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Can a toothache be the reason for someone's cancer? An England based doctor and health content creator @Choji_ES who posts on X, formerly Twitter on reproductive health related content revealed a case where a man went to the dentist due to pain in his jaw and when the tooth was pulled out, a cancer was found in his private part.
The same case also been mentioned by Baridueh Badon (MD, MSc, MBA), who allows posts healthcare content on the same microblogging platform, by the username @BadonB.
In this case, a man went to a dentist for a simple toothache, only to discover that he had cancer. This happened to a 78-year-old healthy man, who suffered pain in his lower jaw and noticed a loose tooth. When he went to the dentist, he decided to get his tooth remove to ease his pain. However, despite the removal, his jaw started to swell again. Confused, the man was recommended for a CT scan and something unexpected happened.
It was Metastatic Prostate Cancer.
As per an African proverb, it is true that the head and the body are one; what affects one may touch the other.
Prostate cancer starts in the prostate gland, which is a part of a man's reproductive system. When it spreads to other parts of the body, like the jaw, it is called metastatic prostate cancer. But, why exactly the jaw? This is because the jawbone is rich in blood and active bone marrow, which makes it a comfortable place for cancer cells to settle and grow.
As per a 2023 study in the Journal of Oral and Maxillofacial Surgery, Medicine, and Pathology, titled Mandibular metastasis from prostate cancer that clinically mimicked osteosarcoma: A case report, noted that in men, 11% of jawbone metastases originated from the prostate gland.
Warning Signs Dentists Look For:
These may seem minor, but they could hint at something serious. Early detection is life-saving.
Prostate cancer is the 4th common cancer globally and is most prone to men who are over 40. Every year, it claims about 400,000 lives worldwide.
Earlier in November, six-time Olympic cyclist Sir Chris Hoy was diagnosed with stage-4 prostate cancer, which was announced in February. This six-time Olympic champion revealed that he had a pain in his shoulder when he was 47, which did not go away. "I was still lifting weights in the gym, still physically active. You are used to having aches and pains, but this one did not go away."
The prostate is a small walnut-shaped gland in men that produces seminal fluid that nourishes and transports sperm. It occurs when abnormal cells form and grow in that gland.
Experts say that not all prostate cancer is deadly. There are cancers that are slow-growing and will not affect a man's lifespan, which is found in 1 in 3 men over 50. Then there is a small number of very aggressive prostate cancers which move quickly and cause harm, this is why regular screening is important.
Chris too has called for more, younger men to be tested, including those with a family history of the disease.
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Smoking, diabetes, high blood pressure, high cholesterol, and obesity have always been recognized as major risk factors for heart disease.
New research has emerged saying these preventable conditions may do more harm than simply contribute to plaque buildup in the arteries. They may also encourage the formation of the most dangerous type of plaque, the kind that is most likely to rupture and trigger a massive heart attack.
The findings, presented at the European Society of Cardiology (ESC) Congress 2026, show that people with a greater number of modifiable cardiovascular risk factors were more likely to have widespread coronary plaque.
They may also have unstable and vulnerable plaques that can suddenly rupture, disrupting blood flow to the heart.
Researchers analyzed coronary artery imaging data to understand how both modifiable and non-modifiable cardiovascular risk factors affect the characteristics of plaque.
The study found that patients with a higher burden of modifiable risk factors had plaques distributed across all three major coronary arteries.
More importantly, these individuals were more likely to develop lipid-rich plaques with thin fibrous caps, a trait of vulnerable plaques that are more likely to rupture.
On the other hand, people whose risk profile was dominated by non-modifiable factors, such as age or genetics, tended to have more stable plaque types.
"Our findings suggest that modifiable cardiovascular risk factors are associated not only with a greater amount of coronary plaque but also with more vulnerable plaque characteristics that are linked to future heart attacks," the researchers said.
Some plaques gradually harden and remain relatively stable for years, causing slow narrowing of the arteries. Others contain large amounts of fat covered by a very thin protective layer known as a fibrous cap.
These unstable plaques can rupture unexpectedly, prompting blood clots to form and suddenly block an artery, leading to a heart attack or stroke.
According to the researchers, individuals with multiple preventable cardiovascular risk factors were significantly more likely to have these high-risk plaques.
Smoking chronically damages the inner lining of blood vessels, making it easier for cholesterol deposits to accumulate while also promoting inflammation and blood clot formation.
High blood pressure places constant stress on artery walls, accelerating plaque development and increasing the likelihood of rupture.
When several of these risk factors occur together, their harmful effects can compound, increasing both the quantity of plaque and likelihood to rupture.
Also read: Vapers & Smokers Have Equally Poor Physical Fitness & Blood Vessel Health, Study Finds
Atherosclerosis is a chronic condition in which fatty deposits made up of cholesterol, inflammatory cells, calcium, and other substances accumulate inside artery walls.
Over time, these deposits narrow the arteries and reduce blood flow to vital organs. The condition often develops silently over decades before causing symptoms.
If a plaque ruptures, a blood clot can rapidly block blood flow, resulting in a heart attack or stroke. Smoking, diabetes, high blood pressure, obesity, and elevated LDL ("bad") cholesterol are among its leading preventable causes.
The researchers said the study highlights the importance of early identification and management of modifiable cardiovascular risk factors through smoking cessation, blood pressure control, diabetes management, cholesterol-lowering treatment, regular physical activity, a healthy diet, and maintaining a healthy weight.
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Sleep disturbances are among the most debilitating symptoms of Alzheimer’s disease. It often appears years before significant memory decline and other symptoms.
A new study from researchers at the University of Kentucky suggests that this sleep loss may not be permanent.
Instead, it could be driven by an immune response in the brain that may be reversible, sparking hope for new treatments.
Published in the journal Alzheimer’s & Dementia, the study found that brain immune cells called microglia, rather than amyloid plaques themselves, are the primary cause of sleep disruption in Alzheimer’s disease.
In mouse-based trials, researchers were able to restore more than two hours of sleep per day by temporarily removing these immune cells, without reducing amyloid plaques.
For years, scientists believed that sleep problems in Alzheimer’s were caused by the accumulation of amyloid plaques or the gradual death of brain cells. However, this study points in a different direction.
Researchers discovered that when amyloid plaques begin forming in the brain, they activate microglia, the brain’s resident immune cells.
Instead of protecting the brain, these cells cause inflammation that keeps brain circuits active, preventing sleep.
Using a drug called pexidartinib (PLX3397), the researchers temporarily depleted around 87% of microglia in Alzheimer’s mouse models.
This restored over two hours of daily sleep, particularly non-rapid eye movement (NREM) sleep, which is essential for tissue repair, memory strengthening, and clearing waste products from the brain.
Notably, the improvement occurred without changing amyloid plaque levels, suggesting that inflammation is manageable.
Lead researcher Dr. Shannon L. Macauley, associate professor of physiology at the University of Kentucky College of Medicine, said, “Basically, we showed that it is not the plaques themselves, or solely dysfunctional neurons, that cause sleep loss but actually microglia.
Microglia are immune cells that, when they respond to plaques, kick off this elaborate cascade of inflammation, as if the microglia are partying all night, and keeping the brain awake.”
She also highlighted why losing restorative sleep can accelerate disease progression.
“That restorative sleep is super important for physical repair, learning and memory and washing out the toxins of the day. When Alzheimer’s patients lose this stage, they lose their brain’s primary cleaning cycle, creating a feed-forward loop that may drive further damage,” she explained.
First author Dr. Nicholas J. Constantino said one of the biggest surprises was that sleep problems did not worsen as amyloid plaques increased.
“I expected that as plaque burden became more severe, sleep disruption would also worsen. The disruptions in sleep… did not worsen by 18 months, despite more than double the amount of plaque burden,” Constantino said.
Also read: What Is Type 3 Diabetes? Insulin Resistance In The Brain That Could Trigger Alzheimer’s
Poor sleep and Alzheimer’s create a vicious cycle. Sleep deprivation reduces the brain’s ability to clear amyloid-beta and tau proteins, which can accelerate disease progression, while worsening sleep.
Sleep disturbances affect up to half of people living with Alzheimer’s disease. The disease disrupts sleep due to various reasons:
Overactive microglia: As shown in the new study, immune cells become chronically activated by amyloid plaques, releasing inflammatory signals that keep the brain in a heightened state of activity.
Damage to sleep-regulating brain regions: Alzheimer’s progressively affects areas like the hypothalamus and brainstem that regulate the sleep-wake cycle.
Loss of NREM sleep: Due to lack of deep sleep, the brain’s ability to clear metabolic waste, including amyloid plagues weakens.
Circadian rhythm disruption: Degeneration of the brain’s internal clock leads to broken sleep and daytime drowsiness. This fuels confusion and agitation associated with the disease.
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Obesity has always been considered as one of the contributors to heart disease, diabetes, and stroke.
Now, growing research suggests that excess body fat, particularly in your 40s and 50s, may also accelerate brain aging and raise the risk of long-term cognitive decline.
Researchers say that obesity is not just linked with memory problems but also to significant changes in the brain structure.
Maintaining a healthy weight, especially during midlife, could help prevent memory problems and overall cognitive decline.
A recent study by researchers at the University of Georgia followed more than 8,200 adults aged 50 years and older for nearly 24 years.
The researchers found that individuals whose body mass index (BMI) increased over time experienced faster declines in cognitive performance than it would with normal aging. Excess body weight affected several aspects of cognition, including memory, planning, decision-making, problem-solving, emotional regulation, and concentration.
Lead author Dr. Claire Sexton (University of Georgia College of Public Health) said, "Maintaining a healthy body weight throughout adulthood may be an important strategy for preserving cognitive health later in life."
The study adds to the evidence that preventing weight gain throughout adulthood could become crucial for reducing dementia risk.
Also read: Grade-1 Fatty Liver: More Indians Are Developing It at Lower BMIs. What's Behind the Shift?
Obesity causes chronic low-grade inflammation, which can potentially damaging neurons essential for learning and memory.
The brain relies on glucose for energy. Insulin resistance, common in obesity, may impair how brain cells use glucose, affecting memory and thinking.
Obesity increases the risk of hypertension, atherosclerosis and vascular disease, reducing blood supply to brain tissue and potentially accelerating cognitive decline.
Experts believe visceral fat, the fat surrounding internal organs, may be more damaging than body weight alone. It produces inflammatory chemicals linked to brain changes and dementia risk.
Also read: Beyond Weight Loss: Scientists Discover How Exercise Can Help Reverse Muscle Aging
The latest findings are supported by several years of research. A large review published in Practical Neurology concluded that obesity is associated with smaller hippocampal volume, temporal lobe atrophy, mild cognitive impairment and increased Alzheimer's disease risk.
Some studies have suggested that obesity during midlife may nearly double the risk of developing Alzheimer's disease or dementia later in life.
Another review on obesity and aging reported that higher BMI is associated with poorer verbal memory, slower information processing and reduced executive function, particularly among older adults.
In January 2026, researchers also used genetic analyses to suggest that obesity and high blood pressure may directly contribute to dementia.
With a few lifestyle improvements, overweight and obese individuals can maintain a healthy BMI, reducing the risk of faster brain ageing and cognitive degradation. Experts recommend focusing on overall metabolic health rather than the number on the weighing scale alone.
Maintaining a healthy weight, regular exercise, controlling blood pressure, cholesterol and diabetes, following a Mediterranean diet, getting adequate sleep, remaining socially and mentally active can help maintain a healthy body weight.
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