Creating a Mt. Rushmore to memorialize those most responsible for the recent advancements in the health care field would be a stone carver’s nightmare - for a reason beyond the monument’s sheer size.

One of the four faces needs to be an amalgamation of millions of them. Plus that amalgamated face requires something super hard to carve: really long whiskers. Because if this new Mt. Rushmore’s done right, a mouse’s face needs to be jackhammered into the granite.

According to the Foundation for Biomedical Research, 95 percent of all lab animals are either mice or rats. And for a whole host of practical reasons.

As Remy Melina notes in an article for Live Science.com, mice live only two or three years, which allows for generational studies. Better still, scientists can breed them so that a large group is virtually genetically identical.

Possibly most importantly, mice behaviorally, biologically, and genetically share much in common with humans. By subjecting them to experimentation, researchers gain valuable information about many conditions and diseases currently plaguing the world.

Like hypertension, cataracts, seizures, cystic fibrosis, muscular dystrophy, Parkinson’s, Alzheimer’s, diabetes, cancer, heart disease, and obesity.

In short, millions upon millions of long-gone laboratory mice deserve your thanks. And to lessen the odds that the still-to-be or burgeoning branches of your family tree become obese - as a well as reinforce a seemingly simple yet so often overlooked aspect of any diet - a recent study using mice merits special note.

Performed at the Baylor College of Medicine and published in the September 2022 issue of Science Advances, this study declares obesity to be “primarily” a disease that adversely affects the nervous system as a result of poor nutrition during pregnancy and early development.

Just to be clear here, the use of “primarily” is especially significant. After all, it means“first and foremost.”

It suggests that someday we could look back and say the research done at Baylor curtailed the obesity epidemic.

To understand why, it helps to know the basics of epigenetics. In an article about it for Live Science.com, Rachael Rettner explains that skin cells, brain cells, and muscle cells all carry the same genetic information.

It’s just that some of it gets “expressed differently.”

That’s it. That’s epigenetics.

In essence, it’s nothing more than the factors or circumstances that turn your genes “off” or “on.”

Two ways you can positively do so is through diet and exercise.

Let’s say your parents, grandparents, and great-grandparents all are or were overweight. That means you are genetically predisposed to be that way, too.

But exceptionally healthy eating and more than the normal amount and intensity of exercise can keep your fat genes from ever turning on - or at least suppress many of them.

While you may never be quite as lean as someone who’s genetically disposed to be that way, you’re not fated to be as heavy as your relatives either. But the Baylor study suggests a different sort of fate could be in store for millions of soon-to-be or burgeoning branches of other family trees.

It led the study’s lead author, Dr. Robert A. Waterland, professor at Baylor College of Medicine, to tell to Medical News Today epigenetics may “play a bigger role in determining an individual’s propensity to obesity” than genetics.

Since it’s a byproduct of whole genome analysis and RNA sequencing done on neuron and glia cells from arcuate nucleus tissue in the hypothalamus of pregnant mice as well as their pups, I’ll assume it’s OK with you if we skip the specifics that led to Waterland’s statement. Instead, we’ll focus on something else Waterland said.

That from this study you can conclude maternal obesity “promote[s] lifelong positive energy balance” in children.

Now Waterland’s being euphemistic, politically correct, or both, so let me undo the doublespeak. “Lifelong positive energy balance” is just another way to say that baby fat on children from fat moms is not, as we believed for years, merely a phase.

That being fat for them is a condition they may not be able to change as they age - at any age. And it’s because family members before them, most likely a mom, did the sorts of things and ate the sorts of foods that not only flipped their fat gene switch to fully on, but also did so to the fat genes being passed along.

Which leads us back to the earlier mention of a seemingly simple yet so often overlooked aspect of any diet: that every morsel of food you place in your mouth counts. That there really is no such thing as a cheat day or even a cheat food - unless you’re referring to cheating yourself out of optimal health.

The Baylor study strengthens that sentiment by extending it. It suggests that if those cheat days and cheat foods make you overweight or obese, you could also be cheating someone other than yourself.

A someone who’s just become or will someday be part of your family tree.