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Aspirin May Fight Cancer – But Not for the Reason You Think

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I’ve written before about the many health benefits of aspirin that many people don’t hear about — from protecting your heart and preventing cancer to boosting your metabolism and balancing your hormones.

But new research is revealing something about aspirin and cancer that changes the story in ways nobody expected. It starts with a completely different way of looking at what drugs actually do to cancer cells. And it ends with a finding that turns decades of assumptions upside down.


How Cancer Drugs Have Always Been Tested — and Why It Misses So Much

For as long as modern cancer research has existed, scientists have tested drugs the same basic way. They put cancer cells in a dish, add the drug, and wait to see if the cells die. If most of them die, the drug is a winner. If they survive, the drug gets tossed.

This sounds perfectly reasonable. But stop and think about what it actually measures. It measures one thing and one thing only: death. Here’s the problem with that.

Cancer isn’t just one thing going wrong — A cancer cell is a normal cell that has gone haywire in many ways at the same time. Think of it like a car where the engine is racing, the brakes are cut, and the steering is locked — all at once. Killing the car — running it into a wall — is one way to stop the problem. But what if you could just fix the engine, unlock the steering, reconnect the brakes, and turn the headlights back on? You would have a working car again.

Cancer cells aren’t alien invaders — They’re your own cells running the wrong program. And a drug that could fix part of that program — slow the engine down, reconnect some of the brakes — would be completely invisible in the standard drug test, because the cells didn’t die. How many valuable drugs have been thrown in the trash because we were only looking at one thing?

Every Cell Runs a Program — Cancer Cells Are Running the Wrong One

To understand the new approach, you first need to understand one simple idea about how your cells work.

Every cell in your body contains the same DNA, the same complete set of instructions — What makes a colon cell different from a brain cell or a skin cell is not which instructions they have, but which instructions they’re actually using. Out of roughly 20,000 genes, each cell type switches on a specific set and keeps the rest turned off. This pattern — which genes are on and which are off — is the cell’s program. It is what gives the cell its identity.

Think of it like a massive mixing board in a recording studio — There are 20,000 sliders. A healthy colon cell has each slider set to a very specific position. The overall setting produces “healthy colon cell.” When a cell becomes cancerous, the sliders get moved. Some that should be turned down get cranked up. Others that should be up get pushed to zero.

The mixing board is still there, the sliders still work, but the overall setting now produces “cancer cell” instead of “healthy colon cell.” This is a crucial point. The cancer cell hasn’t been destroyed or replaced. It’s your cell, running the wrong settings.

A 100-Million-Cell Dataset Made a New Question Possible

Researchers at a company called Tahoe Therapeutics have built something that has never existed before.1 They measured how 1,100 different drugs changed the genetic settings in cancer cells — one cell at a time — across 50 different cancer cell lines. The result is a dataset containing 100 million individual cell measurements from 60,000 separate drug experiments. That’s 50 times more data than everything publicly available before it — combined.

With this enormous dataset, they could finally ask the question that nobody had enough data to answer before — For every drug, does it push the cancer cell’s gene settings back toward the healthy pattern? Here’s how they did it. First, they used data from real colon cancer patients to map out exactly how the gene settings differ between healthy colon tissue and cancerous colon tissue. That gave them the “disease signature” — a precise measurement of what went wrong.

Then, for each drug in their collection, they measured what it did to the mixing board — Did it move the sliders back toward the healthy positions? Or did it push them even further in the wrong direction? Or did it just move them to some random new pattern?

They scored every drug with a simple number — A strong negative score meant the drug was reversing the cancer pattern — pushing the cell back toward normal. They call this “cell-state reversal.”2

The First Test: Does It Match What Doctors Already Know?

Before you trust a new method, you need to check it against reality. If drugs that are already proven to work in colon cancer patients don’t score well on this test, the whole approach is worthless. So, the researchers checked. And the results were clear.

Top-scoring drugs matched the exact mutations driving colon cancer growth — The drugs that scored highest for pushing colon cancer cells back toward normal were exactly the ones that target the specific genetic mutations most commonly found in colon cancer — MEK inhibitors, BRAF inhibitors, KRAS inhibitors, and PI3K pathway inhibitors.

These are the drugs oncologists already use because clinical experience has shown they work. The framework figured this out on its own, from the data alone, without being told which drugs are effective in patients.

It even caught subtleties that match real clinical practice — Among chemotherapy drugs, the ones that target DNA — like 5-fluorouracil and oxaliplatin, which are the backbone of standard colon cancer treatment — scored higher than the ones that target the cell’s internal scaffolding, called microtubule inhibitors. Microtubule inhibitors aren’t part of the standard treatment for colon cancer, and the data reflected that perfectly.

Now Here’s Where It Gets Really Interesting: The Aspirin Surprise

Among all the drugs tested, one result stood out as genuinely unexpected. It involved one of the cheapest, oldest, and most widely available medicines on Earth.

When the researchers looked at aspirin and its close chemical relatives in the dataset, they found that sodium salicylate — which is aspirin with one specific piece removed — produced stronger cancer-state reversal than aspirin itself. To understand why this is such a big deal, you need to know one thing about aspirin’s chemistry. Don’t worry — it is simpler than it sounds.

Aspirin’s chemical name is acetylsalicylic acid — It’s made of two parts: salicylic acid, which comes from willow bark and has been used as medicine for thousands of years, and an acetyl group, which was attached to the salicylic acid by chemists at Bayer in 1897 to make it easier on the stomach.

That acetyl group isn’t just a packaging improvement — It’s the part that gives aspirin its most famous ability — the power to shut down an enzyme called cyclooxygenase, or COX for short. COX produces inflammatory chemicals called prostaglandins. When aspirin blocks COX, inflammation goes down.

That’s how aspirin reduces pain, reduces fever, thins your blood, and — most researchers assumed — fights cancer. Here’s the catch. If aspirin’s anticancer power comes from blocking COX, then removing the acetyl group — the part that does the COX blocking — should make it worse at fighting cancer, not better.

But the Tahoe data showed the exact opposite — Salicylate, without the acetyl group, was better at reversing the cancer cell’s genetic program than aspirin with it. That means the cancer-fighting effect isn’t coming from COX inhibition. It’s coming from the salicylate itself — through a completely different mechanism that nobody was paying attention to.

So, What Is Salicylate Actually Doing? The Answer Is Elegant

The Tahoe data showed what salicylate does to cancer gene patterns. But other research teams have been uncovering how it does it, and the picture is remarkably coherent. Your cells have an energy sensor — think of it as a fuel gauge.

It’s a protein called AMPK, which stands for AMP-activated protein kinase, but all you need to know is that AMPK is the alarm system that goes off when your cell’s energy balance changes.3 It’s one of the most powerful metabolic switches in your body. Salicylate switches AMPK on.4 When AMPK activates, it triggers a chain of events that’s devastating to cancer cells. Here’s the chain, step by step:

Step 1: AMPK shuts down c-MYC — One of the most important genes in cancer is called c-MYC. Think of c-MYC as the gas pedal for cell growth. In a healthy cell, it’s carefully controlled. In many cancers — especially colon cancer — c-MYC is jammed to the floor, driving the cell to grow and divide nonstop. Salicylate-activated AMPK grabs c-MYC and tags it for destruction. The gas pedal gets released.

A 2025 study using a mouse model of colon cancer confirmed this. Mice given salicylate had dramatically lower c-MYC levels in their colon cells, and they developed fewer tumors.5

Step 2: With c-MYC gone, a protective system switches on — Here’s something beautiful about your biology. You already have a built-in tumor defense system — a set of genes that suppress cancer. One of the most important is a group of tiny molecules called miR-34a and miR-34b/c.6 These are microRNAs — small pieces of genetic material that act like off-switches for cancer-promoting genes. They work by silencing specific genes that cancer cells depend on to grow and spread.

Normally, a protein called NRF2 — think of it as your cell’s fire alarm system — is supposed to activate these cancer-fighting microRNAs. But c-MYC sits on top of NRF2 and keeps it silenced. It’s like a bully sitting on the fire alarm so nobody can pull it. When salicylate removes c-MYC, NRF2 is free. It activates miR-34a and miR-34b/c. Your body’s own tumor suppression system comes back online.

Step 3: The cancer cells lose their ability to spread — When researchers blocked miR-34a and miR-34b/c in the lab, salicylate’s ability to stop cancer cell migration and invasion largely disappeared. That tells you these microRNAs are the key weapons. Salicylate isn’t directly attacking the cancer — it’s rearming your body’s own defense system.

And here’s the most important part — Normally, miR-34 depends on a tumor suppressor gene called p53 — often called the “guardian of the genome.” But p53 is the single most commonly broken gene in human cancer. In more than half of all cancers, p53 doesn’t work. Salicylate’s pathway bypasses p53 entirely. It activates miR-34 through NRF2 instead.

This means it could theoretically work in the very cancers that have already lost their most important natural defense, which is exactly the cancers that need help the most. None of this involves COX inhibition. None of it requires the acetyl group. This is the ancient willow bark compound doing something we are only now beginning to understand.

The Clinical Trial That Changed the Guidelines

While these laboratory discoveries were piling up, a major clinical trial was delivering results that would change how oncologists treat colon cancer. The trial used aspirin, not salicylate — but remember, your body rapidly strips the acetyl group off aspirin and converts it into salicylic acid. So, every aspirin patient in this trial was effectively being dosed with salicylate.

The ALASCCA trial, published in the New England Journal of Medicine in September 2025, was the gold standard of medical research — a double-blind, randomized, placebo-controlled trial, meaning neither the patients nor the doctors knew who was getting aspirin and who was getting a sugar pill.7

It was conducted across 33 hospitals in four countries: Sweden, Denmark, Finland, and Norway. The trial focused on patients with stage I through III colon and rectal cancer whose tumors carried mutations in something called the PI3K pathway — a growth-signaling system that, when broken, helps cancer cells multiply unchecked. You don’t need to remember that name.

What matters is that these mutations are found in more than one-third of all colorectal cancers — so this isn’t a rare subtype. It is a big chunk of patients. After surgery, patients were randomly assigned to take either 160 milligrams (mg) of aspirin or a placebo every day for three years.

The results were remarkable — Among patients with the most common type of PI3K mutation, aspirin cut the three-year recurrence rate roughly in half — from 14.1% with placebo down to 7.7% with aspirin.

The benefit held up across every subgroup the researchers checked: men and women, all disease stages, colon and rectal cancer, and regardless of whether patients also received chemotherapy. Lead researcher Anna Martling of the Karolinska Institutet in Stockholm called it “a clear example of how we can use genetic information to personalize treatment and at the same time save both resources and suffering.”8

The National Comprehensive Cancer Network has since updated its recommendations — This organization, which writes the treatment guidelines oncologists follow, now formally recommend genetic testing for PIK3CA mutations in stage II-III colon cancer, and for patients who carry the mutation, three years of low-dose aspirin after surgery.9 This makes aspirin one of the first dirt-cheap, widely available drugs to be officially integrated into precision cancer treatment guidelines.

Aspirin Also Helps Your Immune System See the Cancer

The ALASCCA trial proved aspirin works in patients. But there’s another dimension to the story — aspirin may also be helping your immune system do its own cancer-fighting job. A 2024 study published in the journal Cancer found that regular aspirin use was linked to activation of immune surveillance in colorectal cancer patients.10 Here’s what that means in plain English.

Your immune system is supposed to recognize and destroy cancer cells — That’s one of its main jobs. But cancer cells are sneaky — they learn to hide from your immune system by covering up the markers that would identify them as abnormal.

Regular aspirin use linked to less spread and stronger immune attack — The researchers found that colon cancer patients who regularly used aspirin had two things going for them. First, they had fewer cancer cells that had spread to their lymph nodes. Second, they had more immune cells infiltrating their tumors — meaning the immune system was actually showing up to fight.

Aspirin helps cancer cells reveal themselves to immune system defenses — When they treated colon cancer cells with aspirin in the lab, they found aspirin increased the expression of a protein called CD80 on the surface of the cancer cells. CD80 is like a flag that says “I am abnormal — come get me.”

It helps cancer cells present themselves to your T cells — the soldiers of your immune system — so they can be recognized and destroyed. In simple terms, aspirin was pulling the camouflage off the cancer cells so the immune system could see them.

Aspirin’s Benefits Go Far Beyond Cancer

As I’ve detailed in previous articles, aspirin’s health benefits reach into nearly every major organ system. Here’s an updated picture based on the latest research.

Your liver — A clinical trial found that 81 mg of aspirin daily led to a 17.3% decrease in the amount of fat stored inside liver cells over six months, while patients taking a placebo saw their liver fat increase by 30.3%.11 Aspirin also improved markers of inflammation and scarring in the liver — two key factors in the progression of fatty liver disease.

Your blood sugar — An analysis of 16,209 adults aged 65 and older found that low-dose aspirin was associated with a 15% lower risk of developing Type 2 diabetes and a slower rise in fasting blood sugar levels over time.12

Your survival in critical care — A large study of 146,191 intensive care unit (ICU) patients found that aspirin use during ICU stays was linked to significantly lower death rates within 28 days, particularly in patients with widespread inflammation.13

Your brain — Research found that low-dose aspirin use for more than 10 years was associated with a 31% reduced risk of Alzheimer’s disease, a 69% reduced risk of vascular dementia, and a 54% reduced risk of dementia from any cause — particularly in patients who already had heart disease.14

Your lungs — Aspirin has been shown to reduce the scarring process in lung tissue by switching on a cellular recycling system called autophagy — your cells’ built-in method of cleaning out damaged proteins and preventing scar tissue from building up. When researchers blocked autophagy, aspirin’s anti-scarring effects disappeared, confirming that this recycling process is how aspirin protects the lungs.15

Your metabolism — Aspirin helps your cells burn glucose for energy, reduces the release of linoleic acid (LA) — a harmful omega-6 fat — from your fat stores, lowers your cortisol levels, and increases your metabolic rate by partially uncoupling your mitochondria.16 Think of uncoupling as your cellular engines running a bit hotter and burning more fuel, which is why aspirin may help with weight management.

What About Salicylate and Willow Bark?

The Tahoe finding — that salicylate reversed the colon cancer gene signature more strongly than aspirin — has a practical implication that’s easy to overlook. When you take aspirin, your body quickly strips off the acetyl group and converts it into salicylic acid. That is what circulates in your bloodstream. That is what your cells actually see.

Aspirin’s lasting anticancer effects stem from its salicylate metabolite — The acetyl group does its COX-blocking work during the brief window before it gets removed, but the salicylate metabolite is what sticks around and does the long-term work.

This means the anticancer effects are most likely coming from the part of aspirin that’s identical to what you would get from willow bark — the plant medicine that humans have used for thousands of years, long before Bayer attached an acetyl group to it in 1897.

Willow bark provides the same active compound linked to anticancer benefits — If you’re sensitive to aspirin — if it bothers your stomach or you can’t take it for other reasons — this is important news. A salicylic acid supplement or willow bark extract delivers the very compound that the largest drug-response dataset in history identified as more effective than aspirin at pushing cancer cells back toward normal.

Standardized willow bark dosing approximates common low-dose aspirin effects — For dosage, to approximate the effects of 81 mg of aspirin, you would need 400 mg to 800 mg of willow bark extract standardized to 15% salicin. To match the effects of a full 325 mg aspirin, you would need roughly 1 to 2 grams of standardized extract.

Immediate-release aspirin with minimal additives aligns best with research dosing — If you prefer aspirin, opt for immediate-release, uncoated versions. Avoid coated extended-release formulations because of their additives. Check the inactive ingredients list — corn starch should be the only one listed. A dosage of 81 mg to 325 mg daily, taken with your largest meal, is the range supported by the current research.

Why This Changes How We Think About Medicine

Step back for a moment and consider what’s happened here. For decades, the entire cancer drug discovery pipeline has been built around one question: does this drug kill cancer cells? Billions of dollars, thousands of clinical trials, an entire industry — all oriented around cell death as the primary measure of success.

Now, using the largest dataset of its kind ever assembled, researchers have shown that you can score drugs by a completely different measure — how well they push diseased cells back toward being healthy cells. And when they did this, the results matched known clinical reality with remarkable precision.

More importantly, this approach revealed something that the old method couldn’t see — A simple, ancient, inexpensive compound — salicylate, the active heart of willow bark — is doing something to colon cancer cells that ranks alongside purpose-built targeted cancer drugs. Not by killing the cells. By fixing them.

This framework applies anywhere a disease is fundamentally a cell running the wrong program — Autoimmune conditions where immune cells attack your own body. Brain diseases where neurons lose their specialized function. Scarring diseases where cells produce too much fibrous tissue.

In all of these cases, the right question is not “can we kill the cell” but “can we push the cell back toward normal.” How many other cheap, safe, widely available compounds have cancer-fighting properties that we have completely missed because we were only measuring the wrong thing? We may be about to find out.

The Bottom Line

We’ve spent decades arguing about aspirin and cancer while asking the wrong questions. We asked whether aspirin kills cancer cells. The answer was not very impressive. We asked whether aspirin’s anti-inflammatory COX inhibition reduces tumor-promoting inflammation. The evidence was mixed.

But now, using 100 million cell measurements and a fundamentally different scoring method, we can see that salicylate — the ancient compound at the heart of aspirin, the same molecule found in willow bark — is doing something far more sophisticated than anyone imagined.

It’s not just killing cancer cells or reducing inflammation. It switches on your cells’ energy sensor, shuts down a major cancer-driving gene, reactivates your body’s built-in tumor defense, and pushes cancer cells back toward normal.

And it does all of this through a pathway that has nothing to do with COX inhibition — the mechanism many people assumed was responsible. This is a common, safe, inexpensive medicine whose full power we are only now beginning to understand — and it deserves far more attention than it’s getting.

FAQs About Aspirin and Cancer

Q: Why are researchers rethinking how aspirin affects cancer?

A: A drug-testing framework analyzed about 100 million individual cell measurements to see whether drugs push cancer cells back toward a healthy state rather than simply killing them. Using this method, salicylate — aspirin without its acetyl component — ranked higher than aspirin at reversing the gene patterns associated with colon cancer, suggesting the anticancer effect works through a different mechanism than previously assumed.

Q: What part of aspirin appears responsible for the cancer-related effects?

A: Evidence indicates the salicylate portion — the same compound derived from willow bark — drives the key biological changes. After ingestion, aspirin is rapidly converted into salicylic acid in your body, which persists longer in circulation and is likely responsible for many downstream cellular effects linked to tumor suppression.

Q: How does salicylate influence cancer biology at the cellular level?

A: Research shows salicylate activates AMPK, a cellular energy sensor that suppresses the cancer-promoting gene c-MYC and enables activation of tumor-suppressive microRNAs such as miR-34. This pathway operates even when p53 — commonly impaired in cancer — is dysfunctional, which helps explain broad relevance across tumor types.

Q: What clinical evidence supports aspirin use in colorectal cancer?

A: A randomized clinical trial published in The New England Journal of Medicine found daily aspirin after surgery reduced three-year recurrence from 14.1% to 7.7% among patients with PI3K-pathway mutations.17 These findings contributed to updated guidance recommending genetic testing for PIK3CA mutations and consideration of post-surgical low-dose aspirin in eligible patients.

Q: How do aspirin and willow bark compare in practical terms?

A: Because aspirin is converted into salicylate, both aspirin and standardized willow bark extracts deliver related active compounds. Approximate equivalence described in research discussions suggests 400 to 800 mg of willow bark extract standardized to 15% salicin corresponds to typical low-dose aspirin exposure, while higher extract amounts may approximate full-strength aspirin ranges. Clinical dosing equivalence remains an area of ongoing research.

Test Your Knowledge with Today’s Quiz!

Take today’s quiz to see how much you’ve learned from yesterday’s Mercola.com article.

What is the “Peakspan exit”?

  • When performance drops below 90% of your best

    Peakspan exit marks the point when decline becomes measurable, giving you a chance to act before smaller losses spread across more body systems. Learn more.

  • When a serious disease is first diagnosed
  • When all body systems start failing at once
  • When aging stops responding to treatment

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Getting Older Doesn’t Have to Mean Getting Meaner

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I saw both men laugh off a sad reality: the assumption that age isn’t accompanied by maturity but by a kind of socially acceptable meanness. 

On a recent episode of Pardon the Interruption—a show I’ve been watching faithfully since I was in middle school—co-hosts Tony Kornheiser and Mike Wilbon opened with a lighthearted riff on “National Nothing to Fear Day.”

The show’s cold open proceeded as it often does, with the two friends laughing as Tony rattled off a list of fears—snakes, spiders, emotional intimacy. “None of that,” Tony quipped. I laughed. 

Immediately afterwards, both men—each of whom is over retirement age, Tony considerably so—conceded that their fears lists weren’t the only things increasing with age. No, they both agreed that they’re getting grumpier as they’ve aged. “The list of things that upset you get longer as you get older,” Tony said. “Absolutely, yes,” Wilbon added. 

In what was for most viewers likely an utterly unforgettable moment—part and parcel of the daily lede which ushers the audience into the show’s “A block” as the opening credits roll—I saw both men laugh off a sad reality: the assumption that age isn’t accompanied by maturity but by a kind of socially acceptable craziness and/or meanness. 

What if we aimed instead for something truly countercultural, and thoroughly biblical—becoming older and gentler?

Just think about it. We’re bombarded with stories about grumpy old men, from the 1993 eponymous romcom Grumpy Old Men to Clint Eastwood’s Gran Torino to Disney’s 2009 hit, Up. Though these films’ plots have almost nothing in common, they all attest that old people—and particularly old men—are just plain grumpy. Indeed, whether it’s feuding next-door neighbors competing for the affections of a widow; a racist veteran trying to make sense of his neighborhood’s changing demographics; or curmudgeonly Carl, the adventure-seeking septuagenarian, the films’ main characters possess the same character trait: ill-temperament.

The “grumpy old man,” which has become a popular narrative trope, is also a self-fulfilling prophecy.

But should it be?

I don’t think so. The apostle Paul, in his letter to the Galatians, outlines the fruit of the Spirit: “love, joy, peace, patience, kindness, goodness, faithfulness, gentleness, [and] self-control.” (Gal. 5:22–23). The fruit of the Spirit aren’t meant to be passing traits or youthful ideals. No, they’re the markers of a life shaped by God. “Christian virtues,” as Martin Luther put it.

If we believe sanctification is real (and it is!), then we should expect these traits to ripen and mature, not sour, over time. As we age, we should, in other words, become more virtuous, not less. Insofar as the “fruit” go, we should become more loving, more joyful, more peaceful, more patient, more kind, more good, more faithful, more gentle, more self-controlled.

How often is it the opposite? We’re hateful. Depressed. Quarrelsome. Impatient. Unkind. Unhelpful. Unreliable. Easily provoked to anger. Undisciplined.  

But that’s not what our culture celebrates. We lionize the crank. We chuckle at the retiree who shakes his fist at teenagers and complains about how everything used to be better. We write off bitterness as an earned indulgence of old age.

It ought not be this way.

Yes, the older we get, the more losses we endure. Our health declines, and our friends and loved ones pass away. Institutions disappoint. Dreams fade. Life hits hard in manifold ways. But trials don’t have to make us bitter. They can—and, with Christ’s help—they do, refine us (Rom. 5:3-5; James 1:2-4). 

Now, let me quickly say that I don’t want to attack Mike or Tony. I admire them both. Their banter has been part of my regular rhythm for the better part of two decades. But I do want to challenge the assumption baked into the claim that aging necessarily leads to irritability and detachment. 

In a culture obsessed with youth (and terrified of aging), it’s tempting to reclaim relevance by embracing a caricature: we can’t be young and charming forever, so let’s be old and cantankerous. 

But what if we aimed instead for something truly countercultural, and thoroughly biblical—becoming older and gentler? Older and more patient. Perhaps even older and kinder.

As Christians, we’re not supposed to simply get older; we’re supposed to grow up.

I know it’s fictional, but there’s a moment in The Fellowship of the Ring when Frodo, newly burdened with the knowledge of the Ring’s evil, turns to Gandalf in despair: “I wish it need not have happened in my time,” he says. Gandalf, old and weathered, does not chastise him or stoke his fear. Instead, he answers with profound wisdom: “So do I… and so do all who live to see such times. But that is not for them to decide. All we have to decide is what to do with the time that is given us.” 

Now that’s a portrait of maturity. A picture of what age, guided by grace, can become. You see, Gandalf doesn’t respond to Frodo’s fear with cynicism or irritation. He doesn’t throw fuel on the fire or throw in the towel. No. Gandalf listens. He comforts. He inspires. Let’s hope many of us grow into Gandalfs.

You see, as Christians, we’re not supposed to simply get older; we’re supposed to grow up. On the Christian view, getting older isn’t about voicing opinions, airing one’s grievances, or defending personal irritations. It’s about maturing, about becoming the kind of person whose presence and wisdom can calm rooms, restore relations, even heal. It’s about outdoing others in love, thinking of others more than selves.

I’ll end this way. The world tells us getting older means getting meaner. More easily provoked. More irritable. Crankier. But it doesn’t have to. We don’t have to become grumpy old men. 

In Christ, we can—and should—grow into the kind of “olders” Scripture envisions—warm and wise, charitable yet firm. And not because we’ve seen it all, but because we’re being transformed by the One who sees all of us—and loves us still.



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Yellow Sea Shorebird Conservation: Why These Birds Need Urge…

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National Geographic expert Jing Li has been a notable leader in conservation efforts to protect migratory shorebirds along the coast of the Yellow Sea. But her story didn’t always centre around nature conservation.

Li graduated from Zhejiang University in China with a background in marketing, and worked as a project manager at a leading data mining company for over eight years. It wasn’t until 2006 that she started to contemplate a career change.

National Geographic Signature Expert Jing Li

“I started as a birdwatcher in Shanghai, where I joined a small volunteer group dedicated to bird surveys, especially focusing on shorebirds,” said Li.

“Our team’s work led to the rediscovery of an important shorebird habitat near Jiangsu, where we found a large population of a critically endangered bird.”

This, according to Li, attracted the attention of conservation experts, ornithologists, and the National Geographic team. As of 2024, Li now leads her team as a full-time conservationist in conservation work for the Spoon-billed Sandpiper.

We caught up with Li ahead of her joining National Geographic Signature with G Adventures as an National Geographic Expedition Expert for their 2027 expeditions to China. Here’s what she had to share.

What are your views on the importance of community tourism and how travel can be a vehicle for positive change?

“I believe educating people about caring for the planet is important, and tourism can make conservation more accessible and engaging. Integrating local culture into tourism helps people understand conservation concepts more easily.

In my current project, the main challenge is encouraging people to value birding on tidal flats and helping more locals see the importance of these habitats. The more visitors from outside may sometimes push local people to re-evaluate their own culture, and on a bigger scale. I would say a proper design tourism will benefit both. The local community not only has more income but also will be proud of their land, culture, and themselves.”

A spoon-billed sandpiper on the beach in China

Can you share one travel experience that you hold close to heart?

“I was hiking with my three birding female friends in Hong Kong last week. First, I have known them for over ten years, and never spent so long together. They are from different cities in China and I am so lucky to bring them together. Second, it was my first visit to the hiking route, which is one of the best in the world, the famous MacLehose Trail; we tried only a small part of it, around eight miles. We had a beautiful Hong Kong Spring experience, including blooming trees, many butterflies, stunning ocean views, and a crystal green shining snake. It is a recharge for my friends and me, enjoying the Spring in southern China with friends sharing the same interests.”

What’s one place on earth that reminds you how amazing our planet is?

“I was on an expedition ship trip to the breeding sites for Spoon-billed Sandpiper in 2019. The ship was cruising along the coast of Kamchatka Island, Russia. Most of the coastal areas are non-residency places, but there are volcanoes, bears, lots of far eastern birds, and wonderful views, as well as Orcas and many other cetaceans with us.”

What do you find most rewarding about being a National Geographic expert?

“The best part is meeting more NG explorers, local ones, those in Southeast Asia, and more when I get a chance to explore the festival. Their stories, their projects, and their achievements are beyond my imagination. But we sometimes share the same confusion and difficulties. It feels like another you in a different world and still shining.”

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Your Grammar Was Never Wrong:

How Black Language Built America While America Tried to Bury It

Let me take you somewhere real quick.

Picture a classroom. Third grade. Maybe fourth. Somewhere in the Bronx, or Mount Vernon, or the South Side, or Compton — doesn’t matter, the address changes but the scene stays the same. A little Black child raises their hand and gives an answer in the voice they woke up with. The voice their grandmother used. The voice that got loud at cookouts, that got quiet in church right before the spirit hit, that carried whole novels’ worth of meaning in a single drawn-out *”mannnn.”*

And the teacher — maybe well-meaning, maybe not, maybe just doing what she was trained to do — corrects them. Not the content. The container. Not what was said. How it was said.

That child goes home a little quieter than they left.

Multiply that moment by twelve years of school. By every job interview where someone coached you to “sound more professional.” By every time the way you talked got read as a signal — of your education, your class, your intelligence, your worth. Multiply it by millions of people, across generations, across a country that built entire institutions around the idea that some voices belong in the center and some need to be corrected at the door.

What you get isn’t just a language gap.

What you get is a wound.

I’ve been a writer my whole adult life. With now more than two hundred books. Over two thousand songs. Street narratives, love stories, crime fiction, music that came straight from the gut and hit people exactly where they were living. And I will tell you something that took me longer than it should have to say out loud:

The voice I wrote in was never the problem.

The room was just too small.

What the Research Actually Says

There’s a whole body of scholarly work — serious, peer-reviewed, institution-backed research — that has been making this case for sixty years. It just doesn’t make it into the places most people look.

William Labov went into Harlem in the 1960s, walked the blocks, sat with the people, listened the way nobody official had bothered to listen before. What he found wasn’t what the educational establishment wanted to hear. The children being labeled as linguistically deficient were operating inside a fully systematic, rule-governed language. Complex. Expressive. More capable of certain kinds of precision than Standard American English in specific registers. They weren’t failing because of language. They were navigating a system designed to read their fluency as failure.

Geneva Smitherman took that and made it sing. Her 1977 book documented Black American English as the language of an entire people — tracing it back through the African diaspora, through the slave trade, through the Great Migration, through jazz and gospel and the dozens and the barbershop and the pulpit. She gave it a name — AAVE, African American Vernacular English — and she gave it something the establishment had long withheld: dignity.

More recently, April Baker-Bell has been naming exactly what that constant correction does to a person over time. She calls it linguistic violence. Not metaphorically. She means that the persistent demand that Black students abandon their home language in order to be seen as intelligent is an act of harm. It fractures identity. It teaches children to surveil their own mouths.

And Jonathan Rosa extended the whole conversation outward — showing how what Black communities experience with language is part of a broader pattern. That society has developed a way of hearing people’s voices and immediately filing them by race, by status, by whether they deserve to be believed. He calls it raciolinguistic ideology. The idea that you don’t just speak — you sound like what you are. And what you are gets decided before you open your mouth.

John Russell Rickford tied it all together personally — as a scholar who grew up inside this language, who defended it inside institutions that wanted him to keep it outside the door. His argument is simple and devastating: Black language doesn’t just have rules. It has soul. It carries the weight of how millions of people have loved each other, buried each other, raised children, prayed, grieved, celebrated, and survived.

All five of these scholars — working across decades, from different angles — arrived at the same conclusion.

Your grammar was never wrong. The standard was always political.

What “Standard” Actually Means

Here’s something worth sitting with.

Standard American English — the version you were graded on, the one that gets you the job, the one the news anchor uses, the one teachers spent twelve years trying to install in you — is not neutral. It is not the logical endpoint of language evolution. It is not more precise or more beautiful or more capable of expressing the full range of human experience.

It is the dialect of people who had power when the rules got written down.

That’s it. That’s the whole secret.

Every language has dialects. Every dialect is rule-governed. The difference between a dialect that gets called “standard” and one that gets called “broken” is not linguistic. It is political. It is about who was sitting at the table when the textbooks were printed, whose way of speaking got normalized into the curriculum, whose kids got rewarded for sounding like themselves.

Black people in America built a language out of the wreckage of everything that was taken. They came from hundreds of different African linguistic traditions — Wolof, Yoruba, Akan, Igbo, and more — were stripped of the ability to communicate openly with each other, forced to acquire English under conditions of violence and surveillance, and still produced something that scholars now spend careers trying to fully document. The call-and-response. The tonal semantics. The signifying. The way a single word can carry irony, affection, warning, and praise simultaneously depending on nothing more than how long you hold it.

That’s not broken English.

That’s engineering under impossible conditions.

What This Means for Your Story

I’m not writing this as an academic. I never claimed to be one. I’m writing this as someone who grew up in the Bronx, who spent years in spaces that society had labeled as outside, who put pen to paper and told stories that the literary establishment largely ignored — not because the stories lacked power but because the power showed up in a voice they weren’t prepared to receive.

And what I’ve come to understand, having spent time with these books, is that my whole catalog has been part of something larger than I named it.

Every street narrative I wrote in the vernacular was, whether I called it that or not, a document. Evidence that this language could carry tragedy and humor and moral complexity and desire and grief all at once. Every character I gave a fully realized interior life — in their own voice, not translated into something more “acceptable” — was a small act of refusal.

Refusal to split.

Because that’s what the system asks you to do. Split yourself. Bring your acceptable self to the institution and leave your real self at the door. Code-switch so efficiently that nobody can tell you ever had another language. Make yourself legible to the standard and invisible to your own people simultaneously.

I watched people do that my whole life. And I watched what it cost them.

The ones who split clean — who mastered the standard, who got the degrees and the titles and the corner offices — sometimes made it back to themselves, and sometimes didn’t. The language you perform long enough starts performing you. And one day you realize you’ve spent so many years sounding like someone else that you’ve forgotten what your own voice felt like when it wasn’t trying.

The Ones Who Never Split

Here’s who I want to talk about for a minute.

The ones who never split.

Not because they couldn’t. Because they chose not to.

Think about what it takes to build an art form — hip-hop — inside the most surveilled, policed, and dismissed communities in America, and have that art form eventually become the dominant global music culture. Think about the linguistic architecture in a single Nas verse. The way it moves between street reportage and philosophical reflection without announcing the transition. The density of information per line. The way meaning doubles and triples depending on what you know coming in.

That’s not accidental. That’s craft operating at the highest level — inside a language that was being called broken in classrooms at the exact same time it was being called genius on record labels.

KRS-One built an entire pedagogical theory inside rap music. He wasn’t just rhyming. He was teaching. Every performance was a lecture, a ritual, a demonstration of what this language could do when you took it seriously as a vehicle for transmitting knowledge.

Black Thought has been holding down one of the most technically precise lyrical traditions in the music for thirty-plus years — in the vernacular, with the full range of cultural reference, without apology, without translation.

These weren’t people who succeeded despite their language. They succeeded because of it. Because they understood, even if they didn’t always articulate it in academic terms, that the language itself was the argument.

What the School Never Taught You

Here’s the thing that should make you angry — and then should make you strategic.

There is a direct line from the Harlem Renaissance to AAVE scholarship to hip-hop to contemporary Black literature to your life. A straight line. A tradition. And most of us were never taught it existed.

We were taught to see Black cultural production as a series of isolated incidents — this musician, that writer, this movement, that moment. Never as a continuous tradition with its own internal logic, its own standards of excellence, its own way of measuring what counts as mastery.

But the tradition exists. It has always existed. And the people who’ve spent their careers documenting Black language have been, in their own way, doing the same thing that your favorite rapper does when they drop a verse full of historical reference — they’re insisting that this is real, this matters, this deserves to be taken seriously on its own terms.

What that means for you — right now, wherever you’re sitting as you read this — is that you are not starting from scratch.

You are not an anomaly. You are not an exception. You are not a person who somehow produced meaningful work despite your background, your community, your language.

You are the continuation of something.

The question is whether you know it.

The Violence Was Always Linguistic First

I want to go somewhere a little darker for a moment, because this conversation doesn’t get complete without it.

Baker-Bell’s framework — linguistic violence — is not hyperbole. The assault on Black language has been, since before this country was a country, one of the primary mechanisms of control. You cannot enslave people who can communicate freely with each other. You cannot maintain a caste system if the people at the bottom are allowed to develop and transmit their own knowledge in their own terms. The suppression of language was never incidental to oppression. It was central to it.

And what makes it so effective — what makes it persist long after the formal legal structures of slavery and segregation — is that it gets internalized. You don’t need someone standing over you with a correction anymore. You learn to correct yourself. You learn to hear your grandmother’s voice and wince. You learn to translate your own thoughts before they leave your mouth. You learn to pre-edit your realness.

That internalization is the goal. That’s the mechanism that keeps the system running without obvious enforcement.

And the antidote — the thing that actually works — is not learning to perform the standard more fluently.

The antidote is understanding what your voice actually is.

Not as a consolation prize. Not as a cultural artifact to be preserved behind glass. But as a living, generative, world-making instrument that has always been capable of more than the standard ever gave it credit for.

What I’m Building With This Knowledge

I’m not sharing this just to make a historical argument.

I’m sharing it because it changes how you build.

When you understand that your voice — your actual voice, the one you woke up with, the one your people passed down to you — is not a liability but an asset carrying hundreds of years of accumulated expressive intelligence, you stop asking permission to use it.

You stop code-switching in your art.

You stop writing the Black characters in your stories as translations of themselves.

You stop producing content that gestures at your culture from the outside, that flattens the language into something more universally “accessible,” that trades the full weight of a moment for the comfort of an audience that didn’t earn it.

You write from the inside.

And what comes out when you write from the inside — when you trust the language, trust the tradition, trust the people who built it — is the only thing that lasts. It’s the thing that makes someone set your book down at 2am because they need a minute. It’s the thing that makes a song feel like somebody reached into your chest and named something you didn’t have words for. It’s the thing that makes a story feel less like entertainment and more like testimony.

Testimony. You recognize that word.

Smitherman called it testifyin’. The rhetorical act that is simultaneously personal witness, cultural transmission, and spiritual declaration.

That’s what the best Black art has always been.

That’s what I’ve been doing for two hundred books, whether I named it or not.

And that’s what you can do too — once you stop apologizing for the voice you showed up with.

Where This Leaves Us

The scholars I’ve referenced spent careers inside institutions fighting for the right to say what Black folks have always known at the kitchen table: this language is real, it is complete, it is beautiful, and it belongs.

The artists — the rappers, the novelists, the preachers, the poets — said the same thing with their lives, with their work, with every choice to stay in the voice instead of stepping out of it.

And the people who lived inside this language — your grandparents, your neighbors, the corner, the church, the cookout — they never needed a degree to know their words carried weight.

The research just finally caught up to what they already understood.

So here’s where I land.

Your grammar was never wrong.

Your cadence was never broken.

Your stories — the ones that came out with the music of your actual life in them — were never too much or too little for the page.

The standard was always political.

Which means the decision to ignore it is always personal.

And the most powerful thing you can do — for yourself, for your people, for the tradition that made you — is write like you mean it.

In the voice you were born into.

Without apology.

Without translation.

The whole way through.

*Relentless Aaron is an author, music producer, publisher, and multimedia entrepreneur based in Atlanta, Georgia. His catalog spans 200+ books, 2,000+ music compositions, and an expanding AI-driven content universe. He writes, builds, and moves — always in his own voice.

“Reality Dropout” by Artist Little Thunder

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A series by Hong Kong-based artist Little Thunder. “Reality Dropout” explores the emotional disconnection between our physical presence and digital identity. This collection of images sees Little Thunder taking a look back at her previous body of work before she starts in a new direction:

“Through intimate portraits and subtle surrealism, I depict young women suspended between self-presentation and a yearning for sincerity, fragile yet resilient in their emotions, quietly searching for a place where reality can still feel tender and true.”



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What Black TikTok Means By ‘You the Birthday’ Trend

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TikTok, you the birthday

According to Black TikTok, if you become the center of attention, you might be the birthday.


A new “You The Birthday” trend created by Black TikTok has made its rounds across the internet.

The phrase stands as the latest viral hit started by Black creators on the video sharing platform. However, those not in the know remain confused on what the phrase means, and, furthermore, how to use it.

One TikToker, named The Trill Professor, gave a break down on the how the phrase plays into AAVE’s fluid grammatical structure.

@thetrillprofessor “You the birthday” 🤝 AAVE #aave #english #teachersoftiktok ♬ original sound – Travis

“Just context, intonation and cultural understanding doing all of the work,” explained the TikToker, real name Travis G. Hubbard, on how the phrase came to life.

Hubbard, a current Ph.D. candidate in literacy, language and culture, told TODAY about the term’s new connotations.

“When someone says ‘you the birthday,’ they are positioning the subject as a metaphorical embodiment of everything the word birthday connotes — celebration, joy, the reason everyone showed up,” Hubbard explained. “You are not at a birthday…You are not having a birthday. You are the birthday. The subject becomes the thing itself.”

Forbes further described the phrase as a way to say someone is acting as the main character of a situation, warranted or not.

“The phrase is used to describe a person who is trying too hard, acting over-the-top or expecting fawning, birthday-like attention from everyone in the room, to the point where they embody the whole party,” detailed the publication.

A new term added to the ever-expanding AAVE language, “you the birthday” can be a term of endearment or a jab at the directed individual. Of course, this also depends on the context.

In the video, Hubbard added, “And Black English does this constantly and beautifully.”

For example, some TikTokers have left comments calling someone “the birthday” if they achieve a goal or made a good point on a subject. On the flip-side, users also hurl out the phrase to those exhibiting obnoxious behavior, or who want to stand out unnecessarily.

As the phrase became popular on TikTok and other platforms, elder internet users expressed their confusion. While Gen-Zers eventually came to the rescue, they did clown millennials for not initially keeping up.

The phrase spawned other versions that follow a similar linguistic pattern. Whenever another TikToker does something or expresses a feeling that perpetuates a certain trait, savvy users now call them another word, evolving the phrase while remaining mostly true to its original rules.

TikTokers even played into this expanded trend on Hubbards’ video.

“He explained the birthday, he the birth certificate,” shared one commenter, comparing his explanation of the context to the identification document.

Another stated, “video long, you the birthday month.”

“This is layered, you the birthday cake,” joked another.

However, like many trends, Black TikTok is already aware of the outer world catching onto “you the birthday,” signaling that party may end early in favor of the next viral phrase.

RELATED CONTENT: Lizzo Wants To ‘Bring Back Gatekeeping’ To Stop White People ‘Talking Like Black People’



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The Bootlegging, Blues Singing Star of 1930s Prison Radio

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Filed
1:00 p.m. EDT

04.12.2026

Hattie Ellis was poised for post-prison fame. Then she encountered shotcallers who didn’t value her voice.

This essay is part of Redemption Songs, a limited-run newsletter that spotlights one song each week by incarcerated artists. Sign up now to get a new song each Sunday afternoon until September:

The Bootlegging, Blues Singing Star of 1930s Prison Radio

Listen if you like: Billie Holiday, Buddy Guy, Robert Johnson

My favorite song on the Oscar-winning soundtrack to the movie “Sinners” is “Pale, Pale Moon,” where actress Jayme Lawson channels the great blues women of the 1920s and 1930s like Ma Rainey and Bessie Smith. But the song also reminded me of Hattie Ellis, the imprisoned Dallas vocalist who once earned comparisons to Ella Fitzgerald and Billie Holiday.

Ellis is mostly unknown, perhaps because she left behind only two songs, recorded while she was incarcerated in The Goree State Farm for Women near Huntsville, Texas. But almost a century later, her voice remains mesmerizing through the grit of early phonograph technology. I wish someone would make a movie based on what we do know about her life, because the bare facts are so dramatic.

As Texas Monthly’s Skip Hollandsworth reported, Ellis was involved in Prohibition-era bootlegging at the age of 20. One day, she got into an argument with a customer named Henrietta Murphy, possibly over the cost of whiskey. Murphy, who was likely drunk, urinated on Ellis’s floor. After the argument, Ellis drove to Murphy’s house and shot her in the stomach.

At trial, Ellis said the victim attacked her with a razor. The jury evidently didn’t believe her, since she got a 30-year sentence for murder. She was sent to Goree, a segregated facility named after a former slave owner and Confederate officer. Black women worked in the fields while White women worked in a garment factory.

But each week, some of the women were taken to a male prison nearby to perform on “Thirty Minutes Behind the Walls,” a variety radio show broadcast on Wednesday nights. Scholar Caroline Gnagy writes in her 2016 book “Texas Jailhouse Music: A Prison Band History” that most of the performers were White men, so we can assume it was Ellis’ skill during her debut, in March 1938, that earned her a spot almost every week for three years.

According to Gnagy, Ellis received as many as 3,000 fan letters in a single week, singing hits of the era like “Heart and Soul,” “Stormy Weather” and “Somewhere Over the Rainbow,” since “The Wizard of Oz” came out while she was inside.

I found a 1939 clip from The Echo, the state prison newspaper of the era, that says Ellis would perform for the public at “the Texas Prison System’s big Juneteenth celebration,” which also involved a prisoner baseball game. (She also sang for the public at the annual Texas Prison Rodeo.) She was often introduced in public with condescending monikers that focused on her race, like the “blues-singing Negress,” and the “dusky songstress.”

Among her fans was Texas Gov. Wilbert Lee “Pappy” O’Daniel, who praised the power of the radio show that featured her every week. “Before the advent of radio, prisoners were exiled; citizens outside paid little attention to them,” O’Daniel said on “Thirty Minutes Behind the Walls” in 1939. “But now you hear them talk; you hear them sing; you find out they are sons and daughters of good mothers. You find out they made mistakes, thus proving that they are human.”

A black-and-white photo of a group of musicians dressed in white, with some wearing cowboy hats, standing in a horseshoe shape, while a Black woman in a white dress sings into a microphone. The group is standing on the rodeo grounds, and in the background are the stands where the audience is seated.

Hattie Ellis performs at the annual Texas Prison Rodeo in the 1930s.

O’Daniel went on to pardon Ellis, perhaps seeing it as a canny political move given her popularity (sort of like how President Donald Trump granted clemency to rappers such as Lil Wayne and Kodak Black). The Echo reported that professional talent scouts were interested in her and she wanted to have a music career, but there is no public record to explain why she never succeeded. She returned to prison briefly in the 1950s, after violating her parole, but that’s where the breadcrumb trail ends.

There are no surviving recordings of the radio show, but in 1939, the folklore researchers John and Ruby Lomax captured Ellis singing “I Ain’t Got Nobody,” a classic of the era, and “Desert Blues,” which she said she wrote. A White guitar player named Jack Ramsey played behind her, which is surprising given how segregated prisons were at the time.

John Lomax had previously found success by promoting the music of Huddie Ledbetter — better known by his stage name Lead Belly, a blues singer in a Louisiana prison who had also earned release at one point through his music.

But he wasn’t as impressed with Ellis. Lomax had a paternalistic, conservative view of authenticity and wanted prison music untouched by popular culture. In field notes preserved by the Library of Congress, he wrote, “Hattie’s singing is fast becoming ‘throaty’ as she strives to imitate the professional ‘blues’ singers.”

But her ability to sound like the greats of her era is precisely why I think she could have had a career. We can only guess why she didn’t.

Liner Notes:

Artist: Hattie Ellis | Song: “Desert Blues” | Date: May 14, 1939 | Location: The Goree State Farm for Women, Walker County, Texas | Guitarist: “Cowboy” Jack Ramsey |Producers: John and Ruby Lomax

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Meet the Stars – Hollywood Life

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‘Hunger Games: Sunrise on the Reaping’ Cast Guide: Meet the Stars of the Prequel
Image Credit: Murray Close/Lionsgate

The Hunger Games: Sunrise on the Reaping, directed by franchise veteran Francis Lawrence, is gearing up for its highly anticipated release this year, marking the series’ return to the big screen for the first time since The Ballad of Songbirds & Snakes.

Although it’s the newest installment, the film takes audiences back decades before Katniss Everdeen (played by Jennifer Lawrence) stepped forward as tribute. This prequel dives into the origins of Haymitch Abernathy — portrayed by Woody Harrelson in the original films — and the brutal events of the 50th Hunger Games, better known as the Second Quarter Quell.

“Haymitch has always been a fan favorite, and his origin story is one of the most anticipated in the franchise,”co-president of Lionsgate Motion Picture Group Erin Westerman said in a press release. “We can’t wait for fans to experience the story that shaped one of the most compelling characters in the series.”

Led by Joseph Zada as young Haymitch, the prequel introduces a fresh cast of rising stars and familiar faces stepping into the world of Panem. Among those familiar faces will be Jennifer and Josh, who will reprise their roles as Katniss and Peeta, respectively, according to The Hollywood Reporter

Here’s who is starring in this long-awaited return to the arena.

Jennifer Lawrence as Katniss Everdeen

Though her appearance might be brief, it’s still a huge moment for the original heroine of the franchise. Per The Hollywood Reporter, the actress is reprising her role as Katniss in a “flash-forward scene.” The scene in question likely refers to the epilogue of the book when Haymitch bonds with Katniss and Peeta as they grow up.

Josh Hutcherson

Per THR, Josh is reprising his original role as Peeta in the “flash-forward scene.” The I Love LA actor kept any details of his return a secret while he was hard at work promoting his other projects.

Joseph Zada as Haymitch Abernathy

Zada, an Australian actor, takes on the role of young Haymitch Abernathy, the sole male tribute from District 12 in the 50th Hunger Games. Zada has previously appeared in Australian productions such as Invisible Boys and Total Control. He’s also set to appear in the upcoming series We Were Liars and East of Eden, starring alongside Florence Pugh.

Casting a younger version of such a well-established character was no small task. In a March 2025 interview with Variety, producer Nina Jacobson acknowledged the difficulty of finding someone who could embody the essence of Haymitch without mimicking Harrelson’s original portrayal.

“Nobody can be Woody Harrelson but Woody Harrelson,” she said. “You don’t want somebody who’s impersonating Woody, but you want somebody who very credibly feels like they could be a young version of this character, before the trauma and grief and rage that the fallout of the Games create.”

Whitney Peak as Lenore Dove Baird

Whitney Peak portrays Lenore Dove Baird, Haymitch’s girlfriend and a member of the Covey, a musical group from District 12. Peak is known for her roles in the Gossip Girl reboot and Hocus Pocus 2.

Mckenna Grace as Maysilee Donner

Mckenna Grace plays Maysilee Donner, another tribute from District 12 and a temporary ally of Haymitch during the Games. At just 19, Grace is already a seasoned film and television actor, with standout roles in Ghostbusters: Afterlife, The Handmaid’s Tale, and Young Sheldon.

Jesse Plemons as Plutarch Heavensbee

Jesse Plemons plays Plutarch Heavensbee, a rising figure in the Capitol who becomes crucial to the future of Panem. The 38-year-old actor is known for his acclaimed performances in The Power of the Dog, Breaking Bad, and Fargo.

“Jesse is one of the most talented actors of his generation, with a proven record of picking his roles selectively,” Lionsgate Motion Picture Group Co-President Westerman said in a statement, per Deadline. “We are honored that he has chosen to bring his own take to one of the most fascinating figures in Panem, and feel that his previous collaboration with Philip Seymour Hoffman makes it all the more special. His Plutarch will be both a tribute to the character fans have already come to know and a portrayal he makes his own. We can’t wait for audiences to see it.”

Elle Fanning as Effie Trinket

Ellen Fanning will be playing the younger version of Effie Trinket, the iconic character from the original franchise who lived with the term, “May the Odds Be Ever in Your Favor.” Elle has appeared in a slew of projects, some of which include A Complete Unknown, The Girl From Plainville and Maleficent.

Kieran Culkin as Caesar Flickerman

First played by Stanley Tucci, Caesar Flickerman will now be 24 years younger than when we first met him in The Hunger Games. The buoyant and charismatic show host is known for his on-screen charm as he welcomes tributes onto the stage before they fight to the death. In Sunrise, Caesar will be played by Kieran Culkin.

Kieran has been seen in a variety of roles but has recently earned more accolades for his work. Some of his most notable performances are in Succession and in A Real Pain, for which he won the Oscar for Best Supporting Actor.

Billy Porter as Lucretius “Lucky” Flickerman

Before Caesar Flickerman became the face of Capitol pageantry, there was Lucretius “Lucky” Flickerman—his flamboyant and trailblazing predecessor. In Sunrise on the Reaping, Lucky is the Capitol’s original Hunger Games host, introducing audiences to the twisted spectacle for the first time.

Lucky Flickerman will be portrayed by Billy Porter, whose commanding stage presence and sharp delivery make him a natural fit for the Capitol spotlight. Porter is best known for his Emmy-winning role in Pose, as well as his groundbreaking appearances on Broadway and red carpets.

Glenn Close as Casca Highbottom

Casca Highbottom, the dean of the Academy, is the somber intellectual credited with creating the Hunger Games—though not by choice. In Sunrise on the Reaping, she is portrayed later in life as the Games approach their 50th anniversary.

Veteran actress Glenn Close takes on the role of Casca Highbottom. A seven-time Oscar nominee, Close is revered for her powerful performances in films like Fatal Attraction, The Wife, and Hillbilly Elegy.



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Facing the loss of government disability benefits, Ian wonde…

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Ian currently receives the Canada Pension Plan (CPP) disability benefit, which accounts for $1,600 of his monthly $2,600 income.

Ian is 63 and living with a permanent disability. He wants to make sure his income — largely composed of government benefits and a recent inheritance — will meet his cash flow needs.

He has two key challenges. The first is one that many people who receive government disability pensions often face when they turn 65. It is at this age that disability benefits are typically converted into lesser amounts in retirement pensions.

For example, Ian currently receives the

Canada Pension Plan (CPP)

disability benefit, which accounts for $1,600 of his monthly $2,600 income. This is an age-restricted program and will automatically convert to a likely reduced Canada Pension Plan benefit when Ian turns 65. An annuity that currently pays about $790 a month will also expire in two years.

In addition, he receives the federal disability tax credit of $200 a month.

The second challenge: His rental expenses are expected to double to $2,000 in the next six to 12 months, increasing his total monthly expenses to at least $3,000 and exceeding his current income.

Ian would also like to know how much he can expect to receive in monthly

Old Age Security (OAS)

, and

Guaranteed Income Supplement (GIS)

payments.

He wants to ensure that he is effectively managing his recent inheritance of $143,000 to avoid losing benefits and that he meets his cash flow needs.

To date, he has directed $30,000 of this money into a self-directed

tax-free savings account (TFSA).

The remainder of the inheritance is in a high-interest savings account (HISA). He also has $13,000 in additional TFSAs. He plans to keep $20,000 in the HISA as an emergency fund but would like advice on the most efficient way to invest the remaining assets to minimize the effect on government benefits. For example, should he consider setting up a discretionary trust or specified disability savings plan?

In addition to his inheritance, Ian also has $24,000 in a life income fund (LIF). How can he ensure his investments and government benefits will meet his needs?

What the expert says

One critical tool to ensure Ian maximizes all income sources is to leverage his TFSA, said Graeme Egan, a financial planner and portfolio manager who heads CastleBay Wealth Management Inc. in Vancouver.

But first, it is important to understand his income. Unlike the CPP disability pension, which will revert to his calculated CPP pension benefit at 65, the federal disability tax credit will continue as long as his impairment meets the

Canada Revenue Agency

’s criteria.

“Ian may also be eligible for the GIS payment of up to $1,109 per month if his annual income is below the current threshold,” which is $22,512, said Egan. “GIS is calculated yearly and is based on the previous year’s income. The GIS is non-taxable and would be added on top of his Old Age Security payments. Assuming he meets the criteria, the current monthly maximum OAS benefit is about $817, which is indexed to inflation so it will be higher when he commences OAS at age 65 and will help to offset the loss of his annuity.”

Maximizing his TFSA by contributing $73,000 from his inheritance to use up his remaining contribution room will allow Ian to benefit from tax sheltered growth, Egan said. “In addition, any withdrawals are non-taxable. As such, they do not affect eligibility for GIS and OAS payments.”

“Ian has already invested $30,000 in a high-interest savings

exchange-traded fund

inside his TFSA, but it is only paying a 1.7 per cent yield.” For this reason, Egan suggested investing $103,000 (the $30,000 plus an additional $73,000 TFSA contribution room he has) in a managed pre-selected portfolio with between a 40 per cent equity/60 per cent fixed income to a 20/80 asset mix to ensure he has some equities for long-term growth and a hedge against inflation.

“Or, if Ian wants to self-manage, understanding he wants to maximize income, he could consider an ETF that invests in Canadian banks and distributes a high monthly yield. Canadian banks tend to raise their dividends and be conservative investments over the long term but the extra yield is generated from covered call option strategies to earn extra income in the ETF,” said Egan. “For example, the current yield of the Hamilton Canadian Financials Yield Maximizer ETF (HMAX) is around 12 per cent. He could then arrange to have the monthly income withdrawn from his TFSA quarterly and this would not affect OAS or GIS benefits.”

According to Egan’s calculations, if Ian consolidates his TFSAs into one account ($116,000) and invests this money in an ETF such as HMAX, assuming at least an average eight per cent long-term yield for 25 years, he could extract $900 monthly if he draws down the capital over 25 years. This would be non-taxable.

Egan recommended earmarking $20,000 remaining from the inheritance for emergencies and investing the rest. “One option is to open a … self-directed account alongside his TFSA and invest in a tax-effective, total return index fund, such as Global X Canadian High Dividend Corporate Class ETF.

The managed LIF Ian has will also add to his monthly income as he has to take out a minimum payment each year but is limited to a maximum amount, said Egan, who suggested Ian take out the minimum to keep his income in check. “The LIF should be invested in a balanced mix for the long term and to hedge against inflation. He can opt to change the current aggressive risk profile when he reaches age 65.”

Ian does not need to go to the effort of establishing a discretionary trust, given the amount of money involved and fees associated with setting it up and maintaining it, Egan said. Also, a Registered Disability Savings Plan (RDSP) may not be more advantageous than a TFSA for Ian, he added. “Even though there are government grants and tax-sheltered growth in an RDSP, withdrawals are partially taxable, whereas the TFSA offers tax-free growth and tax-free withdrawals, which do not affect OAS and GIS. ”

*His name has been changed to protect his privacy.

Are you worried about having enough for retirement? Do you need to adjust your portfolio? Are you starting out or making a change and wondering how to build wealth? Are you trying to make ends meet? Drop us a line at wealth@postmedia.com with your contact info and the gist of your problem and we’ll find some experts to help you out while writing a Family Finance story about it (we’ll keep your name out of it, of course).

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Galettes Bretonnes (Britanny Butter Biscuits)

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Galettes Bretonnes are a classic French butter biscuit from Brittany, known for their rich flavour and delicate, sandy crumb. Made with plenty of butter, they’re simple, golden, and melt-in-the-mouth. In France you can buy these at the shops, but I’ve always felt they’re the kind of thing worth making at home. Let’s go!

Galettes Bretonnes - French Butter Biscuits

Galettes Bretonnes

Galettes Bretonnes are traditional butter biscuits from the Brittany region of France (Bretagne in French) that have a deep buttery flavour and a signature short, crumbly texture that’s still snappy and hold its shape despite being thin. Baked into flat rounds with a cross pattern, they sit somewhere between shortbread / French sablé and vanilla biscuits (sugar cookies) and are not to be confused with their more substantial cousin, the Palet Breton.

They’ve always felt familiar to me. My father and grandparents spent many holidays in Brittany and talked about it often, and my grandma would buy Galettes Bretonnes for me when I was a kid. Still takes me right back, so here’s my recipe to make them at home.

Galettes Bretonnes - French Butter Biscuits
Galettes Bretonnes - French Butter Biscuits

Ingredients

You only need 5 ingredients to make these buttery biscuits (milk doesn’t count 😅).

Galettes Bretonnes ingredients
  • Salted butter – This cookie is specifically made with salted butter rather than unsalted which is typical for cooking recipes from the Brittany region of France. If you don’t have salted butter you can use unsalted and add 3/4 tsp of cooking salt / kosher salt.

  • Caster sugar (superfine sugar) – This is a finer grain sugar that dissolves more easily than regular granulated sugar which is larger grains.

  • Egg yolks – One goes into the dough for extra richness and texture you don’t quite get from a whole egg, and another is brushed on top to give the biscuits that golden finish.

  • Flour – These biscuits are made with plain / all-purpose flour.

  • Vanilla extract – This adds flavour so they taste more than just a sweet biscuit.

  • Milk – Added to the egg wash to stretch it out, so you’ve got enough to brush all the biscuits without needing an extra yolk.

How to make Galettes Bretonnes

This is one of those biscuits where the dough is rolled out thinly, biscuits cut out using a round cutter then baked. The dough is easy to work with but once you cut the rounds out, handle them gently using a spatula to move them onto the trays.

make biscuit dough

Galettes Bretonnes steps
  1. Cream butter and sugar – Using an electric beater on medium low speed, beat the butter in a bowl for about 30 seconds until smooth. Add the sugar then beat on medium for about 1 minute until the butter becomes pale in colour.

  2. Yolk and vanilla – Add the egg yolk and vanilla, then beat just until combined then stop beating.

Galettes Bretonnes steps
  1. Add flour in 3 batches – Add one-third of the flour and mix in with the beater on medium low speed. Then add half the remaining flour, mix in again with the beater, then beat in the remaining flour. It will resemble wet sand.

  2. Bring dough together – Turn the mixture out onto the counter, then push the mixture together into a mound.

Galettes Bretonnes steps
  1. Knead into ball – Use your hands to knead the dough so it comes together into a smooth ball.

  2. Fridge 1 hour – Wrap the dough in cling wrap and refrigerate for 1 hour.

CUT OUT AND BAKE

Galettes Bretonnes steps
  1. Roll out dough – Put the dough between 2 sheets of baking paper (parchment paper) then use a rolling pin to roll the dough out to 5mm / 0.2″ thickness. It doesn’t matter what shape it is as long as you get the right thickness.

  2. Cut out biscuits – Use a 7cm/2.8″ round cookie cutter to cut out rounds and use a spatula to transfer to lined baking trays (you will need 3 trays).

Galettes Bretonnes steps
  1. Gather and re-roll scraps – Gather the dough scraps and re-roll out and continue cutting out cookie rounds. You should get 24 cookies in total.

  2. Egg wash – Whisk the egg yolk and milk and brush onto the surface of each biscuit.

Galettes Bretonnes steps
  1. Cross imprint – Using a 4 pronged fork, dip it in water then lightly drag it across the surface (into the dough, not just the egg wash) in a cross formation (per step photo above) for the signature design.

Galettes Bretonnes steps
  1. Bake 15 minutes – Place 2 trays in the oven and bake for 15 minutes at 180°C/350°F (160°C fan-forced) until they are light golden. Keep the 3rd tray aside and cook it after the first 2 trays are done.

  2. Cool – Leave on the trays for 5 minutes, then transfer to a rack to cool completely.

Galettes Bretonnes - French Butter Biscuits

Once cooled, these biscuits can be enjoyed at any moment as a treat, with a cup of tea or coffee, mid-afternoon or whenever you feel like something small yet satisfying. For me, they’ve always been tied to the stories of Brittany that my grandfather used to tell me, along with a few from my childhood, and I hope they find a place in your kitchen too. Bon appétit! – JB


Watch how to make it

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Galettes Bretonnes - French Butter Biscuits

Galettes Bretonnes (Brittany Butter Biscuits)

Servings24 galettes

Tap or hover to scale

Recipe video above. Galettes Bretonnes are classic French butter biscuits from Brittany and one of my favourite! Known for their rich slightly salty flavour, delicate sandy crumb and their melt-in-the-mouth texture, they’re a staple in shops across France. Yet they’ve always felt personal to me because my grandmother would always buy some for me as a child. They still take me right back, so here’s my recipe to make them at home.

Prevent screen from sleeping

Instructions

ABBREVIATED RECIPE:

  • Cream butter and sugar. Beat in yolk and vanilla, then beat in flour in 3 batches. Turn out, knead into ball, refrigerate 1 hr. Roll out into 5mm/0.2″ thickness, cut out 7cm/2.8″ rounds (24 pieces). Brush with egg wash, score cross design with fork, bake 15 min @ 180°C / 350°F (160°C fan).

FULL RECIPE:

  • Cream butter & sugar – Place butter in a bowl and beat for 30 seconds using an electric beater on low speed. Then add sugar and beat for 1 minute on medium until fluffy and slightly paler in colour.

  • Beat in egg yolk and vanilla, just until combined then stop beating.

  • Make dough – Add 1/3 of the flour to the mixture and mix still using the beater on medium low speed. Once incorporated, add half of the remaining flour then mix and repeat with the remaining flour. It will resemble like wet sand. Turn out onto the work surface and use your hands to bring it together, then knead it into a smooth ball of dough.

  • Rest – Wrap in cling film and refrigerate for 1 hour. (Note 4)

  • Preheat oven to 180°C / 350°F (160°C fan-forced).

  • Roll – Using a rolling pin, roll the dough between two sheets of baking paper / parchment paper to 5mm / 0.2″ thickness. It doesn’t matter what shape it rolls out to as long as it’s the correct thickness.

  • Cut – Using a 7cm / 2.8″ round cookie cutter, cut out the galletes. Use a spatula to transfer them onto 3 baking paper / parchment paper lined trays. Re-roll scraps and repeat until all dough is used – you should get 24 biscuits. (Note 5)

  • Egg wash – Mix together egg yolk and milk then brush the galettes lightly with the egg wash.

  • Decorate – Dip a fork in water and use the back of the fork to lightly scrape a cross on the surface of each biscuit, lightly etching a line into the dough, not just the egg wash (watch video, it’s helpful).

  • Bake 2 trays for 14 – 15 minutes until the biscuits are lightly golden (watch the top tray as it might brown faster). Once they are done, bake the 3rd tray.

  • Cool – Leave biscuits on trays for 5 minutes, then transfer to a rack to cool completely.

Recipe Notes:

1. Butter – These biscuits are traditionally made with salted butter, Brittany is famous for it. If using unsalted butter, just add 3/4 tsp of cooking salt / kosher salt.
2. Sugar Regular/granulated sugar works as well but my go-to is caster sugar when it comes to sugar because the grain is finer so you know it incorporates better.
3. Leftover egg whites This recipe uses two egg yolks and I know it can feel a bit annoying to be left with egg whites, but don’t waste them! Here is the perfect cookie recipe for you to use!
4. Make ahead – The dough can be made up to 2 days in advance. Keep it well wrapped in the fridge, then let it soften slightly at room temperature before rolling if it’s too firm.
5. Shape – The normal classic look is more rustic with crinkled edges, but I’ve gone for neat rounds here. Feel free to use either, or both! Hopefully the people of Brittany won’t have a go at me for that one!
Storage – Store in an airtight container at room temperature for up to 1 week (I kept mine even longer!). They stay beautifully crisp and buttery. Not suitable for freezing. 
Nutrition per serving.
 

Nutrition Information:

Calories: 126cal (6%)Carbohydrates: 15g (5%)Protein: 2g (4%)Fat: 7g (11%)Saturated Fat: 4g (25%)Polyunsaturated Fat: 0.3gMonounsaturated Fat: 2gTrans Fat: 0.2gCholesterol: 32mg (11%)Sodium: 49mg (2%)Potassium: 17mgFiber: 0.3g (1%)Sugar: 5g (6%)Vitamin A: 209IU (4%)Calcium: 6mg (1%)Iron: 1mg (6%)

In Memory of Dozer

A little behind-the-scenes moment for you. This was taken while we were shooting the laksa for Nagi’s second cookbook. While we were busy plating, adjusting, and chasing the light, Dozer had found the best spot in the house… fast asleep right under the shooting table, completely unfazed by it all. Classic Dozer. ♥️🦮

Galettes bretonnes Dozer



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