Epigenetics sits above genetics. It changes how genes act without touching the DNA code. Think methyl groups. Small molecules that stick to DNA. They turn genes on or off. Dial up their activity.
Environment fuels this. Stress, bad diet, smoking. These factors rewrite the biological script. The result? Colorectal cancer. Heart disease.
But here is the catch. It is not permanent. Alika Maunakea knows this. He teaches anatomy at the University of Hawaii at Mano. He says these changes can be reversed.
Maunakea grew up subsistence living on a Hawaii homestead. He saw early on. The environment shapes community health. Now he heads the Maunakea Lab. Twenty years in. They look at the molecular root of health disparities.
The Space Between Gene and Environment
Sophie Berdugo asks about the mix of genetics and epigenetics in health.
It’s complicated. Nuanced. Disease risk isn’t just your DNA predisposition. It’s the environment. Lifestyle. Even what your grandparents ate or survived.
Epigenetics is this intermediate state… between the environment and the genome.
You might carry a risk. That doesn’t mean you get the disease. The regions intertwine. Sometimes hard to tell which factor drives the risk. Genetics or epigenetics?
If epigenetics drives the risk? Hope remains. You can change your lifestyle. Reshape the epigeneome. Lower the risk.
Ancient Roots
Maunakea’s great-grandmother was a kahuna la’au lapa’au. A Hawaiian healer. She taught him nā mea Hawai’i. All things Hawaiian. She knew maintaining the land maintained the people.
This history drove Maunakea’s science. He noticed Native Hawaiians face higher rates of chronic disease. Conditions that didn’t exist before Westernization. They appear younger in Native communities than in others. It bothered him. So he went to the cell level. To the gene level.
His goal is practical. Clinical. Community-based tools. Reduce onset. Stop the disorder before it starts.
We know epigenetic processes come before symptoms. Really early. Before the clinical diagnosis. That is the key. Early detection through prevention.
Sweet Blood and Fast Aging
Take Type 2 diabetes. The numbers are stark.
Three times higher in Native Hawaiians than other populations in Hawaii. The onset is earlier too. Ten to fifteen years younger. Mortality is higher.
Pre-colonization, before 1778, this wasn’t a thing. Healers invented new terms. They called Type 2 diabetes mimi koko. Sweet blood. They watched the phenotype and named it.
We don’t know how much is genotype. But environmental shocks drove us here. Colonization. Displacement. Lifestyle disruption. Maunakea wants to see the molecular mechanism behind these outcomes. To prevent them.
The big question: Why so early? Why the young age of onset?
Obesity modifies risk. Sure. But look at molecular aging. Steve Horvath published this in 2013. Epigenetic clocks. Specific DNA sites that correlate with chronological age in healthy people.
Sometimes people age faster biologically. Outliers. Their epigenetic age beats their calendar age. Others age slower.
Maunakea found a similar pattern. Native Hawaiians often show accelerated molecular aging compared to white or Japanese American populations in Hawaii. It correlates with diabetes. With obesity. With poverty. Poor neighborhoods tend toward faster biological aging.
Changing the Course
Here is the good part. It is malleable.
Lifestyle helps. Physical activity. Education. Good nutrition. Even in poor areas. If individuals keep these up? Their biological aging slows down. It approaches the norm.
So the risk is there. But it can be modified.
One pilot study showed it clearly. Native Hawaiians with diabetes joined a lifestyle program. Social support was key. Twelve weeks. Glycemic control improved. Blood glucose managed better.
But look deeper. Inflammatory cells changed. Less inflammation. Their epigenomes shifted toward a nondiabetic state. Inflammation drives the pathology. Taming it might tame the disease.
The Cost of Seeing
We can use this to target interventions. Lower inflammation at the cellular level. Identify issues early. Before the doctor’s office. Especially in high-risk groups. Optimize existing treatments. Hit the epigeneome directly.
The catch? Money.
Checking an individual’s epigenome is resource-heavy. Right now. Expensive. Time-consuming. It won’t happen in clinics tomorrow.
Sequencing costs are dropping. Technologies are getting targeted. Feasibility is rising. But wait is still the order of business.
[Editor’s note: These findings have not yet been published in a peer-review journal.]
So we watch. We wait. The cells change. The clock ticks. But for the first time, maybe, we can hit pause. Or reverse.
Does that sound too hopeful? Maybe. But the data sits there. In the methylation sites. Waiting to be read.
