A portion of this video is sponsored by Radio Code. For centuries, cancer has been thought of as an insidious disease, an insatiable force consuming the body from the inside out. In the 1600s, physicians even tried feeding it, literally.
Applying raw meat to tumor areas in a desperate hope that cancer would select stake over patient. With morbid fascination, the idea of somehow controlling cancer's hunger has permeated everything from old wives tales recommending fasting. I feel like a new man to their modern-day equivalent, your friendly neighborhood wellness guru.
And it was a so-called wellness warrior. Bel Gibson admits she made up the whole story. But is there any meat to this idea?
Well, maybe. And it comes from a kind of unexpected place. Fat.
Those extra holiday pounds may have inspired a team at the University of California, San Francisco, who just published their latest findings in Nature Biotechnology on how fat may be our first weapon capable of starving cancer. No radiation, no chemo, just fat doing what fat does best. Welcome to a series that I'm calling on the shoulders of giants.
Because to me, when you want to peer into the distance and understand the future of what is possible, you need to look down sometimes to see whose shoulders you're actually standing on. So, let's cut the fat, reach for another Dorito, and start at the beginning. How do we understand cancer's hunger for the very first time?
In the early 1900s, German physiologist Otto Warberg was fascinated by how cells generate energy. In particular, the differences between normal and cancerous cells and what allowed cancer to grow so quickly. At the time, scientists knew that cells needed glucose and oxygen to survive.
But the exact process, like glycolysis, the KB cycle, or any of those other things that haunt us from high school biology class, was still reasonably mysterious. Warberg set out to measure how much oxygen cancer cells consumed. In a petri dish, he laid healthy cells and slices of tumor in a carefully prepared nutrient solution and connected them to his customuilt monometer to track their oxygen use.
The results stunned him. Healthy cells consumed oxygen at a rate he had seen time and time again. But the tumor cells barely used any oxygen at all.
Believing this was maybe a mistake, potentially due to lack of nutrients in the solution, he topped up the glucose levels in the petri dishes and ran the experiment again. This time, the results were even more surprising. In the presence of excess glucose, cancer cells stopped using any oxygen at all.
But how could this be? Confused, Wahberg began adding various testing agents to his solution. When he added phenol red, he saw an immediate bright yellow hue filled the petri dish.
His fast growing cancer cells were thriving in a pool of acid. Chemical analysis revealed it to be lactic acid, the compound also produced by muscle cells under extreme exertion. But this wasn't just a minor increase.
In some cases, Wahberg recorded up to a 70fold rise in lactate production compared to normal cells. Then came the real revelation. He measured glucose uptake across both cell types.
Normal tissue consumed about 16 mg of glucose per 100cc of medium. Tumors over 70 mg, a four-fold increase. Wahberg for the very first time had proven that cancer was genuinely a disease of voracious appetite.
But the core mystery remained. If cancer cells weren't oxidizing glucose, what were they doing? In healthy cells, glucose is broken down through glycolysis, then shuttled into the mitochondria, powerhouse of the cell, for oxidative phosphorilation, a highly efficient process that for each molecule of glucose produces over 30 molecules of ATP, the energy used by cells.
But in cancer cells, Warberg saw something else entirely, a reversion to a primitive, inefficient pathway. They were stopping at glycolysis, producing just 2 ATP per glucose, and dumping the rest as lactic acid. Warberg proposed something radical that this switch wasn't a symptom of cancer.
It was the cause. Warber believed that damaged respiration, a defect in the mitochondrial function, forced cells to adopt glycolysis as default and that this shift was what triggered uncontrolled cell growth. This idea would become known as the Warberg effect.
That cancer would throw efficiency to the wind and take a growth at all costs approach. While not completely universal, this increased glucose consumption is seen in 70 to 80% of cancers to varying degrees. We can actually see cancer's hunger in real time thanks to a technique called posetron emission tomography or PET imaging.
It works by injecting a patient with radioactively labeled glucose, essentially glowing sugar, then tracing where in the body that glucose gets consumed most rapidly. That bright spot in the pancreas is a tumor so metabolically active that it's comparable with the brain and heart in terms of glucose usage. It's not just growing, it's feasting.
In this second image taken after several rounds of chemotherapy, that bright spot is gone. The tumor's metabolic signal has vanished. Hopefully a sign that the treatment has worked.
Up until his death, Wahberg was convinced of just one thing. That cancer's hunger could be its greatest weakness. And that became a very compelling idea.
Could the treatment for cancer be as simple as just limiting its energy supply? We'll answer that question, but first I have to thank the most relevant sponsor possible, Radio Code. I've been carrying one of these around while living in Paris for the past few months.
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Now, back to the video. Wberg's research didn't just influence science. It lit a spark in public imagination.
The idea that you could starve cancer by cutting off its fuel supply became deeply appealing, especially to those seeking alternatives to mainstream medicine. The earliest approaches were surprisingly straightforward. If cancer cells thrive on glucose, could removing sugar and carbs from the diet cut off their supply?
Enter the ketogenic diet. Originally developed in the 1920s to treat epilepsy, keto gained a new life among cancer diet advocates. By eliminating carbohydrates and replacing them with fats and proteins, the theory went you could lower blood glucose and starve the tumor.
On the surface, it sounded entirely scientifically possible. But trial after trial failed to show any consistent benefit. Not for tumor shrinkage, not for survival, and that wasn't unique to keto.
Every so-called anti-cancer diet followed the same pattern. big promises, disappointing results. One of the most prominent examples, the Budwig diet, was deeply influenced by Warberg's theories.
Dr Johanna Budwig believed cancer was caused by faulty cellular respiration, specifically that cells weren't absorbing oxygen properly due to a lack of essential fatty acids. Her solution, a blend of flax seed oil and cottage cheese, equal parts delicious, as entirely unlikely to work. She claimed it could restore healthy fat metabolism and oxygen uptake in cells.
But while her recipe may have made headlines, no scientific study ever showed it could impact cancer's outcomes. It was wishful thinking wrapped in scientific language. The alkaline diet went down a similar path.
It claimed that certain foods could shift the body's pH and neutralize the lactic acid buildup around tumors, but it mistood something fundamental that the acidity is a byproduct of cancer metabolism, not the cause. And more importantly, the body tightly regulates pH regardless of what you eat. Again, no evidence of benefit.
And then we got into slightly more dangerous examples like Bel Gibson's whole pantry movement. She built an entire wellness empire on the claim that she'd cured her cancer with diet and lifestyle changes. But in the end, the only whole thing about it was how much she'd made up.
She later admitted she'd never had cancer to begin with. Time and time again, these miracle diets failed the test of scientific evidence. Some were rooted in genuine scientific questions.
Others were pure pseudocience. But none could outsmart the problem at the heart of cancer. It is exceptionally good at finding what it needs.
As a tumor grows, it burns through nutrients faster than its surroundings can provide. The local tissue becomes hypoxic, oxygen starved, and the tumor responds by sending out molecular distress signals, veg F, or vascular endothelial growth factor. This triggers nearby blood vessels to sprout new branches, a process called angioenesis, delivering fresh blood, oxygen, and nutrients straight to the tumor's door.
And this brings us to the brutal truth. This is the fundamental flaw in any whole body approach to starving cancer. Whether through diet, fasting, or anything else.
Even if you put your entire body into a nutrient or energy deficit, cancer cells have evolved to protect themselves, they suffer less than the surrounding healthy tissues. Or put more simply, you starve before the cancer does. And to be clear, this isn't just a problem for alternative medicine.
This is a challenge even for traditional clinically tested therapies. One of the most accidentally fascinating discoveries in this space come from a drug you've probably heard of. Metformin prescribed to lower blood glucose in diabetics.
Metformin is one of the most widely used drugs in the world. Over 86 million prescriptions were filled in the US alone in 2022. When researchers looked at cancer rates among diabetic patients, they noticed something striking.
Those taking metformin were significantly less likely to develop cancer by anywhere from 30 to 50% compared to diabetics who weren't on the drug. But if a patient went on to develop cancer, that benefit disappeared. Metformin didn't improve survival rates, it couldn't stop a tumor that was already entrenched.
So the question became, if cutting supplies off at the whole body level doesn't work, what if we flipped the problem around? What if instead of starving the entire system, we robbed the tumor right at its doorstep just before the nutrients ever arrived? In 2002, a group of radiologists and researchers split between the University Hospital Zurich and the University of Ottawa made an unexpected observation.
While analyzing PET scans, they noticed a consistent strong signal lighting up around the neck and spine in some adults. At first, they assumed it was just muscle activity, which does uptake more glucose when active. But something didn't fit.
The signal got even stronger when the subjects were exposed to cold temperatures. Curious, they compared the PET images with CT scans and realized this tissue wasn't muscle at all. It was brown adapose tissue, also known as brown fat.
Now, brown fat is very different from white fat that most of us familiar with, the kind that simply stores energy. Brown fat burns energy. It generates heat, keeping the body's temperature stable, and is critical for newborns who can't shiver effectively yet.
But the scientific consensus at the time was that brown fat virtually disappeared after infancy. Adults weren't supposed to have it. Yet, there it was, glowing brightly in the scans.
Subsequent studies, particularly by a group of researchers in Japan, confirmed it. When healthy adults were kept in a 19° C room, this is the room. Cool enough to trigger thermogenesis, but not cold enough to cause shivering.
Their brown fat lit up on PET scans. Not only was it still present, it was metabolically active. At the Karolinska Institute in Sweden, researchers decided to take this discovery one step further.
They wanted to understand how brown fats might interact with cancer. They designed a simple experiment. Mice were implanted with tumor cells and then split into two groups.
One group was kept cozy, living at 30° C, a temperature that's warm enough that the body doesn't need to generate extra heat. The other group was moved to a brisk 4° C environment. Cold enough to activate thermogenesis, but not cold enough to cause constant shivering.
Over the next several weeks, the researchers carefully tracked tumor growth and glucose uptake using PET scans, and the results were compelling. In the warm environment, tumors showed strong uptake of radioactive glucose, just as you'd expect. But in the cold exposed mice, it was a different story.
The brown fat activated for thermogenesis, competing aggressively for glucose. And as a result, the tumors became starved with their primary fuel. The impact of which was dramatic.
Tumor glucose uptake dropped significantly. By day 20 after tumor implantation, researchers observed an 80% inhibition of tumor growth compared to the warm group. And even more striking, the overall survival rates of cold exposed mice was double that of the warm group.
But could this cold induced effect actually work in humans? In 2021, researchers tested the idea in a very limited but intriguing human study. They worked with a patient diagnosed with Hodkdins lymphoma, exposing them to mild cold, just 16° C for 4 days.
PET scans showed clear activation of brown fat and more importantly a noticeable decrease in glucose uptake at the tumor sites. It wasn't a cure and it wasn't comprehensive, but it was the first real evidence in a human that brown fat could outco compete cancer for its fuel. effectively starving a tumor.
A glimmer of hope, maybe, just maybe, Wahberg's century old findings could still shape modern cancer therapy. But there was obviously a problem. To maintain the effect, the patient would likely have to stand in what's essentially a walk-in fridge for weeks, possibly months.
Hey, look, a freezer man. While also avoiding sugar or any excess glucose, not a perfect recipe for a body already weakened by battling cancer. So the question became, could we take these ideas and turn them into something practical?
Something targeted, controlled, and therapeutic, something that didn't require living in a freezer. Woohoo! Look at that blubber fly.
Nurse cancel my water clock. Just published in Nature Biotechnology, scientists at the University of California, San Francisco, asked a bold question. Could we skip the freezing cold and still harness brown fat's metabolic power, or more simply, keep the hunger, lose the shivering?
Using crisper, they began genetically engineering white fat cells to behave more like brown fat. By inserting upregulated specific genes from brown fat cells, they aimed to create a new kind of cell, one that could outco compete cancer for nutrients without needing to be cold activated. They called these hybrid cells the slightly unattractive sounding beige fat.
To figure out what genes worked best, they ran a transwell experiment where two different cell populations share the same nutrient pool but are physically separated. One gene in particular stood out. UCP1, a key player in thermogenesis.
When they tested UCP-1 modified fat cells against cancer cells, the results were shocking. At the end of the experiment, almost no cancer cells remained. Meanwhile, the beige fat cells were thriving.
Worried this was an error, they repeated the trial again and again and got the same outcome every single time. They had taken the competitive fuel guzzling metabolism of brown fat, supercharged it, and severed its dependence on cold. From fat, they had made a weapon.
To test it in a living system, they turned the most efficient UCP-1 modified cells into fat organoids, tiny lab grown clumps of tissue that function like miniature fat organs, and they implanted them next to tumor sites, like a set of metabolic love handles poised to siphon off nutrients before they ever reach the tumor. 3 weeks later, they compared tumor growth with a control group. Now, fair warning, if you're a little bit squeamish, you might want to look away, but here's what they found.
Tumors adjacent to the beige fat organoids has shrunk by more than 50%. And they weren't just beating one type of cancer. They outco competed aggressive cell lines from breast, pancreatic, colon, and prostate cancer.
No chemotherapy, no radiation, simply by being better at consuming glucose. Turning one of the body's own metabolic tools into a precision weapon against one of its greatest flaws. The researchers called it living cell therapy.
And fat, it turns out, is a perfect medium for it. Fat cells are easy to extract. We've been doing it through liposuction for decades.
They grow well in a lab, can be genetically modified with precision, and crucially, they're easy to re-implant using wellestablished medical techniques, as evidenced by the myriad of enhanced buttocks that we've seen parading around the earth. Not a topic I thought I'd cover in this video. Most importantly, fat plays nicely with the immune system.
We know this from decades of cosmetic surgery. Reimplanted fat generally integrates smoothly without triggering serious immune rejection. That makes it an ideal candidate for a cell-based therapeutic.
Now, of course, there is still further work to be done, refining the method, scaling it up, and eventually moving through rigorous safety and efficacy trials. And it's very reasonable to ask questions like, "What if the tumors respond by ramping up angioenesis? " Or, "If you manage to starve them a little, many cancers might just switch metabolic gears, burning fat rather than glucose.
" Tackling those problems is maybe for the next generation of scientists to solve. But now, at least you know whose shoulders you're standing on. We aren't there yet, but the concept is here, and the biology broadly is sound.
So imagine a future perhaps not too far off where instead of flooding the body with radiation or chemotherapy, we seed it with enhanced cells engineered not to attack the cancer directly, but to starve it, and we turn one of the body's softest tissues into one of its sharpest medical tools, so that one day in the future, cancer may be left out to starve. There's a quote I often come back to about standing on the shoulders of giants. It's largely how I think about science, and it's the bit that has always been interesting to me.
It's the unbroken chain of curiosity, often stretching back across generations of the smartest folk that we have on the planet. Someone asks a question, someone builds a tool, someone else runs an experiment. There's always full starts, but everything seems impossible until someone actually does it.
That's the part that's always drawn me in. Not just the breakthroughs, but how we actually get there piece by piece, standing on what came before us. I feel super lucky that here on YouTube as well as in my day job, understanding the future of what is possible and working alongside those scientists to actually make it happen is part of what I get to do.
I'm super grateful I get to play a small role and that I get to share a glimpse of those journeys with you guys here. That's the part of this that I love the most. There have been a lot of new folk joining the channel recently since at least my last long video.
I know what you're all actually here [Applause] for. We have some really cool stuff coming up in the next few months. I'm excited to share with you.
The algorithm thinks that you might like this video next, so maybe check it out. Thanks very much for watching and I'll see you guys next time. Goodbye.
I feel like a new man. Not a Dorito. Off-brand Dorito.
