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This transcript has been edited for clarity.

Hello, everyone. This is Dr Bishal Gyawali, from Queens University, Kingston, Canada. Today, I’m back with you to talk about some of the fallacies that I have seen in medicine, oncology, and the drug regulatory space. I wanted to clarify some of these fallacies.

In my last video, I talked about the FDA denying the approval of a new cancer drug. Let me start with one of the fallacies that is pertinent to that, which is that some people make an argument that patients are dying from a certain condition, such as cancer, or even any other disease besides cancer. That is an absolutely true statement, but that does not necessarily mean there should be a lower bar for drug approvals or we should be approving any drug that has a hint of benefit.

In fact, if we have increased mortality rates and our patients are dying from a certain condition, that means we actually need to have good drugs. We need to have drugs that prevent mortality. We need to have drugs that improve outcomes. Just having any drug out there, if we lower our threshold and are letting any drug be used in these patients because the argument is that people are dying, then in fact, it can have negative consequences.

First, there will be opportunity costs. If you can get any lousy drug into the market and make billions of dollars out of it, then there is no strong motivation to produce drugs that actually remarkably improve outcomes.

Second, patients will also be misled. It’s the patient’s opportunity cost in that they will use whatever time they have remaining to pursue these treatments that were not going to improve their outcomes anyway. This is time they could have better spent either in pursuing better treatments, if those treatments are out there, or to prioritize their time accordingly. This rather gives them a false hope, which can be harmful in the long term.

The first fallacy is that just because people are dying does not necessarily mean we should have more new drugs with a lower bar for approval.

The second fallacy I want to talk about, which is also related to this, is that if a certain cancer is rare, the bar for new drug approval should be quite low.

Of course, rare cancers are a special category, and rare cancers should be treated differently from a regulatory perspective. Absolutely. If the cancer is rare, we cannot have trials with large sample sizes to generate evidence. That problem is there, but that does not necessarily translate to the decision that we should approve anything, even something with a small hint of benefit.

There are other methods to make sure that, even in rare cancers, we can generate good-quality evidence. In fact, from an equity perspective, why should patients with rare cancer not deserve drugs that have good-quality evidence?

We can’t tell someone that, “Your cancer is rare, so you should get drugs that only have a benefit in terms of response rate whereas other cancers that are not rare will have drugs based on survival.”

Going back to the point about the difficulty in doing big trials in patients with rare cancers, that is absolutely true and there should be regulatory flexibility in this. I think accelerated approval is a pathway that allows for this regulatory flexibility, which allows access to these drugs early on based on earlier signals of benefit. You can continue to generate evidence in the future and confirm the clinical benefit.

There are also other nuances to this. One is that we should also make sure that this regulatory flexibility with rare cancers should not be misused. What do I mean by that? First, all rare cancers are not the same. There are some cancers that are ultra rare, and then there are some cancers that technically might fit the definition of rare, but trials are possible. Case in point: adrenocortical cancer. It is considered to be a very rare cancer, but there have been randomized trials in adrenocortical cancer.

Our efforts should be to maximize our collaboration globally so that a cancer that is rare locally will still not be so rare globally when we collect all these patients.

In certain situations, like let’s say, based on the molecular subtypes, any common cancer can be sliced and diced into a rare subtype: MSI-high, BRAF-negative, HER2-positive, right-sided colon cancer. If you start to slice cancers into these smaller and smaller molecular subtypes, you can consider anything as a rare cancer. That should not be misused as an excuse to get away from doing proper trials and generating adequate evidence for our patients.

The third fallacy I want to talk about is that increasing cancer incidence in a certain subgroup of population does not automatically translate into, “We should start screening this subgroup of population.”

A certain cancer — let’s say cancer X or cancer Y — is increasing in a young population, so therefore, we should lower the age of the screening of young populations. This cancer is increasing in this ethnic population, so therefore we should start screening this ethnic population more frequently. This cancer is increasing in this type of minority, so therefore, we should start screening this minority more.

No, it does not work like that. Increasing incidence will make us concerned, of course, but that does not necessarily translate into, “We should start screening them.” In order for a screening test to be useful, it has to fulfill a number of criteria.

The goal is not to detect cancers. The goal is to detect cancers that are not indolent enough that they would have never caused problems, nor speed up the diagnosis of aggressive cancers that are going to be lethal pretty soon anyway. The goal is to detect those cancers in the middle, so that by detecting early, we can intervene and improve the outcomes and improve the mortality from that cancer.

This type of intervention requires a thoughtful consideration of the increasing incidence of the cancer, of course, but also the utility of the screening test in that subgroup of population; the life expectancy of this subgroup of patients with and without cancer; the interventions available to address that increasing burden of cancer; and whether by intervening we are going to reduce the mortality rates.

Just because we can detect cancers does not mean we should detect cancers. That’s the third fallacy I wanted to talk about.

The fourth fallacy is related to when someone is asking for more evidence for anything. There is a new drug for this cancer,so what is the evidence? Or there is this new intervention that will detect ctDNA or whatever before the cancer relapses, or before the cancer even shows up as a screening test.

Whenever there is any treatment that is being promoted and someone asks for evidence, people sometimes try to make personal attacks by saying, “Oh, so, you’re okay with patients dying. You don’t want to save lives.”

Absolutely we want to save lives. That’s why we’re in this field, and that’s why we’re asking for more evidence. You should not consider someone who is asking for evidence as evil or that this person does not want this new drug, or this person does not want this innovation. No, that person actually wants to make sure that that innovation actually helps people. That’s why that person is asking for more evidence.

If we stop asking for evidence, then our whole practice becomes based on emotions, faith, and trust rather than science. You could extrapolate it to the other extreme, like if you are not asking for evidence. If it is interpreted as someone who is asking for evidence is evil, or someone who does not want patients to get new drugs, then you could extrapolate these to people also making claims about alternative medicines or ivermectin nowadays, and claiming that this cures cancer.

Science is science. You need to be the same no matter the circumstances. If you are asking for data for ivermectin, you should also be asking data for your cancer drug that you think is going to work. We should always ask for evidence.

Asking for evidence is not a sign that whoever is asking for evidence does not want the patient to have access to the drug. It is showing that the person who is asking for evidence actually wants to make sure that the patients who get this drug are actually being helped by the drug rather than being harmed.

I’m talking about 5 fallacies today. The final, fifth fallacy is that clinical expertise does not equal expertise in making public health decisions or even expertise in critical appraisal. Someone can be a fantastic breast cancer doctor, the best oncologist for breast cancer. That does not automatically make that person the best person to evaluate clinical trials of breast cancer drugs.

Someone can be a fantastic colon cancer doctor. That does not make that person automatically the best person to evaluate whether or not colonoscopy or colon cancer screening is indicated in a certain patient population.

These population-level decisions — including should this drug be approved, should this drug be funded, and should this screening test be made a public health measure, all of these public health decisions that are done at a population level — require different expertise in critical appraisal, clinical epidemiology, and public health.

Just because someone is a fantastic clinician does not make that person a fantastic public health expert. I see on social media often that a famous doctor with expertise in their domain, let’s say a famous neurosurgeon, might say, “I think brain tumors are increasing in incidence in young persons, so we should be targeting an MRI screening for everyone over the age of 30.”

I’m just making this up, but we see examples of things not dissimilar to this. Just because someone is a neurosurgeon does not make them an expert on brain tumor epidemiology, surveillance, or screening. We should separate clinical expertise from public health expertise.

Thank you.

A version of this article first appeared on Medscape.com.

This transcript has been edited for clarity.

Hello, everyone. This is Dr Bishal Gyawali, from Queens University, Kingston, Canada. Today, I’m back with you to talk about some of the fallacies that I have seen in medicine, oncology, and the drug regulatory space. I wanted to clarify some of these fallacies.

In my last video, I talked about the FDA denying the approval of a new cancer drug. Let me start with one of the fallacies that is pertinent to that, which is that some people make an argument that patients are dying from a certain condition, such as cancer, or even any other disease besides cancer. That is an absolutely true statement, but that does not necessarily mean there should be a lower bar for drug approvals or we should be approving any drug that has a hint of benefit.

In fact, if we have increased mortality rates and our patients are dying from a certain condition, that means we actually need to have good drugs. We need to have drugs that prevent mortality. We need to have drugs that improve outcomes. Just having any drug out there, if we lower our threshold and are letting any drug be used in these patients because the argument is that people are dying, then in fact, it can have negative consequences.

First, there will be opportunity costs. If you can get any lousy drug into the market and make billions of dollars out of it, then there is no strong motivation to produce drugs that actually remarkably improve outcomes.

Second, patients will also be misled. It’s the patient’s opportunity cost in that they will use whatever time they have remaining to pursue these treatments that were not going to improve their outcomes anyway. This is time they could have better spent either in pursuing better treatments, if those treatments are out there, or to prioritize their time accordingly. This rather gives them a false hope, which can be harmful in the long term.

The first fallacy is that just because people are dying does not necessarily mean we should have more new drugs with a lower bar for approval.

The second fallacy I want to talk about, which is also related to this, is that if a certain cancer is rare, the bar for new drug approval should be quite low.

Of course, rare cancers are a special category, and rare cancers should be treated differently from a regulatory perspective. Absolutely. If the cancer is rare, we cannot have trials with large sample sizes to generate evidence. That problem is there, but that does not necessarily translate to the decision that we should approve anything, even something with a small hint of benefit.

There are other methods to make sure that, even in rare cancers, we can generate good-quality evidence. In fact, from an equity perspective, why should patients with rare cancer not deserve drugs that have good-quality evidence?

We can’t tell someone that, “Your cancer is rare, so you should get drugs that only have a benefit in terms of response rate whereas other cancers that are not rare will have drugs based on survival.”

Going back to the point about the difficulty in doing big trials in patients with rare cancers, that is absolutely true and there should be regulatory flexibility in this. I think accelerated approval is a pathway that allows for this regulatory flexibility, which allows access to these drugs early on based on earlier signals of benefit. You can continue to generate evidence in the future and confirm the clinical benefit.

There are also other nuances to this. One is that we should also make sure that this regulatory flexibility with rare cancers should not be misused. What do I mean by that? First, all rare cancers are not the same. There are some cancers that are ultra rare, and then there are some cancers that technically might fit the definition of rare, but trials are possible. Case in point: adrenocortical cancer. It is considered to be a very rare cancer, but there have been randomized trials in adrenocortical cancer.

Our efforts should be to maximize our collaboration globally so that a cancer that is rare locally will still not be so rare globally when we collect all these patients.

In certain situations, like let’s say, based on the molecular subtypes, any common cancer can be sliced and diced into a rare subtype: MSI-high, BRAF-negative, HER2-positive, right-sided colon cancer. If you start to slice cancers into these smaller and smaller molecular subtypes, you can consider anything as a rare cancer. That should not be misused as an excuse to get away from doing proper trials and generating adequate evidence for our patients.

The third fallacy I want to talk about is that increasing cancer incidence in a certain subgroup of population does not automatically translate into, “We should start screening this subgroup of population.”

A certain cancer — let’s say cancer X or cancer Y — is increasing in a young population, so therefore, we should lower the age of the screening of young populations. This cancer is increasing in this ethnic population, so therefore we should start screening this ethnic population more frequently. This cancer is increasing in this type of minority, so therefore, we should start screening this minority more.

No, it does not work like that. Increasing incidence will make us concerned, of course, but that does not necessarily translate into, “We should start screening them.” In order for a screening test to be useful, it has to fulfill a number of criteria.

The goal is not to detect cancers. The goal is to detect cancers that are not indolent enough that they would have never caused problems, nor speed up the diagnosis of aggressive cancers that are going to be lethal pretty soon anyway. The goal is to detect those cancers in the middle, so that by detecting early, we can intervene and improve the outcomes and improve the mortality from that cancer.

This type of intervention requires a thoughtful consideration of the increasing incidence of the cancer, of course, but also the utility of the screening test in that subgroup of population; the life expectancy of this subgroup of patients with and without cancer; the interventions available to address that increasing burden of cancer; and whether by intervening we are going to reduce the mortality rates.

Just because we can detect cancers does not mean we should detect cancers. That’s the third fallacy I wanted to talk about.

The fourth fallacy is related to when someone is asking for more evidence for anything. There is a new drug for this cancer,so what is the evidence? Or there is this new intervention that will detect ctDNA or whatever before the cancer relapses, or before the cancer even shows up as a screening test.

Whenever there is any treatment that is being promoted and someone asks for evidence, people sometimes try to make personal attacks by saying, “Oh, so, you’re okay with patients dying. You don’t want to save lives.”

Absolutely we want to save lives. That’s why we’re in this field, and that’s why we’re asking for more evidence. You should not consider someone who is asking for evidence as evil or that this person does not want this new drug, or this person does not want this innovation. No, that person actually wants to make sure that that innovation actually helps people. That’s why that person is asking for more evidence.

If we stop asking for evidence, then our whole practice becomes based on emotions, faith, and trust rather than science. You could extrapolate it to the other extreme, like if you are not asking for evidence. If it is interpreted as someone who is asking for evidence is evil, or someone who does not want patients to get new drugs, then you could extrapolate these to people also making claims about alternative medicines or ivermectin nowadays, and claiming that this cures cancer.

Science is science. You need to be the same no matter the circumstances. If you are asking for data for ivermectin, you should also be asking data for your cancer drug that you think is going to work. We should always ask for evidence.

Asking for evidence is not a sign that whoever is asking for evidence does not want the patient to have access to the drug. It is showing that the person who is asking for evidence actually wants to make sure that the patients who get this drug are actually being helped by the drug rather than being harmed.

I’m talking about 5 fallacies today. The final, fifth fallacy is that clinical expertise does not equal expertise in making public health decisions or even expertise in critical appraisal. Someone can be a fantastic breast cancer doctor, the best oncologist for breast cancer. That does not automatically make that person the best person to evaluate clinical trials of breast cancer drugs.

Someone can be a fantastic colon cancer doctor. That does not make that person automatically the best person to evaluate whether or not colonoscopy or colon cancer screening is indicated in a certain patient population.

These population-level decisions — including should this drug be approved, should this drug be funded, and should this screening test be made a public health measure, all of these public health decisions that are done at a population level — require different expertise in critical appraisal, clinical epidemiology, and public health.

Just because someone is a fantastic clinician does not make that person a fantastic public health expert. I see on social media often that a famous doctor with expertise in their domain, let’s say a famous neurosurgeon, might say, “I think brain tumors are increasing in incidence in young persons, so we should be targeting an MRI screening for everyone over the age of 30.”

I’m just making this up, but we see examples of things not dissimilar to this. Just because someone is a neurosurgeon does not make them an expert on brain tumor epidemiology, surveillance, or screening. We should separate clinical expertise from public health expertise.

Thank you.

A version of this article first appeared on Medscape.com.

This transcript has been edited for clarity.

Hello, everyone. This is Dr Bishal Gyawali, from Queens University, Kingston, Canada. Today, I’m back with you to talk about some of the fallacies that I have seen in medicine, oncology, and the drug regulatory space. I wanted to clarify some of these fallacies.

In my last video, I talked about the FDA denying the approval of a new cancer drug. Let me start with one of the fallacies that is pertinent to that, which is that some people make an argument that patients are dying from a certain condition, such as cancer, or even any other disease besides cancer. That is an absolutely true statement, but that does not necessarily mean there should be a lower bar for drug approvals or we should be approving any drug that has a hint of benefit.

In fact, if we have increased mortality rates and our patients are dying from a certain condition, that means we actually need to have good drugs. We need to have drugs that prevent mortality. We need to have drugs that improve outcomes. Just having any drug out there, if we lower our threshold and are letting any drug be used in these patients because the argument is that people are dying, then in fact, it can have negative consequences.

First, there will be opportunity costs. If you can get any lousy drug into the market and make billions of dollars out of it, then there is no strong motivation to produce drugs that actually remarkably improve outcomes.

Second, patients will also be misled. It’s the patient’s opportunity cost in that they will use whatever time they have remaining to pursue these treatments that were not going to improve their outcomes anyway. This is time they could have better spent either in pursuing better treatments, if those treatments are out there, or to prioritize their time accordingly. This rather gives them a false hope, which can be harmful in the long term.

The first fallacy is that just because people are dying does not necessarily mean we should have more new drugs with a lower bar for approval.

The second fallacy I want to talk about, which is also related to this, is that if a certain cancer is rare, the bar for new drug approval should be quite low.

Of course, rare cancers are a special category, and rare cancers should be treated differently from a regulatory perspective. Absolutely. If the cancer is rare, we cannot have trials with large sample sizes to generate evidence. That problem is there, but that does not necessarily translate to the decision that we should approve anything, even something with a small hint of benefit.

There are other methods to make sure that, even in rare cancers, we can generate good-quality evidence. In fact, from an equity perspective, why should patients with rare cancer not deserve drugs that have good-quality evidence?

We can’t tell someone that, “Your cancer is rare, so you should get drugs that only have a benefit in terms of response rate whereas other cancers that are not rare will have drugs based on survival.”

Going back to the point about the difficulty in doing big trials in patients with rare cancers, that is absolutely true and there should be regulatory flexibility in this. I think accelerated approval is a pathway that allows for this regulatory flexibility, which allows access to these drugs early on based on earlier signals of benefit. You can continue to generate evidence in the future and confirm the clinical benefit.

There are also other nuances to this. One is that we should also make sure that this regulatory flexibility with rare cancers should not be misused. What do I mean by that? First, all rare cancers are not the same. There are some cancers that are ultra rare, and then there are some cancers that technically might fit the definition of rare, but trials are possible. Case in point: adrenocortical cancer. It is considered to be a very rare cancer, but there have been randomized trials in adrenocortical cancer.

Our efforts should be to maximize our collaboration globally so that a cancer that is rare locally will still not be so rare globally when we collect all these patients.

In certain situations, like let’s say, based on the molecular subtypes, any common cancer can be sliced and diced into a rare subtype: MSI-high, BRAF-negative, HER2-positive, right-sided colon cancer. If you start to slice cancers into these smaller and smaller molecular subtypes, you can consider anything as a rare cancer. That should not be misused as an excuse to get away from doing proper trials and generating adequate evidence for our patients.

The third fallacy I want to talk about is that increasing cancer incidence in a certain subgroup of population does not automatically translate into, “We should start screening this subgroup of population.”

A certain cancer — let’s say cancer X or cancer Y — is increasing in a young population, so therefore, we should lower the age of the screening of young populations. This cancer is increasing in this ethnic population, so therefore we should start screening this ethnic population more frequently. This cancer is increasing in this type of minority, so therefore, we should start screening this minority more.

No, it does not work like that. Increasing incidence will make us concerned, of course, but that does not necessarily translate into, “We should start screening them.” In order for a screening test to be useful, it has to fulfill a number of criteria.

The goal is not to detect cancers. The goal is to detect cancers that are not indolent enough that they would have never caused problems, nor speed up the diagnosis of aggressive cancers that are going to be lethal pretty soon anyway. The goal is to detect those cancers in the middle, so that by detecting early, we can intervene and improve the outcomes and improve the mortality from that cancer.

This type of intervention requires a thoughtful consideration of the increasing incidence of the cancer, of course, but also the utility of the screening test in that subgroup of population; the life expectancy of this subgroup of patients with and without cancer; the interventions available to address that increasing burden of cancer; and whether by intervening we are going to reduce the mortality rates.

Just because we can detect cancers does not mean we should detect cancers. That’s the third fallacy I wanted to talk about.

The fourth fallacy is related to when someone is asking for more evidence for anything. There is a new drug for this cancer,so what is the evidence? Or there is this new intervention that will detect ctDNA or whatever before the cancer relapses, or before the cancer even shows up as a screening test.

Whenever there is any treatment that is being promoted and someone asks for evidence, people sometimes try to make personal attacks by saying, “Oh, so, you’re okay with patients dying. You don’t want to save lives.”

Absolutely we want to save lives. That’s why we’re in this field, and that’s why we’re asking for more evidence. You should not consider someone who is asking for evidence as evil or that this person does not want this new drug, or this person does not want this innovation. No, that person actually wants to make sure that that innovation actually helps people. That’s why that person is asking for more evidence.

If we stop asking for evidence, then our whole practice becomes based on emotions, faith, and trust rather than science. You could extrapolate it to the other extreme, like if you are not asking for evidence. If it is interpreted as someone who is asking for evidence is evil, or someone who does not want patients to get new drugs, then you could extrapolate these to people also making claims about alternative medicines or ivermectin nowadays, and claiming that this cures cancer.

Science is science. You need to be the same no matter the circumstances. If you are asking for data for ivermectin, you should also be asking data for your cancer drug that you think is going to work. We should always ask for evidence.

Asking for evidence is not a sign that whoever is asking for evidence does not want the patient to have access to the drug. It is showing that the person who is asking for evidence actually wants to make sure that the patients who get this drug are actually being helped by the drug rather than being harmed.

I’m talking about 5 fallacies today. The final, fifth fallacy is that clinical expertise does not equal expertise in making public health decisions or even expertise in critical appraisal. Someone can be a fantastic breast cancer doctor, the best oncologist for breast cancer. That does not automatically make that person the best person to evaluate clinical trials of breast cancer drugs.

Someone can be a fantastic colon cancer doctor. That does not make that person automatically the best person to evaluate whether or not colonoscopy or colon cancer screening is indicated in a certain patient population.

These population-level decisions — including should this drug be approved, should this drug be funded, and should this screening test be made a public health measure, all of these public health decisions that are done at a population level — require different expertise in critical appraisal, clinical epidemiology, and public health.

Just because someone is a fantastic clinician does not make that person a fantastic public health expert. I see on social media often that a famous doctor with expertise in their domain, let’s say a famous neurosurgeon, might say, “I think brain tumors are increasing in incidence in young persons, so we should be targeting an MRI screening for everyone over the age of 30.”

I’m just making this up, but we see examples of things not dissimilar to this. Just because someone is a neurosurgeon does not make them an expert on brain tumor epidemiology, surveillance, or screening. We should separate clinical expertise from public health expertise.

Thank you.

A version of this article first appeared on Medscape.com.

The fastest way to a new anticoagulation therapy that prevents blood clots without prolonging bleeding or healing time may be a land snail.

A recent preclinical study in ACS Central Science investigating bioactive molecules derived from the land snail Camaena cicatricosa identified a compound that significantly reduced clot formation without prolonging bleeding time and wound healing in rodent models, directly challenging the assumption that effective anticoagulant therapy must inherently disrupt physiologic repair processes.

“I was quite excited,” said Lisha Lin, PhD, lead author on the study and research assistant at the State Key Laboratory of Phytochemistry and Natural Medicines at the Kunming Institute of Botany, Chinese Academy of Sciences, in Kunming, China. “A novel polysaccharide was identified, and more importantly, it showed anticoagulant activity by inhibiting a novel target, with different action mechanism from heparins.”

What Led to the Land Snail?

The choice of C cicatricosa reflects a shift in thinking. The team screened a range of mollusk-derived biomolecules in search of safer anticoagulation strategies, ultimately isolating a novel galactosylated glycosaminoglycan (CCG) from this terrestrial species.

“We compared the anticoagulant activity of glycosaminoglycans from three snail species,” said Lin. They initially studied polysaccharides from C cicatricosa, Achatina fulica, and Helix lucorum — all sulfated glycosaminoglycans with similar structures. “However, we only found CCG from [C cicatricosa] showed anticoagulant activity but not other snail polysaccharides.”

This unexpected selectivity proved crucial. “The result indicated that the galactose branches and special sulfate substitution were important,” she explained, helping to explain why this particular species stood out among structurally similar compounds.

While CCG shares some similarities with heparin-like molecules, it notably lacks the specific pentasaccharide sequence required for antithrombin binding. Researchers hypothesized that this absence could reduce bleeding risk while maintaining antithrombotic activity.

Rather than broadly inhibiting coagulation, the compound selectively disrupts the intrinsic tenase complex, a pathway more closely associated with pathologic thrombosis than with physiologic hemostasis. This mechanism’s selectivity is central to the study’s findings and helps explain why normal wound healing remained intact in preclinical models.

The isolated compound demonstrated a rare combination in anticoagulant research: potent inhibition of pathologic thrombosis with no significant increase in bleeding time and intact wound healing across multiple experimental models. The compound did not act as a broad-spectrum anticoagulant, instead selectively targeting pathways more relevant to disease-associated clot formation.

The Hope of Lowering Bleeding Risk

For decades, anticoagulation therapy has been built on the assumption that inhibiting clot formation inevitably increases bleeding risk. For physicians treating patients with deep vein thrombosis or atrial fibrillation or those requiring postsurgical attention, the balancing act is constant. Prevent clot formation aggressively enough and the bleeding risk rises. Reduce intensity and thrombosis risk returns.

Current therapies, including heparin and direct oral anticoagulants (DOACs), function by broadly targeting the coagulation cascade. This lack of specialty is precisely what limits them. Even when carefully dosed, the treatments interfere with both pathologic clot formation and physiologic hemostasis.

Physicians managing patients on heparin and DOACs frequently encounter recurrent epistaxis, gastrointestinal bleeding ranging from occult to clinically significant, and urogenital bleeding. A degree of mild bleeding after surgery is often expected and usually resolves on its own. However, it’s crucial to evaluate in the context of ongoing anticoagulation to rule out early signs of clinically significant complications.

“There is definitely a lot of interest in the concept of ‘uncoupling’ thrombosis from hemostasis,” said Yazan Abou-Ismail, MD, hematologist and associate professor of medicine at the University of Utah Health in Salt Lake City, who was not involved in the research. “This concept highlights the differences in pathways essential for normal hemostasis at sites of vessel injury, in contrast with those needed for clot propagation and blood vessel lumen occlusion.”

Abou-Ismail noted that this approach has been explored with Factor XI (FXI) inhibitors currently in clinical trials. However, he raised an important mechanistic concern.

“This mechanism may not necessarily accomplish that goal of uncoupling thrombosis from hemostasis, although it might at narrow therapeutic windows,” Abou-Ismail said. “The tenase complex is a central component of coagulation whose deficiency underlies hemophilia A and B, diseases that cause significant bleeding in humans, and it is more essential to hemostasis than [FXI inhibitors]. Tenase inhibition seems like it may pose a higher bleeding risk in humans.”

He explained that FXI inhibitors have a strong mechanistic rationale because they target the feedback loop that amplifies clot propagation, which is less essential for hemostasis. “FXI inhibitors have clinical trial data demonstrating that FXI inhibition is in fact associated with less bleeding compared to current established anticoagulants,” he said. “However, CCG disrupts the FIXa/FVIIIa intrinsic tenase complex itself, which is considered essential for hemostasis.”

Surprises and Confirmations

The researchers were not anticipating such a clear separation between antithrombotic activity and bleeding risk. The preservation of normal wound healing was equally surprising, directly challenging the belief that interfering with clot formation inevitably disrupts tissue repair.

However, the path to these conclusions was not straightforward. “The structural definition of complex macromolecules like sulfated polysaccharides is a common challenge in the research field,” Lin said. “We spent a lot of time to analyze the structure of CCG.”

Even after identifying the candidate compound, the team had to rigorously confirm that its effects were truly anticoagulant in nature, rather than secondary to anti-inflammatory or vascular remodeling properties. Mechanistic studies were essential in demonstrating its targeted disruption of the intrinsic tenase complex, helping to explain how thrombosis could be reduced without broadly impairing coagulation.

Lin is excited but knows patience and skepticism are needed. “Our research is still at the basic stage, but based on the available data, we may provide a potential anticoagulant option with low bleeding risk,” she said. “In the discussion section of our paper, we also stated that ‘the data suggest a wide therapeutic window of CCG, which may offer therapeutic advantages for patients with bleeding contraindication, such as elderly patients and those with renal failure, as well as for safer long-term anticoagulation.’”

A New Direction for Heparin Alternatives?

Despite these concerns, Abou-Ismail acknowledged that the research has genuinely noteworthy aspects. “A future anticoagulant with a novel mechanism of action may be useful in patients who have experienced anticoagulant failure or breakthrough thrombosis from currently established anticoagulants,” he said. “Having another option might be useful when all other options have failed or are not feasible.”

However, he added a note of caution: “If a therapeutic window exists where partial tenase disruption has antithrombotic effect that does not impair hemostasis, then that would definitely be a promising future finding, but it is too early to arrive at that conclusion with this study.”

The search for safer heparin alternatives has been ongoing for decades, but most candidates still operate within the same fundamental paradigm of broad coagulation inhibition. This snail can’t move fast enough.

Abou-Ismail reported having no relevant conflicts. Disclosure information for study authors is available in the original study publication.

A version of this article first appeared on Medscape.com.

The fastest way to a new anticoagulation therapy that prevents blood clots without prolonging bleeding or healing time may be a land snail.

A recent preclinical study in ACS Central Science investigating bioactive molecules derived from the land snail Camaena cicatricosa identified a compound that significantly reduced clot formation without prolonging bleeding time and wound healing in rodent models, directly challenging the assumption that effective anticoagulant therapy must inherently disrupt physiologic repair processes.

“I was quite excited,” said Lisha Lin, PhD, lead author on the study and research assistant at the State Key Laboratory of Phytochemistry and Natural Medicines at the Kunming Institute of Botany, Chinese Academy of Sciences, in Kunming, China. “A novel polysaccharide was identified, and more importantly, it showed anticoagulant activity by inhibiting a novel target, with different action mechanism from heparins.”

What Led to the Land Snail?

The choice of C cicatricosa reflects a shift in thinking. The team screened a range of mollusk-derived biomolecules in search of safer anticoagulation strategies, ultimately isolating a novel galactosylated glycosaminoglycan (CCG) from this terrestrial species.

“We compared the anticoagulant activity of glycosaminoglycans from three snail species,” said Lin. They initially studied polysaccharides from C cicatricosa, Achatina fulica, and Helix lucorum — all sulfated glycosaminoglycans with similar structures. “However, we only found CCG from [C cicatricosa] showed anticoagulant activity but not other snail polysaccharides.”

This unexpected selectivity proved crucial. “The result indicated that the galactose branches and special sulfate substitution were important,” she explained, helping to explain why this particular species stood out among structurally similar compounds.

While CCG shares some similarities with heparin-like molecules, it notably lacks the specific pentasaccharide sequence required for antithrombin binding. Researchers hypothesized that this absence could reduce bleeding risk while maintaining antithrombotic activity.

Rather than broadly inhibiting coagulation, the compound selectively disrupts the intrinsic tenase complex, a pathway more closely associated with pathologic thrombosis than with physiologic hemostasis. This mechanism’s selectivity is central to the study’s findings and helps explain why normal wound healing remained intact in preclinical models.

The isolated compound demonstrated a rare combination in anticoagulant research: potent inhibition of pathologic thrombosis with no significant increase in bleeding time and intact wound healing across multiple experimental models. The compound did not act as a broad-spectrum anticoagulant, instead selectively targeting pathways more relevant to disease-associated clot formation.

The Hope of Lowering Bleeding Risk

For decades, anticoagulation therapy has been built on the assumption that inhibiting clot formation inevitably increases bleeding risk. For physicians treating patients with deep vein thrombosis or atrial fibrillation or those requiring postsurgical attention, the balancing act is constant. Prevent clot formation aggressively enough and the bleeding risk rises. Reduce intensity and thrombosis risk returns.

Current therapies, including heparin and direct oral anticoagulants (DOACs), function by broadly targeting the coagulation cascade. This lack of specialty is precisely what limits them. Even when carefully dosed, the treatments interfere with both pathologic clot formation and physiologic hemostasis.

Physicians managing patients on heparin and DOACs frequently encounter recurrent epistaxis, gastrointestinal bleeding ranging from occult to clinically significant, and urogenital bleeding. A degree of mild bleeding after surgery is often expected and usually resolves on its own. However, it’s crucial to evaluate in the context of ongoing anticoagulation to rule out early signs of clinically significant complications.

“There is definitely a lot of interest in the concept of ‘uncoupling’ thrombosis from hemostasis,” said Yazan Abou-Ismail, MD, hematologist and associate professor of medicine at the University of Utah Health in Salt Lake City, who was not involved in the research. “This concept highlights the differences in pathways essential for normal hemostasis at sites of vessel injury, in contrast with those needed for clot propagation and blood vessel lumen occlusion.”

Abou-Ismail noted that this approach has been explored with Factor XI (FXI) inhibitors currently in clinical trials. However, he raised an important mechanistic concern.

“This mechanism may not necessarily accomplish that goal of uncoupling thrombosis from hemostasis, although it might at narrow therapeutic windows,” Abou-Ismail said. “The tenase complex is a central component of coagulation whose deficiency underlies hemophilia A and B, diseases that cause significant bleeding in humans, and it is more essential to hemostasis than [FXI inhibitors]. Tenase inhibition seems like it may pose a higher bleeding risk in humans.”

He explained that FXI inhibitors have a strong mechanistic rationale because they target the feedback loop that amplifies clot propagation, which is less essential for hemostasis. “FXI inhibitors have clinical trial data demonstrating that FXI inhibition is in fact associated with less bleeding compared to current established anticoagulants,” he said. “However, CCG disrupts the FIXa/FVIIIa intrinsic tenase complex itself, which is considered essential for hemostasis.”

Surprises and Confirmations

The researchers were not anticipating such a clear separation between antithrombotic activity and bleeding risk. The preservation of normal wound healing was equally surprising, directly challenging the belief that interfering with clot formation inevitably disrupts tissue repair.

However, the path to these conclusions was not straightforward. “The structural definition of complex macromolecules like sulfated polysaccharides is a common challenge in the research field,” Lin said. “We spent a lot of time to analyze the structure of CCG.”

Even after identifying the candidate compound, the team had to rigorously confirm that its effects were truly anticoagulant in nature, rather than secondary to anti-inflammatory or vascular remodeling properties. Mechanistic studies were essential in demonstrating its targeted disruption of the intrinsic tenase complex, helping to explain how thrombosis could be reduced without broadly impairing coagulation.

Lin is excited but knows patience and skepticism are needed. “Our research is still at the basic stage, but based on the available data, we may provide a potential anticoagulant option with low bleeding risk,” she said. “In the discussion section of our paper, we also stated that ‘the data suggest a wide therapeutic window of CCG, which may offer therapeutic advantages for patients with bleeding contraindication, such as elderly patients and those with renal failure, as well as for safer long-term anticoagulation.’”

A New Direction for Heparin Alternatives?

Despite these concerns, Abou-Ismail acknowledged that the research has genuinely noteworthy aspects. “A future anticoagulant with a novel mechanism of action may be useful in patients who have experienced anticoagulant failure or breakthrough thrombosis from currently established anticoagulants,” he said. “Having another option might be useful when all other options have failed or are not feasible.”

However, he added a note of caution: “If a therapeutic window exists where partial tenase disruption has antithrombotic effect that does not impair hemostasis, then that would definitely be a promising future finding, but it is too early to arrive at that conclusion with this study.”

The search for safer heparin alternatives has been ongoing for decades, but most candidates still operate within the same fundamental paradigm of broad coagulation inhibition. This snail can’t move fast enough.

Abou-Ismail reported having no relevant conflicts. Disclosure information for study authors is available in the original study publication.

A version of this article first appeared on Medscape.com.

The fastest way to a new anticoagulation therapy that prevents blood clots without prolonging bleeding or healing time may be a land snail.

A recent preclinical study in ACS Central Science investigating bioactive molecules derived from the land snail Camaena cicatricosa identified a compound that significantly reduced clot formation without prolonging bleeding time and wound healing in rodent models, directly challenging the assumption that effective anticoagulant therapy must inherently disrupt physiologic repair processes.

“I was quite excited,” said Lisha Lin, PhD, lead author on the study and research assistant at the State Key Laboratory of Phytochemistry and Natural Medicines at the Kunming Institute of Botany, Chinese Academy of Sciences, in Kunming, China. “A novel polysaccharide was identified, and more importantly, it showed anticoagulant activity by inhibiting a novel target, with different action mechanism from heparins.”

What Led to the Land Snail?

The choice of C cicatricosa reflects a shift in thinking. The team screened a range of mollusk-derived biomolecules in search of safer anticoagulation strategies, ultimately isolating a novel galactosylated glycosaminoglycan (CCG) from this terrestrial species.

“We compared the anticoagulant activity of glycosaminoglycans from three snail species,” said Lin. They initially studied polysaccharides from C cicatricosa, Achatina fulica, and Helix lucorum — all sulfated glycosaminoglycans with similar structures. “However, we only found CCG from [C cicatricosa] showed anticoagulant activity but not other snail polysaccharides.”

This unexpected selectivity proved crucial. “The result indicated that the galactose branches and special sulfate substitution were important,” she explained, helping to explain why this particular species stood out among structurally similar compounds.

While CCG shares some similarities with heparin-like molecules, it notably lacks the specific pentasaccharide sequence required for antithrombin binding. Researchers hypothesized that this absence could reduce bleeding risk while maintaining antithrombotic activity.

Rather than broadly inhibiting coagulation, the compound selectively disrupts the intrinsic tenase complex, a pathway more closely associated with pathologic thrombosis than with physiologic hemostasis. This mechanism’s selectivity is central to the study’s findings and helps explain why normal wound healing remained intact in preclinical models.

The isolated compound demonstrated a rare combination in anticoagulant research: potent inhibition of pathologic thrombosis with no significant increase in bleeding time and intact wound healing across multiple experimental models. The compound did not act as a broad-spectrum anticoagulant, instead selectively targeting pathways more relevant to disease-associated clot formation.

The Hope of Lowering Bleeding Risk

For decades, anticoagulation therapy has been built on the assumption that inhibiting clot formation inevitably increases bleeding risk. For physicians treating patients with deep vein thrombosis or atrial fibrillation or those requiring postsurgical attention, the balancing act is constant. Prevent clot formation aggressively enough and the bleeding risk rises. Reduce intensity and thrombosis risk returns.

Current therapies, including heparin and direct oral anticoagulants (DOACs), function by broadly targeting the coagulation cascade. This lack of specialty is precisely what limits them. Even when carefully dosed, the treatments interfere with both pathologic clot formation and physiologic hemostasis.

Physicians managing patients on heparin and DOACs frequently encounter recurrent epistaxis, gastrointestinal bleeding ranging from occult to clinically significant, and urogenital bleeding. A degree of mild bleeding after surgery is often expected and usually resolves on its own. However, it’s crucial to evaluate in the context of ongoing anticoagulation to rule out early signs of clinically significant complications.

“There is definitely a lot of interest in the concept of ‘uncoupling’ thrombosis from hemostasis,” said Yazan Abou-Ismail, MD, hematologist and associate professor of medicine at the University of Utah Health in Salt Lake City, who was not involved in the research. “This concept highlights the differences in pathways essential for normal hemostasis at sites of vessel injury, in contrast with those needed for clot propagation and blood vessel lumen occlusion.”

Abou-Ismail noted that this approach has been explored with Factor XI (FXI) inhibitors currently in clinical trials. However, he raised an important mechanistic concern.

“This mechanism may not necessarily accomplish that goal of uncoupling thrombosis from hemostasis, although it might at narrow therapeutic windows,” Abou-Ismail said. “The tenase complex is a central component of coagulation whose deficiency underlies hemophilia A and B, diseases that cause significant bleeding in humans, and it is more essential to hemostasis than [FXI inhibitors]. Tenase inhibition seems like it may pose a higher bleeding risk in humans.”

He explained that FXI inhibitors have a strong mechanistic rationale because they target the feedback loop that amplifies clot propagation, which is less essential for hemostasis. “FXI inhibitors have clinical trial data demonstrating that FXI inhibition is in fact associated with less bleeding compared to current established anticoagulants,” he said. “However, CCG disrupts the FIXa/FVIIIa intrinsic tenase complex itself, which is considered essential for hemostasis.”

Surprises and Confirmations

The researchers were not anticipating such a clear separation between antithrombotic activity and bleeding risk. The preservation of normal wound healing was equally surprising, directly challenging the belief that interfering with clot formation inevitably disrupts tissue repair.

However, the path to these conclusions was not straightforward. “The structural definition of complex macromolecules like sulfated polysaccharides is a common challenge in the research field,” Lin said. “We spent a lot of time to analyze the structure of CCG.”

Even after identifying the candidate compound, the team had to rigorously confirm that its effects were truly anticoagulant in nature, rather than secondary to anti-inflammatory or vascular remodeling properties. Mechanistic studies were essential in demonstrating its targeted disruption of the intrinsic tenase complex, helping to explain how thrombosis could be reduced without broadly impairing coagulation.

Lin is excited but knows patience and skepticism are needed. “Our research is still at the basic stage, but based on the available data, we may provide a potential anticoagulant option with low bleeding risk,” she said. “In the discussion section of our paper, we also stated that ‘the data suggest a wide therapeutic window of CCG, which may offer therapeutic advantages for patients with bleeding contraindication, such as elderly patients and those with renal failure, as well as for safer long-term anticoagulation.’”

A New Direction for Heparin Alternatives?

Despite these concerns, Abou-Ismail acknowledged that the research has genuinely noteworthy aspects. “A future anticoagulant with a novel mechanism of action may be useful in patients who have experienced anticoagulant failure or breakthrough thrombosis from currently established anticoagulants,” he said. “Having another option might be useful when all other options have failed or are not feasible.”

However, he added a note of caution: “If a therapeutic window exists where partial tenase disruption has antithrombotic effect that does not impair hemostasis, then that would definitely be a promising future finding, but it is too early to arrive at that conclusion with this study.”

The search for safer heparin alternatives has been ongoing for decades, but most candidates still operate within the same fundamental paradigm of broad coagulation inhibition. This snail can’t move fast enough.

Abou-Ismail reported having no relevant conflicts. Disclosure information for study authors is available in the original study publication.

A version of this article first appeared on Medscape.com.

Approximately 20% of adults screened for early lung cancer met criteria undiagnosed chronic obstructive pulmonary disease (COPD), based on new data from approximately 300 individuals presented at the American Thoracic Society (ATS) 2026 International Conference.

“Patients undergoing lung cancer screening with low-dose CT scans represent a high-risk population for smoking-related lung disease, including COPD,” said lead author Stephen Dachert, MD, assistant professor of clinical thoracic medicine at the Lewis Katz School of Medicine at Temple University, Philadelphia.

“While lung cancer screening programs are well established, COPD remains frequently underrecognized despite many patients having respiratory symptoms, airflow obstruction, and structural lung abnormalities detectable during screening,” Dachert told Medscape Medical News. Currently, the US Preventive Services Task Force does not recommend routine COPD screening, he noted.

To evaluate how often COPD was being missed and whether patients were receiving appropriate therapy, a particular concern in underserved populations, Dachert and colleagues reviewed data from electronic medical record, and pre-bronchodilator spirometry data were collected for 305 adults enrolled in the Temple Healthy Chest Initiative. Symptom burden was assessed using questionnaires about prior inhaler use and the COPD Airway Assessment Test (CAAT). The median age of the participants was 63 years; 182 were women, and 187 were active smokers. Most of the participants (228) self-identified as Black/African American, 42 as non-Caucasian Hispanic, and 31 as White/Caucasian.

About half of the participants (52%) had no previous COPD diagnosis. Of these, 49 (31.2%) had evidence of airflow obstruction, and almost all (97%) had symptoms defined as CAAT scores of > 1 for mucus, cough, or breathlessness.

Overall, “Twenty-one percent met criteria for undiagnosed COPD based on airflow obstruction and positive CAAT symptoms, and many had moderate disease severity by GOLD COPD classification,” Dachert said.

The high prevalence of previously undiagnosed COPD, despite a substantial symptom burden, was a striking finding, Dachert told Medscape Medical News. “We were also struck by the degree of undertreatment, with more than 60% of these patients not receiving any inhaler therapy,” he added. Among the 48 undiagnosed COPD patients in the total cohort, approximately 10% had received short-acting beta 2-agonist-only therapy.

“While prior studies have suggested underdiagnosis in lung cancer screening populations, the magnitude seen in this predominantly minority cohort reinforces how common missed opportunities for diagnosis remain in clinical practice,” Dachert said.

The findings were limited by the use of data from a single region and may not be generalized to other areas. However, the results suggest that lung cancer screening (LCS) programs are an opportunity to identify and treat chronic smoking-related lung disease, Dachert said. “Incorporating spirometry, symptom assessment, and review of respiratory therapies into LCS programs may help identify patients with clinically significant but previously unrecognized COPD, and earlier diagnosis could allow for smoking cessation reinforcement, initiation of evidence-based inhaler therapy, symptom improvement, and potentially reduction in exacerbations and health care utilization,” he said.

“Future studies should evaluate whether systematic COPD screening embedded within lung cancer screening programs improves clinical outcomes such as quality of life, exacerbations, hospitalizations, and healthcare utilization,” Dachert said. Additional work is needed to determine the best combination of screening tools to efficiently identify high-risk patients, which may include spirometry, quantitative CT imaging, symptom questionnaires, and biomarkers, he noted. “Longitudinal studies may help clarify whether earlier identification during lung cancer screening changes disease trajectory over time,” Dachert added.

Value Added for Underserved Populations

The new study’s results suggest that incorporating routine symptom assessment and spirometry into LCS pathways may improve earlier diagnosis and optimization of COPD management, said Jesse R. Sherratt, DO, a pulmonologist and critical care specialist at the University of Texas Health Science Center at San Antonio.

“Individuals undergoing lung cancer screening are at particularly high risk for smoking-related lung disease, yet COPD frequently remains unrecognized and untreated in this population,” said Sherratt, who was not involved in the study. The current study highlights the potential value, particularly among underserved populations, of incorporating spirometry and symptom assessment into LCS programs for earlier identification of patients with clinically significant COPD, he said.

The high rates of undiagnosed COPD and undertreatment were not unexpected, given the substantial smoking exposure and high-risk characteristics of patients undergoing LCS, said Sherratt. “However, the degree of symptom burden and the disproportionate impact on minority populations were especially notable and emphasize ongoing disparities in respiratory healthcare access and diagnosis,” he said.

“Additional studies are needed to determine whether integrating spirometry and structured COPD screening into lung cancer screening programs improves long-term clinical outcomes, healthcare utilization, and quality of life,” Sherratt noted. Further research also should evaluate strategies to reduce disparities in COPD diagnosis and treatment among minority populations, he said.

The study was supported by grants from AstraZeneca and the Temple Lung Center. AstraZeneca collaborators participated in the study as coauthors. Sherratt had no financial conflicts to disclose.

A version of this article first appeared on Medscape.com.

Approximately 20% of adults screened for early lung cancer met criteria undiagnosed chronic obstructive pulmonary disease (COPD), based on new data from approximately 300 individuals presented at the American Thoracic Society (ATS) 2026 International Conference.

“Patients undergoing lung cancer screening with low-dose CT scans represent a high-risk population for smoking-related lung disease, including COPD,” said lead author Stephen Dachert, MD, assistant professor of clinical thoracic medicine at the Lewis Katz School of Medicine at Temple University, Philadelphia.

“While lung cancer screening programs are well established, COPD remains frequently underrecognized despite many patients having respiratory symptoms, airflow obstruction, and structural lung abnormalities detectable during screening,” Dachert told Medscape Medical News. Currently, the US Preventive Services Task Force does not recommend routine COPD screening, he noted.

To evaluate how often COPD was being missed and whether patients were receiving appropriate therapy, a particular concern in underserved populations, Dachert and colleagues reviewed data from electronic medical record, and pre-bronchodilator spirometry data were collected for 305 adults enrolled in the Temple Healthy Chest Initiative. Symptom burden was assessed using questionnaires about prior inhaler use and the COPD Airway Assessment Test (CAAT). The median age of the participants was 63 years; 182 were women, and 187 were active smokers. Most of the participants (228) self-identified as Black/African American, 42 as non-Caucasian Hispanic, and 31 as White/Caucasian.

About half of the participants (52%) had no previous COPD diagnosis. Of these, 49 (31.2%) had evidence of airflow obstruction, and almost all (97%) had symptoms defined as CAAT scores of > 1 for mucus, cough, or breathlessness.

Overall, “Twenty-one percent met criteria for undiagnosed COPD based on airflow obstruction and positive CAAT symptoms, and many had moderate disease severity by GOLD COPD classification,” Dachert said.

The high prevalence of previously undiagnosed COPD, despite a substantial symptom burden, was a striking finding, Dachert told Medscape Medical News. “We were also struck by the degree of undertreatment, with more than 60% of these patients not receiving any inhaler therapy,” he added. Among the 48 undiagnosed COPD patients in the total cohort, approximately 10% had received short-acting beta 2-agonist-only therapy.

“While prior studies have suggested underdiagnosis in lung cancer screening populations, the magnitude seen in this predominantly minority cohort reinforces how common missed opportunities for diagnosis remain in clinical practice,” Dachert said.

The findings were limited by the use of data from a single region and may not be generalized to other areas. However, the results suggest that lung cancer screening (LCS) programs are an opportunity to identify and treat chronic smoking-related lung disease, Dachert said. “Incorporating spirometry, symptom assessment, and review of respiratory therapies into LCS programs may help identify patients with clinically significant but previously unrecognized COPD, and earlier diagnosis could allow for smoking cessation reinforcement, initiation of evidence-based inhaler therapy, symptom improvement, and potentially reduction in exacerbations and health care utilization,” he said.

“Future studies should evaluate whether systematic COPD screening embedded within lung cancer screening programs improves clinical outcomes such as quality of life, exacerbations, hospitalizations, and healthcare utilization,” Dachert said. Additional work is needed to determine the best combination of screening tools to efficiently identify high-risk patients, which may include spirometry, quantitative CT imaging, symptom questionnaires, and biomarkers, he noted. “Longitudinal studies may help clarify whether earlier identification during lung cancer screening changes disease trajectory over time,” Dachert added.

Value Added for Underserved Populations

The new study’s results suggest that incorporating routine symptom assessment and spirometry into LCS pathways may improve earlier diagnosis and optimization of COPD management, said Jesse R. Sherratt, DO, a pulmonologist and critical care specialist at the University of Texas Health Science Center at San Antonio.

“Individuals undergoing lung cancer screening are at particularly high risk for smoking-related lung disease, yet COPD frequently remains unrecognized and untreated in this population,” said Sherratt, who was not involved in the study. The current study highlights the potential value, particularly among underserved populations, of incorporating spirometry and symptom assessment into LCS programs for earlier identification of patients with clinically significant COPD, he said.

The high rates of undiagnosed COPD and undertreatment were not unexpected, given the substantial smoking exposure and high-risk characteristics of patients undergoing LCS, said Sherratt. “However, the degree of symptom burden and the disproportionate impact on minority populations were especially notable and emphasize ongoing disparities in respiratory healthcare access and diagnosis,” he said.

“Additional studies are needed to determine whether integrating spirometry and structured COPD screening into lung cancer screening programs improves long-term clinical outcomes, healthcare utilization, and quality of life,” Sherratt noted. Further research also should evaluate strategies to reduce disparities in COPD diagnosis and treatment among minority populations, he said.

The study was supported by grants from AstraZeneca and the Temple Lung Center. AstraZeneca collaborators participated in the study as coauthors. Sherratt had no financial conflicts to disclose.

A version of this article first appeared on Medscape.com.

Approximately 20% of adults screened for early lung cancer met criteria undiagnosed chronic obstructive pulmonary disease (COPD), based on new data from approximately 300 individuals presented at the American Thoracic Society (ATS) 2026 International Conference.

“Patients undergoing lung cancer screening with low-dose CT scans represent a high-risk population for smoking-related lung disease, including COPD,” said lead author Stephen Dachert, MD, assistant professor of clinical thoracic medicine at the Lewis Katz School of Medicine at Temple University, Philadelphia.

“While lung cancer screening programs are well established, COPD remains frequently underrecognized despite many patients having respiratory symptoms, airflow obstruction, and structural lung abnormalities detectable during screening,” Dachert told Medscape Medical News. Currently, the US Preventive Services Task Force does not recommend routine COPD screening, he noted.

To evaluate how often COPD was being missed and whether patients were receiving appropriate therapy, a particular concern in underserved populations, Dachert and colleagues reviewed data from electronic medical record, and pre-bronchodilator spirometry data were collected for 305 adults enrolled in the Temple Healthy Chest Initiative. Symptom burden was assessed using questionnaires about prior inhaler use and the COPD Airway Assessment Test (CAAT). The median age of the participants was 63 years; 182 were women, and 187 were active smokers. Most of the participants (228) self-identified as Black/African American, 42 as non-Caucasian Hispanic, and 31 as White/Caucasian.

About half of the participants (52%) had no previous COPD diagnosis. Of these, 49 (31.2%) had evidence of airflow obstruction, and almost all (97%) had symptoms defined as CAAT scores of > 1 for mucus, cough, or breathlessness.

Overall, “Twenty-one percent met criteria for undiagnosed COPD based on airflow obstruction and positive CAAT symptoms, and many had moderate disease severity by GOLD COPD classification,” Dachert said.

The high prevalence of previously undiagnosed COPD, despite a substantial symptom burden, was a striking finding, Dachert told Medscape Medical News. “We were also struck by the degree of undertreatment, with more than 60% of these patients not receiving any inhaler therapy,” he added. Among the 48 undiagnosed COPD patients in the total cohort, approximately 10% had received short-acting beta 2-agonist-only therapy.

“While prior studies have suggested underdiagnosis in lung cancer screening populations, the magnitude seen in this predominantly minority cohort reinforces how common missed opportunities for diagnosis remain in clinical practice,” Dachert said.

The findings were limited by the use of data from a single region and may not be generalized to other areas. However, the results suggest that lung cancer screening (LCS) programs are an opportunity to identify and treat chronic smoking-related lung disease, Dachert said. “Incorporating spirometry, symptom assessment, and review of respiratory therapies into LCS programs may help identify patients with clinically significant but previously unrecognized COPD, and earlier diagnosis could allow for smoking cessation reinforcement, initiation of evidence-based inhaler therapy, symptom improvement, and potentially reduction in exacerbations and health care utilization,” he said.

“Future studies should evaluate whether systematic COPD screening embedded within lung cancer screening programs improves clinical outcomes such as quality of life, exacerbations, hospitalizations, and healthcare utilization,” Dachert said. Additional work is needed to determine the best combination of screening tools to efficiently identify high-risk patients, which may include spirometry, quantitative CT imaging, symptom questionnaires, and biomarkers, he noted. “Longitudinal studies may help clarify whether earlier identification during lung cancer screening changes disease trajectory over time,” Dachert added.

Value Added for Underserved Populations

The new study’s results suggest that incorporating routine symptom assessment and spirometry into LCS pathways may improve earlier diagnosis and optimization of COPD management, said Jesse R. Sherratt, DO, a pulmonologist and critical care specialist at the University of Texas Health Science Center at San Antonio.

“Individuals undergoing lung cancer screening are at particularly high risk for smoking-related lung disease, yet COPD frequently remains unrecognized and untreated in this population,” said Sherratt, who was not involved in the study. The current study highlights the potential value, particularly among underserved populations, of incorporating spirometry and symptom assessment into LCS programs for earlier identification of patients with clinically significant COPD, he said.

The high rates of undiagnosed COPD and undertreatment were not unexpected, given the substantial smoking exposure and high-risk characteristics of patients undergoing LCS, said Sherratt. “However, the degree of symptom burden and the disproportionate impact on minority populations were especially notable and emphasize ongoing disparities in respiratory healthcare access and diagnosis,” he said.

“Additional studies are needed to determine whether integrating spirometry and structured COPD screening into lung cancer screening programs improves long-term clinical outcomes, healthcare utilization, and quality of life,” Sherratt noted. Further research also should evaluate strategies to reduce disparities in COPD diagnosis and treatment among minority populations, he said.

The study was supported by grants from AstraZeneca and the Temple Lung Center. AstraZeneca collaborators participated in the study as coauthors. Sherratt had no financial conflicts to disclose.

A version of this article first appeared on Medscape.com.

Military sexual trauma (MST) remained “persistently prevalent” between 2013 and 2026, experiencing a slight overall increase from 7.6% to 8.2% in the time period, according to a research letter written by researchers from Yale University and the Veterans Affairs (VA) Connecticut Healthcare System and published in JAMA Psychiatry. Prevalence among female veterans jumped from 32.4% to 43.3%, with many citing MST as a factor in their decision to leave military service earlier than planned.

The researchers analyzed data from 3 independent nationally representative cohorts of veterans surveyed as part of the National Health and Resilience in Veterans Study. In 2025 and 2026, 189 veterans reported sexual harassment and 80 veterans reported sexual assault. Among female veterans, 128 (42.7%) reported harassment and 55 (21.2%) reported assault; 61 male veterans (3.6%) reported harassment and 25 (1.4%) reported assault. 

Many veterans experienced multiple MSTs. In 2025 and 2026, 61 women and 23 men reported 2 or 3 occurrences of MST, and 57 (42 women, 15 men) reported ≥ 4 occurrences. Most indicated ≥ 1 MST occurrence was perpetrated by a higher-ranking military member. Women were more likely to report ≥ 2 MST occurrences and MST perpetrated by a higher-ranking military member, according to the letter.

MST can have potentially disproportionate consequences for women in terms of military workforce composition, leadership representation, and long-term force readiness, the researchers say. Findings based on 2024 national veteran population data suggest that roughly 1 in 6 women and 1 in 100 men will leave military service after MST. 

History of MST has been independently associated with elevated risk for suicidal thoughts and behaviors, including future suicidal intent. In this study, compared with veterans without MST, those with MST had nearly triple the rates of past-year suicidal ideation and > 4 times the rates of lifetime suicide attempt. They were also significantly more likely to indicate future suicidal intent (6.9% vs 1.2%). Predicted probabilities of suicidal ideation (34.2% vs 28.3%) and suicide attempt (18.5% vs 13.4%) were significantly higher among females than males.

Female service members who experienced MST are also nearly 3 times more likely to have moderate to severe posttraumatic stress disorder (PTSD) symptoms, compared with female service members who did not experience MST. Women veterans who report MST and have PTSD are also more likely to have comorbid mental health diagnoses, including major depression, anxiety, eating disorders, and substance use disorders. 

The researchers claim the research is the first nationally representative characterization of MST contextual features and updated estimates of treatment utilization. They found that fewer than half of survivors received MST-related treatment.

In 2021, President Biden directed the US Department of Defense to establish the Independent Review Commission on Sexual Assault in the Military (IRC). An overview of the IRC commission findings underscored the need for screening. The increased risk of suicidal thoughts and behaviors, it says, makes “integration of crosscutting prevention initiatives within MST care and suicide prevention at VA” critical. 

The Veterans Health Administration universal MST screening program is part of a web of MST-related services. Analysis of medical record data demonstrates that the program yields clinically meaningful information, and increases the likelihood of mental health treatment. Despite the barriers to care for all MST survivors noted in qualitative studies, the commission report says, quantitative research agrees that veterans with a positive MST screen are more likely to engage in health care in VA.

Military sexual trauma (MST) remained “persistently prevalent” between 2013 and 2026, experiencing a slight overall increase from 7.6% to 8.2% in the time period, according to a research letter written by researchers from Yale University and the Veterans Affairs (VA) Connecticut Healthcare System and published in JAMA Psychiatry. Prevalence among female veterans jumped from 32.4% to 43.3%, with many citing MST as a factor in their decision to leave military service earlier than planned.

The researchers analyzed data from 3 independent nationally representative cohorts of veterans surveyed as part of the National Health and Resilience in Veterans Study. In 2025 and 2026, 189 veterans reported sexual harassment and 80 veterans reported sexual assault. Among female veterans, 128 (42.7%) reported harassment and 55 (21.2%) reported assault; 61 male veterans (3.6%) reported harassment and 25 (1.4%) reported assault. 

Many veterans experienced multiple MSTs. In 2025 and 2026, 61 women and 23 men reported 2 or 3 occurrences of MST, and 57 (42 women, 15 men) reported ≥ 4 occurrences. Most indicated ≥ 1 MST occurrence was perpetrated by a higher-ranking military member. Women were more likely to report ≥ 2 MST occurrences and MST perpetrated by a higher-ranking military member, according to the letter.

MST can have potentially disproportionate consequences for women in terms of military workforce composition, leadership representation, and long-term force readiness, the researchers say. Findings based on 2024 national veteran population data suggest that roughly 1 in 6 women and 1 in 100 men will leave military service after MST. 

History of MST has been independently associated with elevated risk for suicidal thoughts and behaviors, including future suicidal intent. In this study, compared with veterans without MST, those with MST had nearly triple the rates of past-year suicidal ideation and > 4 times the rates of lifetime suicide attempt. They were also significantly more likely to indicate future suicidal intent (6.9% vs 1.2%). Predicted probabilities of suicidal ideation (34.2% vs 28.3%) and suicide attempt (18.5% vs 13.4%) were significantly higher among females than males.

Female service members who experienced MST are also nearly 3 times more likely to have moderate to severe posttraumatic stress disorder (PTSD) symptoms, compared with female service members who did not experience MST. Women veterans who report MST and have PTSD are also more likely to have comorbid mental health diagnoses, including major depression, anxiety, eating disorders, and substance use disorders. 

The researchers claim the research is the first nationally representative characterization of MST contextual features and updated estimates of treatment utilization. They found that fewer than half of survivors received MST-related treatment.

In 2021, President Biden directed the US Department of Defense to establish the Independent Review Commission on Sexual Assault in the Military (IRC). An overview of the IRC commission findings underscored the need for screening. The increased risk of suicidal thoughts and behaviors, it says, makes “integration of crosscutting prevention initiatives within MST care and suicide prevention at VA” critical. 

The Veterans Health Administration universal MST screening program is part of a web of MST-related services. Analysis of medical record data demonstrates that the program yields clinically meaningful information, and increases the likelihood of mental health treatment. Despite the barriers to care for all MST survivors noted in qualitative studies, the commission report says, quantitative research agrees that veterans with a positive MST screen are more likely to engage in health care in VA.

Military sexual trauma (MST) remained “persistently prevalent” between 2013 and 2026, experiencing a slight overall increase from 7.6% to 8.2% in the time period, according to a research letter written by researchers from Yale University and the Veterans Affairs (VA) Connecticut Healthcare System and published in JAMA Psychiatry. Prevalence among female veterans jumped from 32.4% to 43.3%, with many citing MST as a factor in their decision to leave military service earlier than planned.

The researchers analyzed data from 3 independent nationally representative cohorts of veterans surveyed as part of the National Health and Resilience in Veterans Study. In 2025 and 2026, 189 veterans reported sexual harassment and 80 veterans reported sexual assault. Among female veterans, 128 (42.7%) reported harassment and 55 (21.2%) reported assault; 61 male veterans (3.6%) reported harassment and 25 (1.4%) reported assault. 

Many veterans experienced multiple MSTs. In 2025 and 2026, 61 women and 23 men reported 2 or 3 occurrences of MST, and 57 (42 women, 15 men) reported ≥ 4 occurrences. Most indicated ≥ 1 MST occurrence was perpetrated by a higher-ranking military member. Women were more likely to report ≥ 2 MST occurrences and MST perpetrated by a higher-ranking military member, according to the letter.

MST can have potentially disproportionate consequences for women in terms of military workforce composition, leadership representation, and long-term force readiness, the researchers say. Findings based on 2024 national veteran population data suggest that roughly 1 in 6 women and 1 in 100 men will leave military service after MST. 

History of MST has been independently associated with elevated risk for suicidal thoughts and behaviors, including future suicidal intent. In this study, compared with veterans without MST, those with MST had nearly triple the rates of past-year suicidal ideation and > 4 times the rates of lifetime suicide attempt. They were also significantly more likely to indicate future suicidal intent (6.9% vs 1.2%). Predicted probabilities of suicidal ideation (34.2% vs 28.3%) and suicide attempt (18.5% vs 13.4%) were significantly higher among females than males.

Female service members who experienced MST are also nearly 3 times more likely to have moderate to severe posttraumatic stress disorder (PTSD) symptoms, compared with female service members who did not experience MST. Women veterans who report MST and have PTSD are also more likely to have comorbid mental health diagnoses, including major depression, anxiety, eating disorders, and substance use disorders. 

The researchers claim the research is the first nationally representative characterization of MST contextual features and updated estimates of treatment utilization. They found that fewer than half of survivors received MST-related treatment.

In 2021, President Biden directed the US Department of Defense to establish the Independent Review Commission on Sexual Assault in the Military (IRC). An overview of the IRC commission findings underscored the need for screening. The increased risk of suicidal thoughts and behaviors, it says, makes “integration of crosscutting prevention initiatives within MST care and suicide prevention at VA” critical. 

The Veterans Health Administration universal MST screening program is part of a web of MST-related services. Analysis of medical record data demonstrates that the program yields clinically meaningful information, and increases the likelihood of mental health treatment. Despite the barriers to care for all MST survivors noted in qualitative studies, the commission report says, quantitative research agrees that veterans with a positive MST screen are more likely to engage in health care in VA.