More Ontarians will be flagged for iron deficiency after doctors advocate for change to guidelines
Coagulopathies: Abnormal Blood-clotting And Bleeding Disorders
Haemostasis is the prevention of unwanted blood loss; this process is interrupted by blood-clotting and bleeding disorders
AbstractPlatelets and blood-clotting factors are critical for haemostasis, which is the prevention of unwanted blood loss, usually following injury or trauma. Coagulopathies can manifest as either abnormal clotting or abnormal bleeding. Pathologies that cause abnormal clotting include thromboses in arteries or emboli from deep vein thromboses; these can both restrict blood flow to vital organs. A hypercoagulable state, such as factor V Leiden, can increase the risk of developing such blood clots. Pathologies that can cause abnormal bleeding include haemophilia and von Willebrand disease. Finally, disseminated intravascular coagulation presents as both abnormal blood clotting and abnormal bleeding; it can be a life-threatening complication of many conditions, including sepsis.
Citation: Nigam Y, Knight J (2024) Coagulopathies: abnormal blood-clotting and bleeding disorders. Nursing Times [online]; 120: 10.
Authors: Yamni Nigam is professor, John Knight is associate professor; both at the School of Health and Social Care, Swansea University.
Haemostasis is the physiological arrest or halting of bleeding, a complex but balanced process that helps stop blood loss. Disruption of this balance can cause bleeding or thrombotic events, which may require clinical intervention (Favaloro et al, 2023).
On injury, when a blood vessel is damaged, it immediately constricts to reduce blood loss. The platelets (tiny cellular fragments that are present in blood) come together to form a plug. This plug is then reinforced by the activation of a cascade of clotting factors (Fig 1), culminating in the conversion of the plasma protein fibrinogen into a strong and tough protein, fibrin. This leads to blood coagulation and the creation of a more robust, permanent clot (Barmore et al, 2023).
This article – the third in a series about the pathophysiology of blood – explores coagulation disorders that affect the body's ability to clot blood, which then manifests as either abnormal clotting or abnormal bleeding.
Platelets and clotting factorsPlatelets (thrombocytes) are tiny, irregular, disc-shaped fragments of larger cells called megakaryocytes, which develop in the bone marrow. Platelets circulate in the blood and are also stored in the spleen. Critically important in the process of haemostasis, an individual's platelet count determines their ability to clot blood effectively when needed.
A normal platelet count ranges from 150,000-450,000 per microlitre (µl) of blood. A platelet count of >450,000/µl is a condition called thrombocytosis and may predispose people to abnormally form clots (Knight et al, 2024). A platelet count of <150,000/µl is known as thrombocytopenia and may lead to abnormal bleeding (Schlappi et al, 2018).
"The complex process of haemostasis results in the formation of a clot"
The platelet plugIn normal conditions, platelets do not stick together or to the walls of healthy blood vessels. However, when a blood vessel is damaged, its inner lining tears, exposing collagen fibres in the tissue beneath. These collagen fibres become covered with a protein called von Willebrand factor, which is released by cells lining the blood vessels. Von Willebrand factor attracts platelets, causing them to stick to the exposed collagen (Cortes et al, 2023). As the platelets stick, they release three key chemicals that help with clotting: serotonin, adenosine diphosphate (ADP) and thromboxane A2 (TxA2) (Knight et al, 2024).
Serotonin helps to stimulate continued vasoconstriction, while ADP and TxA2 attract more platelets to the injury site. This causes membrane changes that render arriving platelets stickier and flatter. These flattened platelets adhere to the platelets that are already stuck to the collagen. Platelets in this second layer now also degranulate, releasing the three main platelet-derived factors mentioned above, thereby attracting even more platelets (Periayah et al, 2017). The resulting positive feedback ensures that layer upon layer of platelets aggregate, leading to the rapid formation of the platelet plug (Fig 2). This plug can be quite fragile and may be washed away if blood flow in the injured vessel is too vigorous, so it needs to be stabilised by the fibrin clot (Barmore et al, 2023).
The fibrin clotTo reinforce the platelet plug and stop blood loss, a more robust clot needs to be formed. This relies on the synthesis of a tough, fibrous, rope-like protein called fibrin. Fibrin forms a meshwork around the platelet plug, sealing the injured vessel and trapping blood cells. Fibrin is formed from the plasma protein fibrinogen in a complex series of reactions involving several blood-clotting factors (I-XIII); this can proceed via the extrinsic or intrinsic pathway (Barmore et al, 2023) (Fig 1).
The extrinsic pathway is triggered by any external trauma that causes blood to exit from damaged vessels. Clotting factor VII interacts with tissue factor, which is a large protein found on the surface of many cells and on the cells lining the blood vessels when they are damaged. The complex of tissue factor plus activated factor VII triggers the clotting mechanisms in seconds, leading to the formation of activated factor X (Knight et al, 2024).
The intrinsic pathway refers to clotting factors that are intrinsic to blood. When blood vessel walls are damaged, collagen fibres are exposed. Contact with collagen fibres activates a protein known as Hageman factor (factor XII). Over several minutes, a sequence of reactions unfolds, wherein each factor activates the next (Barmore et al, 2023) (Fig 1).
The extrinsic and intrinsic pathways meet at a shared point called the common pathway, in which the last part of coagulation can be summarised in three major steps:
This complex process of haemostasis results in the formation of a clot, transforming blood from a free-flowing liquid into a gel-like, solid substance that prevents further bleeding and blood loss. Fibrin then acts as scaffolding, onto which new tissues grow during the healing process (Culvert, 2024).
After the injury is healed, the fibrin clot is dissolved and removed from the body through a process called fibrinolysis. This is essential because, if clots remained in place, they could dislodge, travel in the circulation and get stuck in important blood vessels, thereby impeding blood flow (Risman et al, 2023).
The fibrinolytic system is constantly in operation, removing unnecessary clots. The key enzyme in this cascade of reactions is plasmin. Tissue plasminogen activator (a protein released from cells lining the blood vessels) converts an inactive plasma protein called plasminogen (produced by the liver) into plasmin. Plasmin splits fibrin and fibrinogen into fragments known as fibrin-degradation products (D-dimers), thereby dissolving the clot. A D-dimer blood test is often used to determine whether a patient has recently formed any blood clots (Culvert, 2024).
To limit the formation of clots to the site of injury and prevent them from growing too large, the coagulation cascade is regulated by different anticoagulant mechanisms. Two proteins – protein C and protein S – form a complex that inactivates factors V and VIII. Additionally, a protein called antithrombin III directly decreases the production of thrombin and inactivates factor X (Padda et al, 2023).
Any condition that causes an imbalance between thrombogenic (clot-forming) and antithrombogenic (anticlot-forming) mechanisms predisposes an individual to an increased risk of either abnormal bleeding or abnormal blood-clot formation (Hernández Castillo, 2020). These coagulopathies are conditions that adversely affect the body's normal blood-clotting activities, and are discussed below.
Coagulopathies that can cause abnormal clotting ThrombosisAmong the most significant life-threatening pathologies, thrombosis is a major blood coagulopathy. Thrombosis is the formation of unwanted thrombi (clots) in blood vessels. If anticlotting mechanisms fail, or are overwhelmed, these thrombi – with constituent platelets, fibrin and accumulating blood cells (Fig 3) – can narrow or block a vessel. This can restrict blood supply to the tissues being fed by that particular vessel, which can have serious – even fatal – outcomes, such as strokes or heart attacks. Emboli (fragments of clots) may also break away and lodge in distant vessels, particularly the lungs or brain (Knight et al, 2024).
In arterial thrombosis, a thrombus blocks an artery carrying oxygen-rich blood to an organ. In venous thrombosis, it blocks a vein, causing deep vein thrombosis (DVT). Thrombi and emboli can occlude any part of the circulation, but the coronary and cerebral arteries, and the deep veins of the calf and pelvis are most often affected (Knight et al, 2024).
DVTs are clots that develop in the deep venous circulation of an upper or lower limb and can present as pain and swelling in the affected limb. Emboli can migrate to the lungs, causing a pulmonary embolism. The pathophysiology of DVT formation has not been fully explained, but the current thinking is that the disturbed flow of blood around venous valves makes them uniquely vulnerable to thrombus initiation and formation. This happens through endothelial activation, which allows the adhesion of platelets and leukocytes, contributing to the activation of blood coagulation and trapping blood cells (Navarrete et al, 2023).
There are risk factors that increase the probability of developing DVTs. DVTs are more likely to occur in people:
The risk of DVT is also five times higher during pregnancy and 60 times higher during the first three months after delivery than the risk for non-pregnant women (Pomp et al, 2008).
Studies have shown how leukocytes contribute to DVT. Within six hours of vessel flow being restricted, leukocytes overlay the endothelial surface. Of all leukocytes that are present in a thrombus, 70% are neutrophils; the remaining 30% are monocytes (Swystun and Liaw, 2016).
By releasing their internal nuclear content, neutrophils are capable of producing neutrophil extracellular traps (NETs). This remarkable defence is a network of extracellular strings of DNA that can bind pathogenic microbes. Platelets can stimulate neutrophils to form NETs, and red blood cells also bind to NETs with high affinity. This is thought to be a mechanism by which red blood cells are recruited into venous thrombi. As such, targeting NETs – through either degradation or release prevention – may provide a new way of treating thrombosis (Yao et al, 2023).
"It is believed that a hypercoagulable state occurs in patients with chronic obstructive pulmonary disease"
Hypercoagulable statesA hypercoagulable state (also known as thrombophilia) is a clinical disorder of the blood that increases the risk of developing thromboembolic disease and arterial blood clots. Hypercoagulable states are either primary (inherited) or secondary (acquired) conditions (Hernández Castillo, 2020).
There are many inherited hypercoagulable conditions. Factor V Leiden is the most common, and is more prevalent in people of European descent (Pastori et al, 2024). Under normal conditions, protein C regulates the coagulation cascade by inhibiting factor V. In factor V Leiden, there is a point mutation in the gene coding for factor V, which causes resistance to the anticoagulant effects of activated protein C. The factor V cannot be inactivated, which means it can continuously activate clotting factors downstream. This leads to unregulated production of thrombin and an increased risk of clot formation (Hernández Castillo, 2020).
Acquired hypercoagulable conditions are secondary states caused by conditions or situations that increase the risk of thrombosis, including:
Cancer can cause hypercoagulability due to an increased production of pro-coagulant factors, and due to malignant cells interacting with the inner lining of blood vessels. Smoking, inflammation, surgery and trauma can damage blood vessels, repeatedly triggering activation of the coagulation cascade. Inflammatory disorders can also activate the coagulation cascade, reduce natural anticoagulant mechanisms and impair blood-clot removal (Hernández Castillo, 2020).
It is also believed that a hypercoagulable state occurs in patients who have chronic obstructive pulmonary disease (COPD). It seems this can contribute to an increased incidence of thrombotic events (such as DVTs and venous thromboembolisms), thereby increasing the disease-related morbidity and mortality of COPD (Kyriakopoulos et al, 2021). This can be explained by hypoxia-induced erythropoiesis (red blood cell production) in response to decreased respiratory oxygen levels. Similarly, it has been found that there is a statistically significantly increased likelihood of thromboembolic events occurring at high altitude, where atmospheric oxygen availability is low (Li et al, 2022).
Erythropoiesis requires increased iron transport to the bone marrow, which occurs with the help of transferrin (a small plasma protein). As well as replenishing iron levels for increased red blood cell production, transferrin promotes blood coagulation by increasing thrombin and factor XII activities, and inhibiting antithrombin (Tang et al, 2020); therefore, an increased need for transferrin (and the transport of iron) may play a role in inducing blood coagulation and hypercoagulability.
Coagulopathies that can cause abnormal bleedingAbnormal bleeding disorders can manifest as a variety of clinical symptoms. These include:
Thrombocytopenia is a condition that can be inherited or acquired. It is characterised by a blood platelet count that is too low; this can occur if the bone marrow cannot make enough platelets or it destroys them (Smock and Perkins, 2014). Platelets are stored in the spleen for use when required but, when a person has thrombocytopenia, they remain pooled in the spleen and are not released into the blood. This is often due to an enlarged or overactive spleen, which can be caused by conditions such as liver disease, autoimmune disease or infection (Al-Salem, 2023). Other factors – such as lifestyle habits (for example, overconsumption of alcohol) and certain medicines – can also slow down the production of platelets (Smock and Perkins, 2014).
Heparin-induced thrombocytopenia can also be a serious complication for patients who are exposed to the blood anticoagulant heparin. The immune system causes platelets to clot in the presence of heparin, resulting in a drop in platelet levels (Nicolas et al, 2023).
HaemophiliaAs the various clotting factors all have vital roles to play in the formation of fibrin clots (Fig 1), a missing or deficient factor will seriously hamper an individual's ability to control blood loss. Haemophilia is the most common inherited clotting disorder. There are two major types, both of which are caused by a deficiency in a factor from the intrinsic pathway:
Symptoms of haemophilia include:
Haemophilia can be inherited or acquired.
Inherited haemophilia is caused by a mutation in a gene that provides instructions for making the clotting factor. This mutation can prevent the clotting protein from working properly or cause it to be missing altogether. The mutated gene is located on the X chromosome; therefore, inherited haemophilia is an "X-linked recessive hereditary disorder" that typically affects males, because they have only one X chromosome (Shoukat et al, 2020). As females have two X chromosomes, they are more likely to be carriers of the mutated gene than to develop inherited haemophilia themselves. However, manifestations of inherited haemophilia can sometimes be seen in carrier females. This is a result of an unfortunate skewed inactivation of the normal non-carrier X chromosome, causing the dominant manifestation of the disease. This can be severe enough to cause a life-threatening bleed (Shoukat et al, 2020).
Acquired haemophilia A (AHA) can occur when the body forms autoantibodies (antibodies that react with self-antigens) against blood-clotting factors – most commonly against factor VIII. In 15% of the healthy population, low titres of anti-factor VIII antibodies can be found anyway; these are often asymptomatic in presentation and not caused by an underlying disease (Mingot-Castellano et al, 2022). However, AHA has been associated with:
Patients with AHA may experience acute abnormal bleeding, without previous symptoms or family history. The bleeding pattern is usually subcutaneous bleeds (observed in 80% of patients), followed by muscular, gastrointestinal, genitourinary and retroperitoneal bleeds (Mingot-Castellano et al, 2022).
Haemophilia can be managed by intravenous administration of concentrates of the missing factor. However, non-factor products have recently been developed that facilitate the coagulation cascade (such as emicizumab) or block the anticoagulant pathway (such as concizumab).Clinical trials of these products are ongoing (Nogami and Shima, 2023).
"Haemophilia typically affects males, because they have only one X chromosome"
Von Willebrand diseaseVon Willebrand disease is an inherited bleeding disorder characterised by defects in the concentration, structure or function of von Willebrand factor, a vital molecule in the formation of the platelet plug (Du et al, 2023). Von Willebrand factor is also a carrier glycoprotein for factor VIII, and is synthesised in endothelial cells and megakaryocytes (Sabih and Babiker, 2023).
Low levels of von Willebrand factor are relatively common in the general population; however, not all patients experience clinically significant bleeding issues, so "a significant proportion of the patient population goes undiagnosed" (Sabih and Babiker, 2023). Indeed, a von Willebrand factor level of <30% indicates von Willebrand disease, so most cases are diagnosed only after investigating severe bleeding problems, such as:
Worldwide, it appears that more women than men are affected by von Willebrand disease (Leebeek and Eikenboom, 2016). In a systematic review of literature about the disease, Du et al (2023) found that bleeding was reported in 72-94% of patients, with mucocutaneous, gastrointestinal and oral bleeds being the most common. Life-threatening bleeding involving critical organs was also reported, although this was rare.
Von Willebrand factor replacement can be considered in patients with the most severe type of von Willebrand disease (type 3) (Sabih and Babiker, 2023).
Vitamin K deficiencyVitamins K1 and K2 are very important fat-soluble compounds. Sources of vitamin K1 are leafy greens and cruciferous vegetables; vitamin K2 is found in fermented foods, as well as being synthesised by microbes in the intestine. Many vitamin K dependent proteins are involved in essential processes, such as bone metabolism, cardiovascular health and blood clotting. With regards to this last function, vitamin K is essential for the synthesis of:
As such, vitamin K deficiency can contribute to abnormal bleeding, as well as poor bone development, osteoporosis and increased cardiovascular disease (Eden et al, 2023).
Vitamin K deficiency is present in 8-31% of healthy adults (Eden et al, 2023). However, bleeding or haemorrhage typically occurs in people with malabsorption syndromes (such as coeliac disease or inflammatory bowel disease, which can impede the absorption of vitamin K) or liver disease. Patients on medications such as warfarin (a blood thinner), which interferes with vitamin K metabolism, can also present with vitamin K deficiency and a reduced ability to clot blood if injured. Prolonged use of antibiotics can also disrupt the gut bacteria that synthesise vitamin K (Eden et al, 2023).
Vitamin K deficiency in newborn babies presents a distinct and critical concern for paediatric health care. As vitamin K cannot cross the placenta efficiently, every neonate is born with low-to-undetectable concentrations of it. Newborns with limited vitamin K reserves who do not receive timely intervention are susceptible to developing potentially life-threatening bleeding disorders. Prophylactic treatment for neonates involves administering an intramuscular injection of 0.5-1mg vitamin K1 within the first hour of birth (Ng and Loewy, 2018).
Disseminated intravascular coagulationDisseminated intravascular coagulation (DIC) is a rare but life-threatening condition. The pathological process is characterised by the widespread activation of the coagulation cascade, resulting in the formation of blood clots in the small blood vessels throughout the body. In a stark pathological contradiction, normal blood clotting is compromised and patients also present with considerable bleeding. This is because the body's clotting factors and platelets become consumed and depleted by the coagulation process, forming abnormal blood clots. The presence of both clotting and bleeding (Fig 5) results in a very serious and distressing condition, which can lead to compromised tissue blood flow and, ultimately, multiple organ damage (Iba et al, 2023).
DIC usually occurs as a complicating factor of another underlying condition, most commonly in patients who are critically ill. Causes include:
DIC is of critical concern for patients with sepsis: the mortality rate of sepsis-associated DIC is >30% (Iba et al, 2023). The prognosis for all patients with DIC depends on how much damage blood clots have caused to the body's tissues. Of those patients who survive, some will live with organ dysfunction or the results of amputation (Iba et al, 2023).
ConclusionThis article has explained the process of haemostasis, as well as exploring coagulopathies that cause abnormal blood-clot formation or abnormal bleeding.
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Duolingo's Billionaire Founder Is All In On AI
ByRichard Nieva, Forbes StaffSitting in Duo's Taqueria, a dimly-lit upscale Mexican restaurant in Pittsburgh, Luis von Ahn contemplates the end of work as we know it. In between bites of al pastor tacos and sips of a margarita, von Ahn, founder and CEO of the language learning app Duolingo, talks about how AI will make some jobs disappear, and workers will need to be retrained.
He speaks from experience: Late last year, Duolingo decided not to renew the contracts of about 10% of its contracted workforce who did translations and lesson writing, instead opting to use AI for those tasks in some cases. "Our stance as a company is that if we can automate something, we will," von Ahn said now of the dismissals. "A full time employee's job is very hard to automate. But we had some hourly contractors who were doing pretty rote stuff."
While he firmly believes it was the right call for his company, he's cognizant of the broader problems AI will bring. "It's a tough situation that'll affect the poor, the less educated," he said. "And not just in the U.S., but in poor countries."
From a table in the back of the restaurant, which was originally designed by Duolingo as a place where diners could practice their Spanish, he notes it will require smart regulation from world governments to make sure AI is equitable. But he doesn't have much faith in the U.S., which will have to "get their head out of their ass" to do it. "It's just very hard right now to imagine that the U.S. Is going to legislate this well, given that they can't agree on anything."
"It may put one-on-one human tutors out of business. I understand that. But I think net-net it is better if everybody has access to one."
Luis von Ahn, CEO of DuolingoBut longer term, von Ahn is optimistic that AI could unlock new possibilities for learning, bringing high-quality education to the masses. He thinks languages can help lift people out of poverty, noting that, for non-native speakers, learning English instantly broadens a person's earning potential and opens up a whole new world of jobs. He sees Duolingo on the forefront of the transition to AI-powered learning, with the ultimate moonshot of creating an automated AI tutor that can teach anyone a foreign language.
"That would be generally good for the world," he said. "It may put one-on-one human tutors out of business. I understand that. But I think net-net it is better if everybody has access to one."
Von Ahn isn't afraid to voice strong opinions. He delights in memes that Duolingo's owl mascot (named Duo) might break into the houses of users who missed their language lessons, a corporate brand he calls "wholesome unhinged." He was a staunch critic of Alejandro Giammattei, former president of his home country Guatemala, who he decried as corrupt (he's also the biggest donor for Giammattei's replacement Bernardo Arévalo, who took office in January). And he has said that he thinks AI will make computers better teachers than humans.
On Tuesday, Duolingo unveiled its first step in that direction: An interactive feature in which users partake in "video calls" with Lily, one of Duolingo's beloved mascots — a purple-haired, sarcastic, cartoon woman. Chatting with Lily allows people to practice conversing in other languages as if FaceTiming with an AI friend, with dialogue generated by OpenAI's GPT-4o model. It's part of a $30 a month subscription tier, called Duolingo Max, which the company debuted last year for its premium AI features, including one that tells people why they answered a question wrong during a lesson. Another new AI addition is a mini-game called Adventures, which puts users in interactive situations to practice their language skills, like ordering a coffee from a cafe or getting their passport checked.
The new features are the latest wave of tools from a generative AI push the company began last year. "In my mind, the personalized AI tutor is less like a particular feature that we're building," Klinton Bicknell, Duolingo's head of AI, told Forbes. "And more just kind of a vision for what the whole app as a whole becomes."
The AI push by Duolingo, which went public in 2022, has translated into a surge in users and revenue: Almost 104 million people take language, math and music lessons on the app each month, up 40% year over year. This past quarter, revenue hit $178.3 million, up 41% from last year. The company's stock hit an all-time high on Monday of $270, vaulting the company to a $11.75 billion market cap. Von Ahn, who owns roughly 10% of the company, is now a billionaire, along with his cofounder Severin Hacker.
"It cannot see if a student is experiencing frustration. It cannot see body language. It cannot see joy."
Elizabeth Birr Moje, University of MichiganAnd while business is booming right now, competitors are also investing in AI. Babbel, for example, last year debuted a speech recognition feature that learns a user's voice to evaluate their pronunciation. Rosetta Stone also added AI-powered language assessment exams, used in enterprise settings.
Elizabeth Birr Moje, dean of the University of Michigan's Marsal Family School of Education, said she's excited about the possibilities of Duolingo's new AI features. But she doesn't believe an AI tool will ever be able to replace the intangible skills of human tutors. "It cannot see if a student is experiencing frustration. It cannot see body language," she said. "It cannot see joy."
The Education BillionaireVon Ahn grew up in Guatemala City with his single mom and grandmother, immigrating to the U.S. In 1996 to attend Duke as an undergraduate math major. He then attended Carnegie Mellon University in Pittsburgh for his PhD, where he co-invented the CAPTCHA verification system that distinguishes humans from robots online. He spun the project into a company called reCAPTCHA and sold it to Google for an undisclosed amount in 2009. Two years later, he started Duolingo, along with cofounder Hacker, a Swiss computer scientist he tapped as the company's CTO.
"My net worth growing up was probably close to zero. So was my mom's," said von Ahn, who holds dual U.S. And Guatemalan citizenship. Reflecting on his billionaire status: "It feels cool. But it's not something I think about all the time. I'm proud of it." He's one of few Guatemalan-born individuals to reach the billionaire milestone, including Mario Lopez Estrada, a telecom tycoon who died last year.
Von Ahn's 87-year-old mom Norma now lives with him in Pittsburgh. He said she doesn't realize how much money he has, even though he reminds her they are financially secure. "She asks if it's too expensive to call Guatemala," he said, laughing. "I tell her, call whoever you want!" In 2021, he established the Luis von Ahn Foundation, which seeks to protect and support women and girls in Guatemala, among other causes, and has donated around $13 million so far. One program, called the Visionary Awards, honors individuals making an impact in Guatemala in areas including health and nature conservation, granting them each a $20,000 cash prize.
But his higher profile has also brought some new precautions. He's famous in Guatemala, often getting recognized on the street and stopped for selfies. And because he's been so outspoken about the country's former president, he's also gotten death threats. Now when he visits the country, he travels with the same security detail used by the United Nations mission, which carries packets of blood on hand that match his blood type, in case he gets shot.
"They think that it makes me feel better," he said. "That does not make me feel better. That makes me feel worse."
The Chance Of Going 'Haywire'From the rooftop at Duolingo headquarters, where employees sometimes eat lunch on sunny days, you can see the University of Pittsburgh's Cathedral of Learning, a 42-story Gothic revival church converted to classrooms and labs. It's a distant reminder of Duolingo's roots in academia — von Ahn was a mathematics professor at rival Carnegie Mellon when he incubated the company out of the university, which at one point owned $150 million in Duolingo stock, before divesting after the company went public, von Ahn said.
In addition to its AI tutor efforts, the company has made another big AI investment in its Duolingo English Test (DET), the app's version of TOEFL, or the Test Of English as a Foreign Language, which is widely used to certify English proficiency for university admissions or visa applications. The DET, which costs $59 and first launched in 2016, gained traction during the pandemic because it could be taken remotely. Duolingo now uses AI for every element of the DET exam, von Ahn said, from generating the questions to making sure people don't cheat. One security feature, for example, uses facial recognition to make sure a test taker isn't looking offscreen at notes. Right now, the test accounts for 10% of Duolingo revenue, and von Ahn wants it to become a bigger part of the pie as the company focuses increasingly on non-English speaking users.
"We're prepared. Not in that we have major contingency plans, but I'm prepared for it to happen."
Luis von Ahn, CEO of DuolingoBut creating high-quality AI tools will be a long process. Von Ahn said the company is experimenting with new characters for lessons, created by AI video-generation models, though they are in early prototyping stages. There's also room for improvement with the newly announced "video call" feature. In recorded demos, Lily's voice sounds slow and robotic, and there is sometimes a lag before her response loads. But the dialogue seems natural and casual — important groundwork for von Ahn's vision for a fully automated tutor.
Bicknell, Duolingo's head of AI, said there are three qualities of good private tutors that the company is trying to emulate as it builds out its products: Knowing exactly what the student knows, and how to teach them effectively; being adept enough to answer all of the student's questions; and keeping them motivated to come back.
The video call feature is already trying to tackle the first point. Like a human tutor, the feature learns more about the user with each session. For example, if you told Lily about the wedding you attended during your last call, she might reference that in future calls. Duolingo also tries not to discourage users by having Lily correct their pronunciation or grammar, noting that people get discouraged by their fear of mistakes. As long as the AI "understands" what the user is saying, conversations continue without those reprimands. The company said it intentionally keeps conversations short to keep people engaged, capping them at about one minute for beginners and two and a half minutes for more advanced users.
Von Ahn knows things could get messy. He is concerned an AI tutor could go "haywire," and start "getting into, say, I don't know, some Nazi stuff," he said.
Von Ahn said he's "come to peace" with the possibility of backlash set off by one of the company's interactive AI features. "We're prepared. Not in that we have major contingency plans, but I'm prepared for it to happen," he said. "And that's okay." For the video call feature, the company says it has specific prompting techniques and content moderation guidelines to keep AI responses on the rails.
Matt Skaruppa, Duolingo's CFO, said the company doesn't have to worry as much about pitfalls other companies face when they delve more into AI, because Duolingo is using the technology in a more specialized way. "Our mission is not to solve AI for the world. It's to apply a certain set of things to education," he told Forbes. "So it's a very focused effort we have when we use AI."
Still, von Ahn isn't shying away from the inherent risks — whether that's automating away jobs, or facing down the possibility of its AI saying something inappropriate. "We'll probably have to stick our foot in our mouth," he said. "The benefits outweigh the potential problems."
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Buffalo Bills star linebacker Von Miller was suspended four games for violating the NFL's personal conduct policy, according to multiple reports. Miller will be eligible for reinstatement on October 28 following the Bills' Week 8 game against the Seattle Seahawks.
No reason for the suspension has been confirmed.
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Buffalo Bills linebacker Von Miller (40) during the NFL game between the Buffalo Bills and the Los Angeles Chargers on December 23, 2023, at SoFi Stadium in Inglewood, CA. (Jevone Moore/Icon Sportswire via Getty Images)
Miller has racked up three sacks for the Bills' defense this season as the team is off to a 3-1 start. He's been a steady veteran presence since arriving in Buffalo in 2022.
Miller was previously suspended in 2013 after the NFL learned that he attempted to cheat a drug test. That same year he was arrested for failure to appear for a warrant for driving-related charges in October 2012.
He was arrested last November after being accused of assault, when he turned himself in. The female accuser later recanted the claim. That arrest took place Nov. 30 in Dallas, Texas. The recanted accusations put Miller up against a charge of third-degree felony assault of a pregnant woman, which was later said to be his girlfriend at the time.
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Von Miller #40 of the Buffalo Bills warms up prior to an NFL football game against the Philadelphia Eagles at Lincoln Financial Field on November 26, 2023 in Philadelphia, Pennsylvania. (Perry Knotts/Getty Images)
Miller denied the allegations, saying, "All of it is incorrect. You know, it's not a funny situation, but all of it is incorrect and all of it is untrue. The only thing that is true is we do have a third son on the way."
NFL commissioner Roger Goodell said the league considered putting Miller on the exempt list at the time of the allegations.
"We did consider that," Goodell told reporters in March. "We felt it was not appropriate at the time based on all the facts. I have not gotten an update recently on the status of his case."
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Von Miller of the Buffalo Bills looks on during an NFL football game against the Miami Dolphins at Hard Rock Stadium on September 12, 2024 in Miami Gardens, FL. (Perry Knotts/Getty Images)
Miller has been with the Bills since 2022 after signing a six-year, $120 million deal. However, he took a pay cut this offseason to help the Bills get under the salary cap after missing the first four games of last season as he recovered from a torn ACL that he suffered on Thanksgiving in 2022.
Miller had two tackles and three quarterback hits in 12 games during the regular season and had two tackles against the Kansas City Chiefs in the playoffs.
Miller currently leads all active NFL players in sacks with 126.5.
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Jackson Thompson is a sports writer for Fox News Digital. He previously worked for ESPN and Business Insider. Jackson has covered the Super Bowl and NBA Finals, and has interviewed iconic figures Usain Bolt, Rob Gronkowski, Jerry Rice, Troy Aikman, Mike Trout, David Ortiz and Roger Clemens.
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