— Topics —
Genetic factors vs environmental factors
2025.03.03
The Rise in Obesity is Closely Linked to the Consumption of Ultra-Processed Foods
Summary
1. In 2009, a research group at the University of São Paulo proposed the NOVA classification system, which categorizes foods according to the nature, extent, and purpose of processing. NOVA divides foods into four groups:
・Unprocessed or minimally processed foods
・Processed culinary ingredients
・Processed foods (PFs)
・Ultra-processed foods (UPFs)
2. UPFs are formulations made through multiple industrial processes. They tend to be high in refined carbohydrates, added sugars, salt, and fats, making them highly energy-dense. In contrast, they are often low in dietary fiber and micronutrients.
3. In countries such as the USA and the UK, UPFs account for more than 50% of total daily energy intake. Many studies have shown that a higher proportion of energy intake derived from UPFs is associated with a greater risk of obesity.
In contrast, the consumption of unprocessed foods, such as vegetables, has been inversely associated with obesity.
4. Individuals with higher UPF consumption tend to consume fewer fruits, vegetables, nuts, and fish, and generally have lower overall diet quality.
5. Compared with whole-food meals, processed-food meals may reduce diet-induced thermogenesis (DIT), resulting in greater net energy gain. In addition, UPF-based diets have been shown to increase ad libitum energy intake.
My perspective
6. The global rise in obesity may not be fully explained by an increase in caloric intake alone. I believe that greater attention should be paid to the effects of food processing itself on human physiology.
UPFs are typically low in dietary fiber and have simplified food structures. As a result, they tend to be digested and absorbed very efficiently. As overall diet quality declines, conditions may arise in which undigested matter is less likely to remain in the intestinal tract. I propose that this may contribute to a physiological state that I refer to as intestinal starvation.
【 Full text 】
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Contents
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- Food classification using the NOVA system
- Issues associated with ultra-processed foods
- Consumption of UPFs and its association with obesity
- Impact of UPFs on overall diet
(1)Decline in overall diet quality
(2) Increase in net energy gain
(3) Effects on ad libitum energy intake - How UPFs may contribute to intestinal starvation
The ongoing debates surrounding various dietary approaches—such as low-carbohydrate, ketogenic, paleo, low-fat, and vegan diets—have created considerable public confusion and contributed to growing mistrust in nutritional science.
However, it is less widely recognized that diverse diets recommendations often share a common piece of advice: to avoid ultra-processed foods[1].
In fact, in many countries, rising obesity rates have been reported to closely parallel increases in the consumption of ultra-processed foods[1]. In this article, I would like to examine some of the factors that may underlie this association. Finally, I will also discuss how these issues may relate to my intestinal starvation theory.
1. Food classification using the NOVA system
NOVA (not an acronym) is the food classification system that categorizes foods based not on their nutrient content, but on the nature, extent, and purpose of food processing. It was developed in 2009 by a research group at the University of São Paulo in Brazil [2].
Conventional food classification systems have traditionally categorized foods and ingredients according to their botanical origin or animal species, and according to their nutrient composition.
As a result, whole grains may be grouped together with breakfast cereals and cookies, and fresh chicken or pork may be classified alongside chicken nuggets or sausages.
However, conventional classification systems have had important limitations when evaluating the health effects of foods [3].
The NOVA classification system divides foods into the following four groups according to the nature, extent, and purpose of processing.
(1)Unprocessed or minimally processed foods
Natural foods such as fresh fruits and vegetables, grains, milk, fish, and meat, as well as foods that have undergone minimal processing such as the removal of inedible parts, drying, grinding, pasteurization, refrigeration, freezing, or vacuum packaging.
(2)Processed culinary ingredients
Substances derived from Group 1 foods or from nature through processes that include pressing, refining, milling, or drying, such as oils, butter, sugar, and salt. These processed culinary ingredients are typically not consumed on their own.
(3)Processed foods (PFs)
These are typically made by adding Group 2 substances to Group 1 foods. Examples include canned vegetables, fruit in syrup, canned fish, cheese, and freshly made breads.
(4)Ultra-processed foods (UPFs)
These are formulations made by combining many ingredients and undergoing multiple industrial processes. Examples include breakfast cereals, soft drinks and fruit juices, sweet or savory snack foods, chocolate confectionery, instant foods, reconstituted meat products such as sausages and nuggets, and many fast-food products [3,4].
2. Issues associated with ultra-processed foods
Food processing, in essence, refers to the operations by which raw food materials are made suitable for consumption, cooking, or storage, and virtually all foods undergo some form of processing before being eaten. In other words, processing itself is not inherently harmful.
However, ultra-processed foods may contain little or none of the natural foods classified in Group 1.
Furthermore, because they are formulations produced by combining food-derived substances and additives through multiple industrial processes, they possess characteristics that differ from those of partially modified foods [3].
These foods are typically high in refined grains, added sugars, salt, and fats, making them highly energy-dense. In contrast, they are generally poor sources of dietary fiber, protein, and micronutrients.
In addition, additives such as flavorings, colorings, emulsifiers, and sweeteners are often added to mask undesirable qualities of the final product [5].
Nevertheless, since the 1980s, the consumption of UPFs has increased rapidly not only in developed countries but also in developing nations, largely driven by multinational corporations [3].
Because UPFs are highly palatable, inexpensive, convenient, and have a long shelf life, they have gained widespread popularity among consumers.
Research based on the NOVA classification system has shown that the decline in minimally processed foods and home cooking, together with the increasing replacement of traditional diets by UPFs, is associated with unhealthy nutritional profiles and a higher prevalence of several diet-related diseases [3].
3. Consumption of UPFs and its association with obesity
Studies in adults reporting the proportion of total energy intake derived from ultra-processed foods (UPFs) have shown that the proportion exceeds 50% in the USA and the UK, and reaches approximately 45–52% in Canada.
In contrast, the proportion is relatively lower in countries such as France, Spain, Brazil, and Malaysia, although it still accounts for roughly 20–36% of total energy intake [6].
♦A cross-sectional study (2005–2014) of American adults found that, on average, participants obtained 56.1% of their total energy intake from UPFs. In the highest quintile group (Note 1), UPFs accounted for 84.5% of total energy intake, whereas in the lowest quintile group, the proportion was 25.4% [7].
Note 1: Quintiles divide ranked data into five equal groups.
Increasing consumption of UPFs has been reported to be associated with rising obesity rates in many countries.
♦A cross-sectional study based on data from Brazil’s 2008–2009 Household Budget Survey found that household consumption of UPFs was positively associated with both average BMI and obesity prevalence. Individuals in the highest UPF consumption group were 37% more likely to be obese than those in the lowest consumption group [9].
♦A cross-sectional study using data from the UK National Diet and Nutrition Survey (2008–2016) found that the proportion of total energy intake derived from UPFs ranged from approximately 35% (1st quartile; Note 2) to 74% (4th quartile).
Higher UPF consumption was associated with greater BMI, waist circumference, and obesity prevalence. In addition, for every 10% increase in the proportion of total energy intake from UPFs, obesity risk increased by 18%.
Higher UPF consumption was also more common among men, smokers, younger individuals, and lower socioeconomic groups [10].
Note 2: Quartiles divide ranked data into four equal groups.
♦A prospective cohort study conducted among graduates of the University of Navarra in Spain followed 8,451 participants who were not overweight or obese at baseline for about nine years.
Participants in the highest UPF consumption group had a 26% higher risk of developing overweight or obesity than those in the lowest consumption group. In contrast to their UPF intake, this group had the lowest average vegetable consumption. Overall, higher UPF consumption was associated with lower adherence to the Mediterranean diet [11].
Similar associations have also been reported in studies conducted in 15 Latin American countries, as well as in studies from other countries, including the USA and Canada [4,7,8].
4. Impact of UPFs on overall diet
(1) Decline in overall diet quality
♦A U.S. research group used data from the National Health and Nutrition Examination Survey (2015–2018) to investigate the relationship between UPF consumption and overall diet quality.
The study included 5,919 children and 10,064 adults, and diet quality was assessed using the American Heart Association (AHA) Diet Score and the Healthy Eating Index (HEI)-2015 [12].
The results showed that overall diet quality declined substantially as UPF consumption increased. Among children, the estimated proportion with a poor diet was 31.3% in the lowest UPF consumption group, but rose to 71.6% in the highest consumption group. A similar pattern was observed among adults.
In addition, higher UPF consumption was associated with increased intake of refined grains, sugar-sweetened beverages, and added sugars, while the consumption of healthier foods such as fruits, vegetables, nuts, and fish decreased.
The researchers concluded that higher consumption of UPFs was associated with substantially lower diet quality among both children and adults.
They also noted that these findings were consistent with previous studies conducted in several countries [12].
♦An Italian research group investigated the relationship between meal timing and the degree of food processing.
An analysis of data from 8,688 participants in the Italian Nutrition & Health Survey (2010–2013) found that individuals who ate breakfast, lunch, and dinner at later times tended to consume fewer unprocessed or minimally processed foods and more processed foods and UPFs [13].
Furthermore, later meal timing was inversely associated with adherence to the Mediterranean diet [13]. The Mediterranean diet is a dietary pattern centered on fruits, vegetables, legumes, nuts, olive oil, and fish, and has been associated with a lower risk of weight gain [14].
(2) Increase in net energy gain
♦A U.S. research group conducted a crossover study to compare the effects of processed foods (PF) and whole foods (WF) on energy expenditure. Eighteen participants consumed two isocaloric sandwiches that differed only in their degree of processing.
The WF meal consisted of multigrain bread (containing whole grains and sunflower seeds) and cheddar cheese, whereas the PF meal consisted of white bread and a processed cheese product.
As a result, diet-induced thermogenesis (DIT) (Note 3) following the PF meal was 46.8% lower than that observed after the WF meal. The researchers concluded that this difference in DIT resulted in a 9.7% increase in net energy gain for the PF meal [15].
Note 3: Diet-induced thermogenesis (DIT) refers to the increase in energy expenditure that occurs for several hours following food intake.
The researchers suggested that PFs are structurally and chemically simpler, and therefore easier to digest, than WFs [15,16].
For example, during grain refining, the bran and germ are removed, resulting in the loss of micronutrients, dietary fiber, and phenolic compounds.
As a result, less energy may be required for gastrointestinal activity and metabolism, which could contribute to a reduction in DIT [15,17].
Furthermore, a reduction in dietary fiber decreases the bulk of food, which may delay the onset of satiety and ultimately contribute to an increase in total energy intake [15,18].
(3)Effects on ad libitum energy intake
In 2019, a research group at the U.S. National Institutes of Health (NIH) conducted a randomized controlled trial to examine the effects of UPFs on ad libitum energy intake in 20 weight-stable adults [19].
Participants were admitted to the NIH Clinical Center and consumed an ultra-processed diet and an unprocessed diet for two weeks each. The two diets were designed to be closely matched in presented calories, energy density, macronutrients, and other key nutritional characteristics. They were instructed to eat as much or as little as they desired.
As a result, during the ultra-processed diet period, participants consumed about 459 kcal more per day than during the unprocessed diet period and gained 0.9± 0.3 kg from baseline. In contrast, during the unprocessed diet period, participants lost 0.9± 0.3 kg [19].
Notably, the eating rate was significantly higher during the ultra-processed diet than during the unprocessed diet.
In addition, during the unprocessed diet period, levels of the appetite-suppressing hormone PYY increased, whereas levels of the hunger hormone ghrelin decreased.
The researchers suggested that the oral sensory properties of UPFs—such as their ease of chewing and swallowing—may have increased the eating rate and delayed satiety signals, ultimately leading to greater energy intake [19,20].
5. How UPFs may contribute to intestinal starvation
Until now, the global rise in obesity has often been explained in terms of a relative increase in caloric intake. Indeed, UPFs possess several characteristics that appear to support this view:
・High energy density
・High palatability and ease of consumption
・Potential to increase net energy gain through reduced DIT
・Delayed satiety, which may lead to greater ad libitum energy intake
At the same time, however, studies using the NOVA classification system has begun to highlight factors beyond calories alone.
Studies conducted in many countries have shown that the greater the proportion of total energy intake derived from UPFs, the higher the risk of obesity. However, this association may not be fully explained by an increase in caloric intake alone.
Of particular interest is the finding that lower consumption of unprocessed foods such as vegetables, poorer overall diet quality, and irregular meal timing have all been associated with higher UPF consumption.
In other words, the issue may not be UPF consumption itself alone, but also the fact that it can displace unprocessed foods and contribute to an overall deterioration in dietary balance.
In today's food environment, where efficiency and convenience are highly valued, opportunities to consume ready-to-eat foods such as refined carbohydrates and UPFs have increased. These foods are typically soft, require little chewing, and can be consumed quickly. At the same time, the consumption of unprocessed or minimally processed foods has declined.
As a result, the intake of dietary fiber and other less digestible substances may have decreased, creating conditions in which undigested matter is less likely to remain in the intestinal tract.
The intestinal starvation theory proposes that when ingested food has been completely digested within the intestinal tract, the body may perceive this as a state in which no food is present. I believe that advances in food-processing technology and the increasing availability of ultra-processed foods since the 1970s may have contributed to the occurrence of such conditions.
<References>
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[4]Nardocci M et al. Consumption of ultra-processed foods and obesity in Canada. Can J Public Health. 2019 Feb;110(1):4-14.
[5]Fiolet T et al. Consumption of ultra-processed foods and cancer risk: results from NutriNet-Santé prospective cohort. BMJ. 2018 Feb 14;360:k322.
[6]Elizabeth L et al. Ultra-Processed Foods and Health Outcomes: A Narrative Review. Nutrients. 2020 Jun 30;12(7):1955.
[7]Juul F et al. Ultra-processed food consumption and excess weight among US adults. Br J Nutr. 2018 Jul;120(1):90-100.
[8]Ultra-processed food and drink products in Latin America: trends, impact on obesity, policy implications. Pan American Health Organization, Washington (DC) (2013)
[9]Canella DS et al. Ultra-processed food products and obesity in Brazilian households (2008-2009). PLoS One. 2014 Mar 25;9(3):e92752.
[10]Rauber F et al. Ultra-processed food consumption and indicators of obesity in the United Kingdom population (2008-2016). PLoS One. 2020 May 1;15(5):e0232676.
[11]Mendonça RD et al. Ultraprocessed food consumption and risk of overweight and obesity: the University of Navarra Follow-Up (SUN) cohort study. Am J Clin Nutr. 2016 Nov;104(5):1433-1440.
[12]Liu J et al. Consumption of Ultraprocessed Foods and Diet Quality Among U.S. Children and Adults. Am J Prev Med. 2022 Feb;62(2):252-264.
[13]Bonaccio M et al. Association between Late-Eating Pattern and Higher Consumption of Ultra-Processed Food among Italian Adults: Findings from the INHES Study. Nutrients. 2023 Mar 20;15(6):1497.
[14]Beunza JJ et al. Adherence to the Mediterranean diet, long-term weight change, and incident overweight or obesity: the Seguimiento Universidad de Navarra (SUN) cohort. Am J Clin Nutr. 2010 Dec;92(6):1484-93.
[15]Barr SB, Wright JC. Postprandial energy expenditure in whole-food and processed-food meals: implications for daily energy expenditure. Food Nutr Res. 2010 Jul 2;54.
[16]Fereidoon Shahidi. Nutraceuticals and functional foods: Whole versus processed foods. Trends in Food Science & Technology, Volume 20, Issue 9, 2009, Pages 376-387.
[17]Secor SM. Specific dynamic action: a review of the postprandial metabolic response. J Comp Physiol B. 2009 Jan;179(1):1-56.
[18]Roberts SB. High-glycemic index foods, hunger, and obesity: is there a connection? Nutr Rev. 2000 Jun;58(6):163-9.
[19]Hall KD et al. Ultra-Processed Diets Cause Excess Calorie Intake and Weight Gain: An Inpatient Randomized Controlled Trial of Ad Libitum Food Intake. Cell Metab. 2019 Jul 2;30(1):67-77.e3.
[20] de Graaf C, Kok FJ. Slow food, fast food and the control of food intake. Nat Rev Endocrinol. 2010 May;6(5):290-3.
2024.10.14
The Growing Importance of Body-Weight Set Point Theory: How Can the Recent Rise in Obesity Be Explained?
Summary
(1)The body weight set point model
In 1953, Gordon C. Kennedy proposed that the accumulation of body fat may be physiologically regulated. Later, in 1982, nutritionists William Bennett and Joel Gurin expanded on this concept and developed the “set-point theory.”
(2)Body-weight homeostasis
When an individual loses weight, the body not only reduces energy expenditure beyond what would be predicted from changes in body composition and the thermic effect of food, but also increases appetite through hormonal regulation and alters food preferences. As a result, conditions are created that make weight rebound more likely.
In contrast, temporary weight gain caused by overeating is also thought to trigger compensatory mechanisms that act to return body weight toward its set-point range. However, these mechanisms may be weaker than those that resist weight loss.
A person’s body-weight set point is thought to be established from childhood through adolescence and to remain relatively stable thereafter. However, it has also been suggested that it may shift in response to major environmental changes such as marriage, childbirth, or migration.
Currently, set-point theory has become an important framework for explaining why body weight is not regulated solely by willpower or simple calorie calculations.
(3)Limitations of the set-point model
The set-point model, which proposes that body weight is regulated within a certain range, does not fully explain the sharp rise in obesity observed primarily in Western countries since the 1970s. In response to this limitation, some researchers have suggested that while metabolic resistance to maintaining weight loss is strong, physiological resistance to sustained fat gain may not persist over the long term.
(4)Questions regarding the high-energy diet hypothesis
Animal studies have reported irreversible weight gain following the long-term consumption of high-energy diets. In humans, however, some individuals remain lean despite consuming similarly high-calorie diets, and the hypothesis does not readily account for phenomena such as weight gain associated with social class or major environmental changes.
(5)Intestinal starvation as an alternative perspective
The recent rise in obesity cannot be fully explained by excess energy intake alone. Irreversible weight gain reflecting an upward shift in the body-weight set point may instead be triggered when the body perceives that “food is scarce.”
Since the 1970s, advances in food processing and the resulting changes in the food environment may have increased the likelihood of a physiological state in which the body perceives that ingested food has been completely digested within the intestinal tract—what I refer to as “intestinal starvation.”
【 Full text 】
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Contents
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- Advances in understanding set-point theory
- Limitations of the set-point model
- Environmental and behavioral factors influencing the body-weight set point
I view the human body as possessing a homeostatic system that attempts to maintain body weight within a certain range, and from this perspective, I believe that the concept of a body-weight set point carries important implications.
In this article, I will discuss the background and challenges of set-point theory, which has received renewed attention in recent years. I believe that understanding the environmental and behavioral factors that may contribute to upward shifts in the body-weight set point is important for addressing the growing problem of obesity.
1. Advances in understanding set-point theory
Obesity and weight loss attempts
♦An obese individual who insists that a lean friend has consistently eaten more than the fat person does, may well be telling the truth.（*snip*）
The group of obese patients who are greatly in need of our understanding are those who keep to a calorie intake of perhaps 1,000 kcal per day, yet lose less than one kg per week. There is no doubt whatsoever that such people exist, and can be studied in a metabolic ward under conditions where 'cheating' is virtually impossible without being detected.
Usually these are middle-aged women who have been perhaps 40 kg overweight, and who have already lost about 20 kg. They are often depressed, hypothermic, and have a low metabolic rate. The nature of this metabolic adaptation to a low-calorie diet is not known (as of 1973), but it is a phenomenon that has been recognized since before the 1920s (J S Garrow, 1973)[1].
♦For obese individuals, a certain amount of weight loss is possible through a range of treatments, but long-term maintenance of weight loss is much more challenging, and in most cases, the weight is regained [2]. In a meta-analysis of 29 long-term weight loss studies, more than half of the lost weight was regained within two years, and by five years, more than 80% of lost weight was regained [3,4].
In addition, studies of those who are successful at sustained weight loss indicate that the maintenance of reduced body fat will probably require close attention to energy intake and expenditure, perhaps for life [5].
Energy expenditure in obesity
♦The hypometabolic thesis had fallen out of favor by 1930, when more accurate calculations of body-surface area indicated that the metabolic rates of obese individuals were normal [6].
♦Total energy expenditure (TEE) in a day consists of three components: diet-induced thermogenesis (DIT), physical activity energy expenditure (PAEE), and resting energy expenditure (REE).
When comparing hypothetical men weighing 100 kg and 70 kg, the man weighing 100 kg has a higher TEE [7].
Breakdown of energy expenditure in average 100-kg and 70-kg men
Contrary to popular belief, people with obesity generally have a higher absolute REE compared to leaner subjects. This is because obesity increases both body fat and metabolically active fat-free mass [7,8].
PAEE can be subdivided into "voluntary exercise" and “activities of daily living.” Despite typically engaging in less physical activity, obese individuals often have a daily energy cost for physical activity similar to that of non-obese individuals since PAEE is proportional to body weight [7,9]. Additionally, due to greater food intake, their DIT also tends to be higher [7].
Dynamic changes in energy expenditure
♦Obesity prevention is often erroneously described as a simple bookkeeping matter of balancing caloric intake and expenditure [10].
In this model, energy intake and expenditure are considered independent parameters determined solely by behavior. It is assumed that an obese person can steadily lose weight by eating less and/or moving more at a rate of one pound for every 3,500 kcal (or one kg for every 7,200 kcal) of accumulated dietary caloric deficit [7,11]. This view has been referred to as a “static model” of weight loss, but it has been shown to be physiologically impossible [7,12].
Static model of weight loss
(Despite being recognized as overly simplistic, the 3,500 kcal rule continues to appear in scientific literature and has been cited in over 35,000 educational weight-loss websites as of 2013.) [12,13]
♦It is now understood that energy intake and expenditure are interdependent variables, influenced by each other and by homeostatic signals triggered by changes in body weight [7,14].
Attempts to alter energy balance through diet or exercise are countered by physiological adaptations that resist weight loss [7].
Body weight set point theory
♦In recent years, the influence of homeostatic control has become increasingly recognized, and growing evidence suggests that the body employs physiological mechanisms to regulate energy balance and maintain body weight around a genetically and environmentally determined set point [12].
In 1953, Kennedy proposed that body fat storage is regulated [15]. In 1982, nutritional researchers William Bennett and Joel Gurin expanded on Kennedy's concept when they developed the set-point theory [16]. The model has been widely adopted, and strengthened particularly after the discovery of leptin in the 1990s [7,12].
When an individual loses weight, the body significantly reduces energy expenditure to a degree that is often greater than predicted based on changes in body composition or the thermic effect of food. This process also causes an increase in appetite through hormonal regulation and alters food preferences through behavioral changes, to drive body weight back toward its set-point range[7,16].
Set-point model of weight loss
♦Weight-loss studies have shown that the magnitude of fat stores in the body is protected by mechanisms mediated by the central nervous system, which adjust energy intake (EI) and expenditure (EE) via signals from adipose tissue, the gastrointestinal tract, and endocrine organs to maintain homeostasis and resist weight change as proposed by the set-point model [12,17].
♦The body's protective metabolic mechanism that attempts to preserve energy stores during an energy crisis is known as adaptive thermogenesis (AT) or metabolic adaptation [7,12].
AT is defined as the underfeeding-associated fall in resting energy expenditure (REE), independent of changes in body composition [12].
♦Maintenance of a 10% or greater reduction in body weight in lean or obese individuals is accompanied by about 20 to 25% decline in 24-hour energy expenditure. This decrease in weight maintenance calories is 10–15% greater than predicted based solely on changes in fat and lean mass [17,18].
Since obese individuals also display these compensatory metabolic adjustments in response to dietary restriction, obesity may be considered a natural physiological state for some people. Experimental studies on obesity in animals similarly suggest a view of obesity as a condition of body energy regulation at an elevated set point [19].
♦A meta-analysis of cross-sectional studies investigating adaptive thermogenesis (AT) by comparing formerly obese subjects who had lost weight with BMI-matched subjects who were never obese, found a 3–5% lower resting energy expenditure (REE) in formerly obese subjects compared to never obese controls [20].
This effect means, for example, that if an obese woman reduced her weight from 100 kg to 70 kg, she would have to consume fewer calories to remain at 70 kg than a woman who had consistently weighed 70 kg [6]. Similar results have been confirmed in animal experiments involving obese and normal-weight rats.
This suggests that the frequent claim made by obese people that they eat the same or less than their lean friends but lose no weight, must be given more credence than it is ordinarily accorded [19].
♦On the other hand, as shown in overfeeding experiments on prisoners in Vermont in the 1960s (Doctor Ethan Sims), weight gain due to temporary overeating also triggers compensatory mechanisms that bring body weight back toward its set-point range.
However, some researchers point out that these may be weaker than the mechanisms that resist weight loss.
This asymmetry could be due to the evolutionary advantage of storing fat to survive during periods of food scarcity or starvation [16,17].
♦In addition, hyperphagia (overeating) has been demonstrated following experimental semi-starvation and short-term underfeeding, which is probably the result of homeostatic signals resulting from the loss of both body fat and lean tissue [7,21].
♦This theory also suggests that a person's body-weight set point is established early in life and remains relatively stable unless altered by specific conditions. However, the set point may change throughout one’s life due to factors such as marriage, childbirth, menopause, aging, and disease [16].
On the other hand, the set-point theory remains hypothetical because the molecular mechanisms involved in set-point regulation have not yet been fully elucidated, and some researchers may consider the theory overly simplistic [16].
2. Limitations of the set-point model
On the other hand, some researchers have pointed out important limitations of the body-weight set-point model.
If a homeostatic system truly exists to maintain body weight within a certain range, a fundamental question arises: why do so many individuals in Western countries continue to gain weight gradually throughout majority of their adult lives? In particular, this model does not adequately explain the increasing prevalence of obesity observed in many societies worldwide since around the 1970s [22].
In response, some researchers have suggested that while metabolic resistance to sustaining a reduced body weight is strong, metabolic resistance to sustained increased adiposity may not be physiologically long-lasting. Indeed, the steady increase in obesity prevalence supports the idea that the human body may be physiologically more permissive of weight gain than of weight loss [17,23].
■Animal studies using rats have shown that during the first 3–4 weeks of exposure to a high-fat diet, increases in energy expenditure and activation of the sympathetic nervous system (SNS) can be observed.
However, these compensatory responses were no longer evident after a few months of high-fat diet consumption [17,24].
Furthermore, another rat study has reported that long-term consumption of highly palatable, high-energy diet—such as potato chips and cheese crackers—led to irreversible weight gain, suggesting an upward shift in the body-weight set point [19,25].
These explanations that continuous consumption of high-calorie diet leads to an increase in the body-weight set point may sound plausible at first. However, in my opinion, if body weight changes in only one direction in response to a single external factor, it can no longer be considered a true “set point.”
Moreover, when this hypothesis is applied to humans, it fails to account for the fact that some individuals remain lean despite frequently consuming similarly high-calorie foods. In practice, several contradictions can be identified, including the following:
(1) Obesity is frequently observed among low-income populations in Western countries, as well as among relatively affluent groups in developing countries [22, 27, 28].
(2) Since the 1950s, the coexistence of undernutrition and obesity within poor populations has been documented worldwide [29].
(3) A substantial number of individuals gain weight following major life or environmental changes—such as entering university, marriage, childbirth, or migration from Asia to Western countries [22].
I propose that upward shifts in the body-weight set point are associated with adaptive responses to intestinal starvation.
The next section provides a more detailed explanation of this mechanism.
3. Environmental and behavioral factors influencing the body-weight set point
At present, many international organizations classify obesity as a chronic disease.
Some researchers interested in the body-weight set-point theory have argued that determining whether obesity, as a chronic condition, is treatable requires a clear understanding of how genetic and environmental factors interact to regulate the set point. At the same time, it is also true that many important environmental and social influences remain insufficiently explained [22].
In this article, I will introduce the concept of “intestinal starvation” as a complementary perspective to address these challenges. The key points are outlined below in four parts.
(1) Limitations of the positive energy balance hypothesis
It is generally assumed that weight gain requires a positive energy balance, and the recent rise in obesity is often explained by increased consumption of high-calorie foods and reduced levels of physical activity. Paradoxically, however, the fact that obesity rates have increased in parallel with the growing prevalence of dieting aimed at weight loss [30] suggests that our current understanding of energy balance may warrant reconsideration [12].
What I want to emphasize is that while short-term weight gain due to overeating can be explained by excess energy intake, long-term and potentially irreversible weight gain may instead be triggered by energy deprivation or by the body’s perception that food is scarce. This pattern is also consistent with the phenomenon in which body weight increases beyond its previous level following experimental starvation or weight-loss dieting.
【Related Articles】The Spread of Dieting May Be Fueling the Rise in Obesity
(2) Changes in digestion and absorption brought about by food processing
It is certainly true that high-calorie foods have become increasingly common since the 1970s. However, an even more important factor affecting the human body may be the rise of food processing—particularly ultra-processing. As food processing advanced, hard-to-digest components were gradually removed, while softer and more easily digestible components became increasingly dominant.
As a result, substantial changes may have occurred in the rate of digestion and absorption, as well as in the gut environment.
Intestinal starvation appears to be associated with the frequent consumption of refined carbohydrates and (ultra-)processed foods, and may help explain both the rise in obesity since the 1970s and why obesity can occur frequently not only in developed countries, but also in certain regions of the developing world.
【Related Article】
The Rise in Obesity is Closely Linked to the Consumption of Ultra-Processed Foods
(3) Intestinal starvation as a multifactorial model
Intestinal starvation is a physiological state that is more likely to occur when four factors overlap simultaneously. This concept provides a framework for understanding obesity as a chronic condition arising from interactions between genetic and environmental factors.
【Related Article】Three (+1) Factors That Accelerate “Intestinal Starvation”
(4) Why does the body resist weight loss in obese individuals?
In cases of weight gain that may reflect an upward shift in the body-weight set point through intestinal starvation, the overall efficiency of nutrient absorption may increase. In other words, from the perspective of energy homeostasis, the balance point at which energy intake and expenditure are matched may itself shift to a higher level. This perspective may help explain why even obese individuals with substantial body fat often exhibit compensatory metabolic responses to caloric restriction.
【Related Article】How Intestinal Starvation Can Lead to Weight Gain
As mentioned in the section 2, an animal study in rats reported that 90 days of exposure to a “high-energy diet” resulted in irreversible weight gain suggestive of an upward shift in the body-weight set point (Rolls et al., 1980). However, the “fattening diet” used in this experiment consisted mainly of commercially available, highly palatable foods such as potato chips, cheese crackers, and cookies [25]. At the same time, these foods were also highly refined carbohydrates and (ultra-)processed foods.
In contrast, the solid chow provided to the control group consisted of cracked grains, soybean meal, fish meal, and similar ingredients, and may have contained larger amounts of less digestible matter, such as dietary fiber and the tough cell walls of plants. In this respect, the composition of the control diet may have resembled that of human diets commonly seen more than 50 years ago.
Therefore, I believe that caution is needed before concluding that the long-term consumption of a high-energy diet directly caused weight gain suggestive of an upward shift in the body-weight set point.
<References>
[1]Garrow JS. Diet and obesity. Proc R Soc Med. 1973 Jul;66(7):642-4. PMID: 4741395; PMCID: PMC1645095.
[2]Wu T, Gao X, Chen M, van Dam RM. Long-term effectiveness of diet-plus-exercise interventions vs. diet-only interventions for weight loss: a meta-analysis. Obes Rev. 2009;10(3):313–323.
[3] Hall KD, Kahan S. Maintenance of Lost Weight and Long-Term Management of Obesity. Med Clin North Am. 2018 Jan;102(1):183-197.
[4]Anderson JW, Konz EC, Frederich RC, Wood CL. Long-term weight-loss maintenance: a meta-analysis of US studies. Am J Clin Nutr. 2001 Nov;74(5):579-84.
[5]Wing RR, Hill JO. Successful weight loss maintenance. Annu Rev Nutr. 2001;21:323-41.
[6]Jou C. The biology and genetics of obesity--a century of inquiries. N Engl J Med. 2014 May 15;370(20):1874-7.
[7]Hall KD, Guo J. Obesity Energetics: Body Weight Regulation and the Effects of Diet Composition. Gastroenterology. 2017 May;152(7):1718-1727.e3.
[8]Nelson KM, Weinsier RL, Long CL, et al. Prediction of resting energy expenditure from fat-free mass and fat mass. Am J Clin Nutr. 1992;56:848–856.
[9]Westerterp KR. Physical activity, food intake, and body weight regulation: insights from doubly labeled water studies. Nutr Rev. 2010;68:148–154.
[10] Levine DI. The curious history of the calorie in U.S. policy: a tradition of unfulfilled promises. Am J Prev Med. 2017;52:125–129.
[11] Hall KD, Chow CC. Why is the 3500 kcal per pound weight loss rule wrong? Int J Obes (Lond). 2013 Dec;37(12):1614.
[12] Egan AM, Collins AL. Dynamic changes in energy expenditure in response to underfeeding: a review. Proc Nutr Soc. 2022 May;81(2):199-212. doi: 10.1017/S0029665121003669. Epub 2021 Oct 4. PMID: 35103583.
[13]Thomas DM, Martin CK, Lettieri S et al. (2013) Can a weight loss of one pound a week be achieved with a 3500-kcal deficit? Commentary on a commonly accepted rule. In Int J Obes 37, 1611–1613.)
[14]Hall KD, Heymsfield SB, Kemnitz JW et al. Energy balance and its components: implications for body weight regulation. Am J Clin Nutr. 2012 Apr;95(4):989-94.
[15]KENNEDY GC. The role of depot fat in the hypothalamic control of food intake in the rat. Proc R Soc Lond B Biol Sci. 1953 Jan 15;140(901):578-96.
[16] Ganipisetti VM, Bollimunta P. Obesity and Set-Point Theory. 2023 Apr 25. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2024 Jan–. PMID: 37276312.
[17] Rosenbaum M, Leibel RL. Adaptive thermogenesis in humans. Int J Obes (Lond). 2010 Oct;34 Suppl 1(0 1):S47-55.
[18] Leibel R, Rosenbaum M, Hirsch J. Changes in energy expenditure resulting from altered body weight. N Eng J Med. 1995;332:621–28.
[19] Richard E. Keesey, Matt D. Hirvonen, Body Weight Set-Points: Determination and Adjustment, The Journal of Nutrition, Volume 127, Issue 9, 1997, Pages 1875S-1883S, ISSN 0022-3166.
[20]Astrup A, Gøtzsche PC, van de Werken K, et al. Meta-analysis of resting metabolic rate in formerly obese subjects. Am J Clin Nutr. 1999 Jun;69(6):1117-22.
[21] Dulloo AG, Jacquet J, Girardier L. Poststarvation hyperphagia and body fat overshooting in humans: a role for feedback signals from lean and fat tissues. Am J Clin Nutr. 1997;65:717–723.
[22]Speakman JR, Levitsky DA, Allison DB, et al. Set points, settling points and some alternative models: theoretical options to understand how genes and environments combine to regulate body adiposity. Dis Model Mech. 2011 Nov;4(6):733-45.
[23] Schwartz MW, Woods SC, Seeley RJ, et al. Is the energy homeostasis system inherently biased toward weight gain? Diabetes. 2003 Feb;52(2):232-8.
[24] Corbett SW, Stern JS, Keesey RE. Energy expenditure in rats with diet-induced obesity. Am J Clin Nutr. 1986 Aug;44(2):173-80.
[25] Rolls B.J., Rowe E.A., Turner R.C. Persistent obesity in rats following a period of consumption of a mixed high energy diet. J Physiol. 1980 Jan;298:415-27.
[26](Deleted)
[27] Dykes J et al. Socioeconomic gradient in body size and obesity among women: the role of dietary restraint, disinhibition and hunger in the Whitehall II study. International Journal of Obesity 2004 Feb,:262-68.
[28] Poskitt EM. Countries in transition: underweight to obesity non-stop? Ann Trop Paediatr. 2009 Mar;29(1):1-11.
[29] Gary Taubes. 2011. Why we get fat. New York: Anchor Books. Pages 15-32.
[30] Montani JP, Schutz Y, Dulloo AG. Dieting and weight cycling as risk factors for cardiometabolic diseases: who is really at risk? Obes Rev. 2015 Feb;16 Suppl 1:7-18.
2022.10.10
Does Obesity Run in the Family or Is It Due to the Living Environment?
Contents
- What was the relationship of weight between adoptees and adoptive parents?
- What was the weight of the twins raised apart?
- What do we consider a change in environment?: My thoughts
- Will the shape of your body from childhood continue?
<The bottom line>
Is obesity inherited from parents?
Let us recall our classmates in elementary school. To some extent, we can imagine, if not one hundred percent, that if the parents are thin, their children are often thin, and if the parents are fat, their children are often fat.
The question here is whether this is due to genetics or due to the living environment. Here is one such study I’d like to introduce.
1. What was the relationship of weight between adoptees and adoptive parents?
"Obese children often have obese siblings. Obese children become obese adults. Obese adults go on to have obese children. Childhood obesity is associated with a 200 percent to 400 percent increased risk of adult obesity. This is an undeniable fact. (*snip*)
Families share genetic characteristics that may lead to obesity. However, obesity has become rampant only since the 1970s. Our genes could not have changed within such a short time. Genetics can explain much of the inter-individual risk of obesity, but not why entire populations become obese.
Nonetheless, families live in the same environment, eat similar foods at similar times and have similar attitudes. Families often share cars, live in the same physical space and will be exposed to the same chemicals that may cause obesity–so-called chemical obesogens. For these reasons, many consider the current environment the major cause of obesity.
Conventional calorie-based theories of obesity place the blame squarely on this “toxic" environment that encourages eating and discourages physical exertion. Dietary and lifestyle habits have changed considerably since the 1970s (e.g. car, television, computer, fast food, high-calorie food, sugar, etc.).
Therefore, most modern theories of obesity discount the importance of genetic factors, believing instead that consumption of excess calories leads to obesity. Eating and moving are voluntary behaviors, after all, with little genetic input.
So－exactly how much of a role does genetics play in human obesity?"
(Jason Fung. The Obesity Code. Greystone Books, 2016, Page 21-2.)
"The classic method for determining the relative impact of genetic versus environmental factors is to study adoptive families, thereby removing genetics from the equation.(*snip*)
Dr. Albert J. Stunkard performed some of the classic genetic studies of obesity. Data about biological parents is often incomplete, confidential and not easily accessible by researchers. Fortunately, Denmark has maintained a relatively complete registry of adoptions, with information on both sets of parents.
Studying a sample of 540 Danish adult adoptees, Dr. Stunkard compared them to both their adoptive and biological parents.
If environmental factors were most important, then adoptees should resemble their adoptive parents. If genetic factors were most important, the adoptees should resemble their biological parents.
No relationship whatsoever was discovered between the weight of the adoptive parents and the adoptees.(*snip*)
Comparing adoptees to their biological parents yielded a considerably different result. Here there was a strong, consistent correlation between their weights.
The biological parents had very little or nothing to do with raising these children, or teaching them nutritional values or attitudes toward exercise. Yet the tendency toward obesity followed them like ducklings. When you took a child away from obese parents and placed them into a "thin" household, the child still became obese.(*snip*)
This finding was a considerable shock. Standard calorie-based theories blame environmental factors and human behaviors for obesity. Environmental cues such as dietary habits, fast food, junk food, candy intake, lack of exercise, number of cars, and lack of playgrounds and organized sports are believed crucial in the development of obesity. But they play virtually no role."
(Fung. The Obesity Code. Pages 22-3.)
2. What was the weight of the twins raised apart?
"Studying identical twins raised apart is another classic strategy to distinguish environmental and genetic factors. Identical twins share identical genetic material, and fraternal twins share 25 percent of their genes.
In 1991, Dr. Stunkard examined sets of fraternal and identical twins in both conditions of being reared apart and reared together. Comparison of their weights would determine the effect of the different environments.
The results sent a shockwave through the obesity-research community. Approximately 70 percent of the variance in obesity is familial.(*snip*)
However, it is immediately clear that inheritance cannot be the sole factor leading to the obesity epidemic.
The incidence of obesity has been relatively stable through the decades. Most of the obesity epidemic materialized within a single generation. Our genes have not changed in that time span.
How can we explain this seeming contradiction?"
(Fung. The Obesity Code. Pages 23-4.)
3. What do we consider a change in environment? : My thoughts
I think this is a very interesting study because it compared data from biological parents and adoptive parents.
However, can we assert from the results of this one alone that the influence of genetics was much greater and environmental factors were much less significant?
I believe, as Doctor Fung mentions, the rapid increase in obesity in recent years (since about 1970) has much to do with changes in our living environment (what we eat, irregular lifestyle,etc.),not the genes.
Even those who were slim in their youth may gain five or ten kilos in a short period of time at a certain age, triggered by something (living alone, marriage, parenting, stress from work, etc.). Some people put on weight every time they try dieting to lose weight.
In other words, many of us, in our hearts, have probably noticed that changes in eating habits or our living environment can change our body shape.
■What is the "change in environment" that causes a change in weight here?
The study considers a child living with adoptive parents or twins raised separately to be a "change in living environment," but I think there is a problem with this study.
If a family can afford to take in a child as adoptive parents, don't they have some money to spare and feed their adoptee a somewhat balanced diet three times a day?
Although what they eat and caloric intake may differ from family to family, those changes are not necessarily "environmental changes" that cause changes in weight. Just because the adoptive parents are thin does not mean that adoptees will become thin even if they eat the same diet.
On the contrary, I believe that a fundamental increase in weight and body shape occurs when one’s set-point weight itself goes up, which is induced by intestinal starvation.
And since at least three (+one) factors are required to induce intestinal starvation, living with adoptive parents alone does not necessarily alter one’s set-point weight.
[Related article]
In Japan over the past few decades, our traditional eating habits have been declining. Instead, Westernized eating and diverse work styles have become more prevalent.
Amid these changes, intestinal starvation is more likely to be induced when unbalanced diets (high in easily digestible carbohydrates and ultra-processed foods, and with a lack of vegetables, etc.) combines with irregular lifestyle habits (skipping breakfast, eating late at night, etc.).
This is what I would like to call the "environmental factors and human behaviors" for the recent obesity epidemic, and while genetic factors are, of course, undeniable, I believe that environmental factors are quite significant.
4. Will the shape of your body from childhood continue?
One thing to note here is that the body shape in childhood (say, around three to five years old) tends to continue into adulthood.
When I think back to my classmates in first and second grade, the girls and boys who were fat (although they were not big eaters) often have a similar body shape even decades later.
From my theory, that means that their set-point weight has not changed, and in this study, if there are no environmental factors that cause changes in their set-point for body weight, then wouldn't the body shape from childhood basically continue?
But, I’m simply wondering what the childhood body shape is due to? Whether it is genetic factors or the way food is prepared during childhood－including weaning－is a question that remains unanswered.
The bottom line
(1) In a study regarding adoptive families and examining how genetic and environmental factors influence being overweight, no correlation was found between the weight of adoptive parents and that of their adoptees. On the other hand, when the adoptees were compared to their biological parents, there was a consistent correlation between the weight of both.
A study of twins raised separately also concluded that "genetic influences are far more significant.”
(2) Many researchers had previously blamed "environmental factors and individual behavior” for the recent obesity epidemic, but this study concluded that genetics had far more impact than environmental factors.
However, I find this study problematic. The fact of children living with adoptive parents or twins raised separately is not necessarily an environmental factor that causes changes in weight.
(3) Of course, I do not think we can ignore the genetic factor, but I believe that the recent obesity epidemic is caused by a combination of what we eat－westernized diets, refined carbohydrates, processed foods, etc.－plus lifestyle changes.
A major change in weight and body shape occurs when one’s set-point weight goes up, which is induced by intestinal starvation.
(4) If there is no significant change in one's set-point weight, I think the body shape from childhood is expected to continue. However, I 'm uncertain what determines childhood body shape, whether it is heredity or the way food is prepared during childhood, including weaning.
2022.09.24
Why Does the Body Perceive That It Is More Starved than in the Past?
Contents
- How has our Japanese diet changed over the past fifty years?
- The Pima tribe who gained weight under rations, not prosperity
- The newer the diet in history, the less fit the body is
<End note>
１．How has our Japanese diet changed over the past fifty years?
I was born in 1970, about fifty years ago. That was when twenty-five years had passed since the end of the World WarⅡ, and Japan was in the midst of its rapid economic growth.
In retrospect, I feel that the food scene was quite different from what it is today. My parents were farmers in the country side of Osaka, growing rice and mushrooms. We also had about twenty chickens to get fresh eggs.
On the dining table in the morning, there was usually rice, miso soup, pickles, traditional stewed vegetables, and half-dried fish. I remember the family eating together.
Of course, we sometimes ate bread, but my father did physical labor, so rice was an essential part of breakfast.
(Typical Japanese breakfast we used to have)
■The 1970s, when the dining scene changed dramatically
I think it was after 1970 that our dining landscape slowly changed. I had not been taken to restaurants much when I was a kid, but fast food restaurants and other restaurant chains opened one after another in all corners of Japan, and many people began to eat Western food.
McDonald's (since 1971), Kentucky Fried Chicken (since 1970) and family restaurants called Skylark (since 1970) were the most famous among them. In 1974, the first convenience stores (called Seven-Eleven) opened in Tokyo, followed by a rapid increase throughout the country. Instant foods such as cup noodles and frozen foods also increased rapidly, reflecting busy social conditions.
Even in the 1970s, school lunches already had bread as their side dish rather than rice (apparently at the behest of GHQ, which ruled after the war), and those of us who had grown accustomed to such a diet began to prefer bread, noodles, and other wheat-based foods even as adults.
Along with this, we liked to eat meat and (ultra-) processed foods rather than fish with bones.
We began to prefer soft foods to fibrous and hard foods, and the traditional vegetable stews that had been commonly eaten became less and less common.
Our lifestyles also changed dramatically. More and more people began to work at desks rather than at physical jobs. Nighttime lifestyles became the norm, and more people didn't even eat breakfast.
It was probably around this time that obesity began to increase in Japan. Nowadays, it is not unusual to see women over one hundred-kilograms on the streets.
(Percentage of adults with a BMI of 25 or higher: In both men and women, it has been increasing since 1980
One might think that increased caloric intake was the cause of being overweight.
However, on a caloric basis, the average daily caloric intake of the population in 1970 was twenty-two-hundred kcal, yet in 2010 it had decreased to eighteen-hundred-fifty kcal. [1]
To explain this in my theory, the modern diet is often low in fiber and tends to favor easily digestible refined carbohydrates, processed meat and fish products, and fast food, etc., which can, in turn, induce a state of intestinal starvation based on how we combine the foods.
In particular, with changes in eating habits, such as having only two meals a day (skipping breakfast or lunch), light lunches, or late dinners, as well as dietary restrictions due to dieting, many people experience long periods of hunger, making intestinal starvation more likely to occur.
2. The Pima tribe who gained weight under rations, not prosperity
As an example of how obesity has increased as old traditional eating habits have declined and became westernized, I would like to cite a Native American tribe known as the Pima, although the situation is slightly different.
This is the second time I quote from Mr. Taubes' "Why We Get Fat," but this part is very important and may be the key to solving the problems of obesity, diabetes, and other diseases.
"Consider a Native American tribe in Arizona known as the Pima. Today the Pima may have the highest incidence of obesity and diabetes in the United States. Their plight is often evoked as an example of what happens when a traditional culture runs afoul of the toxic environment of modern America. (*snip*)
Between 1901 and 1905, two anthropologists(Russell and Hrdlička) independently studied the Pima, and both commented on how fat they were, particularly the women. (*snip)
Through the 1850s, the Pima had been extraordinarily successful hunters and farmers.
By the 1870s, the Pima were living through what they called the “years of famine.”(*snip*) The tribe was still raising what crops it could but was now relying on government rations for day-to-day sustenance.(*snip*)
What makes this observation so remarkable is that the Pima, at the time, had just gone from being among the most affluent Native American tribes to among the poorest.
Whatever made the Pima fat, prosperity and rising incomes had nothing to do with it; rather, the opposite seemed to be the case.
And if the government rations were simply excessive, making the famines a thing of the past, then why would the Pima get fat on the abundant rations and not on the abundant food they'd had prior to the famines? Perhaps the answer lies in the type of food being consumed, a question of quality rather than quantity.(*snip*)
So maybe the culprit was the type of food. The Pima were already eating everything “that enters into the dietary of the white man,” as Hrdlička said. This might have been key.
The Pima diet in 1900 had characteristics very similar to the diets many of us are eating a century later, but not in quantity, in quality."
(Gary Taubes. Why We Get Fat. New York: Anchor Books, 2011, Pages 19-23.)
[Related article] Wealthy Ones Get Fat? Poor Ones Get Fat?
In terms of food, I believe that Japanese people in 1970 were eating a lot of different kinds of food than today. There were no convenience stores, and the diet was based on mom's home cooking, with a variety of seasonal vegetables and fish.
In contrast, the modern diet is based on easily digestible carbohydrates and processed meat products, and the variety of food ingredients we eat seems to have decreased dramatically.
Many people are normally worried about gaining weight and are dieting, and then they occasionally splurge and eat high-calorie food as a reward. The situation is different, but if we focus on the inside of the intestines, I can say that it is the same as what happened to the Pima population.
3. The newer the diet in history, the less fit the body is
"The idea is that the longer a particular type of food has been part of the human diet, the more beneficial and less harmful it probably is— the better adapted we become to that food.
And if some food is new to human diets, or new in large quantities, it's likely that we haven't yet had time to adapt, and so it's doing us harm. (*snip*)
The obvious question is, what are the “conditions to which presumably we are genetically adapted”? As it turns out, what Donaldson assumed in 1919 is still the conventional wisdom today: our genes were effectively shaped by the two and a half million years during which our ancestors lived as hunters and gatherers prior to the introduction of agriculture twelve thousand years ago."
(Taubes. Why We Get Fat. Pages 163-4.)
I believe what the author tried to get across was that the modern diet of allowing large amounts of carbohydrates is not genetically compatible with our bodies, and that eating meat and its fat may be more compatible and less harmful to us on a genetic level.
I will quote this passage above to explain my intestinal starvation mechanism.
Suppose (and it makes more sense) that God created a genetic blueprint for people to "store body fat" in case they could not find food.
If the state of "no food" (starvation) was recognized when all food was digested in the entire intestinal tract, then during the hunting-and-gathering age and farming age when people ate wild boar meat, nuts, vegetables with tough cell walls, and unrefined grains, etc., their intestines would not have been in a state of complete starvation even if they couldn’t eat anything for a whole day (because of the long intestines).
In contrast, a modern diet high in quickly digested foods —such as refined wheat and rice, starches, processed meat and fish products, and fast food—can, depending on the combination, lead to a state of intestinal starvation in as little as half a day.
I believe it is the entire intestines (or it may be the small intestine only) that makes all the decisions, and it goes to show that inside the gut, many of us are starving more today than in the past.
End note
People sometimes say, "Japanese food culture is healthy by world standards," but I believe this to be a relic of the past until around the year 2000 at the latest. Now, I feel that traditional Japanese food culture is dying in the average household.
Children who grew up eating fast food are now in their fifties and sixties, and their children are now in their thirties. Thus, in about fifty to sixty years (about two generations), the opportunity to eat traditional foods will have faded away, and the food culture will change greatly.
And, with the shift in diet, it seems like that diseases such as diabetes, kidney disease, heart disease, cancer, and stroke, which were once not as common, are on the rise, just as they are in the Western countries.
References：
[1]Yasuo Kagawa(香川靖雄) , Clock Gene Diet (時計遺伝子ダイエット), 2012, Page 15.
2019.06.22
Obesity as a Multifactorial Condition: Does Intestinal Starvation Act as a Confounding Factor?
-
Contents
- "Overeating causes obesity" is too simplistic
- Most diet methods are "partially correct"
- Can environmental and behavioral factors be systematically organized?
- Intestinal starvation as a confounding factor
The bottom line
1. "Overeating causes obesity" is too simplistic
A 2012 online survey of 1,143 adults in the United States conducted by Reuters and the market research firm Ipsos found that 61% of American adults believed "personal choices related to diet and exercise" were responsible for the obesity epidemic[1,2]. In other words, many Americans still hold the belief that people who become obese lack willpower, overeat, and do not exercise enough[2].
The situation in Japan appears to be similar. Even news anchors and experts frequently make statements such as, “It's only natural to gain weight if you overeat and don’t exercise,” suggesting that many Japanese people likely hold the same view.
However, scientific research indicates that "personal choices" may not account for all cases of obesity[2].
Classical genetic studies based on adoption studies, family studies, twin studies, etc., indicate that about 50–70% of the variance (heritability estimates) in BMI is genetic (Those estimates vary depending on the study design and assessment methods) [3].
Even today, the heritability of obesity is estimated at 40% to 70%[4].
Some researchers point out that numerous different genes have been found to be involved in food selection, food intake, absorption, metabolism, and energy expenditure including physical activity. When considering interactions between gene-by-gene or gene(s)-by-environment(s), the complexity of the mechanisms underlying weight regulation becomes even greater[3].
International Statements Recognizing Obesity as a Chronic Disease
・In 1948, the World Health Organization (WHO) established the International Classification of Diseases (ICD) and classified obesity as a disease. This is considered one of the earliest official frameworks in which obesity was treated as an illness.
However, at the time, this classification received little attention within the medical community and was not widely regarded as clinically important for several decades thereafter[5].
・In 1997, following consultations with the International Obesity Task Force (IOTF, now part of the World Obesity Federation), the WHO clearly identified obesity as a complex and serious chronic disease in an official report[6].
・In 2012, the American Association of Clinical Endocrinologists (AACE) designated obesity as a chronic disease. This designation was based on the recognition that the pathophysiology of obesity is complex, involving interactions among genetic and biological factors, the environment, and behavior, and that obesity meets the definition of a disease as outlined by the American Medical Association (AMA)[7].
・Subsequently, in 2013, the American Medical Association (AMA) formally recognized obesity as a chronic disease[8].
2. Most diet methods are partially correct
If we accept that the human gene pool is unlikely to change substantially over a period of 50 or even 100 years, then the global rise in obesity observed since the 1970’s can reasonably be understood as being strongly influenced by environmental and behavioral factors.
With this in mind, I would like to take a closer look at these factors. An interesting observation about recent popular diets is particularly relevant here and is quoted below.
“What causes weight gain? Contending theories abound:
・Calories ・Food reward・Food addiction
・Sugar・Sleep deprivation ・Stress
・Refined carbohydrates・Wheat
・Low fiber intake・All carbohydrates
・Genetics・Dietary fat ・Red meat
・Poverty ・All meat・Wealth
・Dairy products・Gut microbiome
・Snacking・Childhood obesity
The various theories fight among themselves, as if they are all mutually exclusive and there is only one true cause of obesity. For example, recent trials that compare a low-calorie to a low-carbohydrate diet assume that if one is correct, the other is not. Most obesity research is conducted in this manner.
This approach is wrong, since these theories all contain some element of truth. (*snip*)
THE MULTIFACTORIAL NATURE of obesity is the crucial missing link. There is no one single cause of obesity. (*snip*)
What we need is a frame work, a structure, a coherent theory to understand how all its factors fit together. Too often, our current model of obesity assumes that there is only one single true cause, and that all others are pretenders to the throne. Endless debates ensue.
Too many calories cause obesity. No, too many carbohydrates. No,
too much saturated fat. No, too much red meat. No,
too much processed foods. No, too much high fat dairy. No,
too much wheat. No, too much sugar. No,
too much highly palatable foods. No, too much eating out. No
It goes on and on. They are all partially correct. (*snip*)
All diets (e.g., calorie restriction, low-fat, paleo, vegan) work because they all address a different aspect of the disease. But none of them work for very long, because none of them address the totality of the disease.
Without understanding the multifactorial nature of obesity－which is critical －we are doomed to an endless cycle of blame."
(Jason Fung. The Obesity Code. Greystone Books. 2016. Pages 70, 216-217.)
I find the author’s discussion of the multifactorial nature of obesity to be highly insightful. Obesity is not a simple phenomenon caused solely by overeating; rather, it arises from a complex interplay of multiple factors, and this is a point we must first recognize.
However, at the same time, the sheer number of factors that are often listed suggests another problem: the mechanisms and contributing factors behind weight gain have not been sufficiently organized or clearly conceptualized.
I believe that by introducing the concept of intestinal starvation, some of the environmental and behavioral factors that appear complex can be viewed in a more structured and coherent way. By shifting our focus away from observable eating habits and lifestyle patterns and toward the unseen workings of the intestines, the underlying mechanisms of obesity may become more apparent.
3. Can environmental and behavioral factors be systematically organized?
Here, it is worth reaffirming that the phenomenon commonly described as “gaining weight” actually involves two distinct processes. Introducing this conceptual framework makes it easier to organize and understand the many factors that contribute to weight gain.
【Related article】
The Two Distinct Processes Behind Weight Gain
(1) When body weight returns to its original set point
One type of weight gain occurs when body weight, which has been intentionally kept low, begins to return toward its set point. This process is illustrated in Figure 1A.
Not only the weight gain commonly explained as resulting from overeating or lack of exercise, but also many calorie-restricted diets and traditional weight-loss intervention studies fall into this category.
Fig. 1
Admittedly, regardless of whether fat, carbohydrates, or ultra-processed foods are restricted, body weight tends to decrease temporarily as long as energy intake falls below energy expenditure.
However, because this approach does not alter the underlying body-weight set point, making long-term weight loss maintenance difficult and increasing the likelihood of weight rebound once previous eating patterns resume.
As Dr. Briffa has pointed out, calorie restriction may serve as a temporary remedy, but it is not a fundamental solution to obesity as a whole.
(2) The process by which the set point itself increases
In contrast, the weight gain illustrated in Figure 1B represents a situation in which the body-weight set point itself increases. I propose that this type of weight gain is the result of an adaptive response to the body’s recognition of “starvation.”
One form of this “perceived starvation” is intestinal starvation. Intestinal starvation does not arise from a single cause; rather, it emerges through the simultaneous involvement of multiple factors. This perspective may help clarify the multifactorial nature of obesity, particularly its relationship with environmental and behavioral factors.
【Related article】
Three (+1) Factors That Accelerate “Intestinal Starvation”
4. Intestinal starvation as a confounding factor
Skipping breakfast, eating late dinners, having fewer meals per day, diets high in refined carbohydrates or (ultra-)processed foods, insufficient dietary fiber, and unbalanced diets are often reported to be associated with weight gain and obesity.
What is important, however, is that these factors may not independently cause obesity. Instead, they may influence the occurrence of intestinal starvation.
In other words, I suggest that the core causal factor in obesity may not be individual lifestyle behaviors themselves, but rather intestinal starvation, which is commonly affected by these behaviors.
In this sense, intestinal starvation may be conceptualized as a physiological response that functions as a confounding factor (see Note 1) in obesity research.
Fig. 2. Conceptual framework of intestinal starvation acting in a confounding-like manner
Note 1: A confounding factor is a third variable that influences both the presumed cause (exposure) and the outcome, thereby obscuring the true relationship between them. For example, even if low dietary fiber intake appears to be associated with obesity, intestinal starvation may be an underlying factor that affects both.
The bottom line
(1)Obesity is now widely recognized as a chronic, multifactorial disease driven by interactions among genetic, biological, environmental, and behavioral factors. While many fad diets address specific aspects of obesity, none adequately targets the condition as a whole, which may explain their limited long-term effectiveness.
(2)What is needed now is a conceptual framework that explains how multiple factors interact. By adopting the perspectives outlined below, environmental and behavioral factors related to obesity can be more clearly organized and understood.
(a) There are two distinct processes that lead to weight gain, and one of them—an upward shift in the body-weight set point—is closely associated with the rise in obesity.
(b) Intestinal starvation is involved in this upward shift of the set point itself. It represents an adaptive physiological response that arises at the intersection of genetic factors and the modern food environment and lifestyle, and thus may help explain the multifactorial nature of obesity.
(3) From this perspective, the central causal factor in obesity may not be individual lifestyle behaviors themselves, but rather intestinal starvation, which is commonly influenced by these factors. In this sense, intestinal starvation can be viewed as a biological response that functions as a confounding factor in obesity research.
References
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