On 8 October 2016, Vice‘s food content vertical Munchies covered the findings of a study released that same week in the journal Nature Communications (titled “Divergent effects of central melanocortin signaling on fat and sucrose preference in humans”). Although the word “cheese” was never mentioned in the paper, Munchies went with the headline “Scientists Have Figured Out Why Some People Love Cheese So Much.”
If one were to base their assessment on Internet shareability alone, an outside observer might get the impression that understanding cheese’s “crack-like” hold over humanity is one of the most pressing scientific questions of our time. In the case of this study (and much like its culinary use, in general), the cheese was merely a superfluous addition intended to make the more dense and useful elements of the study palatable to a wider audience.
In reality, the study aimed to test the role of a gene previously linked to obesity in humans with a mechanism that modulates preference for high-fat or high-sugar foods. That gene, MC4R, when mutated in a way that leaves only one viable version of the gene on a person’s chromosome (haploinsufficiency), causes a disease called melanocortin obesity syndrome — the most common cause of early-onset obesity linked to a single gene. Human studies have linked MC4R to obesity, and laboratory studies on animals have investigated possible genetic mechanisms to make that link, as discussed in the study:
Targeted disruption of melanocortin signalling in [laboratory] mice leads to an increase in food consumption and more specifically to increased preference for a high fat diet in food choice experiments. Studies in Mc4r [deficient] mice and rodents harbouring a point mutation in Mc4r, suggest that disruption of melanocortin signalling paradoxically reduces consumption of high sucrose solutions and food. […]
While there is considerable data regarding the contribution of central melanocortin signalling to food preference in rodent models, the relevance of these findings to food preference in humans has not been explored.
In the paper, two separate human experiments were performed. Both used a group of MC4R-defective individuals, and compared them to two control groups, one with a low BMI and one with a high BMI, similar to that of the MC4R group. In both tests, the participants were given access to similar-looking food that varied in fat or sugar content (they used chicken korma curry for the fat experiment and a British pudding called Eton mess for the sugar experiment). After sampling each, they were told to eat as much of any of the options as they wanted until they were full.
These were their results:
Although liking scores for the high-fat meal were comparable to those for the low and medium fat meals, MC4R deficient individuals consumed 95% more of the high fat meal than lean, and 65% more than obese controls. There was no difference in total intake collapsed across fat level between lean controls, obese controls and MC4R deficient individuals for the group comparison.
We found that lean and obese volunteers liked the high sucrose meal more than the low or medium sucrose meals […] In MC4R deficient individuals, […], liking ratings for the high sucrose meal were significantly reduced. Individuals with MC4R variants also consumed significantly less of all three sucrose meals compared with lean and obese controls.
In summary, our findings in MC4R deficient individuals indicate that central melanocortin circuits play a key role in modulating fat and sucrose preference in humans.
In other words, without direct knowledge of the nutritional content of food, MC4R-deficient participants preferred high-fat foods relative to lower-fat foods, and they were significantly less interested in high-sugar foods. The significance of this finding is described in the authors’ own words:
This is to our knowledge one of the first experimental studies to show a direct association between macronutrient preference (other than alcohol) and a specific genetic/molecular mechanism in humans.
The study’s most pertinent contribution to scientific discourse was demonstrating a direct link between a preference for certain groups of food and an individual gene. What Munchies and other outlets reported, however, was that this study elucidated a scientific reason for human’s weakness for cheese:
We’ve all been there. That late night cheese cheese craving so easily escalates from a single Brie sliver to an entire wheel. And when you wake up the next morning, that hankering for a buttery, flaky pastry can never really be sated with just one croissant.
Well, scientists may have cracked your fatty food addiction. And not just because everyone knows fat equals delicious. It may in fact be down to your genes.
That there is a genetic component to food preference (specifically based on different nutrient groups) is not news. Nor is it news that there exists a link between MC4R and obesity (or even a link between MC4R and fat and sugar preference, if you include animal studies).
Further, the notion that this is the cause of “your” fatty food addiction is accurate only in broad (and speculative) terms, or if you suffer from a defect in this specific portion of your genetic code — something that results in significant dietary changes for only about 5 percent of the population.
The authors do suggest relevance to the population as a whole from an evolutionary perspective in their paper’s discussion, but this is a speculative hypothesis that, in essence, boils down to the explanation that when you are starving, you have a desire for high-energy foods:
We hypothesize that the preference for energy-dense high-fat foods in animals and humans may represent part of the adaptive response to nutritional deprivation. Fasting/starvation leads to a fall in leptin levels which triggers physiological and behavioural responses to restore energy homoeostasis. […]
Critical to mediating the response to fasting/starvation is an increase in the endogenous MC4R antagonist AgRP, which potently stimulates food intake, increases fat preference and reduces carbohydrate intake when administered centrally.
Thus, the preference for fat (which delivers twice as many calories/gram as carbohydrates or protein and can be readily stored in adipose tissue), at the expense of sugars/carbohydrates may represent an advantageous behaviour that is expressed in the face of nutritional depletion. Further studies of food preference in the weight reduced/partially-leptin deficient state will be needed to test this hypothesis.
For the other 95 percent of the population with a working MC4R genome, the only direct relevance this study provides is the knowledge that you have a gene in your body that plays a role in how your body perceives and processes the taste of fats and sugars — one gene of many that likely play a similar role.
Ultimately, this study (important as it is) is a far cry from a genetic explanation for a late-night craving for a full wheel of brie. Coverage in that vein essentially conflates late-night munchies with a specific genetic cause of obesity — to no one’s benefit.