An analysis of national data published in the journal Pediatrics earlier this year found the percentage of children ages 2 to 19 who are obese rose from 14 percent in 1999 to 18.5 percent in 2016, an increase of nearly 25 percent. If you consider only the 2-to-5-year-olds during that time, the growth is nearly 36 percent.

I don’t know if your children or grandchildren are obese or not. What I do know is that if they are, it’s no joke.

So don’t do what we once jokingly used to do and blame the caveman.

According to an emerging branch of biology called epigenetics, any accusations that need to be made should be directed towards you. Or your parents.

It is true that our genetic makeup is more than 99.5 percent identical to the Neanderthal’s and that whether or not you are skinny, muscular, or fat is determined to a large extent by which genes you got from your ancestors. Epigenetics argues that your genes can be turned off or on, altering not how they are but how they function.

And what does this turning off and on? Changes in the environment, amount of exercise, and type of diet.

Changes that could have occurred a generation or two ago.

Repeated research with laboratory mice have found this to be true. In one such study, male mice were overfed to the point where they became obese.

Shortly thereafter, they became insulin resistant and glucose intolerant, precursors to type 2 diabetes. Later, an unusually large proportion of the offspring of the overfed mice developed insulin resistance and glucose intolerance — despite being fed a diet designed to keep this from happening.

Evidence in humans suggests undereating presents epigenetic problems as well. When researchers reviewed the harvest and health records of a Swedish town, they found that a string of poor harvests harmed the health of the children — two generations later.

What happened here, according to epigenetics, is that certain genes turned on to get the most energy and nutrition out of the reduced amount of food being consumed. That turn got passed on, so two generations later when harvests were typical, eating what used to be the typical amount led to weight gain for many.

That weight gain led to an increase in diabetes and heart disease and a significantly lower life expectancy — for the grandkids of the kids who didn’t get enough to eat.

Could a similar two-generation lag be why Dr. Sarah Armstrong, an associate professor of pediatrics at Duke University, told NPR’s Rob Stein that despite “pouring research dollars and public health dollars into [the obesity] problem — for at least 20 years . . . we don’t seem to be making a big dent in the situation”?

Could some sort of turn off or turn on of genes be why your kids struggle to lose weight even though they eat well and exercise?

Keep those questions in mind as you consider a key idea in a review written by Dr. Caroline Davis and published in 2013 in the journal Obesity. First, Davis states that obesity is probably the greatest health problem facing your children and the entire world right now despite being the “most preventable.”

Davis, a professor in the Department of Kinesiology and Health Sciences in the Faculty of Health at York University in Toronto, Canada then acknowledges epigenetics. She warns that despite its preventability obesity “will likely . . . become a self-perpetuating problem” because heritable changes increase the odds it will be passed “from one generation to the next.”

In short, epigenetics is as logical an explanation for the 50-year-or-so spike in obesity as you’ll find. It may be hard to accept, however, since it suggests it’s possible that something you did years ago is adversely affecting the weight of your child or grandchild now.

As well as his or her overall health later.

What Dr. Sarah Armstrong expressed to NPR’s Rob Stein is true: “When obesity starts younger, most of these children continue to have obesity throughout childhood and into adulthood.” Excess weight in adulthood is a major risk factor for diabetes and other health conditions, including heart disease and cancer.

But if epigenetics really is part of the obesity problem, it is also part of the solution.

A 2011 meta-analysis of 45 studies totaling more than 200,000 subjects and published in the journal PLoS Medicine found that exercise turned down the expression of what’s called the obesity gene, alpha-ketoglutarate dependent dioxygenase FTO. While having the obesity gene increases your odds of having a higher body mass index, a larger waist circumference, and a higher percentage of body fat, the meta-analysis showed even minimal physical activity reduced the carrier’s chance becoming obese by 27 percent.

That lead the authors to state that physical activity is a “particularly effective way of controlling bodyweight in individuals with a genetic predisposition toward obesity.”