Should We Change Pregnancy Supplements?

Summary of: Is now the time for revisiting supplements for pregnant women?

The Problem:

• Many babies die or face health problems because they are born too early or too small.
• In 2020, about 23 million babies were born underweight or too small, and 13 million were born too early.
• One big reason for this is poor nutrition during pregnancy, especially not getting enough vitamins and nutrients.

What Supplements Do Pregnant Women Get Now?

• The WHO recommends that pregnant women take iron and folic acid to stay healthy.
• Women in poorer areas may also get extra protein supplements.
• But new research suggests a better option: Multiple Micronutrient Supplements (MMSs), which include more essential vitamins and minerals.

What Did the New Study Find?

• MMSs help reduce the number of small, vulnerable newborns, especially among high-risk mothers.
• Another type of supplement, Small-Quantity Lipid-Based Nutrient Supplements (SQ-LNSs), had only a small benefit.
• MMSs are more effective at improving both mother and baby’s health.

Why Aren’t MMSs Used Everywhere?

• WHO has not fully approved MMSs for all pregnant women yet.
• There are concerns about cost, production, and distribution.
• However, studies show MMSs are cost-effective, especially in countries like Bangladesh, India, and Pakistan.

What Needs to Change?

• More pregnant women need access to MMSs—right now, only 5% of those who need them get them.
• Governments and health organizations should update guidelines to include MMSs.
• Local production of MMSs could help make them cheaper and more available.

Bottom Line:

MMSs could save lives and improve health for both mothers and babies. Experts are calling for a global push to replace iron and folic acid with MMSs in pregnancy care.

1. Is now the time for revisiting supplements for pregnant women?

   Das, Jai K et al.
   The Lancet Global Health, Volume 13, Issue 2, e185 - e186

The Climate Crisis and Human Health

The Climate Crisis and Human Health

What’s the Issue?

• Climate change is a major health threat—it’s making people sick in new ways and making existing health problems worse.
• Extreme weather like heatwaves, floods, and storms can lead to new diseases, mental health struggles, and food shortages.
• Poorer countries and small islands suffer the most, even though they contribute the least to climate change.

Why Is This a Problem?

• We’re focusing on reducing pollution (which is important), but we haven’t done enough to prepare for the health risks of climate change.
• People in high-risk areas need better healthcare and support to deal with the changes happening now and in the future.

What’s Being Done?

A group of organizations, including Grand Challenges Canada and Science for Africa, are working together to find solutions by listening to people on the front lines.

How Are They Doing This?

1. Global Climate & Health Survey

   • They’re asking doctors, nurses, and community health workers what climate-related health problems they see and what barriers exist.

2. Online Discussion Event (Teach to Reach 11)

   • Health workers from around the world will share their experiences and ideas in a virtual meeting.

3. Expert Review Panel

   • A team of climate and health experts will look at the results and create a list of the biggest challenges.

4. Sharing the Results

   • The list will be made public so that governments, researchers, and funders can use it to make real changes.
   • It will also help guide funding and new programs to improve health in climate-vulnerable areas.

Why This Matters?

• Climate change is already hurting people’s health—we need to act now.
• By listening to local health workers, we can find practical solutions that actually help communities.
• The goal is to get funding, policies, and innovations that protect people’s health from climate risks.

The climate crisis and human health: identifying grand challenges through participatory research

Sanchez, J JohannaBerry, Peter et al.

The Lancet Global Health, Volume 13, Issue 2, e199 - e200

2022 Sudan Virus Outbreak in Uganda

Summary of 2022 Sudan virus disease outbreak in Uganda: temporal variations in transmission

Figure Inference of Rt during the 2022 Sudan virus disease outbreak in Uganda

What Happened?

• In 2022, Uganda experienced an outbreak of Sudan virus disease, a type of Ebola.
• 164 people got sick, and young children under 10
  years old were hit the hardest.
• Scientists studied how the virus spread and how well public health measures worked.

How Did the Virus Spread?

• The "R₀" number (which shows how many people one sick person can infect) was 1.25—this means each infected person spread it to about 1 or 2 others on average.
• However, this number alone doesn’t tell the full story because virus spread changes over time.

What Happened Over Time?

1. At the Start: The virus spread quickly, with each sick person infecting 2 to 3 others.
2. Government Response: After health teams arrived in late September, the virus spread much less.
3. A Second Wave: A short time later, the virus spread again before it was finally controlled in late October.

What Can We Learn?

• Fast action is key: The quicker health teams respond, the less the virus spreads.
• Tracking the spread helps: Instead of relying on just one number, scientists need to watch how a virus behaves over time.
• Less dangerous than other Ebola viruses: While still serious, Sudan virus is not as likely to cause a big pandemic.

Final Thought

This outbreak shows that quick action saves lives. If we catch future outbreaks early and respond fast, we can stop them before they get worse.

1. 2022 Sudan virus disease outbreak in Uganda: temporal variations in transmission

   de Padua, Bianca et al.
   The Lancet Global Health, Volume 13, Issue 2, e201

How Cancer Outsmarts Your Immune System: The Role of Mitochondrial Hijacking

Imagine your immune system trying to fight off cancer. Normally, your T cells are like soldiers, ready to attack and destroy cancer cells. But cancer cells have sneaky ways to avoid being attacked. They change the environment around them and disrupt the mitochondria—the energy factories—in your immune cells, particularly in tumor-infiltrating lymphocytes (TILs). This makes it harder for your immune system to do its job.

Now picture this: the cancer cells’ mitochondria, which may carry harmful mutations in their DNA, can actually transfer to your T cells. Typically, your T cells can get rid of damaged mitochondria through a process called mitophagy, triggered by harmful byproducts called reactive oxygen species. But cancer mitochondria come equipped with special molecules that prevent this cleanup process. These molecules stick to the cancer mitochondria and hitch a ride into your T cells, replacing your healthy mitochondria.

When your T cells take on these faulty mitochondria, they start to malfunction. They lose energy, stop working properly, and can no longer "remember" how to fight the cancer effectively. This weakens your immune system’s ability to attack the tumor. If your tumor has these mitochondrial DNA mutations, treatments like immune checkpoint inhibitors might not work as well, especially if you have melanoma or non-small-cell lung cancer.

This discovery shows you how cancer can trick your immune system in ways scientists didn’t fully understand before. Knowing this could lead to new, better treatments that help your immune system fight back.

In the study linked below, researchers looked at tissue samples from patients and found that the mitochondria in TILs sometimes carry the same DNA mutations as the cancer cells. The researchers also found that if a patient’s tumor has these mitochondrial DNA mutations, treatments like immune checkpoint inhibitors may not work as well, especially for melanoma or non-small-cell lung cancer.

These findings uncover a new way that cancer tricks the immune system and could help scientists develop better cancer treatments in the future.

From text: Fig. 5: mtDNA-mutated mitochondrial transfer reduces antitumour immunity in vivo.

Ikeda, H., Kawase, K., Nishi, T. et al. Immune evasion through mitochondrial transfer in the tumour microenvironment. Nature (2025). https://doi.org/10.1038/s41586-024-08439-0

A New Way to See Inflammation in the Body

Being able to image inflammation can help doctors diagnose, treat, and predict the outcomes of many diseases. However, there isn’t yet a highly accurate and specific imaging method to detect inflammation. To solve this problem, researchers developed a new technique called CD45-PET imaging. This method provides clear and sensitive pictures of inflammation in different disease models.

One of the key findings is that CD45-PET imaging shows how severe a disease is by producing stronger signals in models of lung and bowel diseases. It works better than the current most-used method, called 18F-fluorodeoxyglucose PET, for detecting inflammation. CD45-PET can also track how inflammation changes over time in specific tissues.

The researchers also created a version of CD45-PET for humans, which successfully detects human immune cells in special mouse models that mimic the human immune system. This new imaging method has great potential to help doctors make better decisions by providing a precise, full-body view of inflammation in patients.

From the text: Fig. 1: 89Zr-CD45 nanobody PET probe clearly visualizes immune-cell-rich organs in vivo.

Salehi Farid, A., Rowley, J.E., Allen, H.H. et al. CD45-PET is a robust, non-invasive tool for imaging inflammation. Nature (2025). https://doi.org/10.1038/s41586-024-08441-6

Improving the Immune System’s Ability to Fight Cancer

The immune system uses a molecule called interleukin-10 (IL-10) to help control inflammation and avoid excessive damage to the body. However, tumors often increase IL-10 levels to suppress the immune system, which helps them grow and spread. Recent studies show that IL-10 production depends on signals from mitochondria, the parts of cells that produce energy.

We discovered that a substance called S3QEL 1.2, which blocks certain chemicals (reactive oxygen species or ROS) from being made in mitochondria, reduces IL-10 levels in immune cells called macrophages. Another substance, myxothiazol, also lowers IL-10 by targeting the same part of the mitochondria. This happens because these substances suppress a protein called c-Fos, which is needed for IL-10 production.

When tested in mice, S3QEL 1.2 lowered IL-10 levels and helped their immune systems fight tumors more effectively, slowing the growth of melanoma. This research shows that blocking specific mitochondrial signals may help improve the immune system’s ability to fight cancer.

From the text: Fig. 2. Complex III inhibition reveals a specific transcriptional signature in activated macrophages

Zotta, A., et al. (2025). Mitochondrial respiratory complex III sustains IL-10 production in activated macrophages and promotes tumor-mediated immune evasion. Science Advances, 11(4), eadq7307. https://doi.org/10.1126/sciadv.adq7307

Understanding How Cells Shape the Immune Response to Food

Our gut's immune system has a tough job—it needs to peacefully handle food and helpful microbes while staying ready to fight harmful germs. Special cells called antigen-presenting cells (APCs) help guide this balance. They "show" food particles to certain immune cells called CD4+ T cells, which can then decide to either calm down (becoming pTreg cells) or gear up for action (becoming Th cells).

To learn more about how this works, researchers used a tool called LIPSTIC to find which APCs present food particles during normal, calming conditions and during inflammation. They also looked at how this balance can be thrown off during infections. They found that worm infections (helminths) upset the gut's ability to tolerate food by changing the balance of APCs. Normally, cells like cDC1s and Rorγt+ APCs help keep the peace, but helminths boosted inflammatory APCs, mostly cDC2s, which didn’t respond to food particles. This prevented the immune system from overreacting to food during infection, avoiding unnecessary allergic responses.

Canesso, M. C. C., Castro, T. B. R., Nakandakari-Higa, S., Lockhart, A., Luehr, J., Bortolatto, J., Parsa, R., Esterházy, D., Lyu, M., Liu, T.-T., Murphy, K. M., Sonnenberg, G. F., Reis, B. S., Victora, G. D., & Mucida, D. (2024). Identification of antigen-presenting cell–T cell interactions driving immune responses to food. Science. https://doi.org/10.1126/science.ado5088