Sweetness, sourness, saltiness, and creaminess are more than just delightful taste qualities: they also reflect key nutritional features that our ancestors needed to survive in a world where food was more than a few steps or clicks away.¹⁷ Sweetness and creaminess signal high levels of sugar and fat, while savory, salty, and sour communicate the presence of essential macro and micronutrients, like sodium, amino acids, and vitamins. We love the taste of these foods because their nutritional properties are salient and rewarding for our brains; they are salient and rewarding because of the synergy between natural selection and the experiences of our ancestors.^17,18 Are we then genetically predisposed to love these types of foods? 

Yes, but there is a twist. While we are genetically programmed to like and eat foods with these taste and nutritional qualities, our preferences– also known as “bliss points”– are shaped by our environment as much as our genes. First, these genetic predispositions are reworked when the sensory system develops.^19–21 In humans, flavor and food preferences are imprinted both before and after birth and depend on the foods eaten by the mother during gestation or lactation and even the type of milk formula consumed by the infant.^22–24 These early preferences are long-lasting and can shape food choices later in life.^25–27

The second way our genetic predispositions are reworked is by the food we eat as adults. Components of food, like salt, sugar, and fat, can influence how we perceive and detect food. In humans and animals, higher levels of dietary sodium decrease people’s perceived intensity for salt, while reducing sodium enhances saltiness perception; these sensory changes also shift the preference for salt concentrations.^32–36 Likewise, high dietary fat lowers the sensitivity to fat taste in humans ^37–39 and decreases the responses of mouse taste cells to sweet ^40,41; in contrast, a restriction in dietary fat enhances fattiness sensation.³⁷ Our own research and that of others shows that this general inverse relationship between the amount of something in the diet and taste sensation also seems true for sugar ^42,43:  lower dietary sugar enhances sweetness,  while higher sugar diminishes it.^44,45 Further, people who consume more sugar-containing foods or drinks have reduced intensity and sensitivity to sweetness.^46–50 Elevated sugar consumption is also associated with a decrease in the responsiveness of the sensory nerves and cells to sweetness in rats and fruit flies,^42,51–54 suggesting that this phenomenon may be a shared or conserved adaptation to the food environment. But it is not just our flavor preference and taste that change with diet: sometimes, the very biochemical and neural mechanisms of sensation are also altered. Indeed, we and others have uncovered differences in the expression of genes important for taste function, as well as epigenetic, cellular, and anatomical changes in response to differences in dietary exposures ^42,43,54,55; although there is evidence that these recover after the diet is removed. ⁵⁴ Thus, this dynamic interplay between genes and diet programs, shapes, and transforms the way we detect and respond to food (Excerpt from for Dus, M. Savor the Flavor, a chapter for the Second Handbook of Food Addiction, 2022.)

Above we explained how taste sensation is shaped by diet. In the lab, we examined the effects of high dietary sugar on taste sensation. Our experiments in flies and rats show that eating elevated sugar levels leads to the desensitization of the taste cells and nerves to sweetness. This decrease in responses of the taste system to some sweet stimuli leads to animals sensing food as less sweet than before, which has significant consequences for food intake through changes in dopamine transmission (see below).

High sugar levels dull taste by enhancing the silencing activity of a nutriepigenetic pathway composed of the conserved nutrient-sensor O-GlcNAc Transferase and the epigenetic repressor Polycomb Repressive Complex 2.1. OGT and PRC2.1 interact at the level of chromatin to instruct changes in chromatin accessibility in response to the dietary environment, which results in the silencing of several hundreds of genes involved in synaptic function, morphology, and plasticity. Recent work shows that neural activity plays an important role in this nutrigenomic silencing by proving the taste cells with the neural activity information.

We propose that nutrigenomic mechanisms can be thought as a new path of information flow in biological systems. Their function is to amplify transient, and often small, variations in nutrient and activity levels, into robust reactions that can orchestrate responses to current and future environmental challenges. 

Consumption of diets high in refined sugar and saturated fat is associated with higher food intake in humans and animal models. Over time, this can lead to metabolic and chronic diseases (diabetes, heart, cancer), which decrease life quality and expectancy. To understand how these foods stimulate eating, we investigated the effects of high sugar on the brain pathways important for regulating food intake.

We found that high sugar desensitizes the responses of the taste cells and nerves to sweet stimuli; this was dependent on diet, not obesity. We further demonstrated that this dulling of sweet taste decreased the activity of dopaminergic neurons and of downstream circuits important for satiety, such as those involved in forming food memories. This led animals to consume longer and larger meals, which over time promoted weight gain and metabolic disease. We showed that these changes in taste, dopamine transmission, and food memories were all dependent on dietary metabolite, not obesity. This suggests that sugar perturbs brain processes early to drive metabolic disease. In these published works we also revealed that the alterations in dopamine and memory circuits are the consequence of taste changes (described above). This is because taste signals are important for many aspects of eating; beyond detecting and savoring foods., taste sensations (and flavor more broadly) also affect satiety.

Indeed, studies have shown that, rather than relying on digestive and hormonal signals, animals use the sensory intensity of food to decide how much to eat during meals. Since foods that are sweeter or creamier, also have more calories, these sensations serve as “cues” to estimate the filling power of food and determine portion size.^11–13,56 When taste and flavor sensations are modified by the high amounts of salt, sugar, and fat, these predictions may no longer function as effective estimates of how much to eat. The formation of food predictions requires dopamine transmission, which occurs when animals eat something salient, such as ice cream.^14,57,58 Lower taste intensity could diminish the responses of dopaminergic neurons and prevent the formation or lower the strength of the predictions.  Our results suggest that is the case: fruit flies fed a high sugar diet showed lower dopaminergic transmission ⁵⁹ and ineffective food predictions, which led to larger meals and obesity; these were entirely dependent on sensory changes. Rodents and humans fed high fat and sugar diets experience similarly profound alterations and disruptions in dopaminergic transmission and reinforcement learning, although the causes remain unknown.^18,60–64 For example, people who consume ice cream daily for two weeks have lower responses in the striatum and insula to milkshakes.⁶⁵ Could some of these disruptions arise from the reshaping of our taste system by dietary exposure to high salt, sugar, and fat? 

Besides weakening the efficiency of food predictions, diet-induced sensory alterations could also enhance our desire for food by creating a mismatch in the number of calories expected versus those actually received.^66,67 Imagine expecting to eat a carrot, only to be served carrot cake: your dopaminergic system would sizzle. In humans, rodents, and even flies, these types of sensory-nutrient mismatches change the reinforcing properties of food and increase our wanting for it (incentive-sensitization).^3,56,68–71 We are currently investigating this question. Finally, since sensory signals also prepare the body to receive food, sensory-nutrient mismatches could also affect its metabolization.^72,73 Indeed, in a recent human study, the uncoupling between sensory and nutrient signals in carbohydrate-containing foods impaired glucose metabolism.⁷⁴

We propose that the reshaping of taste sensation by diets high in salt, sugar, and fat – could drive both a decrease in the satiating power and a higher desire for food. Our results are in line with this hypothesis.

People typically think of food as calories, energy and sustenance. However, the latest evidence suggests that food also “talks” to our genome, which is the genetic blueprint that directs the way the body functions down to the cellular level.

This communication between food and genes may affect your health, physiology and longevity. The idea that food delivers important messages to an animal’s genome is the focus of a field known as nutrigenomics. This is a discipline still in its infancy, and many questions remain cloaked in mystery. Yet already, we researchers have learned a great deal about how food components affect the genome.

The interaction of food and genes

If the idea that food can drive biological processes by interacting with the genome sounds astonishing, one need look no further than a beehive to find a proven and perfect example of how this happens. Worker bees labor nonstop, are sterile and live only a few weeks. The queen bee, sitting deep inside the hive, has a life span that lasts for years and a fecundity so potent she gives birth to an entire colony.

And yet, worker and queen bees are genetically identical organisms. They become two different life forms because of the food they eat. The queen bee feasts on royal jelly; worker bees feed on nectar and pollen. Both foods provide energy, but royal jelly has an extra feature: its nutrients can unlock the genetic instructions to create the anatomy and physiology of a queen bee.

So how is food translated into biological instructions? Remember that food is composed of macronutrients. These include carbohydrates – or sugars – proteins and fat. Food also contains micronutrients such as vitamins and minerals. These compounds and their breakdown products can trigger genetic switches that reside in the genome.

Like the switches that control the intensity of the light in your house, genetic switches determine how much of a certain gene product is produced. Royal jelly, for instance, contains compounds that activate genetic controllers to form the queen’s organs and sustain her reproductive ability. In humans and mice, byproducts of the amino acid methionine, which are abundant in meat and fish, are known to influence genetic dials that are important for cell growth and division. And vitamin C plays a role in keeping us healthy by protecting the genome from oxidative damage; it also promotes the function of cellular pathways that can repair the genome if it does get damaged.

Depending on the type of nutritional information, the genetic controls activated and the cell that receives them, the messages in food can influence wellness, disease risk and even life span. But it’s important to note that to date, most of these studies have been conducted in animal models, like bees.

Interestingly, the ability of nutrients to alter the flow of genetic information can span across generations. Studies show that in humans and animals, the diet of grandparents influences the activity of genetic switches and the disease risk and mortality of grandchildren.

Cause and effect

One interesting aspect of thinking of food as a type of biological information is that it gives new meaning to the idea of a food chain. Indeed, if our bodies are influenced by what we have eaten – down to a molecular level – then what the food we consume “ate” also could affect our genome. For example, compared to milk from grass-fed cows, the milk from grain-fed cattle has different amounts and types of fatty acids and vitamins C and A . So when humans drink these different types of milk, their cells also receive different nutritional messages.

Similarly, a human mother’s diet changes the levels of fatty acids as well as vitamins such as B-6, B-12 and folate that are found in her breast milk. This could alter the type of nutritional messages reaching the baby’s own genetic switches, although whether or not this has an effect on the child’s development is, at the moment, unknown.

And, maybe unbeknownst to us, we too are part of this food chain. The food we eat doesn’t tinker with just the genetic switches in our cells, but also with those of the microorganisms living in our guts, skin and mucosa. One striking example: In mice, the breakdown of short-chain fatty acids by gut bacteria alters the levels of serotonin, a brain chemical messenger that regulates mood, anxiety and depression, among other processes.

Food additives and packaging

Added ingredients in food can also alter the flow of genetic information inside cells. Breads and cereals are enriched with folate to prevent birth defects caused by deficiencies of this nutrient. But some scientists hypothesize that high levels of folate in the absence of other naturally occurring micronutrients such as vitamin B-12 could contribute to the higher incidence of colon cancer in Western countries, possibly by affecting the genetic pathways that control growth.

This could also be true with chemicals found in food packaging. Bisphenol A, or BPA, a compound found in plastic, turns on genetic dials in mammals that are critical to development, growth and fertility. For example, some researchers suspect that, in both humans and animal models, BPA influences the age of sexual differentiation and decreases fertility by making genetic switches more likely to turn on.

All of these examples point to the possibility that the genetic information in food could arise not just from its molecular composition – the amino acids, vitamins and the like – but also from the agricultural, environmental and economic policies of a country, or the lack of them.

Scientists have only recently begun decoding these genetic food messages and their role in health and disease. We researchers still don’t know precisely how nutrients act on genetic switches, what their rules of communication are and how the diets of past generations influence their progeny. Many of these studies have so far been done only in animal models, and much remains to be worked out about what the interactions between food and genes mean for humans.

What is clear though, is that unraveling the mysteries of nutrigenomics is likely to empower both present and future societies and generations.

This article was written by Monica Dus for The Conversation under a Creative Commons license. Read the original article.

During the long seafaring voyages of the 15th and 16th centuries, a period known as the Age of Discovery, sailors reported experiencing visions of sublime foods and verdant fields. The discovery that these were nothing more than hallucinations after months at sea was agonizing. Some sailors wept in longing; others threw themselves overboard. The cure for these harrowing mirages turned out to be not a concoction of complex chemicals, as once suspected, but rather the simple antidote of lemon juice. These sailors suffered from scurvy, a disease caused by a deficiency of vitamin C, an essential micronutrient that people acquire from eating fruits and vegetables.

Vitamin C is important for the production and release of neurotransmitters, the chemical messengers of the brain. In its absence, brain cells do not communicate effectively with one another, which can lead to hallucinations.

As this famous example of early explorers illustrates, there is an intimate connection between food and the brain, one that researchers like me are working to unravel. While we can’t yet prevent or treat brain conditions with diet, researchers like me are learning a great deal about the role that nutrition plays in the everyday brain processes that make us who we are. Perhaps not surprisingly, a delicate balance of nutrients is key for brain health.

Vitamins and mineral deficiencies

As with vitamin C, deficits in other vitamins and minerals can also precipitate nutritional diseases that adversely impact the brain in humans. For example, low dietary levels of vitamin B3/niacin – typically found in meat and fish – cause pellagra, a disease in which people develop dementia.

Niacin is essential to turn food into energy and building blocks, protect the genetic blueprint from environmental damage and control how much of certain gene products are made. In the absence of these critical processes, brain cells, also known as neurons, malfunction and die prematurely, leading to dementia.

In animal models, decreasing or blocking the production of niacin in the brain promotes neuronal damage and cell death. Conversely, enhancing niacin levels has been shown to mitigate the effects of neurodegenerative diseases such as Alzheimer’s, Huntington’s and Parkinson’s. Observational studies in humans suggest that sufficient levels of niacin may protect against these diseases, but the results are still inconclusive. Interestingly, niacin deficiency caused by consumption of excessive amounts of alcohol can lead to similar effects as those found with pellagra.

Ketogenic diet for epilepsy

Not all low levels of something are detrimental to the brain. In fact, studies show that people with drug-resistant epilepsy – a condition in which brain cells fire uncontrollably – can reduce the number of seizures by adopting an ultralow-carbohydrate regimen, known as a ketogenic diet, in which 80% to 90% of calories are obtained from fat.

Carbohydrates are the preferred energy source for the body. When they are not available – either because of fasting or because of a ketogenic diet – cells obtain fuel by breaking down fats into compounds called ketones. Utilization of ketones for energy leads to profound shifts in metabolism and physiology, including the levels of hormones circulating in the body, the amount of neurotransmitters produced by the brain and the types of bacteria living in the gut.

Researchers think that these diet-dependent changes, especially the higher production of brain chemicals that can quiet down neurons and decrease levels of inflammatory molecules, may play a role in the ketogenic diet’s ability to lower the number of seizures. These changes may also explain the benefits of a ketogenic state – either through diet or fasting – on cognitive function and mood. https://www.youtube.com/embed/dLokEBiXgBg?wmode=transparent&start=0 Some foods can negatively affect your memory and mood.

Sugar, saturated fats and ultraprocessed foods

Excess levels of some nutrients can also have detrimental effects on the brain. In humans and animal models, elevated consumption of refined sugars and saturated fats – a combination commonly found in ultraprocessed foods – promotes eating by desensitizing the brain to the hormonal signals known to regulate satiety.

Interestingly, a diet high in these foods also desensitizes the taste system, making animals and humans perceive food as less sweet. These sensory alterations may affect food choice as well as the reward we get from food. For example, research shows that people’s responses to ice cream in brain areas important for taste and reward are dulled when they eat it every day for two weeks. Some researchers think this decrease in food reward signals may enhance cravings for even more fatty and sugary foods, similar to the way smokers crave cigarettes.

High-fat and processed-food diets are also associated with lower cognitive function and memory in humans and animal models as well as a higher incidence of neurodegenerative diseases. However, researchers still don’t know if these effects are due to these foods or to the weight gain and insulin resistance that develop with long-term consumption of these diets.

Time scales

This brings us to a critical aspect of the effect of diet on the brain: time. Some foods can influence brain function and behavior acutely – such as over hours or days – while others take weeks, months or even years to have an effect. For instance, eating a slice of cake rapidly shifts the fat-burning, ketogenic metabolism of an individual with drug-resistant epilepsy into a carbohydrate-burning metabolism, increasing the risk of seizures. In contrast, it takes weeks of sugar consumption for taste and the brain’s reward pathways to change, and months of vitamin C deficiency to develop scurvy. Finally, when it comes to diseases like Alzheimer’s and Parkinson’s, risk is influenced by years of dietary exposures in combination with other genetic or lifestyle factors such as smoking.

In the end, the relationship between food and the brain is a bit like the delicate Goldilocks: We need not too little, not too much but just enough of each nutrient.

This article was written by Monica Dus for The Conversation under a Creative Commons license. Read the original article.