A Compound Made From Shrimp Shells Can Rid The Body Of Microplastics
For those unaware of the extent of the problem, microplastics (MPs) are said to be in essentially every person in every part of the world. Ice samples from the poles and tissue samples from the penis show the extent of penetration. Given that these pieces of plastic have been found in placenta samples and reproductive organs, we can say that children are being subjected to plastic exposure from birth.
To what degree these nano and microplastics will hurt humans is still debated and research is ongoing, and the FDA states that they'll take regulatory action when adverse effects are known. However, the reason that people prefer to avoid becoming plasticized is the conventional wisdom that having small pieces of plastic within our immune cells, nerve cells, and altering which genes are expressed is something we'd want to avoid. There's certainly no known benefit.
Microplastics have ben detected basically everywhere, including the brain and penis.
Recent studies discuss the 'ubiquitous' extent of microplastics and their varied effects. Kidney death, liver inflammation, oxidative stress, cellular toxicity, alterations in gene expression and changes to the DNA itself are some of the observed effects of microplastic exposure.
I will hypothesize that there's potentially a link between nanoplastics and mental wellbeing. Not just from the obvious observation that plastics in the brain are bad, although this is true; I instead refer to the interference that our gastrointestinal microbiota are suffering with their extracellular vesicles because of microplastics. Understanding the brain-gut-microbe axis and the effect that our intestinal flora there have an impact on our neurological function, one may observe that altering this intestinal environment with nanoplastics can have an effect on mental wellbeing. If you do start depressed, try milk aromatherapy. It shows promise in rats depressed because of gut-brain issues.
The Dentist
For those of us who don't enjoy visits to the dentist, we have reasons to be validated. Different materials are used in different dental practices, but a lot of them are plastic or packaged in plastic. By the nature of installing implants that will be subjected to the wear and tear of using one's mouth in daily life, microplastics are created and ingested. Other procedures like polishing restorations, ceramic crowns, using elastics, orthodontic appliances, and so on can generate particles. Think about the plastic fibers on the plastic toothbrush you grind against your teeth twice a day. Should we go back to chewing spruce sap?
Remedies
Chitin is a compound found in mushrooms and the exoskeletons of crustaceans and insects. Chitosan is easily made from chitin. It's used as a dietary supplement and sold to help consumers feel full, block fat absorption and lower cholesterol. Good for wound care as well. We ought to produce more of it and make it mainstream because we have another important reason to like it. A new study has shown that it can benefit our well-being in a novel and needed way: ridding our bodies of microplastics. The study was short but revealing, and I hope it will be reproduced with longer durations and human subjects.
The researchers share two important conclusions. For even short periods of ingestion, microplastics accrue in the digestive tract, primarily the cecum which is the pouch between the small intestine and colon. Assuming that chemicals can leach from these plastics and that the particles themselves will eventually absorb into the wider body, it's clearly advantageous to expel this poison before it accrues/accumulates. The group of rats that was fed a diet supplemented with chitosan expelled more MPs that any of the other groups. Intriguingly and encouragingly for me, over a few days the rats released more MPs than they took in. This suggests that chitosan won't just block absorption of current MPs, but in fact facilitate the cleansing of the colon of recently ingested microplastics. Further, after the rats were euthanized and dissected, the chitosan group had the lightest colons which suggests that they had the least total waste accumulated. As side effects for adding chitosan to one's diet are minimal beyond some stomach upset, UNLESS YOU ARE ALLERGIC TO SHELLFISH OR MUSHROOMS, it seems like a reasonable addition. This is not medical advice and as I said, I look forward to studies done with humans for longer periods to provide us with more information. With said I'm intrigued.
Singapore. Green buildings trap microplastics, clean the air and water, and cool the city.
Prevention
A better way to go than solving a problem is to prevent it. Microplastics come from plastics, and despite some laws and public initiatives, the industry is vital and won't fade away naturally. Proactive investment in alternatives will bring about a whole society shift; personal choice is not an option here. Plastic is ubiquitous and a consumer doesn't have a real option to move away from it. Our tap water and the air we breathe are contaminated, so we must do more than avoid microwaving food in plastic containers, or stop buying items packaged in plastic. If anyone has been to any store ever, they would know that this is impossible. Everything is wrapped in plastic. To exist in the modern world is to be a creator of waste; even the well-intentioned can do little more than be frustrated.
Green roofs are 97.5% effective in removing microplastics. They're generally good for retaining storm water, cleaning the air and runoff, which lessens the work of wastewater treatment plants. Green roofs can contribute to an urban cooling effect, countering the Urban Head Island (UHI) problem. Singapore has been a prime example of this for years. Now, we find another reason to widely adopt the practice in every city, immediately.
Singapore exemplifies greening a city to everyone's benefit.
Great Pacific Garbage Patch
Removing what's already been released is a net benefit. When considering the scale of the undertaking to clean the North Pacific Garbage Patch and the greenhouse gasses that will be released or the marine life that will be interfered with, it isn't immediately clear what the best approach might be. Leaving it and hoping a reef grows on top of it could make sense, given the rubber tire reef projects we've all heard about. A comparative analysis of the Ocean Cleanup shows that while there will be some impact from action, the effect of doing nothing is significantly worse. Proactive action where possible to remove what's been released before it continues to break down into microplastics and nano plastics is a viable strategy for long term environmental health. In the scenario presented, plastic pollution levels drop to below what's considered a safe limit. Inaction has the higher cost.
Leaving plastics in the oceans will be more damaging than removal.
Complex problems can't be solved with simple solutions. Plastics can't be completely replaced, but we can adapt the ways we use them and consider novel strategies to mitigate their harm. When these strategies prove themselves to be effective, they ought to be systematically applied.
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Geek Wire
an hour ago
- Geek Wire
University of Washington celebrates Rubin Observatory's debut — and looks ahead
University of Washington astronomer Zeljko Ivezic talks about the Rubin Observatory — a project in which he played a leading role — with an image of the facility displayed behind him. (GeekWire Photo / Alan Boyle) It's been more than two decades since the University of Washington helped kick off the effort to get the Vera C. Rubin Observatory built in Chile — and now that it's finished, UW astronomers are gearing up to get in on the first decade of discoveries. The university's role in the past, present and future of the Rubin Observatory and its 10-year Legacy Survey of Space and Time, or LSST, literally took center stage in front of a packed house at UW's Kane Hall on Thursday night. UW astronomer Zeljko Ivezic, who served as director of Rubin construction and is shifting his focus to his role as head of science operations for LSST, recalled the night of April 15, when Rubin's first test images came in for fine tuning. 'We were all so happy, and we are still happy,' he said. 'We had been dreaming about this night for two decades, and it finally arrived. And not only that, we quickly obtained beautiful data, but also we continued to do so, and every new image was better and better. The observatory is performing beyond all our expectations.' Ivezic showed off the images of swirling galaxies and colorful nebulas that he first unveiled earlier in the week at a ceremony in Washington, D.C. And he talked up an online tool called Skyviewer that allows users to click around the observatory's 3,200-megapixel images and zoom in on details. 'It's an easy-to-use app,' he told the audience. 'When you go home tonight, then you can spend the next few hours just going around. Turn off the light in your room and then look at your screen, and it will be fantastic.' University of Washington Zeljko Ivezic shows off his Rubin Observatory necktie and matching nail polish. The tie is on sale via the Startorialist website. (GeekWire Photo / Alan Boyle) The University of Washington's involvement in the Rubin Observatory goes back to the early 2000s, when astronomers began considering how a next-generation sky survey might be accomplished. In its early years, the project was known as the Large Synoptic Survey Telescope (which set the precedent for the LSST acronym). UW was one of four founding partners of the LSST Corporation, an entity that was set up to get the project started. (That nonprofit group, which was subsequently renamed the LSST Discovery Alliance, now has 40 member institutions.) In 2008, the project got a huge boost from Microsoft billionaires Bill Gates and Charles Simonyi — who donated $10 million and $20 million, respectively, to support early work on the telescope's 8.4-meter-wide (28-foot-wide) mirror. As the years went on, support for the project grew, fueled by a high rating in the National Research Council's 2010 Decadal Survey. Eventually, the National Science Foundation and the U.S. Department of Energy's Office of Science allocated hundreds of millions of dollars for building the observatory in Chile, where dry air and dark skies made for optimal viewing conditions. In 2019, the observatory was officially named in honor of astronomer Vera Rubin, who analyzed galactic rotation rates to nail down the first convincing evidence for the existence of dark matter. The survey telescope, meanwhile, was named after Simonyi's family in recognition of his early gift. Today, UW's Rubin Observatory team consists of about 75 faculty members and graduate students, plus scores of undergraduates. University of Washington astronomer Mario Juric, the team's principal investigator, noted that UW played an essential role in getting the observatory up and running. 'None of this would be possible without the Rubin team right here at UW,' he told Thursday night's audience. Members of the University of Washington's team for the Rubin Observatory's Legacy Survey of Space and Time pose for a group picture after a presentation at UW's Kane Hall. (GeekWire Photo / Alan Boyle) That essential role will continue into the next decade. In partnership with Princeton University, UW's team is responsible for the software that processes the trillions of bytes of image data that are generated by the observatory on a nightly basis. That work meshes with the leading roles in Rubin operations that are performed by the National Science Foundation's NOIRLab and the Department of Energy's SLAC National Accelerator Laboratory. 'We're here to figure out how to build algorithms to get the most out of data, how to make the software work as well as it can,' Juric told GeekWire. Andrew Connolly, another UW astronomer who is the director of the university's eScience Institute, said the university's researchers are relying on machine learning and other artificial intelligence strategies 'to accelerate our discoveries.' 'We build AI that allows us to study the variability in time series data. We build new tools at U Dub to search for the signatures of a distant planet in the outskirts of our solar system,' he said. 'We even use AI to improve the image quality and the sharpness of the images that you see.' Astronomers expect the data from Rubin to reveal millions of previously undetected asteroids in our own solar system, shed light on the mysteries of dark matter and dark energy, track phenomena including gamma-ray bursts and supernovas, and capture images of billions of galaxies repeatedly over the coming decade. James Davenport — who is the newly named director of the university's DiRAC Institute, taking a handoff from Juric — said it's going to be an exciting 10 years. 'We are going to discover things we don't expect,' he said.
Medscape
2 hours ago
- Medscape
Jun 27 2025 This Week in Cardiology
Please note that the text below is not a full transcript and has not been copyedited. For more insight and commentary on these stories, subscribe to the This Week in Cardiology podcast , download the Medscape app or subscribe on Apple Podcasts, Spotify, or your preferred podcast provider. This podcast is intended for healthcare professionals only. In This Week's Podcast For the week ending June 27, 2025, John Mandrola, MD, comments on the following topics: FDA approves triple-drug polypill, a change of opinion, a deep dive into invasive pulmonary embolism therapies, heart disease trends, and diabetes care is on fire. I learned this week that fellow medical conservative, Andrew Flapan, MD, of Edinburgh, died suddenly. Andrew invited me twice to speak at the Royal College meeting. I enjoyed my time with him immensely. He was a force of nature, and a 'doctor's doctor.' To my colleagues in Edinburgh, I offer my condolences. FDA News in Hypertension The FDA this week approved the three-component polypill for hypertension. It's going to be called Widaplik, which is a silly name. It includes the angiotensin receptor blocker (ARB) telmisartan, the calcium-channel blocker amlodipine and the diuretic indapamide. There will be a polypill with standard doses of the three drugs, but also one with two lower doses. My feelings have changed about the polypill. I used to be dead set against it. I thought it was dumb, and it would be far better to just titrate does of selected drugs. But now I am more open to the whole simplicity thing. As I age, I grow more interested in minimally disruptive care — a concept began by Mayo Clinic endocrinologist Victor Montori, MD. The idea is that life is for living, not for being a patient. Getting prescriptions filled is a huge pain in the butt these days. So the idea of taking one pill that has a better chance of controlling blood pressure (BP) is absolutely minimally disruptive compared to titrating two or three pills, each requiring a prescription. The evidence for polypill efficacy is quite decent. The Lancet published an RCT comparing the triple polypill to three different two-drug combinations. And it fared well — the triple-drug polypill lowered the systolic blood pressure statistically more than any of the other combinations. It was a small efficacy trial but there were no significant differences in hypotension, though more patients in the triple therapy arm had out-of-range sodium or potassium values, but 'very few clinically significant electrolyte abnormalities occurred in any groups.' Also in 2024, JACC published an RCT of about 300 patients with mild to moderate hypertension. This trial randomized patients in a 2:2:1 ratio to polypill quarter-dose (telmisartan 10 mg/amlodipine 1.25 mg/indapamide 0.625 mg), polypill half-dose (telmisartan 20 mg/amlodipine 2.5 mg/indapamide 1.25 mg), or placebo. The BP reductions delta vs placebo was about 7-8 mm Hg. At Week 4, clinic BP control (<140/90 mm Hg) was 37% for placebo, 65% for quarter-dose and 70% for half-dose. Both doses had highly significant P-values. Adverse effects were similar. In 2023, JAMA Cardiology published a meta-analysis of seven trials with 1900 patients looking at 3- and 4-component polypills vs monotherapy or placebo. Again, the polypills were more effective BP-lowering drugs and there were very little adverse effect differences. A word of caution: These trials enrolled 59-year-old patients. They had run-in periods. And in trials, patients are motivated, clinicians are motivated, there are research nurses. IOW the trial environment is seriously protective. The practice of evidence-based medicine (EBM) requires us, the practitioners, to be mindful of the external validity of trials. Giving three drugs in a single pill is not for frail, elderly patients with serious comorbidity. Patients on these drugs should get follow-up. But, again, I stress, the sole point of preventive therapies, like treating hypertension in middle-aged people is so they become old-aged. When patients successfully make it to old age, there is reason for caution. Benefits are less and side effects come more frequently. The thing about the polypill is that it offers a single best chance of getting control of BP. Simple is better not only because it is less work for the patient, but in my experience, early success is more likely to lead to adherence and confidence in the clinician. I don't know how much this drug will cost. The three components are not at all costly but putting them together could be. That would be sad. I am upbeat about polypills. I have changed my mind. We need to talk about a new kid on the block — interventional pulmonary embolism (PE) care. Our two EP labs bookend the three cath labs. I visit our cath labs as a curious person and journalist. I often see the doctors treating PE. The pictures are impressive when a doctor literally sucks a clot out of the pulmonary artery. My former partner for decades, Tom Tu, MD, became the chief medical officer of Inari. I loved working with Tom. Our cubicles in clinic were close. (By the way in private practice, you only get a cubby. My diplomas are not on the way, they're in boxes.). Tom pushed me on evidence. And I once debated him in front of the entire medical staff about percutaneous coronary intervention (PCI) for stable coronary artery disease (CAD). I had all the data; Tom had the stories. And I got crushed. Anyway, I liken endovascular clot aspiration in PE to clot aspiration in myocardial infarction (MI) and embolic protection devices in transcatheter aortic valve replacement (TAVR). Seeing a clot that was once in the body has huge persuasive properties. But scary pictures of clot are not evidence. The European Heart Journal Open has published an eye-opening review on the endovascular treatment of intermediate-risk PE. Now I know what you are thinking: review articles are terrible to read. And I would agree in most cases, but this review however by Arman Shahriar, MD, is superb. Sharp, short sentences; lots of subdivisions. I will link to it, and there are two reasons to read it: (1) if you are interested in PE care, which is increasingly common in cardiology practice; and (2) this is a shining example of the failure of evidence-based practice to determine best therapies. Advocates of EBM should read it for the many lessons. Here is a brief review: PE is obviously a leading cause of CV mortality and morbidity. But the hard part of PE treatment is that PE is not one thing. It's a bit like atrial fibrillation (AF) in that way. PE can be mild, even incidentally discovered on a CT done for other reasons, and it can be severe and devastating, causing shock and collapse. The extremes make for easy decisions. But most people with PE present with 'intermediate' levels of risk. Endovascular procedures have increasingly been used in the past decade. Interesting is that the increased use parallels almost exactly the rise of PE Response Teams (or PERT). Since so few patients present with extremely high-risk PE or extremely low risk, most endovascular therapies are deployed in intermediate risk patients. The problem is that there is little evidence for use of these procedures in intermediate risk. In fact, no guideline gives interventional therapy a Class 1 recommendation because there is not Class-1-level data. A word on risk stratification and basic management: Everyone agrees the first step in PE care is to risk-stratify using clinical, lab, and imaging parameters. The European Society of Cardiology (ESC) defines high-risk PE by hemodynamic instability, which is associated with a 30-day mortality risk exceeding 15%. These patients require immediate adjunctive intervention directed at reperfusion (medical, endovascular, or surgical) to prevent death. By contrast, low-risk PE — characterized by normal BP, low clinical severity, and no evidence of cardiac dysfunction — carries a low early-mortality risk of < 1% and can generally be safely managed with anticoagulation alone in the outpatient setting. Intermediate-risk patients, which encompass 25%-60% of hospitalized PE cases, have stable vital signs but other concerning features, such as cardiac dysfunction. Short-term mortality rates in intermediate-risk PE range from 1%–3% in clinical trials; and 3%–5% in observational studies. According to the ESC, patients with both imaging and laboratory evidence of cardiac dysfunction are deemed intermediate-to- high risk. This is where controversy and uncertainty come in — because of the limited data. The rationale for endovascular therapy of PE stems from a seminal trial called PEITHO in 2014. NEJM published the RCT of systemic lytics + heparin vs heparin alone in 1000 patients with intermediate-risk PE. The study found a small benefit in its primary efficacy endpoint (composite of 7-day mortality and hemodynamic decompensation; 2.6% vs. 5.6%, P = .02) that was outweighed by risks of major extracranial (6.3% vs. 1.2%, P ≤ .001) and intracranial (2.4% vs. 0.2%, P = .003) hemorrhage. Thus, the rationale for endovascular therapies were born. Because systemic lytics worked but were far too dangerous. Lax FDA likely leads to dubious evidence: Five endovascular devices hold indications for PE in the US. In 2014, the EKOS ultrasound-assisted thrombolysis catheter (Boston Scientific) became the first FDA-authorized endovascular therapy in acute PE. This catheter was initially studied in one RCT of 59 intermediate-risk patients (ULTIMA) and a prospective cohort of 150 intermediate and high-risk patients (SEATTLE II), with both studies demonstrating short-term improvements in the right ventricular/left ventricular (RV/LV) ratio. Thereafter, four 'analogous' devices have passed muster in the FDA's 510k pathway, where a device only has to be shown similar to a previous device. These include clot extraction devices of one sort of another. The authors of the review paper in EHJ Open then discuss four important and yet unanswered clinical questions: One question is surrogate validity. Measures of right ventricular (RV) dysfunction, such as RV size > LV size were adopted in earlier studies because it is associated with early mortality. But experts, including the AHA guideline writers, acknowledge uncertainty as to whether rapid improvements in RV dysfunction is a reliable surrogate for outcomes. I would add that RV size is like LDL. No one cares about their echo image. They care about being alive and breathing well. Remaining question number 2 asks whether interventional therapy plus anticoagulation beats simple anticoagulation alone in the short and long term. Only three small trials have addressed this question and the results are mixed. Less than 200 patients have been studied in RCTs with these devices. I know; it's crazy. And again, I remind you FDA allowed these devices based on similarity to others — not evidence of benefit. Remaining question number 3 is whether endovascular therapy added to anticoagulation improves clinical outcomes for patients, including mortality, hemodynamic deterioration, symptom resolution, and sequalae that contribute to long-term mortality such as chronic thromboembolic pulmonary hypertension (CTEPH), post-PE impairment (PPEI), or recurrence of disease. For instance, in intermediate-high risk PE, short-term mortality ranges from 1%–3% and CTEPH develops in 2%–3% of patients, and PPEI in 10%–30%. Despite the rise in endovascular therapy, there have been no RCTs. The good news is that there are now at least three ongoing trials. My hospital participates in one of them and the problem is extremely strict entry criteria, which will limit external validity. The fourth remaining question is the safety of endovascular therapy. While all the devices limit systemic thrombolysis, some involved large-bore catheters. The authors cite a large, real-world, non-industry supported observational study published in the Journal of the Society for Cardiovascular Angiography & Interventions that found much higher rates of major bleeding with endovascular therapy than previously described (10%–15%). The authors devote another section to explaining the popularity of these devices in the absence of evidence. This is quite interesting. One cause is the rise of PERT teams — who are led by interventional-minded doctors. Another, and perhaps stronger, tailwind is reimbursement changes. I did not know this, but following an FDA 510k market approval, insurers independently determine if they will cover a device. The Centers for Medicare & Medicaid Services (CMS) is the largest insurer and its decision influence private insurers. But in 2021, CMS controversially ended its non-coverage policy for PE devices, which allowed local Medicare contractors to decide. This decision accelerated coverage and in turn accelerated use. CMS, the authors wrote, could have required ongoing evidence generation within its CED mechanism — that is, coverage with evidence development . But, alas, they did not. (By the way, a sidebar here, I feel like coverage with evidence—for everything new—could be the most important policy ever employed.) The third reason for rising popularity of these treatments is marketing of observational research. Industry sponsors registries, which of course are voluntary, and produce favorable results, and these get made into ads. Companies than spend money paying doctors to speak and travel. Here is a direct quote from the paper: Until its recent acquisition by Stryker, Inari Medical was a relatively young company that derived two-thirds of its revenue from FlowTriever sales. Since its initial public offering in 2020, the company had rapidly increased its volume and magnitude of general physician payments. In 2020, it made 3500 general payments to physicians amounting to nearly a million dollars. Over the next three calendar years (2021, 2022, and 2023), these figures increased to $2.49 million, $4.86 million, and $6.74 million, respectively, representing 0.9%, 1.2%, and 1.4% of top-line revenues. And it wasn't just physicians. Hospitals too benefited financially via higher diagnosis-related group (DRG) reimbursement rates. Get this: hospitals get paid on severity. Using a device bumps severity. So it's self-fulfilling. Here's another quote from the authors: ' Between 2021 and 2022, for example, the reimbursement for endovascular therapy for PE with major comorbidity or complications (MS-DRG 166) nearly tripled from $9040 to $24,550. Accordingly, an interventional PE service line can generate high revenues for a hospital system .' BOOM—there you go. PERT teams make money. I don't mean to beat up the PE treatment people. I highlight this topic because of its EBM lessons. In the heyday of cardiology, we were leaders in the generation of evidence. Post-MI care, HF care, and in arrhythmias we had CAST and AFFIRM. So, it's weird that that same evidence-generating ethos did not infect the PE world. Which of these devices, if any, is better is a knowable question. But it won't come from observational studies. It has to be via RCTs. And I realize PE patients come in different varieties, but nonetheless, these studies could have been done. And then we would know. And you might say, John, there are ongoing trials now. My counter is that it's largely too late. Equipoise has been injured. When you return from a clot-extracting course on a beach resort, do you think you are going to be energized to randomize a PE patient in a trial or do clot extraction? When reimbursement is favorable, do you think doctors will be keen to randomize or do the procedure? I have already sent multiple notes to my friend Vinay Prasad encouraging him and Marty Makary at the FDA to do something to tighten device regulation. I am not against approving early generation devices, but there must be strong post-marketing requirements for evidence. There currently is not. But, in truth, as professionals and scientists, we should not need FDA to help us. We should want evidence; we should require evidence before exposing our patients to unproven therapy. Sadly, though, the recent experiences with left atrial appendage occlusion, PE, and now tricuspid interventions don't shine a favorable light on the scientific aspects of our profession. The Journal of the American Heart Association published an interesting paper on trends in heart disease mortality. It makes you think. A Stanford-led team used the national vital statistics at the CDC to present data on heart disease mortality over the past 52 years — from 1970 to 2022. The findings: Some good news: Heart disease deaths are decreasing. In 1970, heart disease accounted for 41% of deaths; that has declined to 24% of all deaths. And life expectancy went from 71 years in 1970 to 77.5 in 2022. The proportions of types of heart disease deaths have changed dramatically. Over the past 50 years, overall age‐adjusted heart disease mortality decreased by 66% from 1970 to 2022 (from 761 to 258 per 100,000). In 1970, more than 90% of heart disease deaths were ischemic. Ischemic causes of cardiovascular (CV) death declined to 53% in 2022. One of the reasons may be this statistic: Since 1970, age-adjusted mortality from acute myocardial infarction (AMI) decreased by 89%, from 354 to 40 per 100,000. Since 1970, age-adjusted mortality from any ischemic disease decreased by 81%. But, conversely, since 1970, age-adjusted mortality from other heart disease subtypes increased by 81% with the greatest increases in HF (146%), hypertensive (106%) and arrhythmia (450%). For instance, in 1970, these other subtypes (HF, hypertensive, and arrhythmia) accounted for just 9% of heart disease deaths; now it is 47% of heart disease deaths. First is that the authors rightly acknowledge limitations in the use of coding. For instance, disease names have shifted somewhat. Arrhythmia-related deaths may in fact be related to underlying ischemic heart disease. But limitations aside, it's worth thinking about this data. The fall in deaths from AMI and ischemic heart disease represents a shining example of excellence in both cardiology and public health. The reduction in smoking stands out as a huge success in public policy. Surely this has enhanced the lives of millions of people. I would also laud my interventional colleagues. I spend a great deal of time criticizing the overuse of intervention in stable CAD, but the acute treatment of MI has been one of the most important medical achievements of a generation. Young people cannot appreciate where we were when I began medical school in 1985. MIs then were largely treated with morphine and Swan-Ganz catheters. Now, people come in with an anterior MI and leave with band-aid on their wrist and a normal ejection fraction. So impressive has been the trend in AMI care that it is hard to find an ischemic cardiomyopathy patient who qualifies for a primary prevention implantable cardioverter-defibrillator (ICD). Keep in mind too that this marked reduction in MI deaths bears on screening for heart disease. Namely, the better we get at treating a condition, the less value there is in finding it early. We don't screen for appendicitis or gallbladder disease or pneumonia because we can simply treat those problems when they occur. AMI isn't quite there but it's approaching that. By the way, if you are young and looking for a job that has meaning, I can't think of a better job than interventional cardiology. Nearly every day, you are saving or enhancing a life. The problem of course is that it is hard because like delivering babies, MIs happen at all hours. Another factor in the reduction of death from ischemic heart disease could be statins. Statin use has gone from none to up to 45% of adults over the time frame. Since we know that statins consistently reduce CV events by about 25%, not having an MI in the first place is a good way to not die of ischemic heart disease. I for one think statins play a consequential role in lower ischemic heart disease deaths but smoking and MI care are much larger causal factors. My final comment is the alarming language (both in the paper and online) regarding the rise in other forms of heart disease. Yes, the rise in obesity, which has led to more hypertension and more AF and more heart failure with preserved ejection fraction (HFpEF) is a big concern. I don't want to downplay it. Obesity is a public health crisis, and largely a public health failure. But on the other hand, it's important for doctors to understand that all people die. If you reduce MI deaths, and increase life expectancy, what do you think happens: people die of other diseases, such as heart failure, atrial fibrillation, dementia, cancer, and falls. It's normal. It's still a good thing to extend life, and enhance life, but it's also important to recognize that reducing ischemic heart disease deaths does not magically reduce healthcare costs, because eventually, aging people develop some sort of disease, and if is treated, money is spent. The reason to improve treatment of heart disease is not to save money — it is to extend quality of life. If our therapies do that, then it is worth the money spent. American Diabetes Association (ADA) 85th Scientific Sessions I won't get into specifics, but at the recent American Diabetes Association meeting in Chicago a trove of studies came out that should be on our radar. For instance, a study showed early data on once-weekly insulin. Think about that if you have type 1 diabetes: once-weekly insulin. There were early studies on other GLP-1 drugs as well as combinations of drugs. I think semaglutide and tirzepatide may become the simvastatin of GLP-1's soon. There was even some encouraging data on recombinant gene therapy for type 1 diabetes. The diabetes world is advancing fast. And I think it's only a matter of a short time that cardiologists will be prescribing GLP-1 drugs like we did for SGLT2 drugs. And finally, before I close, I'll say that there's been another BMJ investigation as reported on more potential — emphasis, potential — troubles in the ticagrelor evidence base. I will look into that and have a report on the next TWIC podcast.
Fast Company
2 hours ago
- Fast Company
Your food is full of microplastics—and now we know why
A study published this week delves into the mystery of how the plastic objects we interact with daily shed tiny particles that creep into our bodies, brains and guts. While the scientific focus has long been on how microplastics pollute our environment and impact wildlife, researchers are increasingly raising alarms about how the same contaminants can wreak havoc in the human body. The new research, published in the journal NPJ Science of Food, wove together data from 100 previous papers that studied microplastics, nanoplastics and plastic particles. The results were compiled into an open database published by the Food Packaging Forum, a Swiss nonprofit that examines chemicals in food packaging. Microplastics and nanoplastics are plastic particles in the millimeter to nanometer range, with the latter causing even more concern among scientists because their tiny size makes them able to slip into human cells. 'This is the first systematic evidence map to investigate the role of the normal and intended use of food contact articles in the contamination of foodstuffs with MNPs [microplastics and nanoplastics],' lead author of and Scientific Communication Officer at the Food Packaging Forum Dr. Lisa Zimmermann said. 'Food contact articles are a relevant source of MNPs in foodstuffs; however, their contribution to human MNP exposure is underappreciated.' How we interact with plastic matters The new study looked at a broad range of 'food contact articles' that included water bottles, cutting boards, food processing equipment and packaging ranging from food wrappers to tea bags. Most food packaging contains plastic, even many things that seem like they don't, like the paper that wraps around cold cuts and cheese, cardboard takeout containers and glass bottles and jars, which often have a plastic-coated closure. The authors focused on how everyday objects used as intended can shed microplastics and how that shedding can worsen over the course of repeated interactions. Across 14 different studies, microplastic shedding was found to increase with repeated uses, including screwing a reusable water bottle lid on and off, washing a melamine dish or putting plastic tableware into contact with hot foods 'These findings are relevant for reused plastic [food contact articles] and should be considered when assessing the safety of FCAs across use cycles,' the authors wrote. Based on their research, and its blind spots, they stressed the need for future studies to delve more deeply into how repeated interactions, heating and washing affects how much microplastic is shed by kitchenware and food packaging that most of the world's population might come into contact with countless times each day. The authors also found that the bulk of the research on microplastics focused on only a few kinds of objects that come into contact with food and drinks, like water bottles and tea bags. Similarly, more studies focused on PET and polypropylene over other common plastics, leaving a lot of unknowns about how much plastic is being shed by food packaging made out of other materials. Food and beverage containers can expose the human body to microplastics every time we interact with them but relatively little is still known about how that process works. That mystery is an ominous one considering how ubiquitous plastics are globally in food packaging and preparation and how their presence is increasingly linked to reproductive, digestive and respiratory problems and potentially even colon and lung cancer. Plastics appear to have no trouble finding their way into the human body. Another recent study found that the adult brain can contain a plastic spoon's worth of microplastics and nanoplastics, an amount that's seven to 30 times higher than what might be found in the liver or kidneys. Those kind of findings show that it's imperative for future research to track down how all of that plastic is finding its way into the human body and what exactly it does once it gets there.
