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NOVA (not a acronym) is the food classification that categorizes foods based on the degree and purpose of food processing, rather than their nutritional content. It was developed in 2009 by a research group at the University of São Paulo in Brazil[2].

NOVA classifies foods into four groups based on the nature, extent, and purpose of the industrial processing they undergo.

(1)Unprocessed or minimally processed foods
Fresh fruits and vegetables, and other natural foods (such as grains, milk, fish, and meat) that have undergone processes like removing inedible parts, drying, grinding, pasteurization, chilling, 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 created by combining many ingredients and undergoing a sequence of industrial processes. Examples include breakfast cereals, soft drinks and fruit juices, sweet or savory snacks, confectioneries, instant foods, reconstituted meat products such as sausages and nuggets, and most fast food items[3,4].

Food processing, in essence, refers to “various operations by which raw foodstuffs are made suitable for consumption, cooking, or storage,” and virtually all foods undergo some form of processing before being eaten. Therefore, processing itself is not inherently bad. 

However, ultra-processed foods are not modified foods but formulations made mostly or entirely from substances derived from foods and additives through multiple industrial processes, with little to no Group 1 natural foods[3].

UPFs are highly appealing because they are hyper-palatable and addictive, inexpensive, have a long shelf life, and can be consumed anytime, anywhere[3].

The evidence based on the NOVA classification so far suggests that the decline in minimally processed foods and home cooking, alongside the replacement of food supplies with ultra-processed foods, is associated with unhealthy nutritional profiles and an increase in several diet-related diseases[3].

In studies on adults reporting the proportion of total daily energy intake from UPFs, the highest levels (on average) were reported in the USA (55.1–56.1%), followed by the UK (53–54.3%), Canada (45.1–51.9%), France (29.9–35.9%), Brazil (20–29.6%), Spain (24.4%), and Malaysia (23%)[6].

A cross-sectional study (2005–2014) on American adults, who were found to consume an average of  56.1% of their total energy intake from UPFs, revealed significant differences across quintiles. Those in the highest quintile (Note 1) consumed 84.5% of their total energy intake from UPFs, while those in the lowest quintile accounted for 25.4%[7]. 

 (Note 1: Quintile refers to one of five equal measurements that a set of things can be divided into)

♦A cross-sectional time series study conducted in fifteen Latin American countries revealed that sales of UPFs were associated with changes in body weight in twelve of these countries from 2000 to 2009[8].

A cross-sectional study based on data from Brazil’s 2008–2009 Household Budget Survey found that household availability of UPFs was positively correlated with both the average BMI and obesity prevalence. Those in the highest quartile (Note 2) of household consumption of UPFs were 37% more likely to be obese compared to those in the lowest quartile[9]. 

(Note 2: Quartile refers to one of four equal measurements that a set of things can be divided into)

♦A study involving 6,143 participants from the UK National Diet and Nutrition Survey (2008–2016) classified foods recorded in four-day food diary according to the NOVA system. Consumption of UPFs was associated with increases in BMI, waist circumference, and obesity rates in both men and women. For every 10% increase in UPF consumption, the obesity rate increased by 18%. 

Higher consumption of UPFs was observed among men, white British individuals, smokers, younger people, and those in lower social class groups[10].

♦A cross-sectional study involving 19,363 adults aged 18 and older from the 2004 Canadian Community Health Survey, found that individuals in the highest quintile of UPF consumption were 32% more likely to be obese compared to those in the lowest quintile. Higher UPF intake was associated with being male, younger age, lower educational attainment, physical inactivity, smoking, and being born in Canada[4].

♦A prospective cohort study conducted since 1999 among graduates of the University of Navarra in Spain tracked 8,451 participants who were not overweight at baseline for about nine years. Those in the highest quartile of UPF consumption had a 26% higher risk of developing overweight or obesity compared to those in the lowest quartile.

Moreover, on average, they consumed more fast food, fried foods, processed meats, and sugar-sweetened beverages, while, in contrast, their vegetable intake was the lowest. A higher consumption of UPFs was associated with lower adherence to the Mediterranean diet[11].

♦A U.S. research group analyzed data on 5,919 children and 10,064 adults from the National Health and Nutrition Examination Survey (2015-2018) to investigate the relationship between UPF consumption and overall diet quality. Diet quality was assessed using the American Heart Association (AHA) diet score and Healthy Eating Index (HEI)-2015 score.

The research group concluded that higher consumption of UPFs was associated with substantially lower diet quality among children and adults. These findings were consistent with previous studies conducted in several countries[12].

♦An Italian research group hypothesized that meal timing could also be linked to food processing and conducted a study to test this. They analyzed data on 8,688 individuals from the Italian Nutrition & Health Survey (INHES), conducted between 2010 and 2013. Subjects were classified as early or late eaters based on the population’s median timing for breakfast, lunch, and dinner.

Results showed that late eaters (breakfast after 7 AM, lunch after 1 PM, and dinner after 8 PM) were less likely to consume unprocessed or minimally processed foods compared to early eaters, while they consumed more processed foods (PFs) and UPFs. Late eating was also inversely associated with adherence to the Mediterranean diet[13].

The Mediterranean diet, which primarily consists of fruits, vegetables, legumes, nuts, olive oil, and fish, has been shown to be linked to reduced weight gain[14].

A group of researchers in the U.S. conducted a crossover comparative study to ascertain the net energy intake of two different diets: one consisting of specific processed foods and the other of an isocaloric whole-food (WF) diet. Eighteen subjects consumed two types of sandwiches with the same calorie content but differing in processing levels.

The WF meal consisted of multigrain bread (containing whole sunflower seeds and whole-grain kernels) and cheddar cheese, while the PF meal consisted of white bread and a processed cheese product.

In this study, diet-induced thermogenesis (DIT)(Note 3) after consuming the PF meal was 46.8 % lower than that of the WF meal. The researchers concluded that this difference in DIT led to a 9.7 % increase in net energy-gain for the PF meal[15].

(Note 3)  Diet induced thermogenesis (DIT) is the process by which the body increases its energy expenditure for several hours in response to food intake.

Regarding the significant reduction in diet-induced thermogenesis (DIT) observed with the PF meal, the researchers provided the following analysis:

Compared to whole foods, PFs are characterized by lower nutrient density (a lower content and diversity of nutrients per calorie), less dietary fiber, and an excess of simple carbohydrates. As a result, PFs are structurally and chemically simpler than whole foods, making them easier to digest[15,16].

A group of U.S. researchers conducted a randomized controlled trial to determine the effects of ultra-processed versus unprocessed diets on ad libitum energy intake in twenty adults with stable body weight. Subjects were randomly assigned to either the ultra-processed or calorie-matched unprocessed diet for two weeks, followed by the alternate diet for another two weeks.

In this experiment, participants were allowed to eat additional food after meals. As a result, they consumed more energy (459±105 kcal /day) during the ultra-processed diet and gained 0.4±0.1 kg of body fat. In contrast, they lost 0.3±0.1 kg of body fat during the unprocessed diet.

Fasting blood tests showed that levels of the appetite-suppressing hormone peptide YY (PYY) increased during the unprocessed diet as compared with both the ultra-processed diet and baseline. Also, levels of the hunger hormone ghrelin decreased during the unprocessed diet compared to baseline. This suggests that participants felt less hungry during the unprocessed diet, whereas the ultra-processed diet provided less satiety, making participants feel hungrier[19]. 
           

I would like to explain the link between consumption of UPFs and an increase in obesity from the perspective of intestinal starvation.

Since the development of the NOVA classification, various studies have focused on the degree of food processing rather than calorie content, which is noteworthy.

Through this blog, I have explained that a combination of factors—such as an unbalanced diet leaning toward refined carbohydrates and UPFs, a lack of vegetables, and an irregular lifestyle—can induce intestinal starvation, potentially raising the body's set-point weight.

UPFs are often high in energy density, so they are generally believed to promote obesity when overeaten. However, I believe the biggest issue is the "ultra-processing" itself, as these foods are digested and absorbed more quickly than natural foods.

If the diet is skewed toward refined carbohydrates and UPFs, and the overall diet quality declines, blood sugar levels can fluctuate sharply. Additionally, since these foods leave nothing behind in the intestines after digestion, intestinal starvation can be triggered (Note 5).

The fact that adherence to the Mediterranean diet and the consumption of natural foods like vegetables are inversely correlated with obesity supports my perspective.

In Japan, In my opinion, the consumption of UPFs such as instant foods, cookies, sweet bread, and chocolate confection is not necessarily low. However, one reason Japan’s obesity rate is lower than in Western countries may be its rice-based food culture, and the fact that many Japanese people still follow traditional eating habits. 

(Note 5: Foods high in fat, such as ice cream, take longer to digest and may help prevent intestinal starvation.)

The World Obesity Federation (WOF) warns that if policy directions remain unchanged and no effective measures are taken to prevent and treat obesity, more than half of the global population will be classified as overweight or obese by 2035.

I think this suggests that past policies focused solely on "calories in/ calories out" have not been particularly effective. 

What we need now is a shift in focus from "calories" to factors such as the degree of food processing, the number of chews, and digestibility in policymaking.

However, many people today prefer soft foods that require little chewing and have become overly reliant on refined carbohydrates and UPFs. These diets are low in nutrients and fiber, making them easy to digest, allowing the body to absorb large amounts of energy with minimal effort.

Moreover, once all the food is fully digested in the intestines, a signal that “there is no food” might be sent to the brain.

Such dietary habits were likely rare, if not nonexistent, in human history—at least until around 1970. It is not an overstatement to say that the sharp rise in being overweight, obesity, and many lifestyle-related diseases coincided with the rapid industrialization of food processing in the 1970’s and 80’s.
               

<References>
[1]Katz DL, Meller S. Can we say what diet is best for health?  Annu Rev Public Health. 2014;35:83-103. 

[2]Monteiro CA et al. NOVA. The star shines bright. Food classification. Public Health. World Nutr. J. 2016, 7, 28–38.

[3]Monteiro CA et al. The UN Decade of Nutrition, the NOVA food classification and the trouble with ultra-processing. Public Health Nutr. 2018 Jan;21(1):5-17. 

[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] World Obesity Federation. 
　　　　

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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.

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].

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]. 

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]. 

♦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].

♦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].

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]. 

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: 

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. 

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.

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

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. 

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”

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.
      

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.)

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.
　　　

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.)

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.)

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]. 

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]. 
               

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.

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.
             

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

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. 

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.

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”

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.

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. 

(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

[1]Begley S. America's hatred of fat hurts obesity fight. Reuters. May 11, 2012.

[2]Jou C. The biology and genetics of obesity--a century of inquiries. N Engl J Med. 2014 May 15;370(20):1874-7. 

[3]Speakman JR 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. 

[4]McPherson R. Genetic contributors to obesity. Can J Cardiol. 2007 Aug;23 Suppl A(Suppl A):23A-27A. 

[5]James, W. WHO recognition of the global obesity epidemic. Int J Obes 32 (Suppl 7), S120–S126 (2008). 

[6]Obesity as a Disease.The World Obesity Federation

[7] Garvey WT. Is Obesity or Adiposity-Based Chronic Disease Curable: The Set Point Theory, the Environment, and Second-Generation Medications. Endocr Pract. 2022 Feb;28(2):214-222. 

[8] Garvey WT et al. American Association of Clinical Endocrinologists and American College of Endocrinology Comprehensive Clinical Practice Guidelines for Medical Care of Patients with Obesity. Endocr Pract. 2016 Jul;22 Suppl 3:1-203.