The Sound of Food

We eat with our ears. The noise of food – the crunch of an apple, the pour and fizz of a cold carbonated drink, the sizzle of bacon – is called sonic seasoning, and it adds to the experience of eating.

Oxford professor Charles Spence developed this art within the science of multisensory perception. Celebrity chef Heston Blumenthal, who collaborated with Spence (1), uses very specific sounds to augment the experience of dishes at his famous Fat Duck. I can testify that it is an entirely positive experience.

Food Noise, in contrast, is entirely negative.

Food Noise (FN) is yet another new health problem, like AVPD (Avoidant Personality Disorder), IGD (Internet Gaming Disorder) and VEXAS, which is not like the others and has a definition which runs to an entire paragraph (2).

Whereas IGD and VEXAS were identified and named by medical professionals, the term ‘food noise’ was coined by hoi polloi. It emerged in Weight Watcher groups during the late 1990s and describes the constant, distracting mental chatter about food. Watchers describe FN as a psychological tug-of-war. ‘I’m constantly negotiating the next snack, replaying what I ate earlier and worrying about calories. It crowds out your ability to focus on anything else and makes you eat even when you are not hungry’.

In his melancholic 1944 scrapbook The Unquiet Grave, the essayist Cyril Connolly famously wrote “Imprisoned in every fat man is a thin one wildly signaling to be let out.” Obese himself, he described his physical condition as ‘a disease brought on by boredom and disappointment’; but in these last summer days of food security (3) it is food noise that generally keeps the thin man locked inside.

Hyper-palatable junk and omnipresent food prompts form two walls of the cell. Big Phood uses these to constantly ramp up the noise, creating an emotional Alcatraz for their unhappy and force-fed customers. They focus on the young, implanting unhealthy eating habits which will plague them for life (4, 5). Get them hooked and keep them on the hook is a terrific business model; the third wall is the consumer’s deliberately engineered addiction. The diet culture, bodies beautiful on TikTok and influencers paid by the food companies amplify the noise, and constitute the fourth wall (6).

Thanks to these techniques the incidence of binge eating and other eating disorders rose from 3.5% in 2000 to 7.8% in 2018 (7), and the prevalence of severe obesity doubled (8).

Connolly wrote his book at a time when overweight was uncommon and obesity was rare (9, 10). Pharmaceuticals, diet and lifestyles have changed considerably since then. Amphetamines gave way to orlistat, produce to ultra-processed product. Overweight became endemic, health expectancy plummeted. Connolly’s thin man inside a fat man was reverse engineered, emerging as TOFI (11). And then came the GLP-1 agonists.

Soon after these new drugs went mainstream, members of the Ozempic squad realized that their drug of choice turned food noise off, and started to talk about it online. Big Pharma, scenting a lucrative new sales pitch, coined new and more formal definitions: ‘Unwanted, persistent thoughts about food that cause significant distress.’

Some drug companies (12) now sponsor ‘disease awareness initiatives’ to show how their drugs can ‘quiet the mental chatter that makes weight management difficult.’ Others (13) run education campaigns highlighting food noise as a major cause of obesity, and pump these out on Instagram. All of them stress that food noise is not just a lack of willpower, but has biological roots in brain chemistry and hunger hormones. Which their drugs treat, of course.

Except that they don’t, for long.

A recent paper showed that the initial FN response to one of the new improved GLP-1 / GIP drugs started well, but faded after 5 to 7 months (14). The food noise and cravings came back, as strong as before. This paper looked at a single individual, for reasons which will shortly become clear, but the finding is in line with real-world experience; GLP-1 users commonly hit a weight-loss plateau within a year of treatment. 

The individual whose food noise and eating habits returned was test subject No. 3 in an experiment carried out in the Department of Neurosurgery at the University of Pennsylvania (14). A 60-year-old woman who struggled with food noise, she had developed Type 2 diabetes, severe and treatment-resistant obesity and a bad prognosis. As a last resort, electrodes were surgically implanted in her nucleus accumbens (NAc).

The GLP-1 quieted nervous activity here, together with her appetite, but only temporarily. At 5-7 months the researchers saw activity in the core of the nucleus returning, and as it did the food noise surged back.

The NAc comprises two complementary components, namely an inner core and an outer shell.

The core is a pre-reward center in the brain which lights up with anticipation before a reward arrives, thanks to the familiar neurotransmitter dopamine. The shell is a reward center where we experience pleasure and reinforcement, and here GABA and glutamate are key (15, 16). Dopamine, GABA and glutamate dance together in a neurochemical triad which affects motivation, pleasure and emotions, and therefore a large part of our lives.

Unfortunately, in many people today, the NAc is malfunctioning (17, 18). So are the hippocampus (19, 20) and the hypothalamus (21, 22), both of which connect to the NAc via the mesolimbic pathway. This is the neurocircuitry of survival, motivation, reward, pleasure and the memory thereof.

The hypothalamus signals basic bodily needs and appetites including hunger, thirst and other cravings, the hippocampus links the memory of past experiences to current rewards and the NAc drives action to satisfy those needs (23). This circuit self-evidently shapes a good deal of our behavior and in times gone by it worked well enough; we survived as a species, and even thrived. Until Pringles.

The modern diet causes neuroinflammation (24-26). This lowers levels of dopamine, raises levels of glutamate (27, 28), and disrupts GABA signaling (29). The resulting chemical imbalance limits the brain’s ability to feel pleasure or motivation. It is linked to fatigue, addiction, depression (24-28), and increased impulsivity (30-32), with a host of negative consequences.

Increased impulsivity is not only linked to poor appetite control but poor self-control in general, leading to a host of maladaptive, neuro-psychiatric and anti-social behaviors (33-35).

In addition, and if sustained, chronic neuroinflammation physically degrades the mesolimbic pathway. It is deeply involved in the increasing incidence of neurodegenerative disease (36). The overall data set implies that the junk food diet is degrading us individually and collectively (32, 37, 38), and is likely reducing our average intelligence (37).

Previous research by the U. Penn group (39, 40) had already demonstrated that electrically stimulating the NAc shell (the reward center) reduced over-eating in mice binging on hyper-palatable (cf ultraprocessed) foods. The neuroscientists (14, 39, 40) then began to work on their own Minority Report (41).

In one of their papers (39) they write: ‘Reward hypersensitization is a common feature of neuropsychiatric disorders, manifesting as impulsivity for anticipated incentives. Temporally specific changes in activity within the nucleus accumbens, which occur during anticipatory periods preceding consummatory behavior, represent a critical opportunity for intervention.’

In plain English: ‘We can identify pre-criminal impulses in the brain, and we can modify these before the crime is committed.’

It is not entirely clear if they are proposing pre-emptive brain surgery and/or drugs, but in either case the ethical implications are fascinating – and terrifying.

The fact that it may be possible to pre-screen for and then abort impulsive criminality is complex enough. Crime is not entirely destructive; social responses to criminal acts reinforce social norms and promote needed social change (ie 42, 43).

The usefulness of the concept of impulsivity is itself in question, as it is clearly a composite phenomenon with multiple aetiology and outcomes (44, 45). These are not all negative. Some of them may, in certain situations, confer survival and therefore evolutionary advantages (ie 46).

Then there are the proposed remedies. If prophylactic neurosurgery is too strong for your taste, what about prophylactic next-gen GLP-1 agonists? Plenty of people take this class of drugs voluntarily, and the idea is growing that they may reduce addictive behavior and impulsivity in general (47); and therefore, it may be argued, criminal impulsivity (48-50).

In 2019 a Finnish group showed that a GLP-1 agonist reduced aggression in male mice (51), and just last month, a report out of Rutgers University indicated that men react just like mice. The researchers found that in adults taking GLP-1s, the link between being impulsive and being more prone to violence was noticeably weaker (52).

If we can screen for certain types of pre-criminals, should we pre-prescribe GLP-1 agonists to create a safer (and slimmer) society?

From a purely mechanistic perspective, this makes sense. The GLP-1 agonists modulate dopamine (52), GABA (53) and glutamate (53) chemistry in the brain, and reduce neuroinflammation (54). It’s commercially appealing too, at least to the drug companies, whose business model depends on treating symptoms rather than root causes (55, 56).

But it is not the best solution for us. Rectifying today’s toxic and neuroinflammatory diet would resurface the mesolimbic pathway, and enable more people to yoke their fundamentally divergent impulses with subsequent convergent thinking. As any think tanker will tell you, this is where soil where true creativity grows.

For those unable to drive past the drive-through, the Health Protocol provides an alternative.

Broader issues remain. If we remove impulsivity to what extent do we also impair divergent thinking, creativity and originality? Does that even matter? In a world rapidly shrinking under the impact of AI, are those traits as valuable as they once were?

For anyone interested there are mostly validated Food Noise Questionnaires (ie 57), and behavioral techniques that may help to turn the volume down (58).

References:

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