Thousands of animal species threatened by climate change

 A novel analysis suggests more than 3,500 animal species are threatened by climate change and also sheds light on huge gaps in fully understanding the risk to the animal kingdom.

The study was published today in BioScience.

"We're at the start of an existential crisis for the Earth's wild animals," said Oregon State University's William Ripple, who led the study. "Up till now, the primary cause of biodiversity loss has been the twin threats of overexploitation and habitat alteration, but as climate change intensifies, we expect it to become a third major threat to the Earth's animals."

Ripple, distinguished professor of ecology in the OSU College of Forestry, and collaborators in the U.S. and Mexico used publicly available biodiversity datasets to examine animal data for 70,814 species from 35 existing classes. They categorized the species by class and climate change risks as assessed by the International Union for Conservation of Nature.

The researchers found that at least one-quarter of the species in six different classes are threatened by climate change; these classes include arachnids and chilopodans (centipedes) as well as anthozoans and hydrozoans (marine invertebrates related to jellyfish and corals). Smaller percentages of other classes' species are also directly at risk from a warming climate.

"We are particularly concerned about invertebrate animals in the ocean, which absorbs most of the heat from climate change," Ripple said. "Those animals are increasingly vulnerable because of their limited ability to move and promptly evade adverse conditions."

Sudden impacts on animal communities can take the form of mass mortality from extreme events like heat waves, wildfires, droughts and floods.

"The cascading effects of more and more mass mortality events will likely affect carbon cycle feedbacks and nutrient cycling," Ripple said. "Those effects also likely will have an impact on species interactions such as predation, competition, pollination and parasitism, which are vital for ecosystem function."

The 90% reduction in mollusk populations along Israel's coastline because of escalating water temperatures shows how susceptible invertebrates are, he said. Other examples include the deaths of billions of intertidal invertebrates during the 2021 Pacific Northwest heat dome, and the catastrophic die-off of corals across 29% of the Great Barrier Reef following a severe 2016 marine heat wave.

Mass mortalities have not been limited to invertebrates, Ripple notes. In 2015 and 2016, about 4 million common murres off the west coast of North America starved to death via an altered food web caused by an extreme marine heat wave.

The same heat wave caused a 71% decline in Pacific cod because of an increase in metabolic demand and a reduced prey base, and marine heat waves have likely played a role in the deaths of approximately 7,000 humpback whales in the North Pacific.

Further cause for concern, the authors note, is the comparatively small amount of information that's been gathered regarding climate change risk to wildlife. Most wildlife classes (66 of 101) have not yet had any species assessed by the IUCN, and the 70,814 species that have been assessed represent 5.5% of all described wildlife species alive today.

"Our analysis is meant to be a preliminary effort toward assessing climate risk to wildlife species," Ripple said. "Understanding the risk is crucial for making informed policy decisions. We need a global database on mass mortality events due to climate change for animal species in all ecosystems, and an acceleration in assessing currently ignored species."

The IUCN Red List of Threatened Species, he notes, has a bias toward vertebrates, which make up less than 6% of the Earth's named animal species.

"There is also a need for more frequent climate risk assessments of all species and better consideration of adaptive capacity," Ripple said. "We need the integration of biodiversity and climate change policy planning on a global scale."

Roger Worthington, an attorney in Bend, Oregon, provided partial funding for this study, which also included Christopher Wolf and Jillian Gregg of Terrestrial Ecosystem Research Associates and Erik Torres-Romero of the Biotechnology Engineering-Polytechnic University of Puebla in Puebla, Mexico.

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A step forward in treating serious genetic disorders prenatally

 Injecting medicine into the amniotic fluid staves off progression of spinal muscular atrophy in utero.

Evidence is mounting that clinicians can treat serious genetic disorders prenatally by injecting medicine into the amniotic fluid, thus preventing damage that begins in utero.

A UC San Francisco-led study found that delivering medicine for spinal muscular atrophy (SMA) via the amniotic fluid was safe, and it helped prevent damage to nerve cells in the spinal cord, a part of the central nervous system that is responsible for movement. One experiment was done in mice with SMA -- a neurodegenerative disease that causes muscular weakness, atrophy, and death if untreated. Another followed in sheep that did not have the disease, to demonstrate that the method is safe.

The therapy used molecules called antisense oligonucleotides, or ASOs, that can alter the expression of genes through interactions with RNA, which creates proteins. ASOs are currently given to babies and children with diseases that affect the nervous system, including SMA.

"Children with severe forms of SMA can have irreversible damage by the time they are born, and we wanted to see how we could treat as early as possible, in the least invasive way," said Tippi MacKenzie, MD, a fetal and pediatric surgeon at UCSF Benioff Children's Hospitals and a senior author of the study, which appears in Science Translational Medicine.

Previous research has shown that SMA can be diagnosed before birth, and that expression of the genes involved in the disorder can be manipulated prenatally. This is the first research on treatment for SMA via amniotic fluid -- a less invasive method than the other possible route via the umbilical vein.

One step closer to clinical trial

The researchers found that mice treated prenatally with ASOs fared better in terms of survival, motor function and motor neuron numbers than mice that were treated only after birth or were not treated. In sheep, they confirmed the safety of the treatment and its ability to reach the spinal cord and other organs in therapeutic concentrations via the amniotic fluid.

"This suggests we may be able to use amniotic fluid to deliver therapeutic RNA molecules for other severe, early-onset diseases that affect different areas of the body," MacKenzie said.

This is the first study to test the safety of prenatal administration of therapeutic ASOs in large animals, as well as how the medicine distributes throughout their bodies when injected. Previous studies have looked at intra-amniotic injection of ASOs in mice with Angelman and Usher syndromes.

To apply for FDA approval of a new drug application, researchers must show that the therapy corrects disease -- as happened with the mice in this study -- and that the ASOs were distributed throughout the body with acceptable levels of toxicity -- as happened with the sheep.

"With these results, we are one step closer to testing prenatally in humans an existing treatment for those diagnosed with the disease," MacKenzie said.

An inverse amniocentesis

If eventually approved, the procedure would be given during pregnancy, much like amniocentesis, in which amniotic fluid is collected to test for genetic or chromosomal abnormalities, said first author Beltran Borges, MD, a UCSF post-doctoral scholar and aspiring pediatric neurologist in MacKenzie's lab.

"This is sort of an inverse amniocentesis," Borges said. "Once translated to the clinic, it could be an outpatient procedure."

The researchers were tickled to see through fluorescence that, when the medicine was injected into the amniotic fluid, the fetuses swallowed and inhaled it, which then distributed it to other parts of the body including the lungs, intestines, brain, spinal cord -- and even the nose hairs.

"It is remarkable that you can inject something in the amniotic fluid and let it sit there, and over time a fetus swallows it or sniffs it in, and it gets to the brain and elsewhere," Borges said. "There are likely other routes of entry as well, including through the bloodstream."

The project was special because it brought different research efforts together, MacKenzie said. The sheep study was led by UCSF with significant help from UC Davis; the mouse research was done by colleagues at Johns Hopkins School of Medicine and Cold Spring Harbor Laboratory in New York. Scientists at Ionis and Biogen provided critical guidance, reagents, and experimental support.

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Controlling these 8 risk factors may eliminate early death risk for those with high blood pressure

 A new study led by researchers at Tulane University suggests that people with high blood pressure can significantly reduce -- and possibly eliminate -- their increased risk of premature death by controlling several key health risk factors at once.

The study, published in Precision Clinical Medicine, tracked more than 70,000 people with hypertension and over 224,000 without it, using data from the UK Biobank. Researchers followed participants for nearly 14 years to understand how managing these risk factors affected early mortality -- defined as dying before age 80.

The eight health risk factors evaluated in the study include: blood pressure, body mass index, waist circumference, LDL "bad" cholesterol, blood sugar, kidney function, smoking status and physical activity. Notably, researchers found that hypertensive patients who had addressed at least four of these risk factors had no greater risk of an early death than those without high blood pressure.

"Our study shows that controlling blood pressure is not the only way to treat hypertensive patients, because high blood pressure can affect these other factors," said corresponding author Dr. Lu Qi, HCA Regents Distinguished Chair and professor of epidemiology in the Celia Scott Weatherhead School of Public Health and Tropical Medicine at Tulane University. "By addressing the individual risk factors, we can help prevent early death for those with hypertension."

Hypertension, defined as a blood pressure of 130 mmHg or higher, is the leading preventable risk factor for premature death worldwide.

The study found that addressing each additional risk factor was associated with a 13% lower risk of early death, 12% lower risk of early death due to cancer and 21% lower risk of death due to cardiovascular disease, the leading cause of premature death globally.

"Optimal risk control" -- having 7 or more of the risk factors addressed -- was linked to 40% less risk of early death, 39% less risk of early death due to cancer and 53% less risk of early death due to cardiovascular disease.

"To our knowledge, this is the first study to explore the association between controlling joint risk factors and premature mortality in patients with hypertension," Qi said. "Importantly, we found that any hypertension-related excess risk of an early death could be entirely eliminated by addressing these risk factors."

Only 7% of hypertensive participants in the study had seven or more risk factors under control, highlighting a major opportunity for prevention. Researchers say the findings underscore the importance of personalized, multifaceted care -- not just prescribing medication for blood pressure, but addressing a broader range of health behaviors and conditions.

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Colonic inflammation explains missing link between obesity and beta-cell proliferation

 Researchers at the Tohoku University Graduate School of Medicine have uncovered a key primary step in the hepatic ERK pathway that leads to increased insulin production. While their previous work focused on aspects of the signaling pathway from the liver to the pancreas, this current study shows an even earlier step that begins in the colon when it is inflamed -- triggered by obesity. The present study revealed a novel role the gastrointestinal tract plays in regulating glucose homeostasis.

Insulin is a hormone produced by β-cells in the pancreas. You can think of insulin like a key that unlocks cells to let glucose enter from the blood, so it can be used as energy. However, individuals with obesity can become insulin resistant, which causes the pancreas to secrete more insulin to try to keep up. This occurs through an inter-organ neuronal signal relay originating in the hepatic ERK pathway. Due to the close relationship between obesity and the onset of diabetes, understanding this pathway in depth could help develop new ways to treat or prevent this condition.

"The goal of this study was to define how obesity in particular triggers this cascade," says Junta Imai (Tohoku University). "We theorized that it had to do with inflammation in the colon, since pro-inflammatory factors can play an excitatory role in the hepatic ERK pathway."

The researchers developed a thorough series of experiments to determine if colonic inflammation due to obesity could impact the hepatic ERK pathway. First, the research group analyzed mice without obesity that had been given a drug to cause inflammation in the colon. As a result, they found that simply causing inflammation in the colon activates the ERK pathway in the liver, stimulates the neuronal relay pathway, and increases the number of β-cells even in the mice without obesity. Next, by analyzing colons of mice in which obesity was induced by a high-calorie diet, it was found that colonic inflammation, along with both hepatic ERK pathway activation and increased β-cells, had occurred in these obese mice.

"An exciting finding was when we tried to treat the obese mice with colon inflammation by lowering their inflammation, it actually stopped the ERK pathway in the liver from activating," explains Imai. "Despite the fact the mouse was still obese, targeting colon inflammation was exactly what was needed to alter the ERK pathway."

This research unveils a missing link in the pathway, determining that the liver senses the state of obesity through colonic inflammation, and colonic inflammation serves as the first trigger of β-cell proliferation during obesity development. These achievements will lead to advancements in understanding the mechanism behind β-cells proliferation in order to maintain normal blood glucose levels. In addition, it is anticipated that this research may help progress the development of treatments and prevention methods for diabetes.

These findings were published in JCI Insight on May 8, 2025.This research was supported by the Japan Society of the Promotion of Science (JSPS) KAKENHI Grant-in-Aid for Scientific Research (23K24383, 22K19303, 20H05694); the Japan Science and Technology Agency (JST), Moonshot R&D (JPMJMS2023); and the Japan Agency for Medical Research and Development (AMED), AMED-PRIME (21gm6210002h0004).

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Adult-onset type 1 diabetes increases risk of cardiovascular disease and death

 A new study in the European Heart Journal shows that people who develop type 1 diabetes in adulthood have an increased risk of cardiovascular disease and death, and that those diagnosed later in life do not have a better prognosis than those diagnosed earlier. The study, conducted by researchers at Karolinska Institutet in Sweden, points to smoking, poor glucose control and obesity as the main risk factors.

Type 1 diabetes used to be called childhood diabetes but can start at any time during life. However, research on adult-onset type 1 diabetes is limited. The researchers behind the current study wanted to investigate the risk of cardiovascular disease and death in this group, particularly for those diagnosed after the age of 40.

The registry-based study identified 10 184 people diagnosed with type 1 diabetes in adulthood between 2001 and 2020 and compared them to 509 172 matched people in the control group.

The study shows that these people with adult-onset type 1 diabetes had a higher risk of cardiovascular disease and death from all causes, including cancer and infections, compared to the control group.

"The main reasons for the poor prognosis are smoking, overweight/obesity and poor glucose control. We found that they were less likely to use assistive devices, such as insulin pumps," says first author Yuxia Wei, postdoctoral fellow at the Institute of Environmental Medicine, Karolinska Institutet.

The results emphasise the seriousness of type 1 diabetes, even when it starts later in life, the researchers say.

"But we show that the prognosis can be significantly improved by preventing smoking and obesity and improving glucose control, not least in people diagnosed at older ages," explains senior author Sofia Carlsson, senior lecturer and associate professor at the same department.

The researchers plan to continue investigating adult-onset type 1 diabetes, including risk factors for developing the disease and the prognosis of other outcomes, such as microvascular complications. Optimal treatment in adult-onset type 1 diabetes, including the effect of pump use and other advanced technologies, also needs to be explored.

"We hope to shed light on these issues in the coming years," concludes Sofia Carlsson.

The study was funded by the Swedish Research Council and the Swedish Diabetes Foundation, among others. The researchers report no conflicts of interest.

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Can the brain be targeted to treat type 2 diabetes?

 Successfully treating type 2 diabetes may involve focusing on brain neurons, rather than simply concentrating on obesity or insulin resistance, according to a study published today in the Journal of Clinical Investigation.

For several years, researchers have known that hyperactivity of a subset of neurons located in the hypothalamus, called AgRP neurons, is common in mice with diabetes.

"These neurons are playing an outsized role in hyperglycemia and type 2 diabetes," said UW Medicine endocrinologist Dr. Michael Schwartz, corresponding author of the paper.

To determine if these neurons contribute to elevated blood sugar in diabetic mice, researchers employed a widely used viral genetics approach to make AgRP neurons express tetanus toxin, which prevents the neurons from communicating with other neurons.

Unexpectedly, this intervention normalized high blood sugar for months, despite having no effect on body weight or food consumption.

Conventional wisdom is that diabetes, particularly type 2 diabetes, stems from a combination of genetic predisposition and lifestyle factors, including obesity, lack of physical activity and poor diet. This mix of factors leads to insulin resistance or insufficient insulin production.

Until now, scientists have traditionally thought the brain doesn't play a role in type 2 diabetes, according to Schwartz.

he paper challenges this and is a "departure from the conventional wisdom of what causes diabetes," he said.

The new findings align with studies published by the same scientists showing that injection of a peptide called FGF1 directly into the brain also causes diabetes remission in mice. This effect was subsequently shown to involve sustained inhibition of AgRP neurons.

Together, the data suggest that, while these neurons are important for controlling blood sugar in diabetes, they don't play a major role in causing obesity in these mice, the researchers noted in their report.

In other words, targeting these neurons may not reverse obesity, even as it causes diabetes to go into remission, Schwartz explained.

More research is needed on how to regulate activity in these neurons, and how they become hyperactive in the first place, he said. Once these questions are answered, Schwartz said that a therapeutic approach might then be developed to calm them down.

This approach could represent a shift in how clinicians understand and treat this chronic disease, Schwartz said. He noted, for instance, that Ozempic and other new drugs used to treat type 2 diabetes are also able to inhibit AgRP neurons.

The extent to which this effect contributes to the antidiabetic action of these drugs is unknown. Further research might help scientists to better understand the role of AgRP neurons in how the body normally controls blood sugar, and to ultimately translate these findings into human clinical trials, he added.

Schwartz holds the UW Robert H. Williams Endowed Chair in Medicine and is a UW professor of medicine, Division of Metabolism, Endocrinology and Nutrition, and an adjunct professor of laboratory medicine and pathology. He is also the founding director of the UW Medicine Diabetes and Obesity Center of Excellence.

This work was supported by National Institutes of Health grants (DK083042, DK101997, DK089056, DK124238 S10OD036208, DK114474, DK128383, DoD W81XWH2110635 and P30 DK089507); the NIH-NIDDK funded Nutrition Obesity Research Center (P30DK035816); Diabetes Research Center (P30DK017047) and Diabetes, Obesity and Metabolism Training Grant (T32 DK007247; CLF) at the University of Washington; a Department of Defense grant (W81XWH2110635); and a research agreement between Schwartz and Novo Nordisk, and the Cystic Fibrosis Foundation (SINGH19R0 and SINGH24R0).

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Scientists discover key gene impacts liver energy storage, affecting metabolic disease risk

 A new study published in Science Advances reveals that a single gene plays a big role in how the liver stores energy, a process that's critical for overall health and for managing diseases like type 2 diabetes. Led by Penn Nursing's Kate Townsend Creasy, PhD, Assistant Professor of Nutrition Science in the Department of Biobehavioral Health Sciences, the research focuses on the PPP1R3B gene. This gene tells the liver how to handle energy: store it as glycogen (a form of sugar) or triglycerides (a type of fat).

The research team found that when the PPP1R3B gene is more active, the liver tends to store more energy as glycogen.

The liver stores more energy as fat when the gene is less active.

This shift between glycogen and fat storage is crucial because it affects how the body manages blood sugar and fat levels.

Large scale genomics studies in humans have reported that mutations in the PPP1R3B gene are associated with several metabolic conditions, including type 2 diabetes and fatty liver disease.

However, it was unclear how the gene was involved in these conditions.

"Our research shows that PPP1R3B is like a control switch in the liver," said Creasy.

"It directs whether the liver stores energy for quick use in the form of glycogen or for longer-term storage as fat. We also saw changes in how efficiently mice and cells with genetic manipulations of PPP1R3B could use either glucose or fat for energy. This discovery could help us find new ways to help people with metabolic diseases with precision nutrition approaches, based on their genetics."

Co-authors from the Perelman School of Medicine include: Minal B. Mehta, Joseph Park, David Zhang, and Swapnil V. Shewale (all based in the Department of Genetics), Carolin V. Schneider (Division of Translational Medicine and Human Genetics), John S. Millar (Institute for Diabetes, Obesity, and Metabolism), Marijana Vujkovic (Division of Translational Medicine and Human Genetics and the Institute for Diabetes, Obesity, and Metabolism), Nicholas J. Hand (Department of Physiology), Paul M. Titchenell (Institute for Diabetes, Obesity, and Metabolism and the Department of Physiology), Joseph A. Baur (Institute for Diabetes, Obesity, and Metabolism and the Department of Physiology), and Daniel J. Rader (Division of Translational Medicine and Human Genetics in the Department of Genetics, and the Institute for Diabetes, Obesity, and Metabolism). The National Institutes of Health supported this research.

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Medical myths: Vegetarian and vegan diets

 Following a plant-based diet is becoming increasingly popular. While this is widely regarded as a healthful choice, many myths abound. In this edition of Medical Myths, we dig into the details.

Until fairly recently, vegetarianism was generally considered a fringe lifestyle choice in the United States, and veganism even more so. Anything on the fringes of society tends to inadvertently encourage myths and misconceptions.

Also, deciding to avoid animal products sparks rage in some people. This anger manifests for a range of reasons, which are beyond the scope of this article and discussed in full here. Suffice it to say that if a sizable group of the population is against something, conditions are ripe for myths and half-truths.

Overall, vegetarianism and veganism are misunderstood. As today is World Vegan Day, it seems an appropriate time to address some of the most common myths.

1. Plant-based diets are always healthful

In recent decades, an increasing number of studies have demonstrated links between red meat consumption and poorer health outcomes. For instance, processed and red meat intake is associated with colon cancerTrusted Source, obesityTrusted Source, heart diseaseTrusted Source, and diabetesTrusted Source.

This might suggest that a diet without meat is better for the body. But, just as not all meat is red, not all vegetarian or vegan diets are healthful.

To use an extreme example, if an individual only ate potato chips, they would be vegan, but certainly not brimming with vitality, energy, and health.

As with any other diet, it depends entirely on what an individual consumes.

Additionally, lean white meat and fish are not associated with the same health issues as processed and red meats.

And certain meat substitute products can be high in salt. In 2018, Action on Salt, a “group concerned with salt and its effects on health,” carried out a survey of meat substitutes.

They investigated products from several major retailers in the United Kingdom. When they looked at burgers, they found that the average salt content of beef burgers was 0.75 grams (g), compared with 0.89 g for vegetarian burgers, including bean burgers. According to their findings, a veggie burger has “more salt than a large portion of McDonald’s fries.”

2. Vegetarianism guarantees weight loss

Sadly, no. As the section above makes clear, not all vegetarian and vegan diets are equally healthful. It is incredibly easy to consume thousands of calories each day without any of them being associated with animals.

The key to weight loss is a healthful diet and regular exercise, and neither requires the avoidance of animal products.

It is still worth noting, though, the evidence that following a plant-based diet is associated with weight loss. For instance, a review published in Translational PsychiatryTrusted Source explains:

“We found robust evidence for short- to moderate-term beneficial effects of plant-based diets versus conventional diets […] on weight status, energy metabolism, and systemic inflammation.”

This finding held true for healthy participants, people with obesity, and individuals with type 2 diabetes.

To give another example, another review, published in BMJ Open Diabetes Research and Care, looked at the impact of plant-based diets on people with diabetes. Among other benefits, the authors found that these diets were associated with a “significant improvement” in weight.

3. Vegetarians and vegans cannot get enough protein

This is perhaps the most common of all the myths that we cover today. But it is still a mythTrusted Source. In the world of food, protein abounds.

For people who eat them, dairy products and eggs are high in protein. Vegans also have an array of options, including seitan, tofu, lentils, chickpeas, many types of bean, spelt, spirulina, quinoa, oats, wild rice, seeds, and nuts.

Even some vegetables contain protein, including spinach, asparagus, broccoli, artichokes, potatoes, peas, brussels sprouts, and sweet potatoes.

4. You can’t build muscle without meat

This myth follows on from the protein myth above. In short, the most important nutrient for building muscle is protein, which can easily be found in abundance beyond the animal kingdom.

5. Dairy is essential for strong bones

Dairy is not essential for strong bones, but calcium is. In fact, calcium is important for a number of bodily functions, including maintaining blood pressure, muscle contraction, transmitting signals along nerves, and blood clotting.

Vegans, therefore, need to ensure that they take in enough calcium from plant-based sources.

As with protein, there are plenty of places to pick up calcium, including soy-based foods, beans, lentils, peas, spinach, turnips, figs, flax, chia, sesame seeds, seaweed, and some nuts — almondsTrusted Source, in particular.

6. You cannot get B12 from a vegetarian diet

This is a myth. While vegans often take B12 supplements to ensure that they have adequate levels, vegetarians have a wealth of other options.

Vegetarians can derive B12 from eggs and milk products, including cheese.

Meanwhile, a range of vegan-friendly foods are fortified with B12, including some cereals, tofu, nondairy milks, and spreads.

B12: An interesting aside

Cows need B12, too, and they rely on gut bacteria to produce it.

To produce B12, gut bacteria need cobalt, which a cow normally derives from grazing. However, many cows destined to become meat only spend the beginning of their lives in pasture before being brought inside where they are fed on grain.

Because of this unnatural diet, their gut bacteria are starved of cobalt and cannot produce B12.

But the cow still needs B12 to thrive, so farmers must provide them with either cobalt or B12 supplements.

So even a staunch, dyed-in-the-wool red meat fanatic is likely to derive their B12 from supplements — but in their case, it’s via a cow.

7. Soy increases the risk of breast cancer

As it stands, there is no convincing evidence that eating soy-based foods increases the risk of breast cancer in humans.

This misunderstanding might stem from earlier studiesTrusted Source in rodents. Scientists showed that when these animals received large amounts of soy compounds called isoflavones, they were more likely to develop breast cancer. However, humans process soy differently from rodents.

A study published in February 2020 searched for associations between soy, dairy intake, and breast cancer risk. The scientists had followed 52,795 cancer-free women in the U.S. for an average of 7.9 years.

They found no clear association between soy intake and breast cancer, but they did identify a link between dairy milk and breast cancer.

However, the full picture is, perhaps, slightly more complex. Some women use soy-based supplements as a natural alternative to hormone therapy during menopause. One large studyTrusted Source investigated whether these supplements might be associated with breast cancer risk.

The researchers found “no association between past use of soy supplements and breast cancer.” But, they also found that taking soy supplements, for some women, might increase the risk of breast cancer, particularly for those with a family history.

Overall, as the American Cancer SocietyTrusted Source explain:

“The evidence does not point to any dangers from eating soy in people, and the health benefits appear to outweigh any potential risk. In fact, there is growing evidence that eating traditional soy foods […] may lower the risk of breast cancer, especially among Asian women.”

8. Pregnant people need meat and dairy

During pregnancy, it is important to take in all the nutrients that a growing baby needs. But, as we have seen along the way, plant-based foods can provide the vast majority of them.

Someone who is vegetarian or vegan may need to do a little extra planning to be sure that have enough nutrients, especially at the beginning of pregnancy.

As we mentioned above, it is importantTrusted Source to ensure an adequate intake of vitamin B12, through supplements or fortified foods, and this is especially true during pregnancy and breastfeeding. The American Dietetic Association recommend vitamin B12 supplementation throughout pregnancy and breastfeeding for people with vegan or vegetarian diets.

As the authors of a reviewTrusted Source of research about plant-based diets during pregnancy explain, “The available evidence shows that well-planned vegetarian and vegan diets may be considered safe during pregnancy and lactation, but they require a strong awareness for a balanced intake of key nutrients.”

For people considering plant-based diets, Medical News Today have published useful guides to vegetarian and vegan eating. For anyone with a preexisting condition, it might also be worth discussing the change with a doctor.

Source - Medical news Today

Health misinformation and disinformation: How to avoid it

 In the age of viral content and fast and furious social media communication, disinformation and misinformation, including about health matters, are spreading more widely than ever. Why is this the case exactly, and how can we learn to spot inaccurate and even malicious health information? Why do we fall so easily for false health info, and how can we update our mistaken beliefs? These are some of the questions this episode aims to answer.

Nowadays, thanks to the widespread availability of internet access, almost any piece of information we may want is just one click away. While this is generally a positive development, it can also mean that we become exposed to untrustworthy, unchecked information on any topic, including health.

According to a report issued by the International Panel on the Information Environment (IPIE) in 2024, communication experts are currently most concerned “about the threats to the information environment posed by the owners of social media platforms.”

Such platforms regularly circulate a varied array of videos, articles, and posts on topics including health. However, in the absence of strict rules and regulations around the information shared on social media, there is a clear danger that at least some of what we see being shared online amounts to misinformation or even disinformation.

Misinformation occurs when communication is laden with inaccuracies, either because the original information was misinterpreted or misunderstood or because someone picked up a piece of erroneous information by mistake and kept sharing it.

Disinformation is an even more concerning phenomenon. It occurs when a bad actor disseminates fake information on purpose, manipulating their audience to support a hidden agenda.

In this episode of In Conversation, we look at why health misinformation and disinformation spread, how we can identify mis- and disinformation, and what it takes for people to update their views after they have assimilated incorrect information.

Our special guest is Prof. Stephan Lewandowsky, PhD, Chair in Cognitive Psychology at the School of Psychological Science, University of Bristol, United Kingdom, and Project Lead of PRODEMINFO (Protecting the Democratic Information Space in Europe) at Potsdam University in Germany.

Prof. Lewandowsky is a cognitive scientist with an interest in computational modeling who has extensively studied decision-making processes, the persistence of misinformation in society, the ways in which myths and misinformation can spread, and how people update their memories if the notions they believe in turn out to be false.

We also hear from our trusted expert, Jenny Yu, MD, FACS, Chief Health Officer at RVO Health, the parent company of Medical News Today and Healthline. Dr. Yu advises on key strategies to ensure we are accessing the most accurate and trustworthy sources of health information.

Please listen to our podcast episode in full below or on your preferred streaming platform.

Source - Medical News Today

Could eating chicken heighten cancer risk? Experts weigh in on latest claims

 

• A recent study found that eating 300 grams of poultry per week was linked to an increased risk of gastrointestinal cancer and death from all causes.
• The findings have caused concern among consumers as they challenge traditional beliefs that poultry such as chicken and turkey is a healthier choice of protein.
• Medical News Today speaks to experts to investigate whether these findings lack nuance or whether there is a genuine need for more caution regarding diets and cancer risk.

A recent study conducted in southern Italy presented some surprising findings that linked the regular consumption of poultry to potential increases in gastrointestinal cancers and all-cause mortality. This has caused one question to arise — is eating chicken really as healthy as we think it is?

The study’s findings indicated that exceeding the weekly recommended amounts — that is, eating more than 300 grams (g) of poultry, such as chicken and turkey, per week — resulted in a 27% higher risk of all-cause mortality compared to eating moderate amounts.

Moreover, the research suggested that higher poultry intake was linked to a 2.3% increase in the risk of gastrointestinal cancers, with a higher observed risk among men at 2.6%. The findings were published in the journal Nutrients.

What has concerned consumers is that these findings contrast with current established dietary guidelines, such as the Mediterranean diet, of which poultry is an important component.

However, should such results make people reconsider their diets? Could the results be overestimated? What should consumers watch out for when interpreting the results of similar studies on nutrition?

Medical News Today spoke to two experts — Wael Harb, MD, board certified hematologist and medical oncologist at MemorialCare Cancer Institute at Orange Coast and Saddleback Medical Centers in Orange County, CA, and Kristin Kirkpatrick, MS, RD, dietitian at the Cleveland Clinic Dept of Department of Wellness & Preventive Medicine in Cleveland, OH, and senior fellow at the Meadows Behavioral Healthcare in Wickenburg, AZ, to find out more.

Causation vs. correlation when interpreting findings

Both experts reiterated that an association from an observational study is not enough to draw definitive conclusions about a dietary item and its links to cancer.

“The findings are interesting, but as this is an observational study, it doesn’t prove causation. The broader body of evidence still supports moderate poultry consumption as part of a balanced diet,” Harb told MNT.

Harb underscored that poultry played an important role in healthy diets and advised caution when interpreting the results.

“This study raises important questions, but we need to interpret it with caution. Poultry has long been a core part of healthy eating patterns like the Mediterranean diet, which is associated with reduced cancer and heart disease risks.”
— Wael Harb, MD

Another important point to consider is that cancer, as a disease, is very complex and multifactorial, meaning it is hard to pinpoint its causes to one factor.

“Studies show that the development of cancer from one person to another is complex and encompasses multiple factors, including but not limited to genetics, environment, diet, physical activity, exposure to toxins, and even age and inflammation. Therefore, we need to look at any study and try to assess how it can be translated to our lifestyle,” said Kirkpatrick.

“If you smoke, for example, the first step before cutting chicken out may be quitting smoking. This is just one example of how we can assess data,” she added.

Is it the poultry itself or the additives causing cancer?

How food items are cooked or whether other additives such as oils and spices are added can change the ‘healthiness’ of a food source. The two experts said the potential cancer risks associated with eating poultry could be more closely connected to those aspects, rather than the poultry itself.

“When poultry is grilled, fried, or cooked at high temperatures, it can form compounds like heterocyclic amines (HCAs) and polycyclic aromatic hydrocarbons (PAHs), which have been linked to cancer risk. However, these compounds also occur in red meat and processed meats, so the issue may lie more in cooking methods than the type of meat itself,” Harb explained, highlighting that how a good is cooked could result in the release of cancer-causing chemicals.

Kirkpatrick further explained how a food item is processed and cooked can impact the potential benefits or risks of consuming it.

“For example, a frozen chicken nugget may be considered ultra-processed, and breaded and fried chicken may pose risksTrusted Source from the process of high-heat frying as well. Both may differ in their impact on health when compared to a plain chicken breast that is baked,” she said.

White vs. red meat: Which is healthier?

The study has also fed into a long-standing debate about whether white meat is healthier than red meat.

Although white meat, such as chicken and turkey, has lower fat content and a higher protein-to-fat ratio than red meat, this does not necessarily translate into lower cholesterol levels.

In fact, a 2019 study found that white and red meat may both have similar effects on blood cholesterol levels, specifically LDL or “bad” cholesterol and apolipoprotein B (apoB).

The current study also fails to identify the specific type of poultry consumed and its links to heightened cancer risk.

“The study was not able to identify the specific type of poultry (for example, was the consumed protein processed deli meat or was it a grilled chicken breast). The processing of meats in general may change their health risks. We would need more studies assessing various types of poultry and various types of red meat to truly assess significant differences between the two,” Kirkpatrick said.

What should future studies on food and cancer investigate?

The study did have several limitations, such as not accounting for the sources of the poultry consumed, the potential impacts of pesticides on plant and animal crops, antibiotic and hormone usage in industrially raised poultry, as well as cooking methods, meat preparation, and dietary patterns.

“Limitations the authors cited was lacking information on specifics of the poultry consumed/ cooking methods, as well as lack of data on physical activity — which shows positive impact to mortality from other studies,” Kirkpatrick said.

Harb said that the type of follow-up research needed would have to address multiple unanswered questions.

“We need well-designed prospective studies that account for cooking methods, levels of processing, and overall dietary habits. It would also help to examine biological markers of carcinogen exposure in people with high poultry intake. Given that the risk was higher in men, gender-specific research would be important too,” he said.

How much poultry is it safe to eat per week?

Kirkpatrick said that these results are not enough to change current recommendations for healthy eating.

“This study would not cause me to stop recommending poultry to my patients, especially in those patients that are making other beneficial lifestyle changes alongside poultry consumption — such as a dietary pattern high in fruits, vegetables, fiber, whole grains, healthy fats, and other forms of protein such as beans and lentils, or wild fatty fish,” she told us.

Regarding what is considered healthy and safe by the United States, Harb reminded that current guidelines recommend no more than 300 g per week as a limit.

“Based on what we know, the current guideline of 300 grams of poultry per week is reasonable — especially if the poultry is skinless, minimally processed, and not cooked at high temperatures.”
— Wael Harb, MD

However, for those with certain health conditions or a family history of cancer, a lower intake may be more appropriate.

“For those who are particularly health-conscious or have a family history of cancer, staying closer to 200 grams per week and incorporating more fish, legumes, and plant proteins may be a prudent option,” Harb said.

Source - Medical News Today