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Diet and nutrition

Is it genes that make us fat, or what’s on our plate?

Sources: 15 · Article: 18 109 characters

Genes affect our susceptibility to weight gain, but they do not explain the rise in obesity on their own; food and the environment matter too.

  • Some rare genetic changes can cause severe obesity, but many genes affect weight only slightly.
  • Ewa Dąbrowska identifies an unhealthy lifestyle, especially processed food and lack of exercise, as the main cause of obesity.
  • Diet and physical activity can also change how genes work without changing their structure.
  • In short: genes can increase susceptibility, while eating habits and other conditions can affect whether weight increases.

What the authors write

prof. David Ludwig

Many genes affect weight, usually only slightly, while rare mutations can cause severe obesity.

„Recent research indicates that dozens of genes affect body weight to some degree, most by only a tiny amount. Together, however, they significantly influence how likely you are to gain weight. Rarely, mutations in certain genes cause massive obesity, typically from early in childhood.”Recent research indicates that dozens of genes affect body weight to some degree, most by only a tiny amount. Together, however, they significantly influence how likely you are to gain weight. Rarely, mutations in certain genes cause massive obesity, typically from early in childhood.
Do Genes Make Us Fat?
prof. David Ludwig

The obesity epidemic has grown too quickly to be explained by genetic changes; the author points to changes in the environment and processed food.

„The obesity epidemic developed far too fast to be attributable to genetic changes. Although genes haven’t changed rapidly, the environment has. The most obvious culprit in our environment is all the highly processed carbohydrate that flooded the food supply during the low-fat craze of the last forty years.”The obesity epidemic developed far too fast to be attributable to genetic changes. Although genes haven’t changed rapidly, the environment has. The most obvious culprit in our environment is all the highly processed carbohydrate that flooded the food supply during the low-fat craze of the last forty years.
Do Genes Make Us Fat?
Ewa Dąbrowska

Diet and physical activity can switch genes on or off without changing their structure.

„It has been discovered that diet and physical activity can activate or silence genes without changing their structure. This is a revolution in medicine. We become ill not at the level of our organs, but at the level of our genes. Lifestyle can “reprogram” how they work—from promoting disease to promoting health.”Odkryto, że sposób odżywiania i aktywność fizyczna mogą aktywować lub wyciszać geny, nie zmieniając ich struktury. To rewolucja w medycynie. Chorujemy nie na poziomie narządów, ale genów. Styl życia może „przeprogramować” ich działanie — z pro-chorobowego na prozdrowotne.
Dieta warzywno owocowa
Ewa Dąbrowska

An unhealthy lifestyle, especially too much processed food and too little exercise, is identified as the main cause of obesity.

„The main cause of obesity is an unhealthy lifestyle—above all, excessive consumption of processed food and lack of physical activity. A vegetable-and-fruit fast, combined with exercise, directly addresses the causes of disease: excess calories and too little physical activity.”Główną przyczyną otyłości jest niezdrowy styl życia – przede wszystkim nadmierne spożycie przetworzonej żywności i brak aktywności fizycznej. Post warzywno-owocowy, połączony z ruchem, działa bezpośrednio na przyczyny chorób: nadmiar kalorii i niedobór ruchu.
Dieta warzywno owocowa
Ewa Dąbrowska

An unhealthy lifestyle, including too much processed food and too little physical activity, is identified as the main cause of obesity.

„The main cause of obesity is an unhealthy lifestyle—above all, excessive consumption of processed food and lack of physical activity. A vegetable-and-fruit fast, combined with exercise, directly addresses the causes of disease: excess calories and too little physical activity.”Główną przyczyną otyłości jest niezdrowy styl życia – przede wszystkim nadmierne spożycie przetworzonej żywności i brak aktywności fizycznej. Post warzywno-owocowy, połączony z ruchem, działa bezpośrednio na przyczyny chorób: nadmiar kalorii i niedobór ruchu.
Schorzenia i świadectwa
Ewa Dąbrowska

A diet high in processed carbohydrates can raise insulin levels, and excess insulin may promote fat storage.

„A diet high in processed carbohydrates (e.g. pizza, white bread, sweets) raises insulin levels. Too much insulin can reprogram metabolism toward storing fat. During fasting, insulin levels fall, triggering processes that reduce body weight and reverse metabolic diseases.”Dieta bogata w przetworzone węglowodany (np. pizza, białe pieczywo, słodycze) prowadzi do wzrostu poziomu insuliny. Nadmiar insuliny może przeprogramować metabolizm w kierunku odkładania tłuszczu. W czasie postu poziom insuliny spada, co uruchamia procesy redukcji masy ciała i cofania się chorób metabolicznych.
Dieta warzywno owocowa
Paul Clayton

Eating habits and living conditions, such as poverty, access to fresh food, and heat that limits physical activity, are identified as factors associated with obesity.

„All of this applies to the people of Glasgow, too. Here are some of the reasons why poverty and obesity have gone hand in hand over the past half-century (11–14), although the rising tide of ultra-processed food is now tipping the balance across all social classes (13–15).”To wszystko dotyczy również mieszkańców Glasgow. Oto niektóre z powodów, dla których bieda i otyłość przebiegały równolegle przez ostatnie pół wieku (11–14), chociaż rosnąca fala ultraprzetworzonej żywności przechyla teraz szalę we wszystkich klasach społecznych (13–15).
Dieta a nasze przeznaczenie
Paul Clayton

Eating habits, marketing, and social norms can make it harder to return to a healthy diet.

„Add to this the conditioning of our palates, aggressive marketing, and social norms. Once you’ve sold your soul to ultra-processed food, it’s hard to return to healthy eating (19–20). In the background, Big Food’s constant marketing of its rubbish flows through the media like an oil slick.”Dodaj do tego aklimatyzację podniebienia, agresywny marketing i normy społeczne. Kiedy sprzedasz swoją duszę ultraprzetworzonej żywności, trudno jest wrócić do zdrowego jedzenia (19–20). W tle nieustanny marketing wydalin Big Food płynie przez media jak plama oleju.
Dieta a nasze przeznaczenie
Paul Clayton

More frequent adoption of a Southern diet and lifestyle, rather than Southern genes, was identified as an explanation for differences in residents’ health.

„The idea that genes in the southern United States were responsible for people’s disability was disproved a quarter of a century ago in the DanishTwin study (9), when a team led by the formidable James Vaupel established that diet and lifestyle account for 80 percent of health and lifespan.”Pomysł, że geny południa USA są odpowiedzialne za ich niepełnosprawność, został obalony ćwierć wieku temu w badaniu DanishTwin (9), kiedy zespół kierowany przez budzącego grozę Jamesa Vaupela ustalił, że dieta i styl życia są odpowiedzialne za 80 proc. zdrowia i długość życia.
Dieta a nasze przeznaczenie
Bracia Rodzeń

According to Bracia Rodzeń, carbohydrates raise insulin levels, and insulin signals the body to store energy; consuming more carbohydrates is said to promote weight gain.

„After eating carbohydrates, insulin levels in the blood rise significantly. Insulin is a hormone that signals the body to store energy. The more carbohydrates in your food, the faster and more you will gain weight and develop insulin resistance and other metabolic diseases.”Po spożyciu węglowodanów poziom insuliny we krwi znacznie wzrasta. Insulina to hormon, który daje sygnał do magazynowania. Im więcej węglowodanów w Twoich pokarmach, tym szybciej i bardziej przytyjesz, zachorujesz na insulinooporność i inne choroby metaboliczne.
Bracia Rodzeń
Jerzy Jaśkowski

The statement quoted attributes the rise in obesity to environmental changes, which may trigger disease in people with a genetic predisposition.

„The recent rise in chronic diseases such as diabetes, childhood asthma, obesity, and autism cannot be caused by changes in the human gene pool, because such changes take much longer. They must be caused by environmental changes that can trigger disease in people who are genetically predisposed.”Niedawny wzrost chorób przewlekłych, takich jak cukrzyca, astma u dzieci, otyłość czy autyzm nie może być spowodowany zmianami w puli genów ludzkich, ponieważ zmiany te wymagają znacznie więcej czasu. Muszą być spowodowane zmianami w środowisku, które mogą spowodować choroby u osób predysponowanych genetycznie.
Autyzm – czyli jak nas podstępnie uszkadzają i okradają
M. Williamson i N. Moustaid-Moussa i L. Gollahon

The effect of saturated fats on obesity risk may depend on the APOA2 gene variant.

„Saturated fatty acids from the diet interact with the promoter of APOA2, thereby influencing risk of obesity depending on gene variant (). The underlying mechanism reveals significant changes in methylation status at a particular gene location according to saturated fat intake ().”Saturated fatty acids from the diet interact with the promoter of APOA2, thereby influencing risk of obesity depending on gene variant (). The underlying mechanism reveals significant changes in methylation status at a particular gene location according to saturated fat intake ().
Frontiers | The Molecular Effects of Dietary Acid Load on Metabolic Disease (The Cellular PasaDoble: The Fast-Paced Dance of pH Regulation)

Research from PubMed · Europe PMC

We selected 8 studies with the best, positive results. This is a selection, not a full review of all research.

Total number of studies on this topic in PubMed: 4 114.

A review found that, in children, eating when not hungry is associated with more body fat, and its development may be partly influenced by genetics.

Aim of the study: Eating in the absence of hunger (EAH) has been extensively studied over the past two decades and has been associated with excess body weight and the development of obesity. However, determinants of EAH remain uncertain.

Results: Moreover, EAH development seems to be influenced by genetics. In adolescence, the number of studies is limited; yet, studies show that EAH slightly increases or remains stable with age, is not clearly different between sexes, and findings for overweight or obesity are less consistent across studies in adolescence. For familial factors, parental restrictive feeding practices are positively associated with EAH during childhood, mostly for girls. Studies assessing environmental factors are lacking and robust longitudinal studies spanning from early childhood to adolescence are needed.

Factors Associated with Eating in the Absence of Hunger among Children and Adolescents: A Systematic Review. · Nutrients 2022
Money for the studygovernment, public institutions · Research Center of the Centre Hospitalier Universitaire Sainte-Justine, Canadian Institutes of Health Research
Do the authors have ties to companies?no — the authors say so
Did a manufacturer help with the study?NO
Type of studyreview of many studies

“Not stated” does not mean nobody paid — the database does not always record it.

A review indicates that genes affect BMI and eating behaviors, but the environment and eating habits matter too.

Aim of the study: Obesity has dramatically increased during the last decades and is currently one of the most serious global health problems. We present a hypothesis that obesity is a neuro-behavioral disease having a strong genetic background mediated largely by eating behavior and is sensitive to the macro-environment; we study this hypothesis from the perspective of genetic research.

Results: Obesogenic environments at both childhood family and societal levels reinforce the genetic susceptibility to obesity. Genetic factors have a clear influence on macro-nutrient intake and appetite-related eating behavior traits. Results on the gene-by-diet interactions in obesity are mixed, but emerging evidence suggests that eating behavior traits partly mediate the effect of genes on BMI. However, more rigorous prospective study designs controlling for measurement bias are still needed.

Obesity and eating behavior from the perspective of twin and genetic research. · Neurosci Biobehav Rev 2020
Money for the studynot stated
Do the authors have ties to companies?not stated
Did a manufacturer help with the study?unknown
Type of studydiscussion of other studies

“Not stated” does not mean nobody paid — the database does not always record it.

A review indicates that genes have a moderate influence on eating habits, while the environment matters as well.

Aim of the study: Humans show remarkable variability in their eating styles. Reasons for this variability are poorly understood, but carry important implications for the onset of obesity and its comorbidities.

Results: This review highlights what is known about the genetics of food preferences and selection in humans. Data from family and twin studies suggest a moderate genetic contribution to eating style, with clear environmental effects emerging as well. Select studies show support for gene-environment interactions and common genetic bases for certain dietary patterns, obesity, and/or metabolic complications. Genetically informative designs that infuse innovative behavioral measures may help explain individual differences in eating styles and hopefully promote more effective obesity treatments.

Genetics of eating and its relation to obesity. · Curr Atheroscler Rep 2002
Money for the studygovernment, public institutions · NIDDK NIH HHS, NIMH NIH HHS
Do the authors have ties to companies?not stated
Did a manufacturer help with the study?unknown
Type of studydiscussion of other studies

“Not stated” does not mean nobody paid — the database does not always record it.

A review describes how emotional eating may contribute to later weight gain, and how genes may partly affect weight through eating behaviors.

Aim of the study: Stress and other negative emotions, such as depression and anxiety, can lead to both decreased and increased food intake. The term 'emotional eating' has been widely used to refer to the latter response: a tendency to eat in response to negative emotions with the chosen foods being primarily energy-dense and palatable ones.

Results: First, studies implying that emotional eating may be one behavioural mechanism linking depression and development of obesity. Secondly, studies highlighting the relevance of night sleep duration by showing that adults with a combination of shorter sleep and higher emotional eating may be especially vulnerable to weight gain. Thirdly, an emerging literature suggesting that genes may influence body weight partly through emotional eating and other eating behaviour dimensions. The review concludes by discussing what kind of implications these three avenues of research offer for obesity prevention and treatment interventions.

Emotional eating and obesity in adults: the role of depression, sleep and genes. · Proc Nutr Soc 2020
Money for the studynot stated
Do the authors have ties to companies?not stated
Did a manufacturer help with the study?unknown
Type of studydiscussion of other studies

“Not stated” does not mean nobody paid — the database does not always record it.

A review indicates that successful weight loss depends not only on biology, but also on behaviors and psychological factors.

Aim of the study: There is a large variability between individuals in the weight loss response to any given diet treatment, which fuels interest into personalized or precision nutrition. Although most efforts are directed toward identifying biological or metabolic factors, several behavioral and psychological factors can also be responsible for some of this interindividual variability.

Results: There are many factors that can influence the response to dietary weight loss interventions, including factors related to eating behavior (emotional eating, disinhibition, restraint, perceived stress), behaviors and societal norms related to age and sex, psychological and personal factors (motivation, self-efficacy, locus of control, self-concept), and major life events. The success of a weight loss intervention can be influenced by many psychological and behavioral constructs and not merely by physiological factors such as biology and genetics. These factors are difficult to capture accurately and are often overlooked. Future weight loss studies should consider assessing such factors to better understand the underlying reasons for the large interindividual variability to weight loss therapy.

Behavioral and Psychological Factors Affecting Weight Loss Success. · Curr Obes Rep 2023
Money for the studynot stated
Do the authors have ties to companies?not stated
Did a manufacturer help with the study?unknown
Type of studydiscussion of other studies

“Not stated” does not mean nobody paid — the database does not always record it.

A review found that children with overweight or obesity are more likely to eat after becoming full, and some studies point to a genetic basis for this behavior.

Aim of the study: Eating in the Absence of Hunger (EAH), or consuming highly palatable foods when satiated, is one behavioral pathway that may lead to childhood obesity. EAH is an objective, laboratory-based measure. A more comprehensive understanding of potential determinants of EAH could inform childhood obesity programs outside of a laboratory setting.

Results: 12 cross-sectional, six prospective, and one behavioral-intervention studies were included in the review. EAH was observable among boys and girls; absolute levels of EAH increased with age; and maternal feeding styles were associated with EAH among girls. The most consistent evidence supported increased levels of EAH among overweight and obese versus normal weight children, both cross-sectionally and prospectively. Two studies supported a genetic component to EAH. Studies enrolling independent samples support a positive association between weight status and EAH among children; studies addressing causality are needed. Other various individual, genetic, and familiar characteristics were associated with EAH, yet studies among more heterogeneous sample populations are needed to confirm findings. Studies addressing societal-level factors related to EAH were absent.

Understanding eating in the absence of hunger among young children: a systematic review of existing studies. · Appetite 2015
Money for the studygovernment, public institutions · NICHD NIH HHS, NIEHS NIH HHS, NIGMS NIH HHS
Do the authors have ties to companies?not stated
Did a manufacturer help with the study?unknown
Type of studyreview of many studies

“Not stated” does not mean nobody paid — the database does not always record it.

A review indicates that children’s eating habits are shaped by their family and social environment, and that genetics may also matter in obesity.

Aim of the study: To investigate the relationship between the biopsychosocial environment and eating habits and behaviors that lead to the selection and consumption of certain food from the earliest stages of life. To clarify whether there is an interaction between genetic and epigenetic factors, and how they shape eating habits.

Results: Eating habits are transmitted from parents to children in different ways: environmental, emotional, social, and educational. In cases of obesity, a greater association of genetic influence can be observed.

Transgenerational transmission of eating habits. · J Pediatr (Rio J) 2024
Money for the studynot stated
Do the authors have ties to companies?yes — the authors reported it
Did a manufacturer help with the study?YES
Type of studydiscussion of other studies

“Not stated” does not mean nobody paid — the database does not always record it.

In a rat study, excessive consumption of high-calorie, tasty food was associated with the development of obesity and compulsive eating.

Aim of the study: We found that development of obesity was coupled with emergence of a progressively worsening deficit in neural reward responses. Similar changes in reward homeostasis induced by cocaine or heroin are considered to be crucial in triggering the transition from casual to compulsive drug-taking.

Results: Striatal dopamine D2 receptors (D2Rs) were downregulated in obese rats, as has been reported in humans addicted to drugs. Moreover, lentivirus-mediated knockdown of striatal D2Rs rapidly accelerated the development of addiction-like reward deficits and the onset of compulsive-like food seeking in rats with extended access to palatable high-fat food. These data demonstrate that overconsumption of palatable food triggers addiction-like neuroadaptive responses in brain reward circuits and drives the development of compulsive eating. Common hedonic mechanisms may therefore underlie obesity and drug addiction.

Dopamine D2 receptors in addiction-like reward dysfunction and compulsive eating in obese rats. · Nat Neurosci 2010
Money for the studygovernment, public institutions · NIDA NIH HHS
Do the authors have ties to companies?not stated
Did a manufacturer help with the study?unknown
Type of studyanimal study

“Not stated” does not mean nobody paid — the database does not always record it.

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