on August 22, 2026
Food texture is part of its physiology
When talking about nutrition, the focus tends to be almost exclusively on the chemical composition of foods: calories, carbohydrates, proteins, fats, vitamins, and minerals. However, there is an often underestimated dimension: the physical structure of the food.
A whole, crunchy, or fibrous food requires longer oral processing than a liquid, creamy, blended, or highly refined food. This changes the duration of sensory exposure to the food, the number of chewing strokes, the speed at which it is ingested, and potentially the neuroendocrine signals that regulate satiety and energy intake.
Contemporary research on eating behavior does, in fact, show a consistent association between eating quickly and greater adiposity. A meta-analysis of 23 studies found that individuals who ate faster had a higher average BMI and about twice the probability of obesity compared to those who ate slowly. However, these are mainly observational data: the association does not prove that slowing down a meal alone is sufficient to cause weight loss.
Experimental studies also suggest that chewing plays a role. In a controlled study conducted on young men with normal weight and obesity, increased chewing activity reduced energy intake during the meal and altered some gastrointestinal hormones involved in appetite regulation.
A systematic review and meta-analysis dedicated to oral processing, that is, the processes that occur in the mouth during food consumption, also found that greater oral exposure and prolonged chewing can promote satiety processes and, under certain experimental conditions, reduce food intake.
This makes a very simple rule interesting: do not rush to swallow.
The principle of so-called “putting down the cutlery” makes physiological sense: bring the bite to your mouth, put down the cutlery, and only pick it up again after you have finished chewing and swallowing. There is no need to turn chewing into a rigid ritual or count jaw movements; the goal is simply to break the automaticity of fast eating.
Hunger, stomach, and neuroendocrine signals: there is no single “switch”
However, a common oversimplification needs to be corrected: satiety does not simply depend on the stomach being “filled”.
Ghrelin is indeed one of the main signals involved in hunger regulation, but the control of food intake is the result of the interaction between numerous systems: gastric distension, intestinal nutrient sensing, cholecystokinin, GLP-1, PYY, insulin, leptin, vagal signals, and hypothalamic and mesolimbic circuits.
Food texture also plays a role through a more complex mechanism: a food that requires more chewing tends to slow down consumption and increases sensory exposure to the food, giving satiety systems more time to act.
However, the idea that prolonged chewing necessarily produces a “weight-loss signal” through a single brain receptor is too simplistic to represent current physiology.
The literature suggests an interaction between chewing, the autonomic nervous system, gastrointestinal hormones, and brain reward circuits. It is therefore not correct to attribute an independent and guaranteed anti-obesity effect to chewing.
The whole grain: germ, bran, and endosperm
Simply put, a whole grain is composed of three main components:
germ, that is, the embryo of the seed;
bran, consisting mainly of the outer layers of the grain;
endosperm, the storage part that is especially rich in starch and contains proteins.
During the refining of grains, the germ and much of the bran are removed, leaving mainly the endosperm.
This profoundly changes the nutritional composition of the food. The germ contains unsaturated lipids, vitamin E, B vitamins, minerals, and other bioactive compounds; the bran provides fiber, minerals, vitamins, and numerous phytochemical substances.
For this reason, the comparison between a whole grain and the corresponding refined grain should not be reduced to the simple amount of carbohydrates.
The fundamental point is that whole grain preserves the original matrix of the seed, while refined grain mainly preserves its starchy component.
However, it is important to avoid generalized numbers such as “iron is 5 to 20 times higher” or “vitamin B2 is five times higher” as if they were valid for any flour. The composition varies considerably depending on the species, cultivar, agronomic conditions, milling, and possible fortification.
The terminology also needs clarification: niacin is vitamin B3, not B5. Vitamin B5 is pantothenic acid.
Whole grain does not simply mean “more bran”
The concept of whole food involves preserving the main components of the grain, not simply adding bran to a refined matrix.
From a nutritional point of view, in fact, the grain matrix matters.
Bread or pasta made from whole grain has a different structure compared to a refined product to which a certain amount of fiber has subsequently been added.
This does not mean that a product with added bran is necessarily “fake” or lacking nutritional value. Rather, it means that it should not automatically be considered equivalent, in every respect, to a food obtained from the whole grain.
The difference becomes particularly interesting when considering blood sugar, satiety, intestinal fermentation, and nutrient metabolism.
Fiber: much more than intestinal regularity
Dietary fiber represents one of the most important characteristics of whole plant foods.
Not all fiber is the same. There are soluble and insoluble fibers, viscous and non-viscous, fermentable and poorly fermentable. Their physiological properties can be very different.
Some fibers increase the viscosity of the intestinal contents and slow down gastric emptying and nutrient absorption; others are metabolized by the intestinal microbiota with the production of short-chain fatty acids, including acetate, propionate, and butyrate.
Fiber can therefore influence:
- intestinal transit;
- stool consistency;
- microbial fermentation;
- production of intestinal metabolites;
- glycemic response;
- satiety;
- bile acid metabolism.
But even here, absolutes should be avoided.
A systematic review of 44 publications highlighted that the effects of fiber on satiety are heterogeneous: only a part of the interventions resulted in a significant reduction in hunger or energy intake. Some categories, such as beta-glucans, rye fiber, and some fiber-rich mixtures, showed more consistent results.
A more recent review of 48 randomized studies on cereal fiber confirmed favorable effects on some measures of satiety, but with more limited effects on spontaneous energy intake.
Therefore, saying that “fiber satiates” is reasonable; saying that “any fiber automatically prevents overeating” is not.
Whole grain and cardiovascular health: the epidemiological evidence is interesting
The habitual consumption of whole grains is one of the aspects of diet with particularly consistent epidemiological literature.
A dose-response meta-analysis published in the BMJ, including 45 prospective studies, observed that greater consumption of whole grains was associated with a reduction in the risk of cardiovascular disease, cardiovascular mortality, all-cause mortality, and, to a lesser extent, cancer mortality.
Another meta-analysis estimated that every increase of 50 g/day of whole grains was associated with a relative risk of about 0.78 for total mortality, 0.70 for cardiovascular mortality, and 0.82 for cancer mortality.
This is important data, but it must be interpreted correctly: these are mainly prospective observational studies. They do not prove that simply adding a certain amount of whole grains to the diet automatically reduces mortality.
Those who consume more whole grains may simultaneously consume more fruit and vegetables, less processed meat, exercise more, smoke less, and have other favorable behaviors.
The scientifically most solid message is therefore that a diet overall rich in whole plant foods and whole grains is associated with better health outcomes.
The problem is not only white flour: it is the food matrix
A refined food does not automatically become “toxic”.
White bread, white rice, or refined pasta can easily be part of a balanced diet. The problem arises when a very high proportion of the diet consists of refined, energy-dense products, low in fiber and easily consumed in large quantities.
The difference compared to a whole grain is not only about fiber content.
Refining changes the physical structure of the food, the speed of consumption, the glycemic response, and the ratio between energy and micronutrients.
It is therefore more correct to talk about the overall quality of the food matrix rather than demonizing a single flour.
From refined food to ultra-processed
The concept becomes even more relevant when moving from simply refined foods to ultra-processed foods.
Ultra-processed foods do not coincide with all industrial foods, and not all packaged foods are necessarily unfavorable. Furthermore, the NOVA classification has limitations and areas of scientific discussion.
However, the epidemiological picture is now very broad.
An umbrella review published in the BMJ in 2024 brought together 45 pooled analyses involving almost 9.9 million participants. Greater exposure to ultra-processed foods was associated with numerous adverse outcomes, with particularly relevant evidence for type 2 diabetes, cardiovascular mortality, obesity, and general mortality. However, the same authors emphasize that much of the evidence has low or very low quality and that epidemiological association does not automatically equate to causality.
This point is fundamental.
The problem is not the presence of a single “bad” molecule, but frequently the combination of high energy density, high palatability, rapid consumption, low fiber content, easily ingestible texture, and formulations that promote high energy intake.
Sugars: “sugar-free” does not necessarily mean metabolically neutral
The “sugar-free” label must be interpreted by reading the entire list of ingredients and the nutritional table.
Glucose, fructose, maltose, sucrose, and syrups can have different characteristics, but they all belong to the family of available carbohydrates and can contribute to energy intake.
The glycemic index also cannot be used in isolation to judge a food.
The metabolic response depends on the amount consumed, the composition of the meal, the presence of fiber, fats, and proteins, the processing of the food, and individual response.
It is therefore simplistic to claim that replacing sucrose with glucose syrup always represents a metabolically irrelevant change or, conversely, that any replacement with an artificial sweetener necessarily increases hunger.
In fact, the most recent literature on non-nutritive sweeteners is much more complex. A 2026 meta-analysis of randomized trials evaluated weight, metabolism, and appetite within weight control programs, showing the need to distinguish the effects of different sweeteners, doses, and dietary context.
Sweeteners and hunger: a more complex relationship than it seems
The hypothesis that sweet taste without energy intake could alter appetite regulation systems is biologically interesting.
The brain receives information not only from glucose present in the blood, but also from taste receptors, the gut, the vagus nerve, and reward circuits.
However, studies on humans do not allow us to conclude that all artificial sweeteners systematically increase hunger or cause obesity.
The most prudent conclusion is that their impact depends on the type of substance, overall eating behavior, and whether they are used to replace sugars or simply added to an already high-calorie diet.
Trans fats: here the evidence is much clearer
The story is different for industrially derived trans fatty acids.
Partial hydrogenation of vegetable oils can generate trans fatty acids. These compounds have unfavorable effects on the lipoprotein profile, increasing LDL cholesterol and reducing HDL cholesterol, and are associated with an increased cardiovascular risk.
Intervention studies have also shown biological effects consistent with inflammatory activation. In a 16-week randomized study conducted in postmenopausal women with overweight, the consumption of industrial trans fats increased TNF-α compared to the control, although not all inflammatory markers changed.
However, it is important to correct a statement present in older popular literature: it is not correct to say that trans fats accumulate in the arteries simply because our body “does not have the enzymes to break them down”.
Cardiovascular risk is more complex and involves alterations in lipoproteins, endothelial function, cellular metabolism, and inflammatory processes.
PPAR: a real biological mechanism, but not a simple “consumption/accumulation” switch
PPAR receptors, peroxisome proliferator-activated receptors, are indeed important regulators of gene transcription.
PPAR-α, PPAR-γ, and PPAR-δ participate in the control of lipid metabolism, carbohydrate metabolism, adipogenesis, and the inflammatory response.
But even in this case, physiology is more complex than a simple distinction between “natural fats” that activate consumption and “altered fats” that induce accumulation.
The response of PPARs depends on the nature of the fatty acids, the concentration, the tissue involved, and the metabolic state of the organism.
The useful concept to keep in mind is therefore this: the composition of fatty acids can modulate cellular metabolic signaling, but there is no single molecular switch that determines whether the organism should accumulate or burn fat.
Glutamate: do not confuse presence, dose, and toxicity
Monosodium glutamate is often included in the list of substances to avoid indiscriminately.
The scientific situation is more nuanced.
Glutamate is an amino acid naturally present in numerous foods and is also an important neurotransmitter. However, dietary glutamate does not automatically equate to glutamate acting as a neurotransmitter in the central nervous system: there are important barriers and metabolic processes that separate these compartments.
This does not mean that high amounts of an ingredient cannot be problematic for some people or in certain contexts, but it is not scientifically correct to state that the normal dietary consumption of glutamate “excites neurons” because ingested glutamate directly enters the brain.
Even the so-called “Chinese restaurant syndrome” is now considered an insufficiently robust description to generically attribute headaches, sweating, or other symptoms to monosodium glutamate.
Nitrites and nitrates: the risk depends on the context
Nitrites and nitrates deserve attention, but they cannot simply be presented as substances to eliminate.
Nitrates are naturally present in many vegetables, especially leafy greens. Nitrites are used, in regulated quantities, mainly in the preservation of processed meats.
The problem arises from the metabolism of nitrogenous compounds and the possible formation of N-nitrosamines, some of which have carcinogenic activity.
The nutritional risk is therefore linked to the source, the quantity, the preparation method, and the overall consumption of processed meats.
Methemoglobinemia is a real toxicological condition associated with excessive exposure to nitrites, but using it as a general argument against the normal regulated quantities present in foods does not represent a correct interpretation of risk in the general population.
Eating peacefully: the brain participates in digestion
The meal is not just a mechanical process.
Digestion is regulated by the autonomic nervous system, the vagus nerve, gastrointestinal hormones, and a complex bidirectional communication between the brain and the gut.
Stress and sympathetic activation can alter motility, gastrointestinal secretions, and the perception of digestive symptoms.
This does not mean that a phone call during lunch “blocks digestion,” but it suggests that eating distractedly, quickly, and under conditions of high stress can alter eating behavior and gastrointestinal perception.
For this reason, a calm environment, reducing distractions, and paying greater attention to food represent reasonable behavioral strategies.
The principle of “putting down the cutlery” then becomes interesting not as a medical prescription, but as a simple tool to slow down the pace of eating and increase awareness of the meal.
Fiber and bloating: a fundamental distinction
A common mistake is to conclude that, if a high-fiber food causes bloating, then fiber is “the cause of the problem.”
In reality, the sudden increase in fiber intake can temporarily increase fermentation, gas production, and abdominal distension, especially when the previous diet was low in fiber.
This does not mean that fiber is harmful.
The gut microbiota uses many fibers as a metabolic substrate, and the production of short-chain fatty acids represents one of the main links between diet, microbiota, and host physiology.
The most rational strategy is therefore to gradually increase high-fiber foods, accompanying them with adequate hydration and assessing individual tolerance.
In the presence of persistent gastrointestinal symptoms, pain, diarrhea, weight loss, blood in the stool, or other clinical manifestations, however, it is not correct to automatically attribute everything to fiber: a medical evaluation is required.
And alcohol?
On this point, scientific knowledge has evolved significantly compared to many popular publications from the 1990s and 2000s.
It is no longer correct to present the classic “glass of red wine” as necessarily protective behavior.
Alcohol is classified as a group 1 carcinogen, and the World Health Organization emphasizes that no level of consumption has been identified as free from oncological risk. The risk increases with the quantity, but it can also increase with relatively low consumption.
This does not mean that someone who occasionally drinks a glass of wine should automatically consider themselves sick. It means that it is not scientifically correct to prescribe alcohol as a cardiovascular prevention strategy.
Grape polyphenols, such as resveratrol and quercetin, can be consumed through grapes, berries, vegetables, and other plant-based foods, without having to introduce ethanol.
Inflammation is not always an enemy
Even the term “inflammation” requires precision.
Acute inflammation is a fundamental biological response. It is part of the processes through which the organism recognizes damage, recruits immune cells, and initiates tissue repair.
The problem is different when we talk about low-grade chronic inflammation, characterized by a persistent alteration of immunometabolic homeostasis.
Visceral obesity, metabolic alterations, sedentary lifestyle, smoking, sleep disorders, and certain dietary patterns can contribute to this state.
However, it is not correct to state that repeatedly eating “the same foods” automatically causes a pathological immune response or that a supposed “food inflammation” is indiscriminately responsible for diabetes, tumors, dementia, and autoimmune diseases.
IgE-mediated allergies, autoimmune diseases, enzymatic intolerances, celiac disease, and other adverse food reactions have different biological mechanisms and must be diagnosed with appropriate tools.
The word “intolerance,” used generically, can therefore create more confusion than clarity.
The real goal: recover the structure of the food
The most interesting lesson is not that we should only eat “hard” foods or eliminate any soft food.
A healthy diet cannot be built on the consistency of an isolated food.
The point is to recover, when possible, a greater presence of whole and minimally processed foods: whole grains, legumes, vegetables, whole fruit, nuts, seeds, tubers, fish, eggs, and protein sources suitable for individual needs.
Whole fruit, for example, is different from juice not because juice is necessarily “poison,” but because the physical structure of the food, the fiber, and the time required for consumption alter the physiological response.
The same applies to a whole grain compared to highly refined flour.
And it also applies to a meal prepared from recognizable ingredients compared to a product industrially formulated to be extremely palatable, easily consumed, and densely energetic.
A simple rule: eat what requires a little work
Modern food physiology therefore suggests an interesting perspective: our organism does not only receive nutrients; it receives information.
Consistency, chewing, ingestion speed, fiber, energy density, taste, smell, and food structure participate in the construction of that information.
Eating slowly does not magically “turn on” metabolism.
Fiber does not “cleanse” the gut of all toxins.
Whole grain is not a cure for chronic diseases.
Gluten is not a glue that automatically makes wheat harmful.
Refined food is not poison.
And an industrial food is not automatically harmful because it contains an additive.
But, looking at the overall evidence, a much more solid principle emerges: a diet based predominantly on whole plant foods, whole grains, adequate fiber, simple preparations, and mindful consumption is consistent with better metabolic and cardiovascular health. The evidence on whole grains is particularly consistent on the epidemiological level, while that on chewing and meal speed indicates a possible role in regulating energy intake.
The direction, therefore, is not necessarily “eat less.”
It is about learning to eat better, more slowly, and with foods that retain their original structure.
Bibliographic references
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- Chen GC, Tong X, Xu JY, et al. Whole-grain intake and total, cardiovascular, and cancer mortality: a systematic review and meta-analysis of prospective studies. American Journal of Clinical Nutrition. 2016;104(1):164-172.
- Benisi-Kohansal S, Saneei P, Salehi-Marzijarani M, et al. Whole-Grain Intake and Mortality from All Causes, Cardiovascular Disease, and Cancer. Advances in Nutrition. 2016;7(6):1052-1065.
- Clark MJ, Slavin JL. The effect of fiber on satiety and food intake: a systematic review. Journal of the American College of Nutrition. 2013;32(3):200-211.
- Sarkar A, et al. Influence of oral processing on appetite and food intake – A systematic review and meta-analysis. Appetite. 2018;125:253-264.
- Li J, Zhang N, Hu L, et al. Improvement in chewing activity reduces energy intake in one meal and modulates plasma gut hormone concentrations in obese and lean young Chinese men. American Journal of Clinical Nutrition. 2011;94(3):709-716.
- Ohkuma T, Hirakawa Y, Nakamura U, et al. Association between eating rate and obesity: a systematic review and meta-analysis. International Journal of Obesity. 2015;39:1589-1596.
- Lane MM, Gamage E, Du S, et al. Ultra-processed food exposure and adverse health outcomes: umbrella review of epidemiological meta-analyses. BMJ. 2024;384:e077310.
- Bendsen NT, Stender S, Szecsi PB, et al. Effect of industrially produced trans fat on markers of systemic inflammation: evidence from a randomized trial in women. Journal of Lipid Research. 2011;52(10):1821-1828.
- Smit LA, Katan MB, Wanders AJ, et al. A high intake of trans fatty acids has little effect on markers of inflammation and oxidative stress in humans. Journal of Nutrition. 2011.
- World Health Organization Regional Office for Europe. No level of alcohol consumption is safe for our health. 2023.
- WHO Europe/IARC. Joint statement on the link between alcohol and cancer. 2023
