Evolutionary Psychiatry

The hunt for evolutionary solutions to contemporary mental health problems.

Crisco and Cocaine

…or a fun Saturday night.

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Heart disease wasn’t a huge killer in the United States until the end of the 1920s.  Cigarette smoking really took off at the beginning of the 20th century, but did you know Crisco was released in 1911 and came into general use over the next 10 years for pie crusts and biscuits and everything baked?  There are no early studies of eating red meat and saturated fats that aren’t confounded by the generous use of Crisco and the utterly unnatural trans fatty acids it contained.  Even now, years after the FDA required manufactures to list trans fats on a label as they were found to be unsafe in any amount, some studies are still released with “high fat diets” equated to “high trans fat diets”  (1). 

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With that in mind, let’s look at A History of Bingeing on Fat Increases Cocaine Seeking and Taking.  (In case you were wondering, rodent researchers really know how to make an intriguing combination of industrial lubricants "heart healthy vegetable oil" and cocaine sound boring.) 

Song—an oldie but a goodie—The Dandy Warhols:  Bohemian Like You (right click to open in new tab)

I've discussed the rodent bingeing literature before:  see here and here and a little bit here. Rats and mice, like humans, will binge on sugary snacks.  Unlike humans, rats and mice will binge on Crisco alone, whether it is the old fashioned trans-fat kind or the modern however-it-is-they-make-vegetable-oil-solid-at-room-temperature kind we can buy in the supermarket now.  The sugar-fat combo seems to be the most damaging—though in all of these studies, a variety of vegetable oil was the fat used, so it is hard to know whether it is an omega 6 thing or a fat thing in general.

A little reminder:  not all binge-eaters are obese, but 67% of them are.  And not all obese people are binge-eaters, far from it.  It seems that about 1/3 of those who seek medical treatment for obesity have binge-eating behavior, however.  If we are considering the prospect of disordered "food reward" pathways, perhaps looking at binge-eaters will help us to understand one extreme of the continuum.  Or perhaps the pathology behind binge-eating and the supposed disordered food reward leading to obesity are really different concepts.  I suspect they aren't entirely separate, but it isn't a simple comparison, either.  And certainly, exploration of binge-eating and addiction can hopefully inform our treatments of those disorders.

In this new study, researchers added the interesting twist of seeing if a history of fat-bingeing made their rodents more vulnerable to becoming addicted to cocaine in the future.  As I've noted from my clinical experience (and as is noted in the literature), binge eaters can (but don't have to) have a hard time controlling behaviors in several areas—bulimia and binge-eating often occur together with substance abuse in humans.  

Let's start with what all the folks agree upon—massive doses of sugar (really, sugar—sucrose, meaning glucose + fructose) are a bad idea, particularly in those who are vulnerable to addiction of bingeing behaviors.

Rat researchers know their bingeing and drugging.  A correlation between liking sweets and drugs of abuse (including alcohol, cocaine, and amphetamines) is known in humans, and in rats, repeated exposure to sucrose seems to enhance behavioral susceptibility to cocaine later on.  Sucrose is, in this paradigm, a "gateway drug."  Let's not forget that in sugar-bingeing rats, taking away the sugar leads to opiate-like withdrawal syndromes and worsens the withdrawal from morphine.  So let's say you are a binge-eater withdrawing from a sugar-fest—are you more likely then to have a bottle or two of wine, some meth, or cocaine?  Could be.  Even though these different drugs of abuse affect different reward neurotransmitters, they all end at one common pathway, which makes sorting out some of the specifics rather difficult.

Here is the money excerpt from the paper:

Offering further support for the connection between the intake of sugar and fat and the intake of drugs of abuse are several studies investigating the neuroanatomical and neurochemical changes that accompany sucrose and fat consumption. Not surprisingly, these sugar and fat consumption-induced changes occur in the mesocorticolimbic dopamine system, a major component of the brain’s reward pathway, and many of the changes mimic those that occur after exposure to drugs of abuse, including turnover and release of DA, D2 receptor binding and expression, and dopamine transporter binding and expression. In addition, differential responsiveness in rats bingeing on fat has been reported when a D2 receptor antagonist is administered peripherally, or directly into the prefrontal cortex.

In short, eating fat and sugar seems to engage our reward systems in the same way that drugs of abuse do.  This is not terribly unsurprising—we have a reward system for our survival.  Protein is easy to find in the paleolithic world (ask any bug or lean rabbit)—but what about our fuels of sweet and fat?  We need it, we love it, and our big brains encourage us to find it and consume it, and drives us to find it and consume it again.  My suspicion (not first thought of by me in any respect!) is that, like cocaine, Snackwells, Oreos, Big Gulps, potato chips, peanut M&Ms and deep-fried twinkies stimulate our reward centers in ways our brains were never designed for, like a magnitude 9 earthquake taking out at magnitude 7-rated nuclear reactor.  To parse matters even further, the actual substances may be less important than the manner in which they are consumed.  A sugar binge (with all the sweaty anticipation, consumption, aching stomach and crashing blood sugar later on) is a far more worrisome issue than eating the same amount of sugar over the course of a day, at least in rats.  Here we separate those who are (for whatever reason, environment, genes, etc.) vulnerable to addiction and those who are not.  

So what happened to these rats with the cocaine and the crisco, anyway?  The methods are a bit boring, but in short, we have some rats on standard rat chow, and then some rats on standard rat show plus access to fully hydrogenated Crisco (which technically should be less toxic than the old partially hydrogenated kind)  All the rats were then transported to another lab 90 miles away (in Hershey, PA, which is a lovely community of nostalgia and chocolate), where there was no Crisco, but there was some high quality blow (actually it was IV cocaine, and the rats could control the administration by licking a certain spout, leading to an infusion of the drug.  Interestingly enough, a study was once done on humans comparing IV cocaine, IV amphetamines, and IV caffeine, and the humans could not tell the difference.)


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You will not be surprised to learn that the indulgent, gluttonous crisco-bingeing rats were mostly the same ones who had a bit too much affection for the cocaine.  The other, abstaining rats were rather like Meg Ryan in "When Harry Met Sally"  "I don't like to eat between meals."  So superior, so sure that all you have to do is exercise some self control, as they do, and you could wear size 2 jeans, no problem.

I know, it is a big leap from a few crisco-loving, coke-addled rats to 60% of the population being overweight or obese.  But certainly there is something there.  And for the love of all that is precious and good, DO NOT EAT CRISCO (even though the new fully hydrogenated stuff is likely far less deadly than the partially hydrogenated stuff**).  

Ever.

** In the US, anything less than 0.5mg trans fat per serving can be listed as "0g trans fat."  Does anyone know the fully hydrogenating process for New Crisco and how good it is at getting all the double bonds saturated?  Or are quite a few missed and you end up with a small dollop of trans fat each time, still?

Image credit

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Copyright Emily Deans, MD

Emily Deans, M.D., is a psychiatrist with a practice in Massachusetts.

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