The article highlights a disturbing trend in the United States – cancer deaths linked to obesity have tripled over the past two decades. A study presented at the Endocrine Society’s annual meeting in San Francisco examined more than 33,000 deaths from obesity-associated cancers and revealed sharp increases in cancer deaths, particularly among women, older adults, Native Americans, and Black Americans.

“Obesity is a significant risk factor for multiple cancers, contributing to significant mortality,” said lead researcher Faizan Ahmed. “This research underscores the need for targeted public health strategies such as early screening and improved access to care, especially in high-risk rural and underserved areas.”

The study used mortality data from the Centers for Disease Control and Prevention (CDC) to analyze U.S. deaths from obesity-associated cancers between 1999 and 2020. The results showed age-adjusted mortality rates increased from 3.73 to 13.52 per million over two decades, with steep increases among certain groups.

Obesity is a complex disease resulting from multiple genetic, physiological, hormonal, environmental, and developmental factors. It raises the risk of developing serious chronic conditions such as high blood pressure, high cholesterol, prediabetes, type 2 diabetes, heart disease, and chronic and end-stage kidney disease.

In addition to certain types of cancer, obesity is associated with a higher risk of developing 13 types of cancer, according to the CDC. These cancers make up 40% of all cancers diagnosed in the United States each year.

The regions with the highest rates of obesity-related cancer deaths were identified as follows:

* The Midwest had the highest rate.
* Vermont, Minnesota, and Oklahoma had the highest state-level rates.
* Utah, Alabama, and Virginia had the lowest state-level rates.

This research emphasizes the need for targeted public health strategies to combat the growing epidemic of obesity-related cancer deaths. Early screening and improved access to care are crucial in reducing mortality rates among high-risk groups.

The UC Davis Comprehensive Cancer Center has made a groundbreaking discovery that may explain why certain immune cells in humans are less effective at fighting solid tumors compared to non-human primates. This finding could lead to more powerful cancer treatments.

Researchers have uncovered an evolutionary change that makes the Fas Ligand (FasL) protein, essential for triggering programmed cell death and killing cancer cells, vulnerable to being disabled by plasmin in humans. This genetic mutation is unique to humans and not found in non-human primates, such as chimpanzees.

“The evolutionary mutation in FasL may have contributed to the larger brain size in humans,” said Jogender Tushir-Singh, senior author for the study and an associate professor in the Department of Medical Microbiology and Immunology. “But in the context of cancer, it was an unfavorable tradeoff because the mutation gives certain tumors a way to disarm parts of our immune system.”

The team discovered that a single evolutionary amino acid change – serine instead of proline at position 153 – makes FasL more susceptible to being cut and inactivated by plasmin. Plasmin is often elevated in aggressive solid tumors, such as triple negative breast cancer, colon cancer, and ovarian cancer.

This means that even when human immune cells are activated and ready to attack the tumor cells, one of their key death weapons – FasL – can be neutralized by the tumor environment, reducing the effectiveness of immunotherapies. The findings may help explain why CAR-T and T-cell-based therapies often fall short in solid tumors.

Blood cancers often do not rely on plasmin to metastasize, whereas tumors like ovarian cancer heavily rely on plasmin to spread the cancer.

Significantly, the study also showed that blocking plasmin or shielding FasL from cleavage can restore its cancer-killing power. This finding may open new doors for improving cancer immunotherapy.

By combining current treatments with plasmin inhibitors or specially designed antibodies that protect FasL, scientists may be able to boost immune responses in patients with solid tumors.

“Humans have a significantly higher rate of cancer than chimpanzees and other primates,” said Tushir-Singh. “There is a lot that we do not know and can still learn from primates and apply to improve human cancer immunotherapies.”

The Rutgers Health researchers have made a groundbreaking discovery about how our brains process hunger and fullness cues. Two new studies, published in Nature Metabolism and Nature Communications, have mapped the first complementary wiring diagram of hunger and satiety in ways that could refine today’s blockbuster weight-loss drugs and blunt their side effects.

One study, led by Zhiping Pang of Robert Wood Johnson Medical School’s Center for NeuroMetabolism, pinpointed a slender bundle of neurons that runs from the hypothalamus to the brainstem. This pathway, known as GLP-1 receptors, is mimicked by weight-loss drugs such as Ozempic. When Pang’s team used optogenetics to fire axons with laser light, well-fed mice quit eating; when they silenced the circuit or deleted the receptor, the animals packed on weight.

The cells in this pathway bristle with GLP-1 receptors, which are proteins that play a key role in regulating energy balance. The study found that fasting weakened the connection until a burst of natural or synthetic GLP-1 restored it. Pang warns that drugs that keep the signal high around the clock could disrupt the brain’s normal rhythm and create some of the side effects of GLP-1 drugs, such as nausea, vomiting, constipation or diarrhea and muscle wasting.

For the other paper, Mark Rossi, who co-leads the Center for NeuroMetabolism with Pang, charted the circuit that triggers hunger. His group traced inhibitory neurons in the stria terminalis to similar cells in the lateral hypothalamus. When researchers triggered the connection, a suddenly hungry mouse would sprint for sugar water; when they blocked it, the animals lounged even after a long fast.

Hormones modulated the effect. An injection of ghrelin, the gut’s hunger messenger, revved food seeking, while leptin, the satiety signal, slammed it shut. Overfed mice gradually lost the response, but it returned after diets made them thin again.

Pang’s pathway shuts things down,” Rossi said. “Ours steps on the accelerator.” Although the circuits sit in different corners of the brain, members of both teams saw the same principle: Energy state rewires synapses quickly. During a fast, the hunger circuit gains sensitivity while the satiety circuit loosens; after a meal, the relationship flips.

It is the first time researchers have watched the push-pull mechanism operate in parallel pathways, a yin-yang arrangement that may explain why diets and drugs that treat only one side of the equation often lose power over time. The studies suggest a therapy targeting only the brainstem circuit and sparing peripheral organs might curb eating without the side effects.

Conversely, Rossi’s work hints that restoring the body’s response to the hunger-regulating hormone ghrelin could help dieters who plateau after months of calorie cutting. Both projects relied on the modern toolkit of neural biology – optogenetics to fire axons with laser light, chemogenetics to silence them, fiber-optic photometry to watch calcium pulses and old-fashioned patch-clamp recordings to monitor single synapses.

Follow-up work from both teams will explore more questions that could improve drug design. Pang wants to measure GLP-1 release in real time to see whether short bursts, rather than constant exposure, are enough to calm appetite. Rossi is cataloging the molecular identity of his hunger-trigger cells in hopes of finding drug targets that steer craving without crushing the joy of eating.

“You want to keep the system’s flexibility,” Rossi said. “It’s the difference between dimming the lights and flicking them off.”