Category: 8. Health

Given the seriousness and increased frequency of strokes, many studies have been conducted to assess the relationship between hysterectomy and/or bilateral oophorectomy and the risk of stroke with varying results. A new study suggests women having a hysterectomy and/or bilateral oophorectomy have higher risks of stroke compared with those who did not have surgery. Results of the study are published online today in Menopause, the journal of The Menopause Society.

Stroke is the third dominant cause of death and the fourth dominant cause of disability around the world, representing a significant public health challenge. Therefore, ongoing prevention efforts that address modifiable risk factors are essential to reduce the burden of this disease.

Estrogen levels play a major role. Women of reproductive age have a lower stroke risk, whereas postmenopausal women are roughly two times more likely to have a stroke within a decade of menopause. Both hysterectomy and oophorectomy significantly affect estrogen levels. Hysterectomy may result in lower ovarian sex steroid levels, resulting in earlier menopause. An oophorectomy can reduce premenopausal serum estradiol by up to 80% and androgen levels by about 50% in both premenopausal and postmenopausal women.

Although multiple studies have previously been conducted around the relationship between surgery and stroke risk, results have been mixed. This latest study using data from the National Health and Nutrition Examination Survey (NHANES) included more than 21,000 women, with an average of 8.3 follow-up years, documenting 193 stroke-related deaths. The analysis of these results found an increased risk for hysterectomy with bilateral oophorectomy but not for hysterectomy alone or hysterectomy with unliteral oophorectomy. A pooling analysis of this study’s results with other cohorts, however, revealed an 18% higher risk of stroke for hysterectomy with bilateral oophorectomy, and a 5% higher risk of stroke for hysterectomy alone.

Although the new study lacked surgical indication data, meta-analysis studies show that there is no connection between a benign or malignant diagnosis when determining the associated risk of surgery. Similarly, current evidence does not differentiate the amount of risk based on specific indications (ie, endometriosis, adenomyosis, fibroids, abnormal uterine bleeding, prolapse, or other rare conditions).

Additional studies with a large sample size and longer follow-up period are needed to address the disparities of type of stroke, age at surgery, surgical techniques, and menopause status on the association between stroke risk and hysterectomy and/or bilateral oophorectomy.

Survey results are published in the article “Stroke risk in women with or without hysterectomy and/or bilateral oophorectomy: evidence from the NHANES 1999-2018 and meta-analysis.”

The results of this study demonstrate increased stroke risk related to hysterectomy and/or bilateral oophorectomy, highlighting that these common procedures carry longer-term risks. They also call attention to an opportunity for more careful assessment of cardiovascular risk and implementation of risk reduction strategies in women who undergo these surgeries.”

Dr. Stephanie Faubion, medical director, The Menopause Society

The organic process is neither viable nor sustainable but a new paper would like to change that. By allowing modern gene editing. The only way Europe can reach the goal of 25% Organic™ farmland that its government-funded environmental groups demand, a 250% increase, is by moving into the 21st century, they argue.

When the organic process was the only thing available, the food-rich were rich and the poor were poor and the only difference was being born into a natural breadbasket. Cycles of famine were common.

Science and technology gradually changed all that. First the heavy plow was introduced, then synthetic fertilizer, then synthetic pesticides. Each improvement made agriculture safer and more efficient, and that made food more affordable. Along the way, hybrids were created but in the 20th century science was able to speed genetic engineering up quite a lot. By 1980, the Malthusian beliefs in Population Bombs, Soylent Green, and need for global sterilization promoted by Paul Ehrlich and John Holdren were shown to be paranoid nonsense. 

Once food became affordable for all, every Sneetch now had a Star, so it needed new virtue signaling. The organic movement, and its cousin, the anti-vaccine movement, were ready to sell those new stars to Sneetches. They only became true movements 25 years ago, but had their modern origins in the 1940s, when anti-everything activist J. I. Rodale started publishing magazines for rich white people who distrusted science.

We can’t fault Rodale’s gift for marketing. He knew what his target audience wanted; models happy being up to their knees in garbage. But Rachel Carson, author of “Silent Spring”, thought him a weird creep and denied it flatly when he tried to claim she was part of his movement because she didn’t want so much DDT used. Carson was not right about much, but she was right about Rodale. His campaigns against both agricultural science and vaccines live on today.

In 2000, President Clinton, arguably the most anti-science American president ever, told his US Department of Agriculture to create a special marketing panel inside USDA and let them decide what products could be “USDA Organic.”

Boomer Environmentalism had reached its apex. He killed nuclear energy, he diverted government science funding to acupuncture, he freed supplement marketing from FDA oversight, but most importantly he gave Organic™ food a government seal. Now it’s a $135 billion industry but the demographic is the same. It is still for wealthy white progressives but also includes those who want to seem like wealthy white progressives. What it still lacks is sustainability.

Yet if the European Green Deal is going to be sustainable, and reach that 25% Organic™  agricultural land goal they want by 2030, the only way is science. And that means genetic engineering. Yet Europe continues to call everything modern a “GMO.” Creating class warfare around food is bad for the poor and it’s scientifically illiterate.

GMO was a trademarked name for one genetic engineering technique, long off patent. That Europeans continue to call everything “GMOs” shows they are far behind America in scientific literacy and, when it comes to France, why they also lead the world in vaccine denial.

Anti-science hippies love hemp. Like with GMOs, it is impossible for any person without a $20,000 machine to detect any difference between an Organic™ plant and a modern genetically engineered one. So maybe go slow, let Europeans grow CRISPR hemp first. Then when they have learned to crawl, scientifically speaking, they can tackle more important things.  Credit: Justus Wesseler

The organic process in both America and Europe does allow gene editing, just not the modern kind. Mutagenesis, for example, an older form of genetic modification that used chemical baths and radiation to force mutations, is the basis of thousands of products, many of them government-certified as Organic™.

Like this Spanish clementine? It was genetically modified in a lab using fast neutron radiation to generate induced mutations. It’s certifiedOrganic™.

GMOs were not banned by Europe for any science or health reason, it was geopolitics.

GMOs only became controversial after they pivoted from niche products like insulin to the Rainbow Papaya, where a gene gun saved the entire industry in Hawaii. That sailed through regulatory approval without issue but it can’t be dismissed as coincidence that Monsanto, an American company, suddenly had a genetic engineering tool for food better than Mutagenesis, made by BASF, a European company, and suddenly European activists began to call it “Frankenfood”, and that European media outlets joined in.

When Europe banned GMOs they specifically exempted European Mutagenesis. It was clearly a tariff on American products, economic protectionism they resent when it happened back toward them in 2025.

“If mutagenesis had not been exempted from GMO legislation, the estimation is that 80%–90% of the cereal products on the European market would have been subject to GMO labeling,” notes the paper’s senior author Professor Kai Purnhagen of the University of Bayreuth.  

2001 was a long time ago. Hopefully now even environmentalists know that Frankenstein was not a GMO, he was a grafted hybrid and would be certified Organic™ today.

Which means the authors of the new paper saying the European left needs to embrace pre-market authorization for new genomic techniques. CRISPR-Cas9, Cisgenesis and Intragenesis didn’t exist when Europe banned modern science. Even Targeted Mutagenesis is illegal now.

Without science, Europe’s Green Deal will be a black eye for food like they have received by pivoting to solar and wind for energy. It will mean 100% higher costs for food just like spiritual beliefs in alternative energy caused in electricity bills.

Europe is ready. Today, GMOs are as old and therefore time-tested as Mutagenesis was when Europe exempted it from their ban. That’s right, GMOs have fed a trillion cows and billions of humans without a single stomach ache or harmful effect on the environment, just like Mutagenesis.

Europe can continue to block GMOs, if that concession will placate their green NGOs, because it is a legacy product just like Mutagenesis and Bayer, a European company, now owns the former Monsanto. They only need to allow techniques invented after the ban, which are even better than GMOs, to get Europeans back into the science conversation worldwide. And they are not. Europeans don’t have a top company in any industry. They are not even close to being vital in any science output.

Or they could reposition genetic engineering, give it a new name. The anti-science left that hated vaccines until 2021 now claims to love them, so perhaps the easiest solution to get environmentalists on board is to rebrand genetic engineering as ‘vaccines against pests‘. Sure, Republicans in America will then object but their hearts aren’t really in it. The entire Republican party today has fewer kids being exempted from vaccines today than California alone had in 2014. So we’ll be fine.

Hank Campbell is the founder of Science 2.0 and the author of Science Left Behind. Follow Hank on X @HankCampbell

A version of this article was originally posted at Science 2.0 and is reposted here with permission. Any reposting should credit both the GLP and the original article. Find Science 2.0 on X @science2_0

For the new study, researchers sought to better understand these relationships by using a pure source of placenta cells, unlike in previous studies that looked at either whole animals or isolated mouse placentas. To do so, they first purified human cytotrophoblasts, which are the stem cells that make all the cells of the placenta. They then added serotonin to those cells to see where it would go and discovered it concentrated in the nucleus. Next, they used a selective serotonin reuptake inhibitor (SSRI) that blocked SERT — the antidepressant escitalopram, commonly known by the brand name Lexapro — to show that the normal growth, function, and differentiation of these cells was completely blocked. 

They also used another inhibitor called cystamine to block serotonylation, or the process by which serotonin is added to proteins like histone 3, which turns genes “on” and “off.” Again, that completely blocked the normal growth of the cells. 

Blocking either SERT or serotonylation led to significant changes in gene expression of RNAs in the cytotrophoblasts, they found. Some genes — including ones involved in making, moving, and growing cells — became downregulated, or less active, when serotonin couldn’t enter the cell. Other genes — including ones that help cells stay alive and protect them — became upregulated, or more active. According to the researchers, these findings show that serotonin is critical for the growth of the cytotrophoblasts, the placenta, and by extension, the fetus. 

Additionally, researchers discovered that the cytotrophoblasts don’t contain tryptophan hydroxylase (TPH-1), or the enzyme that makes serotonin, indicating the cells within the placenta can’t produce serotonin on their own. 

“This suggests that factors that either inhibit serotonin transport through the placenta, or increase it, may have a significant impact on the placenta, embryo, fetus, and ultimately, the newborn and its brain,” Kliman said.

For example, Kliman says this explains why taking SSRIs — which decrease the levels of serotonin into the placenta — leads to smaller babies, and why, conversely, increased levels of serotonin may lead to bigger babies, with bigger brains, who may be at increased risk for developmental disabilities like autism.

Kliman and his lab have long investigated the link between placentas and children with autism, specifically the number of trophoblast inclusions (TIs) in the placenta. TIs are like wrinkles or folds in the placenta, caused by cells multiplying more than they should, typically only seen in pregnancies where there are genetic problems with the fetus. 

This new study is the culmination of research first published in 2006 that found significantly more TIs in the placentas from children with autism, and later in 2021, that the genetics of the fetus — and not the parent’s uterine environment — determine how many TIs are in the placenta. 

“This puts a big nail into the theory that vaccines cause autism,” suggested Kliman. “Autism, in essence, starts in the womb, not after delivery, and is most likely due to the genetics of the placenta and to a lesser extent, the maternal environment the placenta finds itself in.”

Kliman is also the director of the Reproductive and Placental Research Unit at YSM. 

Other Yale authors include Gary Rudnick, a professor emeritus of pharmacology at YSM, and Seth Guller, a senior research scientist in obstetrics, gynecology, and reproductive sciences and director of the Gyn/Endocrine Laboratory at YSM. 

This study was supported by grants from the Fulbright-Monahan Foundation, the University of Paris Cité, and the Reproductive and Placental Research Unit at Yale School of Medicine.

People in the world are living longer than before, but they are not always living healthier lives during those extra years. A recent study by researchers at the MayoClinic found that while life expectancy keeps rising, the number of years people spend in good health does not increase as much. The study has been published in the journal Communications Medicine.Basically, scientists are seeing that just because people are living longer these days (that’s what we call “lifespan”), it doesn’t mean they’re living all those extra years in good health (“healthspan”). So, life is getting longer, but not necessarily better, because more people are spending a lot of their “golden years” dealing with sickness or disabilities instead of being healthy and active.

How did they figure this out?

The research team did a massive study that looked at health and life expectancy data from 183 countries all over the world. They used information from the World Health Organization and other big international sources to figure out two things for each country:Life expectancy: How long, on average, people live in that country.Health-adjusted life expectancy (HALE): Basically, how many years, on average, someone lives in good health, not hampered by illness or disability.The “healthspan-lifespan gap” is just the difference between those two numbers. So if the average life expectancy is 80, but the average healthy lifespan is 70, that means people spend around 10 of their years dealing with health problems.

What did they find?

Globally, there’s now a gap of about 9 years between lifespan and healthspan — and that gap is getting wider, not smaller! But it’s not the same everywhere. For instance, people in Europe and North America tend to live the longest, but they also spend more years in poor health. Meanwhile, people in parts of Africa may have shorter lifespans overall, but spend a higher percentage of those years in good health.One interesting part is what causes people to lose those healthy years. In wealthier regions like the Americas and Europe, most of the gap is because of chronic, non-infectious diseases — think heart disease, cancer, diabetes, and things like that. In poorer regions, people tend to die younger, but more often from infectious diseases or conditions related to childbirth and nutrition. However, chronic diseases are on the rise everywhere as people adopt more modern lifestyles.

What about mental health?

Another thing the study pointed out is that problems like depression and substance abuse are pretty common across all regions. These mental and behavioral issues don’t explain the differences between places, but they’re a big deal just about everywhere.

Why does it matter?

This growing gap between how long people live and how long they’re healthy is worrying. It means more folks are facing years of poor quality of life, with pain, disability, and all the stress (and cost) that comes with illness.Even more, the researchers noticed that economic factors (like a country’s wealth and health spending) and patterns of disease in that society can predict this gap. Richer countries tend to have more years of chronic illness, probably because people survive longer with disease management, but don’t necessarily cure the illness. Poorer countries, on the other hand, are catching up as their populations age.

So, what now?

The main takeaway is we can’t just focus on making people live longer, we’ve got to think about helping them live healthier, too. Each region of the world has its own challenges, so there’s no single solution. The study says we need to tailor health policies and disease prevention strategies to the specific problems in each place, rather than treating everyone the same.In short: More years doesn’t always mean better years. The world has some homework to do if we want those golden years to actually be golden!

Pumpkin seeds might be small, but their health benefits are mighty. While many people know these crunchy green seeds help balance blood sugar levels, there’s a lot more to them than meets the eye. According to U.S.-based gastroenterologist Dr. Pal Manickam, pumpkin seeds are one of the most underrated superfoods you can easily include in your diet, and they’re surprisingly affordable too.

In a recent Instagram video and a post on X (formerly Twitter), Dr. Pal shares seven science-backed reasons to add pumpkin seeds to your daily routine. “If you’re not including pumpkin seeds in your diet, you’re seriously missing out,” he said.

So, what makes these little seeds so powerful? Let’s break down the seven benefits he shared, including one he calls his personal favourite.

1. Boosts Immunity

Pumpkin seeds are rich in zinc, a key mineral that strengthens the immune system and helps your body fight infections more effectively. Including them in your meals can be a tasty way to keep seasonal illnesses at bay.

2. Supports Heart Health

Thanks to their high magnesium content, pumpkin seeds help maintain a steady heartbeat and regulate blood pressure. Magnesium is also known to support overall cardiovascular health.

3. Improves Mood and Relaxation

Pumpkin seeds contain tryptophan, an amino acid that converts into serotonin, the “feel-good” hormone. This can help improve mood, reduce anxiety, and promote better sleep, something many people overlook when managing stress.

4. Strengthens Bones

These seeds also offer a good dose of phosphorus and magnesium, which are essential for bone strength and density. Regular consumption may reduce your risk of conditions like osteoporosis later in life.

5. Balances Blood Sugar

Perhaps the most well-known benefit, pumpkin seeds help regulate insulin levels and keep blood sugar in check, thanks again to their magnesium content. This makes them a smart snack option for people managing diabetes or prediabetes.

6. Helps with Cravings and Weight Loss

Dr. Pal’s personal favourite benefit: curbing cravings. Packed with healthy fats and protein, pumpkin seeds keep you full for longer, making it easier to avoid mindless snacking and overeating.

7. Protects Skin and Eyes

Loaded with antioxidants like vitamin E and carotenoids, these seeds help reduce inflammation, slow signs of aging, and protect your eyes and skin from damage caused by environmental stress.

Who is Dr Pal Manickam?

For the unversed, Dr. Pal Manickam is not your average doctor. Known for mixing health advice with humour, he has built a large following across social media. He shares easy-to-understand, science-based health tips, often focusing on gut health, intermittent fasting, and holistic wellness. Dr. Pal completed his MBBS at PSG Medical College, Coimbatore, India, then a Master’s in Public Health at the University of Massachusetts, Boston and an MD in Internal Medicine at Wayne State University, Detroit, before steeping into gastroenterology fellowship.

Pumpkin Seeds vs Flax and Chia seeds?

According to Healthline, flaxseeds and chia seeds are also loaded with fiber and omega-3 fats, pumpkin seeds bring something unique to the table, they’re easier to eat (no grinding required), and they offer a broader range of nutrients like zinc, magnesium, and protein. That makes pumpkin seeds an excellent all-rounder for anyone looking to boost their health with minimal effort.

Difference between flax seeds, chia seeds and pumpkin seeds.

So, next time you’re looking for a budget-friendly superfood, skip the supplements and reach for a handful of pumpkin seeds instead.

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For years, health authorities have warned against red meat consumption, with the World Health Organization’s cancer research arm classifying it as “probably carcinogenic to humans”. But a controversial new study challenges that position, suggesting that animal protein might protect against cancer deaths rather than cause them.

The International Agency for Research on Cancer (IARC), part of the WHO, has long classified red meat, including beef, pork, lamb and mutton, as probably carcinogenic. And processed meats such as bacon and sausages are classified as definite carcinogens. This judgment reflects multiple studies linking red meat to colorectal cancer, forming the basis of dietary advice to limit intake.

Yet the new research by Canada’s McMaster University suggests the opposite: that people who consume more animal protein may actually have lower cancer mortality rates. But, before you rush out to buy a pack of sausages, there are some important points you should note.

The study’s methods contain important nuances that complicate its headline-grabbing conclusions. Rather than examining red meat specifically, the researchers analysed consumption of “animal protein”, a broad category that includes red meat, poultry, fish, eggs and dairy products. This distinction matters significantly because fish, particularly oily varieties such as mackerel and sardines, are associated with being cancer-protective.

By grouping all animal proteins together, the study may have captured the protective effects of fish and certain dairy products rather than proving the safety of red meat.

Dairy products themselves present a complex picture in cancer research. Some studies suggest they reduce colorectal cancer risk while potentially increasing prostate cancer risk. This mixed evidence underscores how the broad “animal protein” category obscures important distinctions between different food types.

The study, which was funded by the National Cattlemen’s Beef Association, America’s primary beef industry lobbying group, contains several other limitations. Crucially, the researchers didn’t distinguish between processed and unprocessed meats – a distinction that countless studies have shown to be vital.

Processed meats such as bacon, sausages and deli meats consistently show higher cancer risks than fresh, unprocessed cuts. Additionally, the research didn’t examine specific cancer types, making it impossible to determine whether the protective effects apply broadly or to particular cancers.

Interestingly, the study also examined plant proteins, including legumes, nuts and soy products such as tofu, and found they had no strong protective effect against dying of cancer. This finding contradicts previous research suggesting that plant proteins are linked to decreased cancer risk, adding another layer of complexity to an already confusing picture.

These findings don’t diminish the established health benefits of plant-based foods, which provide fibre, antioxidants and other compounds associated with reduced disease risk.

Not a green light

Even if the study’s conclusions about animal protein prove accurate, the study shouldn’t be interpreted as a green light for unlimited meat consumption. Excessive red meat intake remains linked to other serious health conditions, including heart disease and diabetes. The key lies in moderation and balance.

The conflicting research highlights the complexity of nutrition science, where isolating the effects of individual foods proves remarkably difficult. People don’t eat single nutrients in isolation – they consume complex combinations of foods as part of broader lifestyle patterns. It’s more important to focus on overall dietary patterns rather than fixating on individual foods.

A balanced plate approach, featuring a variety of protein sources, plenty of vegetables and fruits, and minimally processed foods, remains the most evidence-based path to optimal health.

While this latest study adds a new dimension to the meat debate, it’s unlikely to be the final word. As nutrition science continues to evolve, the most prudent approach remains the least dramatic: moderation, variety and balance in all things.

Ahmed Elbediwy, Senior Lecturer in Clinical Biochemistry / Cancer Biology, Kingston University and Nadine Wehida, Senior Lecturer in Genetics and Molecular Biology, Kingston University

This article is republished from The Conversation under a Creative Commons license. Read the original article.

With support from the Commonwealth of Virginia’s Alzheimer’s and Related Diseases Research Award Fund (ARDRAF), Fralin Biomedical Research Institute at VTC scientists Sharon Swanger and Shannon Farris are working to understand why this area is especially vulnerable.

Swanger studies how brain cells communicate across synapses in disease-susceptible brain circuits, while Farris focuses on how different circuits in the brain’s memory center function at the molecular level. Their overlapping expertise made the collaboration a natural fit.

“We’ve both been studying how circuits differ at the molecular level for a while,” said Swanger, an assistant professor at the research institute. “This new collaborative project brings together my work on synapses and Shannon’s on mitochondria in a way that addresses a big gap in the Alzheimer’s disease field.”

“This kind of state-level support is critical,” Farris said. “It gives researchers in Virginia the chance to ask questions that may eventually make a difference for people living with Alzheimer’s. It’s meaningful to be part of research that could help people facing that journey.”

A key focus of their research is mitochondria — tiny structures inside brain cells that provide the energy needed for a variety of cellular functions in neurons including synaptic transmission. In Alzheimer’s disease, mitochondria stop working properly in the course of the disease.

Farris and Swanger are investigating whether mitochondria in a vulnerable memory-related circuit may become overloaded with calcium, a key signaling chemical for multiple neuronal and synaptic processes. That overload could contribute to the early breakdown of memory circuits.

“The connection between these cells is one of the first to fail in Alzheimer’s,” Farris said. “We found that this synapse has unusually strong calcium signals in nearby mitochondria — so strong we can see them clearly under a light microscope. Those kinds of signals are hard to ignore. It gives us a model where we can really watch what’s happening as things start to go wrong.”

To test their hypothesis, the researchers will study brain tissue from healthy mice and mice with certain aspects of Alzheimer’s pathology. By comparing how mitochondria function and how brain cells communicate across synapses in each group, they hope to find early signs of stress or failure in the entorhinal cortex-hippocampus circuit.

Swanger and Farris are members of the Fralin Biomedical Research Institute’s Center for Neurobiology Research and also faculty in the Department of Biomedical Sciences and Pathobiology of the Virginia-Maryland College of Veterinary Medicine.

A new study from the University of Sydney has revealed how type 2 diabetes directly alters the heart’s structure and energy systems, offering vital insights into why people with diabetes are at greater risk of heart failure.

Published in EMBO Molecular Medicine, the research was led by Dr. Benjamin Hunter and Associate Professor Sean Lal from the School of Medical Sciences. The researchers analysed donated human heart tissue from patients undergoing heart transplantation in Sydney and found that diabetes causes distinct molecular changes to heart cells and structural changes to the muscle, especially in patients with ischaemic cardiomyopathy, the most common cause of heart failure.

“We’ve long seen a correlation between heart disease and type 2 diabetes,” said Dr. Hunter, “but this is the first research to jointly look at diabetes and ischaemic heart disease and uncover a unique molecular profile in people with both conditions.

“Our findings show that diabetes alters how the heart produces energy, maintains its structure under stress, and contracts to pump blood. Using advanced microscopy techniques, we were able to see direct changes to the heart muscle as a result of this, in the form of a build-up of fibrous tissue.”

Heart disease is the leading cause of death in Australia and over 1.2 million people live with type 2 diabetes.

Our research links heart disease and diabetes in ways that have never been demonstrated in humans, offering new insights into potential treatment strategies that could one day benefit millions of people in Australia and globally.” 

Sean Lal, Associate Professor, School of Medical Sciences, University of Sydney

Getting to the heart of the problem

The researchers examined heart tissue from transplant recipients and healthy donors. 

The study discovered that diabetes is not just a co-morbidity for heart disease – it actively worsens heart failure by disrupting key biological processes and reshapes the heart muscle at a microscopic level.

“The metabolic effect of diabetes in the heart is not fully understood in humans,” said Dr Hunter.

“Under healthy conditions, the heart primarily uses fats but also glucose and ketones as fuel for energy. It has previously been described that glucose uptake is increased in heart failure, however, diabetes reduces the insulin sensitivity of glucose transporters – proteins that move glucose in and out of cells – in heart muscle cells. 

“We observed that diabetes worsens the molecular characteristics of heart failure in patients with advanced heart disease and increases the stress on mitochondria – the powerhouse of the cell which produces energy.”

The researchers also observed reduced production of structural proteins critical for heart muscle contraction and calcium handling in people with diabetes and ischaemic heart disease, along with a build-up of tough, fibrous heart tissue that further affects the heart’s ability to pump blood.

“RNA sequencing confirmed that many of these protein changes were also reflected at the gene transcription level, particularly in pathways related to energy metabolism and tissue structure, which reinforces our other observations,” said Dr Hunter.

“And once we had these clues at the molecular level, we were able to confirm these structural changes using confocal microscopy.”

Associate Professor Lal said the discovery of mitochondrial dysfunction and fibrotic pathways could help guide future therapies.

“Now that we’ve linked diabetes and heart disease at the molecular level and observed how it changes energy production in the heart while also changing its structure, we can begin to explore new treatment avenues,” said Associate Professor Lal.

“Our findings could also be used to inform diagnosis criteria and disease management strategies across cardiology and endocrinology, improving care for millions of patients.”

Sep 2 2025

Heart rate is one of the most basic and important indicators of health, providing a snapshot into a person’s physical activity, stress and anxiety, hydration level, and more. 

Traditionally, measuring heart rate requires some sort of wearable device, whether that be a smart watch or hospital-grade machinery. But new research from engineers at the University of California, Santa Cruz, shows how the signal from a household WiFi device can be used for this crucial health monitoring with state-of-the-art accuracy-without the need for a wearable.

Their proof of concept work demonstrates that one day, anyone could take advantage of this non-intrusive WiFi-based health monitoring technology in their homes. The team proved their technique works with low-cost WiFi devices, demonstrating its usefulness for low resource settings.

A study demonstrating the technology, which the researchers have coined “Pulse-Fi,” was published in the proceedings of the 2025 IEEE International Conference on Distributed Computing in Smart Systems and the Internet of Things (DCOSS-IoT) .

Measuring with WiFi

A team of researchers at UC Santa Cruz’s Baskin School of Engineering that included Professor of Computer Science and Engineering Katia Obraczka, Ph.D. student Nayan Bhatia, and high school student and visiting researcher Pranay Kocheta designed a system for accurately measuring heart rate that combines low-cost WiFi devices with a machine learning algorithm. 

WiFi devices push out radio frequency waves into physical space around them and toward a receiving device, typically a computer or phone. As the waves pass through objects in space, some of the wave is absorbed into those objects, causing mathematically detectable changes in the wave. 

Pulse-Fi uses a WiFi transmitter and receiver, which runs Pulse-Fi’s signal processing and machine learning algorithm. They trained the algorithm to distinguish even the faintest variations in signal caused by a human heart beat by filtering out all other changes to the signal in the environment or caused by activity like movement. 

“The signal is very sensitive to the environment, so we have to select the right filters to remove all the unnecessary noise,” Bhatia said. 

Dynamic results

The team ran experiments with 118 participants and found that after only five seconds of signal processing, they could measure heart rate with clinical-level accuracy. At five seconds of monitoring, they saw only half a beat-per-minute of error, with longer periods of monitoring time increasing the accuracy. 

The team found that the Pulse-Fi system worked regardless of the position of the equipment in the room or the person whose heart rate was being measured-no matter if they were sitting, standing, lying down, or walking, the system still performed. For each of the 118 participants, they tested 17 different body positions with accurate results

These results were found using ultra-low-cost ESP32 chips, which retail between $5 and $10 and Raspberry Pi chips, which cost closer to $30. Results from the Raspberry Pi experiments show even better performance. More expensive WiFi devices like those found in commercial routers would likely further improve the accuracy of their system.

They also found that their system had accurate performance with a person three meters, or nearly 10 feet, away from the hardware. Further testing beyond what is published in the current study shows promising results for longer distances.

“What we found was that because of the machine learning model, that distance apart basically had no effect on performance, which was a very big struggle for past models,” Kocheta said. “The other thing was position-all the different things you encounter in day to day life, we wanted to make sure we were robust to however a person is living.”

Creating the dataset 

To make their heart rate detection system work, the researchers needed to train their machine learning algorithm to distinguish the faint detections in WiFi signals caused by a human heartbeat. They found that there was no existing data for these patterns using an ESP32 device, so they set out to create their own dataset. 

In the UC Santa Cruz Science and Engineering library, they set up their ESP32 system along with a standard oximeter to gather “ground truth” data. By combining the data from the Pulse-Fi setup with the ground truth data, they could teach a neural network which changes in signals corresponded with heart rate.

In addition to the ESP32 dataset they collected, they also tested Pulse-Fi using a dataset produced by a team of researchers in Brazil using a Raspberry Pi device, which created the most extensive existing dataset on WiFi for heart monitoring, as far as the researchers are aware. 

Beyond heart rate

Now, the researchers are working on further research to extend their technique to detect breathing rate in addition to heart rate, which can be useful for the detection of conditions like sleep apnea. Unpublished results show high promise for accurate breathing rate and apnea detection.

Those interested in commercial use of this technology can contact Assistant Director of Innovation Transfer Marc Oettinger: [email protected].