Kurt and Robin are substantially overweight (in mid-October 2012), whereas their similarly built cousin was skinny for years on a nearby pasture that was by all standards very green and lush.

I have often heard researchers refer to a “thrifty” gene in horses that develop laminitis.

Researchers say this gene may be the reason that some horses founder and some don’t. My farm is surrounded by pastures far larger than my own that are dotted with horses — some relatives of my horses — that haven’t foundered, so I’m skeptical of this thrifty gene, but it would explain some things.

I’ve heard a couple of laminitis researchers theorize that horses that traveled from Europe to America by boat as America was colonized had to be able to get by on little food to survive. The researchers suggested we owe the birth of our country to those horses’ thriftiness.

The website of the International Museum of the Horse paints a grim picture of Spaniards shipping their horses to the New World in the 1600s, and let’s remember that this was only 400 years ago. Hard to believe.

Apparently, horses were shipped in slings. This took their weight off their feet and allowed them to swing with the roll of the ship. The dark, damp atmosphere in the boats and lack of exercise often killed half the horses, and the dead animals were buried at sea. Some say this is how the section of the Atlantic Ocean named the Horse Latitudes got its name, though others say this is folklore.

Getting the horses off the ship was hazardous, as well. They were lowered by sling into the water and made to swim ashore by people in row boats.

Laminitis researchers suggest that the same thrifty genes that served horses well in hardship are now killing them because the improved grass and hay created for cows is too rich for the systems of these horses, and they develop laminitis (as do cows).

I would buy the thrifty gene theory more if I could explain why none of my parents’ Connemaras (the ancestors of my horses) foundered. Similarly, I don’t know of any siblings of my horses that have foundered, though many live on pasture. My mare Angel moved to my current farm as a 3-year-old in 1997 and got very fat in a year. I sent her to Ohio for three years as a broodmare, and immediately she dropped a tremendous amount of weight, even though she got pregnant. She was stalled some of the time but she also got out on pasture each day. I don’t think her access to grass there was much different than her life at my farm, because, here, she had almost no grass, sharing a 2-acre pasture with four other horses round the clock. One could argue she got more grass while away. She was very thin when she returned home from Ohio at the end of 2001. She got fat and foundered by February 2004, a little over two years later, in the middle of winter even as I worried about laminitis from having problems with my other horses and tried to maintain an appropriate diet for all of the horses.

At any rate, I’ve been searching online for this equine thrifty gene. Mostly, it seems like the thrifty gene is a theory, and scientists are trying to find which gene is the culprit.

I saw a few references to a likely thrifty gene in an article by laminitis researcher Philip Johnson at the University of Missouri’s vet school. He wrote the article in 2009 for the Journal of Diabetes Science and Technology.

Johnson’s article covers the fact that horses that evolved naturally would go through the process of putting on excess weight during the fall in the form of stored fat to get through harsh winters.

He says herbivores, including horses, contain a critical survival mechanism — increased secretion of proopiomelanocortin (POMC) peptides in the fall — that stimulates the appetite and leads to other changes that result in fat storage in preparation for winter, when food tends to be relatively scarce.

This short-term addition of fat was fine historically. Johnson says it’s the chronic persistence of fat that leads to problems, and owners today generally keep their horses too fat.

He talks about how wild horses survived by covering a great distance daily to find little grass that was relatively low in sugar. He says today there is good evidence that providing higher sugar rations leads to diminished insulin sensitivity.

Higher sugar combined with less exercise and “grossly excessive” feed rations is what is getting horses in trouble today, he says. And he points out that today’s forage is designed to make farm animals gain weight quickly.

He says there are few statistics on current horse obesity, but one study found 45 percent of 319 randomly selected horses to be fat or very fat. That compares to 25.8 percent rate of obesity in cats and 25.2 percent rate in dogs, he says. I’ve seen other numbers that put cat and dog obesity much higher in 2012.

Johnson points out that laminitis is seen in two forms: one that leads to separation of the hoof lamellar interface, the tissue that connects the hoof to the bone inside the foot; and one due to chronic remodeling of the foot resulting from endocrine disorders (others have compared this remodeling to cancer-like growth).

Johnson says the endocrine abnormalities that are most often seen in horses with chronic laminitis are insulin resistance and excessive levels of corticosteroids. He says insulin resistance is likely an important component of thriftiness — horses with insulin resistance can survive on far less food.

As for corticosteroids, the corticosteroid named cortisol, a glucocorticoid due to its role in sugar metabolism, is secreted by the adrenal glands. Its primary roles are to increase blood sugar, suppress the immune system and aid in metabolism. Stress can lead to elevated cortisol levels, which can lead to weight gain.

Johnson said that an enzyme called 11-hydroxysteroid dehydrogenase-1 (11-HSD1), which converts inactive circulating cortisone to cortisol in localized tissue, is an important component of human metabolic syndrome and it is seen in increased amounts in the hoof lamellar interface (the connective tissue between the hoof and the bone) in laminitic hooves as well in the cresty necks of horses with equine metabolic syndrome. He said this enzyme is likely one of these thrifty genes.

Johnson also reviews the fact that insulin itself is toxic to the hoof lamellar interface, and raising a horse’s insulin level can result in laminitis.

My feeling is that, yes, all of these thrifty genes may behave in a way that leads to laminitis, but something has to trigger them to behave in that manner. If horses of similar genetic background can live on grass nearby, what is triggering these thrifty genes to behave in a problematic manner in my horses? What is triggering them in the horses of others?