis usually peaks during winter months and early spring. Outbreaks in kindergartens and schools are common. GAS pharyngitis is diagnosed by rapid antigen tests (Rapid Strep) or bacterial culture and is treated with antibiotics and supportive care. Good hand hygiene and general personal hygiene can help control transmission.
However, in rare instances, GAS infection can lead to invasive GAS, which can cause life-threatening conditions, such as necrotizing fasciitis, streptococcal toxic shock syndrome and other severe infections, as well as post-immune mediated diseases, such as poststreptococcal glomerulonephritis, acute rheumatic fever and rheumatic heart disease.
Public health response
Enhanced surveillance activities have been implemented in the countries reporting an increase in iGAS cases, together with public health messages addressing the general population and clinicians, in order to enhance early recognition, reporting and prompt treatment initiation of GAS cases. An alert has been issued to other countries to be vigilant for a similar rise in cases and to report any unexpected increased national or regional incidence of iGAS infections to WHO.
WHO continues to support countries in assessing and responding to the epidemiological situation across the region and to provide recommendations to the public.
WHO risk assessment
WHO currently assesses the risk for the general population posed by the reported increase in iGAS infections in some European countries as low, considering the moderate rise in iGAS cases, GAS endemicity, no newly emerging emm gene sequence types identified, and no observed increases in antibiotic resistance.
The risk will be continuously assessed based on available and shared information.
WHO advice
The reports of these events do not change the current WHO recommendations on public health measures and surveillance of iGAS.
General recommendations
WHO recommends continued close analysis of the epidemiological situation in countries throughout the European region, which will be critical to assess ongoing risk and to adjust risk management measures in a timely manner.
WHO recommends that all countries be vigilant for a similar rise in cases, particularly in light of the ongoing increase in respiratory virus circulation that is now occurring across Europe.
Given the potential for severe cases, it remains important that GAS-related infections, including scarlet fever, streptococcal toxic shock syndrome, are identified and treated promptly with antibiotics to reduce the risk of potential complications such as iGAS and reduce onward transmission.
Countries should report any unexpected increased national or regional incidence of iGAS infections to WHO through IHR or equivalent mechanisms either as notifications or consultations, as applicable and driven by the decision-making instrument in Annex 2 of the IHR (2005).
Clinical recommendations
WHO encourages countries to undertake public health communication activities and messaging to healthcare providers to ensure proper clinical assessment and diagnostic testing of patients with symptoms consistent with GAS infection, and prompt treatment of patients with GAS. In addition, healthcare providers should be reminded that for iGAS infection, early recognition and prompt initiation of specific and supportive therapy for patients can be life-saving.
Healthcare providers should maintain a high degree of clinical suspicion for GAS infection when assessing patients, particularly those with preceding viral infection (including chickenpox) and those who are close contacts of scarlet fever or iGAS patients. In case of hospital admission, droplet precautions should be implemented. Healthcare workers should always follow standard precautions and perform a risk assessment to evaluate the need for additional precautions.
Healthcare providers should also be reminded of the increased risk of invasive disease among household contacts of scarlet fever and iGAS cases. Close contacts of these cases should be managed according to national guidance. In addition, adequate hand and respiratory hygiene and adequate indoor ventilation should continue to be emphasized as important protective measures during this winter season.
Laboratory and Surveillance recommendations
Clusters of cases of iGAS should be reported to local, regional or national health authorities to prompt further investigation.
In addition, laboratories should be encouraged to submit invasive disease isolates and also non-invasive isolates from suspected clusters or outbreaks to national reference laboratories for further characterization and antibiotic susceptibility testing.
Travel
WHO does not recommend any restrictions on travel and/or trade for any affected countries based on available information about this event.
World Health Organization. (2022). Transmission-based precautions for the prevention and control of infections: aide-memoire. World Health Organization. https://apps.who.int/iris/handle/10665/356853. License: CC BY-NC-SA 3.0 IGO
World Health Organization. (2022). Standard precautions for the prevention and control of infections: aide-memoire. World Health Organization. https://apps.who.int/iris/handle/10665/356855. License: CC BY-NC-SA 3.0 IGO
Light carries with it the secrets of reality in ways we cannot completely understand.
Key Takeaways
Light is the most mysterious of all things we know exist.
Light is not matter; it is both wave and particle — and it’s the fastest thing in the Universe.
We are only beginning to understand light’s secrets.
This is the third in a series of articles exploring the birth of quantum physics.
Light is a paradox. It is associated with wisdom and knowledge, with the divine. The Enlightenment proposed the light of reason as the guiding path toward truth. We evolved to identify visual patterns with great accuracy — to distinguish the foliage from the tiger, or shadows from an enemy warrior. Many cultures identify the sun as a god-like entity, provider of light and warmth. Without sunlight, after all, we would not be here.
Yet the nature of light is a mystery. Sure, we have learned a tremendous amount about light and its properties. Quantum physics has been essential along this path, changing the way we describe light. But light is weird. We cannot touch it the way we touch air or water. It is a thing that is not a thing, or at least it is not made of the stuff we associate with things.
If we traveled back to the 17th century, we could follow Isaac Newton’s disagreements with Christiaan Huygens on the nature of light. Newton would claim that light is made of tiny, indivisible atoms, while Huygens would counter that light is a wave that propagates on a medium that pervades all of space: the ether. They were both right, and they were both wrong. If light is made of particles, what particles are these? And if it is a wave propagating across space, what’s this weird ether?
Light magic
We now know that we can think of light in both ways — as a particle, and as a wave. But during the 19th century the particle theory of light was mostly forgotten, because the wave theory was so successful, and something could not be two things. In the early 1800s Thomas Young, who also helped decipher the Rosetta Stone, performed beautiful experiments showing how light diffracted as it passed through small slits, just like water waves were known to do. Light would move through the slit and the waves would interfere with one another, creating bright and dark fringes. Atoms couldn’t do that.
But then, what was the ether? All great physicists of the 19th century, including James Clerk Maxwell, who developed the beautiful theory of electromagnetism, believed the ether was there, even if it eluded us. After all, no decent wave could propagate in empty space. But this ether was quite bizarre. It was perfectly transparent, so we could see faraway stars. It had no mass, so it wouldn’t create friction and interfere with planetary orbits. Yet it was very rigid, to allow for the propagation of the ultra-fast light waves. Pretty magical, right? Maxwell had shown that if an electric charge oscillated up and down, it would generate an electromagnetic wave. This was the electric and magnetic fields tied up together, one bootstrapping the other as they traveled through space. And more amazingly, this electromagnetic wave would propagate at the speed of light, 186,282 miles per second. You blink your eyes and light goes seven and a half times around the Earth.
Maxwell concluded that light is an electromagnetic wave. The distance between two consecutive crests is a wavelength. Red light has a longer wavelength than violet light. But the speed of any color in empty space is always the same. Why is it about 186,000 miles per second? No one knows. The speed of light is one of the constants of nature, numbers we measure that describe how things behave.
Steady as a wave, hard as a bullet
A crisis started in 1887 when Albert Michelson and Edward Morley performed an experiment to demonstrate the existence of the ether. They couldn’t prove a thing. Their experiment failed to show that light propagated in an ether. It was chaos. Theoretical physicists came up with weird ideas, saying the experiment failed because the apparatus shrunk in the direction of the motion. Anything was better than accepting that light actually can travel in empty space.
And then came Albert Einstein. In 1905, the 26-year-old patent officer wrote two papers that completely changed the way we picture light and all of reality. (Not too shabby.) Let’s start with the second paper, on the special theory of relativity.
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Einstein showed that if one takes the speed of light to be the fastest speed in nature, and assumes that this speed is always the same even if the light source is moving, then two observers moving with respect to each other at a constant speed and making an observation need to correct for their distance and time measurements when comparing their results. So, if one is in a moving train while the other is standing at a station, the time intervals of the measurements they make of the same phenomenon will be different. Einstein provided a way for the two to compare their results in a way that allows these to agree with each other. The corrections showed that light could and should propagate in empty space. It had no need for an ether.
Einstein’s other paper explained the so-called photoelectric effect, which was measured in the lab in the 19th century but remained a total mystery. What happens if light is shined onto a metal plate? It depends on the light. Not on how bright it is, but on its color — or more appropriately stated, its wavelength. Yellow or red light does nothing. But shine a blue or violet light on the plate, and the plate actually acquires an electrical charge. (Hence the term photoelectric.) How could light electrify a piece of metal? Maxwell’s wave theory of light, so good at so many things, could not explain this.
The young Einstein, bold and visionary, put forth an outrageous idea. Light can be a wave, sure. But it can also be made of particles. Depending on the circumstance, or on the type of experiment, one or the other description prevails. For the photoelectric effect, we could picture little “bullets” of light hitting the electrons on the metal plate and kicking them out like billiard balls flying off a table. Having lost electrons, the metal now holds a surplus positive charge. It’s that simple. Einstein even provided a formula for the energy of the flying electrons and equated it to the energy of the incoming light bullets, or photons. The energy for the photons is E = hc/L, where c is the speed of light, L its wavelength, and h is Planck’s constant. The formula tells us that smaller wavelengths mean more energy — more kick for the photons.
Einstein won the Nobel prize for this idea. He essentially suggested what we now call the wave-particle duality of light, showing that light can be both particle and wave and will manifest differently depending on the circumstance. The photons — our light bullets — are the quanta of light, the smallest light packets possible. Einstein thus brought quantum physics into the theory of light, showing that both behaviors are possible.
I imagine Newton and Huygens are both smiling in heaven. These are the photons that Bohr used in his model of the atom, which we discussed last week. Light is both particle and wave, and it is the fastest thing in the cosmos. It carries with it the secrets of reality in ways we cannot completely understand. But understanding its duality was an important step for our perplexed minds.
If you gave me $400 and I gave you $3.15, would you consider yourself wealthier? That’s a financial analogy for the supposed fusion power “breakthrough.”
Key Takeaways
In 2021, NIF’s laser fusion energy output jumped by 2,500%, a legitimate breakthrough.
This year, NIF reports that it has achieved “ignition” — that is, it has achieved slightly more fusion energy output than laser energy input.
However, to produce commercial fusion power, NIF would need to increase the fusion output of each experiment by at least 100,000%. The technological hurdles are absolutely enormous.
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Here we go again. In 2021, the National Ignition Facility (NIF) announced a scientific breakthrough in its pursuit of fusion power technology. One year later, they’re making another announcement, heralded as “game-changing,” “transformative,” and “a moment of history.” But this is not a meaningful breakthrough for practical, commercial fusion power: NIF still drains at least 130 times more energy from the power grid than it produces.
A legitimate breakthrough in 2021
Last year’s big news was that NIF dramatically increased the fusion output of its experiments. At the time, I wrote about NIF and the scientific background of its accomplishment. They earned most of their hype. Here’s a quick recap:
“[NIF] was built for two missions. Performing research in support of the Stockpile Stewardship Program is the foremost duty, but the sign over the door doesn’t say “National Stockpile Research Facility.” NIF is named after its other task: to further our quest to understand and harness energy from nuclear fusion. A recent breakthrough in this fusion mission has made headlines across the scientific community.”
…
“One of two critical parts of NIF’s fusion mission is “ignition“: release of a quantity of fusion energy greater than the laser energy required to drive the implosion. After the failure of the National Ignition Campaign, many scientists believed that ignition at NIF was impossible. That goal remains just beyond our grasp, but it is now far closer than before. The bigger news is that we may have seen the first sign of the other important fusion goal: thermonuclear burn.”
A hyped breakthrough in 2022
In that work, NIF’s laser fusion energy output — measured in megajoules, MJ — jumped by 2,500%, a sign of a significant physics breakthrough on the crucial problem of thermonuclear burn. This week’s announcement is an increase in fusion energy output, relative to laser energy input, from 70% in 2021 to 154% in 2022. This incremental, possibly incidental, progress toward thermonuclear burn is not a breakthrough.
The facility has, at last, achieved slightly more fusion output than laser input: ignition. On paper that is a major symbolic victory. In practice, it’s of little consequence. Here’s why.
The laser energy delivered to the target was 2.05 MJ, and the fusion output was likely about 3.15 MJ. According tomultiplesources on NIF’s website, the input energy to the laser system is somewhere between 384 and 400 MJ. Consuming 400 MJ and producing 3.15 MJ is a net energy loss greater than 99%. For every single unit of fusion energy it produces, NIF burns at minimum 130 units of energy.
In terms of electrical power, 3.15 MJ would not quite power one 40-watt refrigerator light bulb for a day. Charging NIF steadily over the same day would draw 4,600 watts from the power grid. (NIF is actually charged much more quickly, but at the cost of a much higher draw in watts — more energy per unit time, over less time — but the total energy is the same.)
Getting to viable fusion power
To produce useful power, NIF would need to increase the fusion output of each experiment by at least 100,000%. That’s an enormous scientific challenge to resolve before commercial operation can even be considered.
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The scientific challenge is equaled and possibly exceeded by others. A power plant needs to produce steady power. NIF currently executes, at best, one experimental blast per day. A commercial plant would need to blast fusion-producing capsules at a rate of tens of thousands per day.
Each blast requires strict conditions: temperatures a few degrees (Kelvin) above absolute zero; a spherical capsule, mechanically perfect in shape with an error of less than 1% the width of a hair; and a vacuum chamber environment. Most blasts suffer from slightly imperfect conditions and produce less fusion.
Either way, the machine takes hours to recover from each experiment. The fact that NIF is able to do this once per day is a technical achievement that took years to perfect. Making it happen 10,000 times faster is absurdly difficult. If it could be done, still more engineering then would be required to extract the energy in the form of heat for practical electricity generation.
Finally, there is a supply problem. The pellets contain deuterium and tritium. Deuterium is plentiful, but the world’s entire supply of tritium is something like 50 pounds. In 2020, the market cost of tritium was nearly $1 million per ounce. Livermore scientists estimate that a commercial operation modeled on NIF would require two pounds per day. Producing more tritium itself will be a challenge.
Celebrate responsibly
As in 2021, we should laud the scientific accomplishments of NIF. Many years (and careers) of hard work are producing progress on one of the most difficult applied science problems ever tackled. Scientifically, it’s symbolic progress. But it’s not a breakthrough, a game-changer, or the herald of imminent clean fusion power. NIF is still decades away from economically viable fusion.
A group of prominent scientists shares how research has changed them.
Key Takeaways
Engaging in science does not only tell us about the world around us.
It can change us personally — how we think, how we act, and who we are as humans.
Several scientists tell Big Think how science has changed their understanding of the Universe and themselves.
Science speaks truth. But it is not a truth that is always easy to see. We live our lives, oblivious to the inner world of bacteria within us. Subatomic particles move in ways that seem magical and counterintuitive. The Universe goes on and on, stretching farther than our minds can comprehend. Somehow, the language of math ties everything together, bringing beauty and symmetry to the spiral of the galaxy and the unfolding of a fern leaf.
This is science to me. It is beautiful, yet it constantly reminds me that while we are part of this world and this Universe, we are observers that are far from all-knowing. There is so much we are learning, but even more that we do not know how to look for — truths hidden from our eyes and our ears, far beyond our experience yet every bit as real as the world we perceive.
Science has transformed how I see the world, and I wanted to know how it has done so for others. So I took the opportunity to speak to prominent scientists and thinkers in a range of fields to ask them one simple question: How has science changed how you think about the world? This is what they had to say.
Always new questions
Dr. Carlo Rovelli, Physicist
Professor of Physics at the Centre de Physique Theorique de Luminy, Distinguished Visiting Research Chair at the Perimeter Institute
“I am not two separate persons — one a scientist and the other a normal human creature. I am just a single one, and my worldview changes continuously, like for all of us, including because of what I do in my science. Since my adolescence I have posed to myself questions about reality, about myself, about the nature of thinking, about life and death, the nature of knowledge, the nature of time and space, history, and politics. In the course of my scientific life, these questions have guided my quest, and my work in various areas of quantum gravity, general relativity and the history and philosophy of science has continuously altered my views about all these matters. I have discarded naive ideas, got clarity about something and have been puzzled by new questions.”
Science needs art
Dr. Lekelia Jenkins, Marine sustainability scientist and science dance choreographer
Associate Professor, School of the Future of Innovation in Society, Arizona State University
“Great science or innovative leaps are creative processes, so engaging in art feeds our creativity and helps find connections and solutions that the scientific process alone might not have led us to. I think that science art speaks to people at an emotional level that impacts how our minds and the biochemistry of our bodies work. We can harness science art to build empathy with environments and species in need of protection. We can also use science art to uplift people in the midst of dealing with overwhelming issues like climate change. I believe delivering a message about climate or the environment through art allows people to sit with these difficult issues longer, and the longer people can sit with and process a problem, we are more likely to find and agree on solutions.”
The brain and the mind
Dr. Jorge Morales, Psychologist
Assistant Professor of Psychology and Philosophy and Director of the Subjectivity Lab, Northeastern University
“Becoming a scientist completely changed my understanding of uncertainty. What we understand about the human mind and brain, and what we don’t, is much more nuanced and interesting than I used to think. Certain things that used to seem obvious to me about the human mind now completely baffle me. At the same time, perhaps paradoxically, I constantly find myself impressed by how much we do know and how well we understand many aspects of how the human mind and brain work.”
Science and equality
Rev. Gregory Simpson, Ph.D., Chemist
Pastor, Nauraushaun Presbyterian Church and Co-Founder & Chair of the Board, Green Community Consulting, Inc.
“First, as a natural-product chemist, I saw the critical role that natural remedies (teas, tinctures, etc.) played in ethnic identity, health, and well-being in rural life. Second, related to my research on environmental contaminants in communities of color, in both the Caribbean and upstate New York, where those most affected were least able to advocate for themselves for several reasons, including a more nuanced understanding of the medical threats faced. Both explorations pointed to the challenge of helping communities use scientific approaches when front-line communities are unaccustomed to such practices daily. For me, the lack of access to appropriate scientific knowledge is the greatest injustice in a heavily scientific and technological world. Not only does it disenfranchise communities in terms of economic, physical, and psychological wholeness, but it also generally reinforces a state of distrust in the sciences. The result has been my advocacy, and a more profound commitment to science education reforms that transform rather than stifle society in a global sense.”
Boundaries are dissolved
Dr. Eiichiro Komatsu, Astrophysicist
Director of the Department of Physical Cosmology, Max-Planck-Institut für Astrophysik
“There were many occasions in which I felt that my view of the world had been changed by science education. Probably the greatest impact was the realization that the same physical laws operate on Earth and in the whole Universe. I felt, suddenly, that borders and boundaries became meaningless to me. I still understand the importance of respecting cultural differences between regions on Earth (or in the Universe), but in the end, the idea that all obey the same physical laws has somehow enabled me to see much further, in space and time, than those without a scientific background.”
What it means to be human
Dr. Maya Ackerman, AI researcher and opera singer
CEO & Co-Founder of WaveAI
“Research substantially impacts my worldview. Paradoxically, it brings both more rigor and more wonder and creativity into my understanding of the universe. You can tell you are approaching the truth when order and beauty emerge. More specifically, doing research in generative AI has been a wonderful journey. Generative AI enables an aggregation of human creativity, elevating that creativity to previously unimaginable heights. My research and industry work in generative AI has foundationally transformed my worldview, allowing me to experience firsthand the critical role that researchers have in creating our societies, as well as the need to focus on socially responsible and ethical developments for powerful innovations. In a very real way, science creates science fiction. Combining scientific rigor with great imagination has led to the greatest transformations in humanity, and we are only just beginning.”
It’s all one big piece
Br. Guy Consolmagno, Ph.D., Astronomer of the Pope
Director of the Vatican Observatory, President of the Vatican Observatory Foundation
“I’ve been a scientist all my adult life, for fifty years now, and a Catholic for even longer. Of course my worldview has changed over the years. How much of that had to do with science? That’s impossible to say since I see everything, including my religion and my hobbies, in the light of being a scientist, just as I understand what it means to be a scientist in light of my religious faith.”
What is the Universe up to?
Dr. Brian Green, Ethicist
Director of Technology Ethics, Markkula Center for Applied Ethics, Santa Clara University
“First, biochemistry and genetics led me to marvel at the deep complexity of life and of any Universe that could create such life. Second, science lays out a causal trail to the origin of the Universe and then stops at a question mark — a place it can no longer investigate. And yet we know that this non-investigable place must have an ability to cause effects, otherwise our Universe could not exist. Together, both are profoundly suspicious. The Universe came into existence from a cause outside itself and it seems to be doing something, developing from simplicity towards complexity. This was enough to tell me that what we can see through science is only the tip of the iceberg. The Universe is doing something and, as parts of the Universe, we each have a place in that activity. The next step is to consider what the Universe is doing and what our part might be, and that — our own better and worse behavior when confronted by this realization — is the question of ethics. This is why I changed my career to what I do now.”
On being an explorer
Dr. Seth Shostak, Astronomer
Senior Astronomer and Institute Fellow at the SETI Institute
“I’ve been fortunate to have the opportunity to investigate a truly profound question: Is Homo sapiens the only intelligent species in the universe? This is very unlike the usual research program that tries to refine an experimental result of physics, biology, or some other discipline. In fact, SETI is more exploration than traditional science research. If we were to find evidence of others out there, that would be a result that humanity would forever know and celebrate. It’s truly a ‘big picture’ question that we’re trying to answer, and it’s a privilege to be part of that effort.”
Look for the evidence
Dr. Briana Pobiner, Paleoanthropologist
Research Scientist at the Smithsonian Institution
“The other day, my brother — who is not a scientist — sent me a message with a link to a story about eggs evolving before chickens. In our exchange, he said ‘You always taught me to do my research; don’t take someone’s word, find out the facts and if it’s backed up by real research. I’ll always remember that.’ Without me even realizing it initially, my exploration of science has changed my worldview in that it has led me not only to ‘think like a scientist’ — to look for reliable evidence when I have a question about the natural world, and to figure out how to frame questions to be answerable with this kind of evidence — but to also encourage others around me to do the same.”
A recent Swedish study found children born with heart defects are 8.7 times more likely to die of heart failure.
The study, published in the AHA journal Circulation, followed 89,532 people born with heart defects between 1930 and 2017 with a control group of 890,469 born without heart defects.
“Though heart failure is extremely rare in young people, any occurrence in young congenital heart defect survivors signals a need for better screening and follow-up, starting early and continuing throughout their lifetime,” study author Dr. Niklas Bergh, a cardiologist at Sahlgrenska University Hospital in Sweden, told the American Heart Association. “Increased awareness of the high risk of heart failure in this population may lead to an earlier diagnosis as well as more appropriate treatment, which may have implications for survival.”
Here are four study findings:
During an average 25 year follow-up, 7.8 percent of people with congenital heart defects were diagnosed with heart failure, compared with 1.1 percent in the control group.
The lifetime risk for heart failure was 8.7 times higher for people born with heart defects.
People born with more complex defects faced threefold higher risk of heart failure compared to those with less complex defects.
Age makes a big difference. Those 17 and younger with heart defects faced 220 times higher risk than their peers, while those aged 60 to 69 only had five times higher risk.
“When I see a patient who is 40 years old, they are basically a 66-year-old in terms of cardiovascular risk,” Curt Daniels, MD, director of the Adult Congenital Heart Disease Program at Ohio State University and Nationwide Children’s Hospital, both in Columbus, said in the article. He was not involved in the study. “There is such a lack of attention to this population. We need to understand that these patients are unique and different. We need research for how to evaluate and treat heart failure in this group earlier in life.”
Cardiologists at Wellspan York (Pa.) Hospital are working to change the standard of care for patients with heart complaints thanks to a new 4D cardiac CT scan machine.
Currently, patients who experience symptoms of heart disease typically have at least three points of contact with the health system, Stewart Benton, MD, director of the cardiac catheterization lab at WellSpan York Hospital, said. Diagnosis and treatment can take an average of two to four weeks if everything goes well, and longer if insurance preauthorization issues arise or there are delays getting appointments.
“It starts when a patient has a complaint of chest discomfort, shortness of breath, something like that. Typically, they see their primary care provider or come into the emergency department. That’s when a referral is made to a cardiologist. That’s the first touchpoint and the first delay in treatment,” Dr. Benton said. “From there patients are referred for a noninvasive stress test. That’s the second touchpoint where there’s a delay: You see the cardiologist, they refer you for a stress test and the patient waits to do the test then waits again to get the results. Then there’s the third touchpoint where patients go in for an invasive study in the cath lab. That’s the point where the diagnosis of coronary disease would be confirmed. If the disease is amenable to PCI or stenting, it would be treated at that time.”
But with the new CT scan machine, Dr. Benton has diagnosed and treated some patients in as little as five hours.
Recently, he had a virtual office visit with a patient concerning intermediate risk chest pain. He asked the patient to come to the hospital the next day to undergo a 4D CT scan. The single scan showed one artery was critically blocked. “That scan allowed me to quickly convert from the diagnostic procedure to the therapeutic one,” Dr. Benton said. He proceeded with a stent treatment and after a four-hour observation, the patient went home. The entire process took around five hours and in a single room.
The cardiac CT scans are helpful for more than just diagnosis. They can help with preclinical disease that would not be caught in a traditional stress test.
“It’s kind of akin to a mammogram for breast cancer or a screening for colonoscopy. You catch the disease before it’s clinically apparent,” Dr. Benton said. “As things are now, we can tell patients, ‘Your stress test was normal because the disease may be preclinical.’ The patient hears that and they’re less motivated to change their lifestyle. But that disease will continue untreated until one day they may come in with a heart attack. At that point it’s too late.
“But with these scans we can say, ‘The atherosclerosis is worse and you’re at higher risk of a heart attack. This is an important window to change your future outcomes.’ We can start lowering blood pressure and cholesterol and talk about diet and lifestyle to modify that disease so the patient doesn’t have to suffer a heart attack to find out they had it.”
The traditional pathway is inefficient, he said.
“During the pandemic we had to maximize efficiency and rethink how we provide treatment to patients,” Dr. Benton said. “We had to ask, ‘How can we scale this path of treatment with CT scans? How could this be operationalized?’ We could start changing the paradigm of what standard care might be.”
He said it starts with doing what is best for patients and designing a care pathway that meets that goal.
“A hospital could place two or three of these suites in an emergency department and service all chest pain syndromes that come through,” Dr. Benton said. “You could have a point of care where patients are diagnosed and treated, then discharge to close outpatient follow-up. It could be the new standard in heart care.”
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