The findings of a recent study has discovered the link between a sense of smell and the rolls under one’s chin. In fact, the better it smells, the less calories we burn.
We all have that friend, that one friend who tells you about how “just the smell of food” makes them put on weight, before they dig into their kale-packed quinoa super salad. Much as it may hurt you to strain a disingenuous laugh at your fitness-savvy friend, there may actually be some truth to their done-to-death office-room joking.
Researchers at the University of California Berkeley have found that obese mice who have lost their sense of smell do in fact lose weight.
Surely that’s because without their ability to sniff out their delicious fatty food – which one can only assume is some kind of deep fried cheese and not the local RatDonald’s or similar rodent-based fast food chain – bulkier mice lose any desire to eat their problems away, right?
Interestingly enough, that’s not exactly right.
These nostril-y lacking mice ate just as much fatty food as their normal-smelling peers, yet only the mice that retained their sense of smell gained any weight. What’s more, mice that were given a boosted sense of smell – perhaps the most useless superpower one could ever hope for – grew even fatter on the same high-fat diet than ordinarily-nosed mice.
This suggests that the odor of our food has great importance in how our bodies deal with calories. If you were to lose your ability to smell your food, much like our rodent friends above, your body may burn it, rather than store it.
The results of this study show a key connection between the olfactory (or smell) system and regions of the brain that regulates metabolism, particularly the hypothalamus. It should be noted, however, that the neural circuits involved are still unknown.
Céline Riera, a former UC Berkeley postdoctoral fellow now at Los Angeles’ Cedars-Sinai Medical Center, described the study as one of the first that demonstrates how “we can actually alter how the brain perceives energy balance and how the brain regulates energy balance” by manipulating olfactory inputs – our noses.
Indeed, humans who lose their sense of smell because of age, injury, or diseases such as Parkinson’s often become anorexic, but until this point the cause has been unclear. This is because loss of pleasure in eating also leads to depression, which in itself can cause a loss of appetite.
This study, published in this week’s Cell Metabolism journal, indicates the loss of smell itself plays a role and suggests possible interventions for both those who have lost their sense of smell as well as those having trouble losing weight.
“Sensory systems play a role in metabolism,” explains senior author Andrew Dillin, the Thomas and Stacey Siebel Distinguished Chair in Stem Cell Research, professor of molecular and cell biology and Howard Hughes Medical Institute Investigator. “Weight gain isn’t purely a measure of the calories taken in; it’s also related to how those calories are perceived. If we can validate this in humans, perhaps we can actually make a drug that doesn’t interfere with smell but still blocks that metabolic circuitry. That would be amazing.”
Riera notes that mice, like humans, are more sensitive to smells when they are hungry than after they have eaten and that, as a result, it is possible that the lack of smell tricks the body into thinking it has already eaten. While we search for food, our bodies store calories in case it is unsuccessful. Once food has been successfully found, however, our bodies feel free to burn those calories away.
In order to avoid condemning their furry friends to a scent-free life, researchers made use of gene therapy to destroy olfactory neutrons in the mice’s noses while sparing their stem cells. This meant the mice would only lose their sense of smell for about three weeks before the olfactory neutrons reset. The mice turned their beige fat cells – the subcutaneous fat storage cells that accumulate around our thighs and midriffs – into brown fat cells which burn fatty acids to produce heat. In fact, some turned almost all of their beige fat into brown fat, making them as lean as any of your workplace gym junkies.
White fat cells – the storage cells that cluster around our internal organs and are associated with poor health outcomes – also shrank in size. The formerly chunky mice, which had also developed glucose intolerance – a condition that leads to diabetes – also regained normal glucose tolerance, in addition to their weight loss.
It’s not all good news, though. The loss in smell was accompanied by a large increase in levels of the hormone noradrenaline – a stress response tied to the sympathetic nervous system. In humans, this sustained hormone rise could lead to a heart attack.
As Dillin notes, though eliminating smell in humans wanting to lose weight would be a drastic step to take, it could be a viable alternative for morbidly obese people contemplating stomach stapling or bariatric surgery, even in spite of the increase noradrenaline line. “For that small group of people, you could wipe out their smell for maybe six months and then let the olfactory neutrons grow back, after they’ve got their metabolic program reworked.”
Dillon and Riera developed two different techniques in blocking the sense of smell in adult mice – one involving genetically engineering mice to express a diphtheria receptor in their olfactory neutrons, which reach from the nose’s odor receptors to the olfactory center in the brain. When diphtheria toxin was sprayed into their nose, the neurons died, rendering the mouse smell-free until their stem cells regenerated them.
While eliminating smell in humans wanting to lose weight would be a drastic step to take, it could be a viable alternative for morbidly obese people contemplating stomach stapling or bariatric surgery.
In method two, they engineered a benign virus to carry the receptor into olfactory cells only via inhalation. Once inhaled, the diphtheria toxin would again take down their sense of smells for around three weeks. Regardless of how the mouse lost their sense of smell, they ate the same amount of high-fat food as their scent-appreciative cousins. However, while the smell-deficient mice gained at most 10% more weight – going from 25-30 grams to 33 grams – the stock standard mice gained about 100% of their normal weight, climbing up to 60 grams and giving up any hope of a summer beach bod.
The smell-free mice retained a normal insulin sensitivity and response to glucose – both of which are disrupted in metabolic disorders like obesity.
Better still, mice that were already chunky lost weight after their smell was knocked out, slimming down to the size of normal mice while still eating their high-fat diet. Only fat weight was lost, with no impact on muscle, organ, or bone mass.
The UC Berkeley researchers then teamed up with colleagues in Germany who had developed a super-smelling strain of mice, complete with more acute olfactory nerves, where they made the discovery of their increase in weight gain.
“People with eating disorders sometimes have a hard time controlling how much food they are eating and they have a lot of cravings,” explained Riera. “We think olfactory neurons are very important for controlling pleasure of food, and if we have a way to modulate this pathway, we might be able to block cravings in these people and help them with managing their food intake.”
Of course, before you go rushing to your shed in hopes of removing your bothersome nose, it should be noted that research is still ongoing and that mice are, believe it or not, not identical to your average human being.
Still, if all it takes to meet your shredding goals is a few weeks without your overrated sense of smell, it might be time to cancel that gym membership. Again.