Category: 8. Health

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.”

Reference: Hunter B, Zhang Y, Harney D, et al. Left ventricular myocardial molecular profile of human diabetic ischaemic cardiomyopathy. EMBO Mol Med. 2025:1-42. doi: 10.1038/s44321-025-00281-9

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Caffeine and other common substances can influence bacterial defenses, reducing the effectiveness of some antibiotics.

Compounds found in our daily diets, including caffeine, can influence how bacteria respond to antibiotics. This conclusion comes from a new study led by Professor Ana Rita Brochado and her team at the Universities of Tübingen and Würzburg.

The researchers showed that bacteria such as Escherichia coli (E. coli) use complex regulatory networks to detect chemical cues from their surroundings, and these responses can alter the effectiveness of antimicrobial drugs.

To explore this effect, the team conducted a systematic screen of 94 substances, including antibiotics, prescription medicines, and dietary ingredients. They examined how these compounds influenced the activity of key genetic regulators and transport proteins in E. coli, a bacterium that can cause disease.

Transport proteins act as channels and pumps in the bacterial membrane, controlling the flow of substances into and out of the cell. Because bacterial survival depends on maintaining a precise balance in these transport systems, changes in regulation can have major consequences.

Antagonistic interaction with caffeine

“Our data show that several substances can subtly but systematically influence gene regulation in bacteria,” says PhD student Christoph Binsfeld, first author of the study. The findings suggest even everyday substances without a direct antimicrobial effect – e.g. caffeinated drinks – can impact certain gene regulators that control transport proteins, thereby changing what enters and leaves the bacterium.

“Caffeine triggers a cascade of events starting with the gene regulator Rob and culminating in the change of several transport proteins in E. coli – which in turn leads to a reduced uptake of antibiotics such as ciprofloxacin,” explains Ana Rita Brochado.

This results in caffeine weakening the effect of this antibiotic. The researchers describe this phenomenon as an ‘antagonistic interaction.’

Broader implications for antibiotic treatment

Interestingly, this weakening effect was not observed in Salmonella enterica, a close relative of E. coli. This indicates that even related bacterial species may react differently to the same environmental cues, likely due to variations in transport pathways or their role in drug uptake. President Prof. Dr. Dr. h.c. (Dōshisha) Karla Pollmann remarks: “Such fundamental research into the effect of substances consumed on a daily basis underscores the vital role of science in understanding and resolving real-world problems.”

The study, which has been published in the scientific journal PLOS Biology, makes an important contribution to the understanding of what is called ‘low-level’ antibiotic resistance, which is not due to classic resistance genes, but to regulation and environmental adaptation. This could have implications for future therapeutic approaches, including what is taken during treatment and in what amount, and whether another drug or food ingredient – should be given greater consideration.

Reference: “Systematic screen uncovers regulator contributions to chemical cues in Escherichia coli” by Christoph Binsfeld, Roberto Olayo-Alarcon, Lucía Pérez Jiménez, Morgane Wartel, Mara Stadler, André Mateus, Christian Müller and Ana Rita Brochado, 22 July 2025, PLOS Biology.
DOI: 10.1371/journal.pbio.3003260

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Researchers at MUSC Hollings Cancer Center have discovered a potentially powerful weapon in the fight against head and neck cancers. The new drug, still in preclinical studies, attacks cancer cells from within by damaging their mitochondria, the cells’ energy factories.

The study, published in Cancer Research, was led by Besim Ogretmen, PhD, associate director of Basic Science at Hollings and director of Hollings’ Lipidomics Shared Resource.

The multidisciplinary research team aimed to suppress tumor growth in head and neck squamous cell carcinoma, a cancer that develops in the cells lining the head and neck, such as the nose, mouth and throat. This highly aggressive form of cancer is treatment resistant, and a significant number of patients who receive standard care see their cancer return. Even when effective, these standard treatments can have broad impacts, killing noncancerous as well as cancerous cells and triggering debilitating side effects.

To overcome these issues, the researchers developed and tested a new compound called LCL768. LCL768 is a synthetic form of ceramide, a fat molecule naturally found in cells.

Ceramides are important for healthy cell function and have been shown to induce cell death under stress. Many head and neck cancers are low in this helpful fat, which relates to poorer outcomes in patients and contributes to the tumors’ aggressive growth.

The drug’s actions hinged on its ability to increase levels of a specific ceramide called C18-ceramide inside the mitochondria of cancer cells. When C18 levels increased, it set off a process called mitophagy, by which cells remove damaged or unnecessary mitochondria. Cancer cells’ growth relies heavily on mitochondria, and when they are destroyed, the cancer cells run out of energy and die.

“LCL768 essentially cuts off the power supply to cancer cells,” Ogretmen said. “Once their mitochondria are gone, the cells can no longer grow or survive.”

In addition to breaking down mitochondria, LCL768 disrupted a key metabolic pathway. It did so by blocking fumarate, an important molecule in the cell’s energy cycle. Without fumarate, cancer cells were further impaired in their energy production. Together, the combination of C18-ceramide buildup and fumarate depletion created a dual attack that induced cancer cell death.

“Our results reveal a metabolic weakness in these cancer cells,” Ogretmen explained. “By triggering mitophagy and depleting fumarate, LCL768 shut down cancer cell survival mechanisms on two fronts, targeting both their mitochondria and metabolism.”

The team tested LCL768 in mouse models of head and neck cancer and lab-grown tumors made from actual patient tissue. In both cases, the drug led to a significant increase in mitochondrial C18-ceramide.

After treatment, cancer cells showed clear signs of mitophagy and metabolic collapse, which led to slowed tumor growth. In support of this finding, providing the cells with fumarate almost completely reversed the inhibitory effects of LCL768 and led the tumors to regrow rapidly.

The researchers highlight LCL768 as a potential new way of targeting a vulnerability in head and neck cancers. What makes this approach unique is its efficiency – LCL768 both builds up tumor-killing ceramide and disrupts a key part of cancer cell metabolism. Importantly, the drug had little effect on healthy tissues, suggesting it may offer a safer alternative to chemotherapy and radiation.

“This precise targeting could lead to fewer side effects than chemotherapy or radiation, which often damage healthy cells as well as cancer cells,” Ogretmen said. “The new drug homes in on a process cancer cells use to avoid normal cell death. Because healthy cells do not rely as heavily on these pathways, they are left mostly untouched.”

The researchers are optimistic that the results could open new doors in cancer therapy, especially for tumors resistant to standard treatments. Reduced ceramide is a hallmark of many cancers, and boosting its levels via compounds like LCL768 could be part of a new class of treatments designed to target the metabolism and stress system of tumor cells.

“These findings represent a new frontier in cancer therapy,” Ogretmen said. “We’re not only targeting cancer cells, we’re dismantling their internal infrastructure and exploiting a fundamental weakness in how those cells manage energy and stress. That could make this treatment useful for a range of tumors.”

Although LCL768 is still in preclinical testing, meaning it hasn’t yet been used with patients, the early results are promising. The team is now working to advance LCL768 toward clinical trials, with the hope that the novel approach may one day offer a lifeline to patients with hard-to-treat cancers.

“This research lays the foundation for developing a new class of anti-cancer agents that exploit mitochondrial vulnerability,” Ogretmen said. “We are exploring how to optimize this approach for clinical use so that LCL768 or drugs like it could one day offer a safe, effective option for cancer patients who currently have few available treatments.”

Reference: Oleinik NV, Atilgan FC, Kassir MF, et al. Ceramide-induced metabolic stress depletes fumarate and drives mitophagy to mediate tumor suppression. Cancer Res. 2025;85(17):3313-3334. doi: 10.1158/0008-5472.CAN-24-4042

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This breakthrough uncovers a potentially powerful new therapeutic option, with further work ongoing to delineate the specifics.

Macrophages are a type of white blood cell with several high-profile roles in our immune system. They patrol around the body, surveying for bugs and viruses, as well as disposing of dead and damaged cells, and stimulating other immune cells – kicking them into gear when and where they are needed.

However, their actions can also drive local inflammation in the body, which can sometimes get out of control and become problematic, causing more damage to the body than repair. This is present in lots of different diseases, highlighting the need to regulate macrophages for improved patient outcomes. 

In the new study, just published in the international journal Cell Reports Physical Science, the Trinity team worked with human macrophages isolated from heathy donor blood samples provided via the Irish Blood Transfusion Board, St James’s Hospital. They stimulated these cells using a custom bioreactor to apply electrical currents and measured what happened.

“We have known for a very long time that the immune system is vital for repairing damage in our body and that macrophages play a central role in fighting infection and guiding tissue repair,” said Dr Sinead O’Rourke, Research Fellow in Trinity’s School of Biochemistry and Immunology, and first author of the research article. 

“As a result, many scientists are exploring ways to ‘reprogramme’ macrophages to encourage faster, more effective healing in disease and to limit the unwanted side-effects that come with overly aggressive inflammation. And while there is growing evidence that electrical stimulation may help control how different cells behave during wound healing, very little was known about how it affects human macrophages prior to this work.”

“We are really excited by the findings. Not only does this study show for the first time that electrical stimulation can shift human macrophages to suppress inflammation, we have also demonstrated increased ability of macrophages to repair tissue, supporting electrical stimulation as an exciting new therapy to boost the body’s own repair processes in a huge range of different injury and disease situations.”

The findings from the interdisciplinary team led by Trinity investigators, Professor Aisling Dunne (School of Biochemistry and Immunology) and Professor Michael Monaghan (School of Engineering) are especially significant given that this work was performed with human blood cells (showing its effectiveness for real patients); electrical stimulation is relatively safe and easy in the scheme of therapeutic options; and the outcomes should be applicable to a wide range of scenarios.

Corresponding author Prof. Monaghan added: “Among the future steps are to explore more advanced regimes of electrical stimulation to generate more precise and prolonged effects on inflammatory cells and to explore new materials and modalities of delivering electric fields. This concept has yielded compelling effects in vitro and has huge potential in a wide range of inflammatory diseases.”

Reference: O’Rourke SA, Suku M, Petrousek S, Hoey DA, Dunne A, Monaghan MG. Electromodulation of human monocyte-derived macrophages drives a regenerative phenotype and impedes inflammation. Cell Rep Phys Sci. 2025:102795. doi: 10.1016/j.xcrp.2025.102795

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Dr. Karen Zaghiyan, a prominent colorectal surgeon at Cedars-Sinai in Los Angeles, recently shared vital advice on bowel cancer in a widely viewed Instagram video. She offers straightforward guidance for anyone concerned about or diagnosed with colorectal cancer. Dr. Zaghiyan stresses the life-saving importance of early screening, particularly colonoscopies, and urges patients to seek second opinions to ensure accurate diagnoses. She warns against unverified remedies and emphasizes taking prompt, informed action when symptoms arise. Her advice highlights how timely medical decisions can dramatically improve outcomes, highlighting the critical role of awareness, professional consultation, and early intervention in combating colorectal cancer.

5 hard truths about colon cancer

1. Get a colonoscopy early

Dr. Zaghiyan stresses that everyone should begin colorectal cancer screening at age 45, even if they feel healthy or have no family history. Colonoscopies allow doctors to visually inspect the entire colon and remove precancerous polyps before they develop into cancer. Unlike at-home stool tests, which can miss a significant number of polyps, colonoscopies are more than 95% effective at detecting and preventing colorectal cancer. Proper preparation, including dietary adjustments and the use of laxatives, is essential for an accurate examination. Patients should also plan for post-procedure transport due to sedation. Starting screenings early can dramatically increase the chances of detecting cancer at a curable stage.

2. Take screening and diagnosis seriously

Early detection is critical in improving survival rates for colorectal cancer patients. Dr. Zaghiyan notes that patients diagnosed at stage one have around a 90% chance of surviving at least five years, while those diagnosed at stage four have only a 10% five-year survival rate. Symptoms like rectal bleeding, changes in bowel habits, abdominal pain, fatigue, or unexplained weight loss should never be ignored. Delaying medical attention or dismissing these signs as minor issues can allow the disease to progress, making treatment far more complicated and reducing the likelihood of a positive outcome. Taking diagnosis and screening seriously can be the difference between life and death.

3. Seek second opinions

Dr. Zaghiyan strongly recommends getting a second opinion for any diagnosis or if symptoms are concerning. Misdiagnoses are not uncommon, and consulting multiple experts ensures that patients receive the most accurate assessment and treatment plan. For instance, rectal bleeding might be incorrectly attributed to hemorrhoids without proper examination. Patients should feel empowered to ask questions, challenge their care plans, and consult additional specialists if necessary. Taking the extra step to verify your diagnosis can prevent mistakes and provide access to the latest treatment options, potentially saving lives.

4. Avoid unverified remedies

Online advice and alternative treatments can be misleading or harmful. Dr. Zaghiyan warns against trusting unproven cures, such as extreme diets, supplements, or home remedies promoted online. Instead, patients should rely on evidence-based medical treatments and consult registered cancer dietitians to safely complement conventional therapy. For those seeking innovative approaches, enrolling in clinical trials with rigorous oversight is far safer than following anecdotal or unverified claims. Sticking to verified medical advice increases the likelihood of successful treatment and minimizes unnecessary risk.

5. Act timely and follow medical guidance

Delaying treatment is one of the most dangerous decisions a patient can make. Dr. Zaghiyan emphasizes that once concerning symptoms appear or a diagnosis is confirmed, timely action can mean the difference between curable and advanced disease. Following your doctor’s recommendations without unnecessary delay, adhering to medication schedules, and attending follow-up appointments is crucial. Patients should avoid waiting to “see if it goes away” and instead act promptly, as early intervention substantially increases survival chances.

Symptoms and risks of colon cancer

Colorectal cancer often develops silently, showing few or no symptoms in its early stages. Being aware of both warning signs and risk factors is crucial, as early detection can dramatically improve survival rates. Individuals should pay attention to changes in their digestive health and seek prompt medical evaluation if they notice unusual patterns or persistent discomfort.Common symptoms:

Risk factors:

Disclaimer: This article is for informational purposes only and does not constitute medical advice. Always consult a qualified healthcare professional before making any changes to your health routine or treatment.

Researchers at the Icahn School of Medicine at Mount Sinai have identified three monoclonal antibodies against monkeypox (also commonly referred to as mpox) that block viral spread and protect against severe disease. The findings provide a potential basis for developing targeted therapies for orthopoxvirus infections.

The findings, published in Cell, reveal that the antibodies – isolated from an individual previously infected with mpox – target a protein called A35. In laboratory studies, the antibodies not only halted viral spread but also shielded rodents from severe illness and prevented death entirely. Importantly, analysis of patient samples showed that people who had been infected with mpox naturally carry high levels of these antibodies and that their presence is linked to milder disease and fewer hospitalisations.

A virus in urgent need of treatment

Mpox has been a global health concern since a multi-country outbreak in 2022. The virus, a close relative of smallpox, is transmitted primarily through direct contact and causes rash, lymphadenopathy and fever. Although most cases resolve, infection can result in permanent scarring and, in severe instances, be life threatening.

Despite repeated warnings from the World Health Organization, which has declared mpox a public health emergency of international concern twice since 2022, there is still no approved drug to treat the disease. Clinical trials of the most advanced candidate therapy have failed to demonstrate effectiveness, highlighting the urgent need for alternatives.

That urgency is precisely what drove the Mount Sinai team.

“A previous study published in 2023 by our team showed that human antibodies targeting the viral protein A35 were unusually increased in sera in response to mpox infection compared with vaccination for smallpox or antibodies against other viral proteins,” explained Dr Camila Coelho, Assistant Professor of Microbiology at Icahn Mount Sinai.

“Based on this earlier finding, we hypothesised that antibodies targeting A35 from mpox-infected individuals would be highly protective against orthopoxviruses, since the viruses in this family share high genetic similarity. We aimed to address the urgent unmet need for effective treatments for orthopoxviruses, and with the help of our outstanding collaborators, I am very proud to say that we are close to achieving that goal.”

What makes the discovery particularly compelling is the antibodies’ binding site. The researchers found that the antibodies latch onto a region of A35 that is highly conserved across not just orthopoxviruses – including mpox – but the entire poxvirus family. As this site is unlikely to mutate, the antibodies are less vulnerable to immune escape, making them robust drug candidates.

“Ours is the first report of the crystal structure of a human antibody bound to an mpox virus protein, providing a detailed map of a vulnerability in the virus,” said Dr Raianna Fantin, postdoctoral researcher and first author of the study.

“It is also the first time that monoclonal antibodies against orthopoxviruses were quantified in human sera. We were surprised by how consistently people recovering from mpox infection produced antibodies targeting the same A35 epitope of the virus as the antibodies we discovered.”

Next steps towards therapy

The Icahn School of Medicine has already patented the antibodies, signalling confidence in their potential clinical use. However, the team is clear that the work is still in its early stages. The antibodies must undergo rigorous preclinical safety checks and eventually human clinical trials before becoming available as a therapy.

For now, the researchers are focusing on two tracks: advancing the antibodies through further testing and leveraging their insights into the immune response to guide future strategies. Their dual approach could yield not only a treatment for mpox but also a foundation for tackling related viruses.

The discovery comes at a critical time. Mpox cases continue to be reported globally and no approved treatments are available. The identification of targeted antibodies offers a potential path toward effective therapy.

Usually, this 8 percent of your DNA — the viral bits — are kept silent. Scientists call it part of the “dark matter” in your genome.

Now scientists at La Jolla Institute for Immunology (LJI) have published a first look at a key viral protein. In a study published in Science Advances, LJI researchers revealed the first three-dimensional structure of a protein from one of these ancient “human endogenous retroviruses (HERVs).”

The team mapped the surface envelope glycoprotein (Env), the antibody target of the most active HERV, marking a milestone in structural biology. “This is the first human HERV protein structure ever solved — and only the third retroviral envelope structure solved overall, after human immunodeficiency virus (HIV) and simian immunodeficiency virus (SIV),” says Erica Ollmann Saphire, Ph.D., MBA, LJI President, CEO, and Professor.

This discovery opens the door to new strategies for diagnosing and treating disease. Back in the evolutionary past, HERV-K Env proteins studded the outside of the HERV-K retroviruses. But in modern humans, HERV-K Env proteins show up on the surface of certain tumor cells and in patients with autoimmune and neurodegenerative diseases, making them a valuable target for developing novel diagnostics and therapies.

“In many disease states, like autoimmune diseases and cancer, these genes re-awaken and start making pieces of these viruses,” says Saphire. “Understanding the HERV-K Env structure, and the antibodies we now have, opens up diagnostic and treatment opportunities.”

An unexpected “twist”

Until now, HERV proteins had been invisible. They’ve proven too mobile — and too twitchy — to be seen with even the most sophisticated imaging techniques. Solving the structure of HERV-K Env was especially challenging because the LJI team needed to capture the protein’s delicate “pre-fusion” state.

Envelope proteins are full of potential energy — they’re essentially spring-loaded to merge with a host cell to start the infection process. This means pre-fusion proteins are prone to spontaneous switching to their later, post-fusion state. “You can look at them funny, and they’ll unfold,” says LJI Postdoctoral Fellow Jeremy Shek, who spearheaded the study as co-first author with LJI Postdoctoral Fellow Chen Sun, Ph.D.

To study the three-dimensional structure of HERV-K Env, the researchers introduced small substitutions to lock the protein’s structure in place, while preserving its natural shape. Saphire and her team have used this approach before to reveal the structures of key proteins on Ebola virus, Lassa virus, and more. The researchers also discovered and characterized specific antibodies that helped anchor different versions of the viral proteins.

After stabilizing their HERV-K Env structures, the LJI team used a high-resolution imaging technique called cryo-electron microscopy to capture 3D images of HERV-K Env at three key moments: cell surface, in the act of driving infection, and when it locks together with antibodies.

Many viral envelope glycoproteins have a trimer structure, but HERV-K Env is different from anything scientists had seen before, including trimers from other retroviruses. Unlike the shorter, squatter trimers made by HIV and SIV, the HERV-K Env is tall and lean. Further, the protein’s fold — the weaving together of strands and coils that build the working machine — is unlike any other retrovirus.

A new path for clinical research

The new LJI study opens the door to using HERV-K Env to our advantage. Understanding the HERV-K Env structure, and how antibodies target it, may prove useful for developing diagnostic tools or new therapeutics.

For example, many types of cancer cells — from breast cancers to ovarian cancers — but not healthy cells, are dotted with HERV-K Env proteins. This means antibodies against HERV could distinguish cancer cells from healthy cells. As Sun explains, scientists could develop cancer immunotherapies that zero in on HERV-K Env to track down tumor cells. “We can use it as a strategy to specifically target cancer cells,” says Sun.

People with autoimmune diseases such as lupus or rheumatoid arthritis also express HERV-K Env on their cells. Some scientists suspect that patients’ immune cells see these strange proteins and think the body is under attack. Just like during a normal viral infection, their B cells start making antibodies against HERV-K Env proteins.

“Understanding how antibodies recognize these proteins was challenging because there was no structure and precious few good antibodies yet available,” says Saphire.

So the LJI team made their own panel of antibodies to reveal how the immune system can target the different subunits of the molecule in all its different shapes. Once scientists understand how these antibody attacks work, they can try to intervene and stop harmful inflammation.

The scientists also tested the idea that their antibodies may also be useful tools for diagnosing many autoimmune diseases. They used the antibodies to try and hunt down immune cells in samples from patients with rheumatoid arthritis and lupus. When Saphire and her colleagues tagged these antibodies with a molecular flag, they were able to quickly detect HERV-K Env on neutrophils, a type of immune cell that can cause inflammation.

“These antibodies marked aberrant HERV display on neutrophils from rheumatoid arthritis and lupus patients, but not healthy controls,” says Saphire.

The interest in HERVs is quickly growing, and scientists are finding more and more diseases where HERV-K Env crops up. “We can really pick whatever disease we’re interested in and go down that route,” says Shek.

These projects may someday advance clinical care — and our fundamental understanding of human biology. After all, we’re all part virus. It’s time to get to know that part of ourselves.

Additional authors of the study, “Human endogenous retrovirus K (HERV-K) envelope structures in pre- and postfusion by cryo-EM,” were Elise M. Wilson, Fatemeh Moadab, Kathryn M. Hastie, Roshan R. Rajamanickam, Patrick J. Penalosa, Stephanie S. Harkins, Diptiben Parekh, Chitra Hariharan, Dawid S. Zyla, Cassandra Yu, Kelly C.L. Shaffer, Victoria I. Lewis, Ruben Diaz Avalos, and Tomas Mustelin,

This study was supported by a Curebound Discovery Grant (13502-01-000-408) and by LJI & Kyowa Kirin, Inc. (KKNA-Kyowa Kirin North America; and a Kirin North America Accelerator Grant [18030-01-000-408]).

Nutrition professionals significantly influence consumer choices, and recent research looks at how perceptions of plant-based dairy alternatives shape their inclusion in a healthy diet. We speak to the European Food Information Council (EUFIC) to learn about challenges and opportunities in this space.

The study examined 259 various Spanish nutrition professionals. It shows that they often misunderstand the nutrient value of plant-based dairy alternatives due to their highly variable nutrient profiles, inconsistent fortification levels, and reliance on food-based dietary guidelines.

Their own habits can shape their advice, and they may exclude children and older adults from consuming plant-based dairy alternatives, the study suggests. 

Meanwhile, it warns that nutrition professionals overestimating fortification may cause consumers to miss key nutrients. 

Those who recommend plant-based dairy alternatives believe they are more sustainable and promote a diverse diet, as they are another way of consuming legumes and nuts.

Misunderstandings amok 

EUFIC’s senior research manager, Dr. Katerina Palascha, tells Nutrition Insight why some nutrition professionals may misunderstand plant-based milks.

“Firstly, their nutrient profile is highly variable, as it depends both on the ingredient they are made from (e.g., soy, oats, or coconuts) and the type of product (e.g., drink, yogurt, or cheese), so they cannot be treated as one homogenous group,” she explains.

“Secondly, their level of fortification can be inconsistent across products and brands. Thirdly, some plant-based dairy alternatives in Spain and Portugal contain a mix of different plant-based sources, further increasing the difficulty of making precise recommendations.”

Palascha adds that some of these professionals may focus more on foods included in food-based dietary guidelines because there is more guidance about them. 

The study found that over 70% of professionals want information on fortification, bioavailability, and nutritional composition of plant-based dairy alternatives. Over 60% wanted processing, additives, and environmental impact data.

The availability bias

The research notes that health professionals consider plant-based products compatible with a healthy diet and support their fortification. However, as there is no consensus on their nutritional value compared to dairy products, they believe this brings confusion, including among consumers. 

Palascha explains the availability bias and assures: “If they are professional, they are not likely to give advice that goes against the science. But whatever they are familiar with may come more readily to their minds as a potential option, as it does to everyone.”

“Both our study and previous studies show that health professionals who consume plant-based dairy alternatives themselves are more likely to recommend these products to their clients.”

The study found that those who thought PBDA was nutritionally equivalent to dairy recommended it more frequently than those who were uncertain.

Although 34% of the sample would advise plant-based dairy alternatives to all consumers, the majority of nutritionists would, based on particular demographics, such as adults (52%), those on restricted diets (75%), or those who currently use these products (49%). 

Other target groups include those with allergies, autoimmune diseases, or digestive problems, or those who value sustainability, and menopausal women. 

Age-specific nutrition

Palascha notes that children and older adults need specific nutrients from dairy products, such as protein, calcium, vitamin B12, and iodine. They are also more susceptible to deficiencies in these nutrients.

“Given that milk and dairy tend to provide more bioavailable sources of these nutrients than plant-based dairy alternatives, it needs to be considered whether making PDBA recommendations for these groups may potentially increase the risk of these deficiencies.”

The study shows that most nutrition professionals thought plant-based dairy alternatives were most frequently fortified with calcium (92%), vitamin D (85%), and vitamin B12 (61%), but this is an overestimation. 

According to Palascha, consumers may not be aware that nutrients added to products tend to be less bioavailable than the same nutrient level that is found in food. 

“This is normally not a problem in a balanced, varied diet, but it can be a problem otherwise. But if consumers think they are absorbing more of a nutrient than they are, they may not seek other sources of the same nutrients, which can lead to a nutrient deficiency.”

Previous research shows that animal protein helps early life survival, while plant-based protein is more linked to adult longevity and overall life expectancy.

Question of sustainability

The study reveals that nutrition professionals are curious to learn more about the environmental impact of plant-based dairy alternatives. This highlights the importance of transparency in informing dietary guidelines and supporting professional recommendations.

Those who saw plant-based dairy alternatives as more environmentally friendly than dairy and believed they could completely replace dairy when fortified strongly supported their inclusion in the Spanish dietary guidelines. 

Palascha believes that the decision to use plant-based milk is personal. “Since it is possible to have a nutritious diet that is also environmentally friendly, there is no need to have a trade-off between environmental and personal health.” 

“Effective fortification of plant-based dairy alternatives presents both a challenge and an opportunity to deliver products that are both nutritionally adequate and environmentally friendly,” she concludes.

Alpro funded the research, which was carried out independently by EUFIC from February to August 2025.

In July, the UK called for better plant-based milk fortification. Despite growing consumer interest in these alternatives, the UK’s Scientific Advisory Committee on Nutrition and the Committee on Toxicity of Chemicals in Food, Consumer Products and the Environment concluded that no almond, oat, or soy drink available in the UK was nutritionally equivalent to cow milk as of early 2022.