— Topics —
Basic theory of gaining weight
2024.10.14
The Increasingly Important "Set-Point" Theory of Body Weight: What are the Environmental and Behavioral Factors?
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Contents
- Advances in understanding “set-point” theory
- Problems with the set-point model
- Environmental and behavioral factors influencing weight set-point
- Why intestinal starvation increases one’s set-point weight
<How to prove my theory>
- Advances in understanding “set-point” theory
As I've explained in previous blog posts, I believe that each person has an individual “set-point” for their weight, and that understanding how this set-point increases is the key to addressing the issue of obesity.
This time, I would like to share my thoughts on recent advances in research regarding the set-point theory of body weight, as well as the environmental and behavioral factors that influence it.
1. Advances in understanding “set-point” theory
<Obesity and weight loss attempts>
♦A fat person 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 1000 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 which has been known since before 1920. [1](J S Garrow, 1973)
♦For obese individuals, a certain amount of weight loss is possible through a range of treatments, but long-term sustainability of lost weight 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 a reduced degree of body fatness will probably require close attention to energy intake and expenditure, perhaps for life[5].
<Metabolic values of obese individuals>
♦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 a model case of men with an average weight of 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 a 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].
<Set-point theory of body weight>
♦In recent years, the influence of homeostatic control has been recognized, and there is growing evidence that the body employs physiological mechanisms to manipulate energy balance and maintain body weight at 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 1990’s [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. It also causes an increase in appetite through hormonal regulation and alters food preferences through behavioral changes, to drive the 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 tissue to maintain homeostasis, and resist weight change (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 adaption[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 reduction in weight maintenance calories is 10 to 15% lower than what is predicted based solely on alterations (/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, reported 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 100kg to 70kg, she would have to consume fewer calories to remain at 70kg than a woman who had consistently weighed 70kg[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 1960’s (Doctor Ethan Sims), weight gain due to temporary overeating also triggers compensatory mechanisms that bring body weight back into a set-point range.
However, some researchers point out that these may be weaker than those protecting weight loss. This asymmetry could be due to the evolutionary advantage of storing fat to survive during periods of caloric restriction, such as prolonged 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 set-point for body weight 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 a theory because all the molecular mechanisms involved in set-point regulation have not been elucidated, and some researchers may consider this theory to be overly simplistic[16].
2. Problems with the set-point model
However, some researchers have pointed out problems with the set-point model of regulation.
If such a powerful biological feedback system regulating the state of our body fat exists, then why do many individuals in most Western countries gain weight throughout majority of their lives？ In particular, they argue that this model cannot explain the increasing prevalence of obesity that has been observed in many societies worldwide since the 1970’s[22].
In response, some researchers argue that while metabolic resistance to sustaining a reduced body weight is strong, metabolic resistance to sustained increased adiposity may not be physiologically long-lasting. The steadily increasing prevalence of obesity in humans also suggests that the state of body fat is facilitated more vigorously than losing weight[17,23].
Animal studies in mice demonstrated increased energy expenditure and increased sympathetic nervous system (SNS) tone during the first 3-4 weeks of consuming a high-fat diet, while these changes were no longer evident after a few months of high-fat diet consumption[17,24].
Another animal study in mice reported that long-term consumption of palatable, high-energy diets such as potato chips, cheese crackers, cookies, etc., caused irreversible weight gain, suggesting an increase in the set-point weight[19,25]. This effect is believed to be due to the increases in the number of fat cell[19,26].
■These explanations may sound reasonable at first, but in my opinion, this is no longer a "set-point" and it fails to explain why the body stubbornly shows metabolic resistance to maintaining weight loss, even at a higher set-point weight.
When applied to humans, not everyone who frequently consumes high-calorie foods becomes obese. This brings up several contradictions, such as:
(1)Why is obesity more prevalent among the lower-income groups in Western societies[22,27] and relatively wealthier groups in developing societies?[28];
(2)The coexistence of undernutrition and obesity in poor populations, observed globally since the 1950’s[29];
(3) Why do some people gain weight after environmental changes such as entering college, getting married, having children, or moving from Asia to Western countries?[22]
As I have mentioned repeatedly in this blog, I believe that an increase in set-point for body weight is due to inducing intestinal starvation, and that I can explain all these contradictions.
In the following section, I will explain that more specifically.
3. Environmental and behavioral factors influencing weight set-point
In 2012, the American Association of Clinical Endocrinology (AACE) designated obesity as a chronic disease. One of the rationale for that designation is that, like other chronic diseases, the pathophysiology of obesity is complex, involving interactions of genetic, biological, environmental, and behavioral factors[30].
Some researchers interested in the body weight set-point theory argue that understanding how genes and the environment interact to regulate the set-point is essential to determining whether obesity, as a chronic disease, can be cured. However, they struggle to explain the many significant environmental and social influences[22].
■ I also believe that the set-point of body weight changes due to the interaction between (1) genetic and biological factors, and (2) environmental and behavioral factors, but this time, I will mainly discuss (2) in this article.
When considering changes in living environment since the 1970’s, most researchers blame the rise in obesity on the increased availability of high-calorie foods and a decrease in physical activity as society became more affluent. In other words, they believe that a positive energy balance is necessary for weight gain.
However, paradoxically, the fact that the increasing prevalence of obesity coincides with an increase in weight-loss attempts[31] suggests that our understanding of energy balance may be flawed[12].
As suggested by overfeeding experiments, “temporary weight gain from overeating” and “irreversible weight gain occurring over many years ” are different. In my view, obesity as a chronic disease arises rather from signals of negative energy balance or "food scarcity" in the body, as in the cases where people gain more weight than before after starvation or dieting.
[Related article]
The Overfeeding Study Suggests That "Overeating" Is Not the Cause of Obesity
■Despite its impact on our bodies due to changes in our living environments since the 1970’s, "intestinal starvation" remains unrecognized.
Intestinal starvation refers to a state where everything consumed is fully digested throughout the entire intestinal tract, and it can occur in today's affluent developed countries, developing countries, or even among the poor. When there is little or no fiber and everything has been digested, our bodies perceive it as having "no food."
【Related Article】
The Body Perceive That It Is More Starved than in the Past
Perhaps in many parts of the world before 1970, even if people went a whole day without eating until their next meal, there were likely still undigested substances like fiber and tough plant cell walls left in their intestines. However, in today’s society, with its abundance of easily digestible, refined carbohydrates, processed foods, and fast food, intestinal starvation can occur in as little as eight to ten hours, depending on eating habits.
Intestinal starvation is more likely to occur with frequent consumption of easily digestible refined carbohydrates (bread, noodles, rice, etc.), industrially processed meat or fish products, fast food, and snacks, etc., combined with a lack of vegetables and long periods of prolonged hunger (such as skipping breakfast, late-night meals, or irregular eating habits).
【Related Article】
■In the animal experiments on rats described in section 2 above, it was reported that consuming a "high-energy diet" for 90 days led to irreversible weight gain, suggesting an increase in the set-point. However, the "fattening” diet used in this experiment (Rolls et al., 1980) primarily consisted of highly palatable items like potato chips, cheese crackers, and cookies sold in supermarkets. Those foods contained 47.5% industrially processed refined carbohydrates (fat: 42%, protein: 10.5%) on an energy basis[25]. Moreover, rats only eat when they’re hungry, and they are capable of eating the same food repeatedly.
In contrast, the “chow” fed to the control rats may have been made from ingredients like ground wheat, ground corn, soybean meal, and fish meal, etc. In other words, just as our diets from over fifty years ago, it likely contained a high amount of indigestible components, such as fiber and tough plant cell walls.
Therefore, I question the conclusion that highly palatable "high-energy diets" alone caused the irreversible weight gain.
4. Why intestinal starvation increases one’s set-point weight
Below, I will explain the mechanism by which the set- point for body weight increases due to the induction of intestinal starvation. While some of it involves speculation, it is based on events that have happened to me several times. You may not believe it, but at least for me, it is 100% accurate.
■Let's assume there is a man who has maintained a weight of 70 kg for many years. Even though his weight may fluctuate slightly during busy periods or after overeating, his weight revolves around 70 kg, so his set-point would be considered 70 kg.
When intestinal starvation occurs, a signal that 'there is no food' is transmitted from the intestines (or small intestine) to the brain.
As a result, the body tries to absorb more nutrients, causing microscopic substances attached to the villi (or microvilli) in the small intestine to detach (Figure 1), thereby increasing the surface area for absorption and raising the absolute absorption ability.
In other words, I believe that weight gain, at least to some extent, involves not only an increase in body fat but also lean tissue such as muscle.
(Fig. 1 )
(Normally, a few undigested fiber or fats may remain, but when all food is perfectly digested, 5 to 10 kg of weight gain over a short period is possible.)
As a result, I believe the weight balancing point (the set-point) increases and reaches equilibrium within just a few days (Figure 2).
Weight gain does not occur from the gradual accumulation of excess calories each day, but rather in one sudden jump, possibly 0.3kg or 0.5g.
When dieting, the set-point can unknowingly rise, so you may gain a few pounds more than before once the diet ends.
(Fig. 2 )
Once the body’s balance point rises, it becomes harder to lose weight because the overall absorption ability has increased. As mentioned in reference in section 1 , I agree with the idea that obesity is a “state of energy regulation at a higher set-point,” and is "a natural physiological condition" for obese individuals.
For more details, please refer to the article below.
【Related Article】
Gaining Weight by Intestinal Starvation; What Does It Mean?
<How to prove my theory>
It may be difficult to determine the exact cause when someone gains a few kg in a year, meaning their highest weight ever. However, I believe that, even with reduced calorie and carbohydrate intake from the meals I provide, it is possible to significantly increase a person's weight (by around 5 to 10 kg) within a few months, setting a new high set-point weight. By observing the data before and after, I think it is possible to investigate what changes have occurred inside the body.
<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]Faust I.M., Johnson P.R., Stern J.S., Hirsch J. Diet-induced adipocyte number increase in adult rats: a new model of obesity. Am. J. Physiol., 235 (1978), pp. E279-E286
[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 31-40.
[30]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.
[31]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.
2024.06.20
The Overfeeding Experiment Suggests That "Overeating" Is Not the Cause of Obesity
Contents
- Can overfeeding experiments make people obese?
- Subsequent overfeeding experiments
- Can metabolism explain this weight regain?
- Difference between obesity and overfeeding experiments: My thoughts
1. Can overfeeding experiments make people obese?
According to George A. Bray (as of 2020, an emeritus professor at Pennington Biomedical Research Center), until the 1960’s, obesity was viewed as a "lack of will power," and many people thought, and some said "if only these patients would push themselves away from the table, they would not have this problem."
With this view of obesity, he reflects that the turning point for obesity being accepted as a bona fide area of academic interest were the studies on overfeeding. Overfeeding studies began to provide valuable insights into the biology of obesity. For Doctor Bray, who was a postdoctoral fellow at the New England Medical Center Hospital in Boston at the time, the excitement that was generated when the Vermont overfeeding studies were first presented in 1968 was unforgettable[1].
This was the case with the overfeeding experiments conducted by Doctor Ethan Sims in the late 1960’s. Until then, it was commonly believed that, "overeating obviously leads to obesity," so few such experiments had been conducted.
According to Dr. Jason Fung, the author of “The Obesity Code,” Dr. Sims recruited lean students at the nearby University of Vermont and encouraged them to eat a lot to gain weight. However, despite what both he and the students had expected, the students did not become obese.
Suspecting that the students might have been increasing their exercise, Dr. Sims changed course. He then recruited convicts at the Vermont State Prison as subjects. Physical activity was strictly controlled, and attendants were present at every meal to ensure the calories－4000 per day－were eaten.
Although the prisoners’ weight initially rose, it then stabilized. While some prisoners gained more than twenty percent of their original body weight, the extent of weight gain varied significantly among them[2] .
Over two hundred days on this overfeeding regimen, twenty inmates gained an average of twenty to twenty-five pounds. (About 10 kg.) However, once the experiment ended and their caloric intake returned to normal, the men had difficulty maintaining the weight gain, and most shed all the weight they had gained relatively easily. The exceptions were two inmates who struggled to lose that weight[3].
At the time, Dr. Bray was allowed to participate as a co-researcher in Dr. Sims' experiment to examine the metabolic changes occurring in adipose tissue during the weight gain that followed overfeeding.
Later, in 1972, he conducted his own overeating experiment, using himself as a guinea pig. Initially, he tried to double what he usually ate at each meal, but he couldn't finish, so he switched to energy-dense foods, such as ice cream.
Over the next ten weeks, he gradually gained ten kilograms, and repeated his tests such as measuring the thermic effect of foods.
But once he stopped stuffing himself, his weight rapidly decreased, returning to his original seventy-five kilograms six weeks later, and he has maintained this weight with no trouble ever since.
Following his self-experiment, the other four volunteers in this study began overeating in the summer of 1972. When the experiment ended, all the volunteers returned to their baseline weight.
Dr.Bray states that this rapid return to normal weight contrasts with the difficulties people with spontaneous obesity have in losing weight, and the even more difficult task of a maintaining a lower weight. Many who develop obesity over years suffer from a different kind of pain than those of us who acutely gain weight by overfeeding. For them, the obesity “slips up” on them and once present, is difficult to reverse.
The history of overfeeding and underfeeding trials and other lines of evidence clearly show that obesity prevention and treatment cannot simply rely on the advice to "eat less and exercise more." [1]
2. Subsequent overfeeding experiments
Alex Leaf (Western States University) and Jose Antonio (Nova Southeastern University) reviewed overfeeding studies conducted up to 2017 that evaluated various combinations of macronutrient overfeeding and its effects on body composition.
They found twenty-five overfeeding studies that reported changes in fat mass (FM) and fat-free mass (FFM), in addition to changes in body weight. The study durations ranged from nine to one hundred days, and all but four were conducted in sedentary populations[4]. Notably, the objectives of each study varied, and not all mentioned weight loss following the end of the experiments.
To give a few examples, a study on identical twins was published in 1990.
■Bouchard (Laval University, Canada) et. al. recruited twelve pairs of young adult male identical twins (twenty-four individuals) with no exercise habits. Each participant's energy requirements were measured during a two-week base-line period, and after that, they were overfed by 1000 kcal per day (comprising 15% protein, 35% fat, and 50% carbohydrates), six days per week, for a total of eighty-four days during a one hundred-day period. The men were housed in a closed section of a university dormitory, and were under supervision by staff all day.
The mean weight gain was 8.1 kg, of which 67% was fat mass (FM). However, the weight gain varied widely among participants, ranging from 4.3 to 13.3 kg[5].
Four months after the experiment ended, the twins' average weight was 61.7 kg, which was only 1.3 kg higher than their baseline weight of 60.4 kg, indicating they had almost returned to their original weight[1].
■Conford (University of Michigan) et. al. conducted a study in 2012 involving nine healthy, non-obese adults (seven men and two women). The participants were admitted to the hospital for two weeks, during which time they ate 4000 kcals per day (comprising 15% protein, 35% fat, and 50% carbohydrates). Their energy requirements were determined during a one-week baseline period before the start of the experiment. In addition to three main meals, they had four snacks each day. The average weight gain was 2.1 kg, of which 67 % was fat mass (FM).[6]
The summary of this review indicates that overfeeding healthy, sedentary adults with a diet moderately high in both carbohydrates and fats (35-50% energy intake each) and low in protein (11-15%) primarily results in a gain in fat mass (FM), which accounts for 60-70 % of the weight gain. Additionally, the increase in fat-free mass (FFM) may be due to an increase in body water content rather than skeletal muscle tissue. In contrast, diets with significantly increased protein intake showed favorable changes in body composition, even with increased energy intake[4].
3. Can metabolism explain this weight regain?
Why did the participant’s weight rapidly return to normal over the ensuing weeks when they stopped overeating?
According to Dr. Bray, one of the striking findings in this Vermont study was that to maintain the weight they gained after overfeeding, they required more energy per unit surface area than before weight gain. When Dr. Bray moved to the University of California in 1970, his new lab began operating to explore his hypothesis about why extra energy was required to maintain the increased weight[1].
■Leibel (Rockefeller University) et. al. conducted a study in 1995 involving eighteen obese (BMI of 28 or higher) subjects (Group A) and twenty-three subjects who had never been obese (Group B).
They measured changes in energy expenditure under three conditions: at their usual body weight, after losing more than 10 percent of their body weight by underfeeding, and after gaining 10 percent of their body weight by overfeeding.
When maintaining a body weight at a level 10% or more below their initial weight, the total energy expenditure decreased by 8±5 kcal per kilogram per day in Group A and by 6±3 kcal in Group B.
Conversely, when maintaining a body weight at a level 10% above their initial weight, total energy expenditure increased by 8±4 kcal in Group A and by 9±7 kcal in Group B.
The study concluded that maintenance of a reduced weight or elevated body weight is associated with compensatory changes in energy expenditure, which resist maintaining the altered body weight and function to restore the original weight. This suggests that the long-term effectiveness of obesity treatment through caloric reduction may be limited[7].
4. Difference between obesity and overfeeding experiments: My thoughts
As Dr. Bray mentioned, I also believe that weight gain from temporary excessive caloric intake is due to body mechanisms entirely different from those underlying fundamental obesity. If compensatory metabolic mechanisms resist changes in body weight, why do some people continue to gain weight?
As I have repeatedly mentioned through this blog, the difference between people who are overweight and lean can be explained by the difference in set-point for body weight. (One's set-point weight goes up through intestinal starvation.)
For example, suppose a person who normally weighs a stable sixty kg is temporarily overfed and reaches sixty-three kg.
This can be compared to a glass of water that is usually filled to about 97% now being filled to 100%, and then surface tension causing the water to rise above the rim.
Conversely, maintaining a weight of fifty-six kg by eating less is like the water level temporarily decreasing, causing a dip in the surface of the water.
In both cases, the set-point weight has not changed.
In contrast, if a person who originally weighs sixty kg gradually gains weight over several years, and then maintains a stable weight of ninety kg, this indicates that the set-point weight itself has increased, meaning the glass has grown larger, with energy balancing at a higher level.
Today, we are sometimes said to be living in an "obesogenic environment" that promotes obesity, but that does not necessarily mean consuming high-calorie foods or living sedentary lifestyles. As some researchers have already mentioned, calorie counting is clearly of little significance. Changes in caloric intake only lead to temporary weight gain or loss.
Rader, the "obesogenic environment" in my opinion is related to foods that are overly digestible foods (refined carbohydrates, fast food, processed foods, etc.) and an imbalanced diet (lack of vegetables, etc.). When these factors overlap with some other conditions such as skipping breakfast or eating late dinners, intestinal starvation is more likely to be induced.
Of course, researchers will say that in order to gain weight, more energy must be taken into the body than before. For more on why intestinal starvation leads to greater energy intake and weight gain, please refer to the article below.
[Related article] Gaining Weight by Intestinal Starvation; What Does It Mean?
<References>
[1]Bray GA. The pain of weight gain: self-experimentation with overfeeding. Am J Clin Nutr. 2020 Jan 1;111(1):17-20.
[2] Fung J, The Obesity Code, Greystone books, 2016, P114-116.
[3] Jou C. The biology and genetics of obesity--a century of inquiries. N Engl J Med. 2014 May 15;370(20):1874-7.
[4] Leaf A, Antonio J. The Effects of Overfeeding on Body Composition: The Role of Macronutrient Composition. Int J Exerc Sci. 2017 Dec 1;10(8):1275-1296.
[5] Bouchard C et al. The response to long-term overfeeding in identical twins. N Engl J Med. 1990 May 24;322(21):1477-82.
[6] Cornford AS et al. Rapid development of systemic insulin resistance with overeating is not accompanied by robust changes in skeletal muscle glucose and lipid metabolism. Appl Physiol Nutr Metab. 2013 May;38(5):512-9.
[7] Leibel RL et al. Changes in energy expenditure resulting from altered body weight. N Engl J Med. 1995 Mar 9;332(10):621-8.
2019.08.14
Gaining Weight by Intestinal Starvation; What Does It Mean?
Contents
- Hunger in Africa and hunger in the modern era
- Why do we gain weight during periods of starvation?
- What happens when one’s set-point weight is elevated?
Let me explain something about the core of this blog.
Perhaps for most of you it is hard to believe me, but I’ll just write the facts as they are, as I experienced them. I did not write this from my imagination, but based it on my own analysis of what actually happened to me.
When I got into college, my total body weight fell down to the thirty-kilo range, so I knew exactly why I gained almost five kilos so rapidly in a few days, even though I didn’t eat much.
1. Hunger in Africa and hunger in the modern era
The idea of storing fat in the body as a reserve against starvation is something every researcher considers at one time or another.
However, it is said that this theory is an idea that has been rejected by researchers throughout history. This is because many overweight people often eat more, and many African refugees are thin and malnourished.
One might say, “If starvation makes us fat, then African refugees would be obese.”
However, please understand that this is a true state of starvation (malnutrition) in which the people can’t eat even if they want to, and I’m stating that it is different from what I call “intestinal starvation.”
African refugees do not have access to digestible food, and malnutrition even diminishes their ability to digest food and nutrients.
In contrast, many of us in developed countries are more likely to eat westernized foods made from wheat, meat, eggs, etc., which provide good nutrition and are easier to digest. Therefore, if we focus on the inner workings of our intestines, we are more prone to inducing intestinal starvation.
The reality is that being overweight has become a problem even among the poor populations in the world. What is common in these cases is not the excessive intake of calories or sugars, but rather a diet that is low in nutritional value and unbalanced, often due to a reliance on inexpensive refined carbohydrates and a lack of vegetables.
2. Why do we gain weight during periods of starvation?
In my blog, I mentioned that one’s set-point for body weight goes up by inducing intestinal starvation, and I want to explain what it means here. For the sake of explanation, I will use plants as an example.
(1) For plants, eating food and gaining weight is done by adding "fertilizer." This fertilizer is the equivalent to our diet, and of course, we need to use fertilizer periodically for growth.
However, using too much fertilizer doesn’t usually result in producing a bigger plant, and if we use it too often, it may sometimes have a negative effect.
The same goes for humans, and just eating a lot of calories doesn’t necessarily mean we all gain weight and become overweight. Even if we eat only one meal a day, as long as it’s well-balanced, there will be enough nutrition left in the intestines to be absorbed.
(2)Using an example of a plant, weight gain by inducing intestinal starvation and an increase in set-point for body weight could be explained in the same way as a plant that is extending its roots and taking in more nutrients. (See figure below)
When there is not enough nutrition, plants grow their roots deeper into the ground seeking more nutrients, and the same phenomenon occurs when we humans digest all the food in our entire intestines (or it may be the small intestine only), and intestinal starvation is induced.
(It is said that “the small intestine is the second brain” or that “it has a will,” and I clearly felt the will of my small intestine.)
Actually the villi (*1) of the intestines do not grow, but I believe that the following phenomena occur:
(*1)In order to absorb more nutrients efficiently, the interior of the small intestine has a folded structure, with numerous protrusions called villi on its surface (Fig. 1). Additionally, microvilli develop on the surface of these villi.
It is sometimes said that if all of these were spread out, the surface area inside the small intestine would be equivalent to that of a tennis court.
(Fig. 1: Villi of the small intestine)
First, I believe that the intestines (especially the small intestine) is the first organ to sense whether or not food is present. This is determined not only by the amount of energy, but also by how far the food has been digested. (For this reason, even if you eat a large amount, if your diet is heavily skewed towards easily digestible carbohydrates, intestinal starvation can be induced.)
When undigested substances, including fiber, remain in the intestines to some extent, the body perceives that “there is still food,” even if you're hungry. However, when all the food is digested (or very close to it), the small intestine sends a signal to the brain that “there is no food.”
In response, the body attempts to absorb more nutrients, and microscopic substances attached to the villi (or microvilli) of the small intestine detach (Fig. 2). This, in turn, increases the surface area for absorption, thereby boosting absolute absorption ability.
This causes weight gain, suggesting an increase in the set-point for body weight, and reaches a new equilibrium at a higher set-point within just three to four days.
( Fig.2 )
In other words, weight doesn't gradually increase due to excess calories being stored bit by bit. Instead, the body normally maintains a stable set-point weight, but at some point, it suddenly jumps, whether by 300 grams or 500 grams, all at once (Fig. 3).
In summary, I believe that one of the key factors in the fundamental difference between obese and lean people involves their absorption ability.
[Related Article]
( Fig.3 )
In Japan, obese individuals sometimes say things like, “I gain weight even just by drinking water.”
Of course, water alone does not make them fat, but I don't think it is totally wrong. It reflects just how efficient their absorption rate is.
3. What happens when one’s set-point weight is elevated?
(1) Once you gain weight, it becomes more difficult to lose weight
When your set-point for body weight goes up and you gain weight, it means that the balancing point, in terms of "energy- in, energy-out," has gone up, which can generate a more positive energy cycle and make it more difficult to lose weight.
When dieting, temporarily reducing the caloric intake to lose weight means reducing the "fertilizer" in the example of a plant. However, it is only a temporary weight loss, and you will likely return to your original weight when you start eating a normal diet again (the rebound effect).
Moreover, the reason why each time some people diet, they rebound and gain more weight than before is that skipping meals or eating light meals (not enough vegetables) can lead to intestinal starvation, which can further increase your set-point weight.
(2) More muscle, too
It is not that after you get fat, you gain muscle to support it. Since the overall absorption of nutrients increases, I believe that weight gain, at least to some extent, involves not only an increase in body fat but also lean mass such as muscle.
When a fat person loses body fat, they often have a thick, muscular chest or thighs. After body fat is gained, would the muscles around the chest and neck thicken to support that weight? (This varies widely from person to person.)
(3) Cause-and-effect reverse phenomenon
The increased intake of nutrients as a whole, including protein, creates a positive cycle of energy, which leads to the following phenomena.
Since digestive enzymes, hormones, etc. are also made from proteins (amino acids), it could enhance the ability to digest food and potentially bring about changes in the hormonal systems that regulate appetite and other functions. So, it is no wonder that people with larger bodies or stronger stomachs generally eat more than others.
There exists a cause-and-effect reversal phenomenon: people do not gain weight because they eat more, but because the bigger they are, the hungrier they become, and in turn, they eat more.
(4) Those who are overweight are prone to gaining more weight
Even if everyone eats exactly the same amount, people with big bodies－big, meaning large with some extra body fat or muscularly built－, or obese people, are more likely to feel hungry, which means that they eat relatively less, and they tend to gain more weight little by little.
It may be a vicious circle where a person eats modest amounts and gains weight, and if they skip meals or eat less to lose weight, they gain even more weight in the long run.
【Related article】→What Does It Mean to Eat Relatively Less?
On the other hand, if a lean person eats balanced meals three times a day, every day, he or she doesn’t induce intestinal starvation. And there is a good chance they will stay the same weight and have the same appearance for the rest of their life, regardless of caloric intake.
Therefore, "fatness" and "non-fatness," in this regard, are not due to obesity genes.
Also, for people like me who are very thin, being thin itself can reduce the amount of protein and other nutrients that can be taken in, thus a negative energy cycle continues. In turn, the muscles that support the stomach and intestines become weak and droopy, and the ability to digest food is also diminished by not secreting enough digestive enzymes.
This is a vicious circle where thin people can’t gain weight and remain thin.
2019.06.22
Is Obesity a Multifactorial Disease?
Contents
- The view that obesity is "multifactorial"
- Various factors intertwined...
<The bottom line>
１. The view that obesity is "multifactorial"
It is said that obesity is related to many factors, but why? I will quote an interesting description that is relevant to my blog.
“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."
(Jason Fung. The Obesity Code. Greystone Books, 2016, Page 70.)
"THE MULTIFACTORIAL NATURE of obesity is the crucial missing link. There is no one single cause of obesity.
Do calories cause obesity? Yes, partially.
Do carbohydrates cause obesity? Yes, partially.
Does fiber protect us from obesity? Yes, partially.
Does insulin resistance cause obesity? Yes, partially. Does sugar cause obesity? Yes, partially.
(*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 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. Pages 216-217.)
I think the author provides a keen insight into the multifactorial nature of obesity. We must first understand that being overweight is not as simple as "it happens when we consume more calories than we expend," but is caused by a complex interplay of various factors.
However, what I want to say is that based on my intestinal starvation idea, the various factors can be aggregated to some extent, which means that obesity can be complicated and intertwined with factors and theories we can see, and cannot be completely explained, but when we focus on the unseen workings of the intestines, the cause of weight gain would be mostly specific.
2. Various factors intertwined...
As I’ve already explained, please understand that the phrase “gaining weight” has two meanings.
【related article】
Two Meanings to the Phrase "Gaining Weight"
The mechanism that many people refer to as “get fat by eating a lot” is in the range of (A) in the graph below. I think that most of the Intervention studies on obesity so far have only been comparative studies that involve reducing the intake of calories, regulating the amount of carbs or fat, or increasing exercise, etc. The experiment they are doing is also in the range of (A).
Of course, everyone will lose some weight if they reduce their caloric intake and incorporate exercise, although individual differences may vary.
However, that is not the fundamental way to deal with being overweight, as Dr. Fung mentioned, so regaining weight (the rebound effect) is inevitable if you eat as before.
▽In contrast, when (B) the 'set-point' for body weight goes up by intestinal starvation, there are various interrelated factors.
For instance, it is said that the following affects weight gain:
・Skipping breakfast ・Late dinner ・How many meals you eat
・Refined carbohydrates ・Processed food
・Lack of fiber intake ・Unbalanced diets
These are some of factors that are related to part (B) of the graph.
The important thing here is that each of these factors seems to be linked to weight gain, but there is no causality between each factor and outcome. Rather, they are related to inducing intestinal starvation. (In this case, some may say intestinal starvation can be “confounding factors.”)
As I’ve already explained in another article, a combination of some of these factors below (from category 1 to 4 of the table) happening simultaneously or overlapping, can cause intestinal starvation, and the occurrence of intestinal starvation may be pinpointed in the unseen workings of the entire intestinal track (or it may be the small intestine only).
[Related article]
Three (+one) Factors to Accelerate “Intestinal Starvation”
The bottom line
(1) Many theories that are believed to make us fat fight among themselves, as if there is only one true cause of obesity, as Dr. Fung mentioned. Researchers may be well versed in their own areas of research (e.g. resistant starch, the value of eating breakfast, the effects of carbohydrate restriction, hormones, gut bacteria, etc.), but that does not necessarily capture obesity as a whole, so each theory can stand alone.
What we need now is a framework for how each theory is intertwined, and I'd like to believe my theory can be helpful in that regard.
(2) The root cause of being overweight, I believe, is the increased set-point weight, which is caused by intestinal starvation. Intestinal starvation is caused by a combination of at least four factors, and since "what kind of food we eat" and "how we eat them (lifestyle)" are such important factors, many things seem to have something to do with weight gain－intestinal starvation can be a "confounding factor."
In other words, I believe the causes of weight gain would be mostly specific in the unseen workings of the intestines.
2016.10.17
Three (+one) Factors to Accelerate “Intestinal Starvation”
Contents
- An unbalanced diet and irregular eating rhythm can cause intestinal starvation
- This last, but not least important factor, what is “+one? ”
１. An unbalanced diet and irregular eating rhythm can cause intestinal starvation
I’ve stated before that what increases your set-point weight is the hunger mechanism (intestinal starvation) and here, I want to talk about three(+one) factors that accelerate intestinal starvation.
【Related article】→My Definition of “Intestinal Starvation”
In Japan, the reasons for gaining weight with the exception of calories are often said to be associated with:
■an unbalanced diet
・fast food/junk food
・too many carbohydrates
・lack of vegetables, etc.
■ irregular eating rhythm
・eating dinner late at night
・skipping breakfast or lunch
・snacking or not
When there is only one of the situations from above, the intestinal starvation mechanism hardly occurs. However, when there are three and the +one factor which I will discuss later, the mechanism for intestinal starvation happens more often.
The 3 factors are as follows :
- What you eat (quality and balance of food);
- the time you stay very hungry between meals;
- the ability to digest (stomach acid, digestive enzymes, etc).
Some say they gained weight from eating too many carbohydrates, but others won’t seem to gain weight even if they eat a lot of carbs.
Some say they gained weight by eating junk foods late at night, but others don't gain at all, even if they eat in the same way.
These differences exist since intestinal starvation is decided by the composition of various factors.
Explanation of (1)
1)What you eat (quality and balance of food)
・Low fiber intake ・Refined carbohydrates ・Digestible protein
・Processed food ・Fast food ・Junk food, etc.
Meals with mainly refined carbohydrates (starch) and some good protein (a small amount is enough) and less fiber intake from vegetables, make people fat most easily. It seems with less fat in the diet, intestinal starvation is more likely to be induced. It’s because dietary fat slows digestion.
It doesn’t depend on the amount of calories you eat but the quality and balance of food you eat.
For example, eating a variety of foods and having a good balance vs a bad balance may lead to gaining weight, even if you eat in small amounts.
In contrast, balanced meals including vegetable fiber, dairy products, low G.I. foods, meat, and fat, etc., prevent inducing intestinal starvation.
*Eating speed, how many times you chew your food, or hydration during the meal, are also related to the above.
Explanation of (2)
2) The time you stay very hungry between meals
・Skipping breakfast or lunch ・Late dinner
・Number of meals per day ・Snacking or not
When we say we got fat due to an irregular eating rhythm such as late dinners or not eating breakfast, it means the problem is because of the time span between meals.
In other words, experiencing being hungry for a long period of time.
Eating late at night won’t automatically make you fat. If you have to eat a late dinner, you can snack (milk, chocolates, or sandwiches, etc.) between meals in order to prevent intestinal starvation.
Explanation of (3)
3) Digestive ability
・Strong/weak stomach ・Gastroptosis
・Difference of digestive enzymes
Those with strong stomachs and high digestive ability tend to induce intestinal starvation more rapidly than those with slow digestion.
This is because intestinal starvation doesn’t depend on the amount of food intake, but how fast the food is processed in the entire intestinal tract (or it might be a small intestine only).
It differs from person to person, but Individuals with a droopy stomach, or poor digestion might not be able to even induce intestinal starvation.
If there are genetic factors, the difference of digestive ability will be the first thing I will bring up as the factors. And it may vary between races as well as between families. (Of course, it may change after birth.)
２. This last, but not least important factor, what is “+one ?”
I stated that an important factor other than the above three factors is “+one,” but this can be explained by a “continuity,” which is whether you had an unbalanced diet (or a light meal) for your previous meal and the meals before that.
(Japanese typical breakfast we used to eat)
For example, you eat a light meal such as a hamburger and coffee for lunch, and then you can’t eat until 9 p.m. that night.
If you had also eaten a heavy breakfast with dairy, salad, seaweed, beans, or butter, you won’t experience a intestinal starvation (it depends on the person).
The reason for this is that the intestines are as long as seven to eight meters, so it takes the food more than ten hours to pass through.
Intestinal starvation is determined by the entire intestinal tract (or it might be the small intestine only), so the previous meal or the meals before that also affect it.
2016.10.17
My Definition of “Intestinal Starvation”
If you haven’t read these articles below, please read them first.
A Set-Point Weight; The Precondition Regarding the Rebound Effect
Two Meanings to the Phrase 'Gaining Weight'
In my previous article, "Two meanings to the phrase 'gaining weight' ," I wrote that your set-point weight increases by the hunger mechanism－strictly speaking, intestinal starvation. I would like to explain it simply.
Of course, in order to gain weight, you need nutrition such as carbohydrates, protein, or fat.
However, it’s what happens later on...because there is a time lag between the emergence of the cause of gaining weight and the actual gaining of weight by eating.
What I mention here as “intestinal starvation” is different from the situation such as when you don't eat anything over a few days.
Definition
(1) It happens when you eat and when your gastrointestinal tract is working.
(2) It refers to the situation between meals, such as between breakfast and dinner, or lunch and late dinner, or dinner and the next lunch, where every substance in the entire intestines from a range of seven to eight meters has been digested.(It might be small intestine only.)
In other words, the stomach and intestines are working to nourish the body, but all the food eaten has been digested, and the body perceives it as “there is no food.” It’s different from simple hunger in that:
(a) basically, everything, including protein, fat, and even water, is digested;
(b) there is no fiber or anything close to it (※This is why it is said refined carbohydrates make you fat).
▽Over the course of evolution, humans stored nutrition in the liver, bones, muscles, and fat cells in order to prepare for cases of starvation. This is because they didn’t know when they could eat the next time.
From this aspect, getting fat should be the mechanism of the body trying to store energy. Then this mechanism of storing nutrition should work strongly with those who don’t eat a lot.
However, in this era with an abundance of food, it seems like those who eat a lot are obese and those that don't eat much are thin, and this tends to lead to a misunderstanding.
There is a reason for this, and it is my own theory based on my personal experience.
The question here is : "In what way do our bodies perceive starvation ?" Starvation is not decided by the amount of how much we’ve eaten, but rather, how the digestion process in the intestines proceeds.
That is to say, even if you eat a lot, if your diet is skewed toward easily digestible carbohydrates and some protein, and you end up being very hungry for hours, you will be close to a starvation situation.
On the other hand, even if you eat a little, if you eat a well-balanced diet including vegetables, dairy, meat, and fat every five to seven hours, then your body won’t perceive you as being in starvation mode. When there are some undigested substances in your intestines, your body perceives them as "there is still food." In other words, your intestines decide everything.
A long time ago, our ancestors had nuts, meat, or root vegetables, and then, even if they had nothing after that for a whole day, their bodies didn’t perceive it as starvation.
On the other hand, our current bodies sometimes perceive us in starvation mode depending on what we eat for as little as seven to eight hours.
This is an important message to convey that the increase in obesity that has been occurring worldwide since around 1980 is not necessarily due to increased caloric intake, but rather is related to (1) refined carbohydrates and easily digestible food, and (2) irregular eating habits－skipping breakfast or late night meals, etc.－associated with lifestyle changes.
[Related article] Why Does the Body Perceive That It Is More Starved than in the Past?
2016.03.15
Two Meanings to the Phrase "Gaining Weight"
Contents
- When your weight goes back to your set-point weight (A)
- When your set-point weight itself increases (B)
Please check out my blog below before reading this one.
→ A Set-Point Weight; The Precondition Regarding the Rebound Effect
I would like to define this term first. There are two meanings of the expression "gaining weight" which we use daily. I think the confusion of these meanings causes a lot of misunderstandings.
For example, “you'll gain weight if you eat a lot of calories” or "despite dieting and eating less, you gain even more weight when you rebound,” etc.
I realized this when I got really thin, but I think the confusion of these two meanings results in various misunderstandings and false information, and most people are dieting in the wrong way.
1. When your weight goes back to your set-point weight (A)
The first one is “gaining weight” meaning to go back to your set-point weight based on the mechanism of maintaining your present condition.
Many of those who are overweight try to keep their weight low by reducing their daily caloric intake and/or doing some exercise, because they do not want to gain weight.
In such cases, the body always tries to go back to its set-point. Therefore, it is no surprise that if they stop calorie restriction and return to their previous eating habits, they will gain weight.
(Note: Temporary overeating may cause a slight increase in weight beyond the set-point, but the set-point itself remains unchanged, and the weight gain can be considered temporary.)
When people say, "If I eat high-calorie foods, I gain weight easily," or "If I eat sweets or cake, I gain weight," they are mostly talking about this meaning.
Sometimes I hear women say, "I have a body type that gains weight easily as soon as I eat a little more."
But, in my opinion, it means that the body is repeatedly going through a “mini-diet” and a “mini-rebound” by the mechanism to preserve its current stasis.
▷Toru Watanabe, a Japanese actor, used to be heavy, but with a diet, he weighed around 70kg when he appeared on a television show.
However, when he got married at twenty-six, he couldn't maintain his diet anymore and ate a lot and he went back to 130kg. (It is said that he made a new record for his weight change every time he dieted.)
Again with the help of his wife’s home cooking, he succeeded in losing 40kg.
However, in the end, he repeated rebounding. It’s quite a famous story in Japan.
(You can imagine a glass in which water is increasing and decreasing.)
2. When your set-point weight itself increases (B)
On the other hand, the second “gaining weight” expression means that your set-point weight itself increases.
Though I have reduced the amount of my food intake, I shattered my previous weight level and gained three kilograms in the last year which means I’ve gained ten kilograms in the last three years... meaning my maximum weight has increased.
This is not due to the amount of food eaten or caloric intake, but by the mechanism of hunger (strictly speaking, I have defined it as “intestinal starvation” ).
I believe that this makes a fundamental difference between fat people and thin/lean people. (You can imagine a glass of water that the glass itself is growing larger.)
[Related article]
My Definition of “Intestinal Starvation”
For example, someone who has never been more than sixty kilograms has become sixty-three kilograms in the last year. In this case, it means that his/her set-point weight itself increased from sixty to sixty-three kilograms.
When you gain weight to your set-point weight from a rebound after a diet, it's the (A) mechanism, but if you gain weight naturally more than your set-point weight, it is the (B) mechanism. This is because a calorie-restricted diet can create a situation of intestinal starvation.
It is generally believed in Japan that eating when your metabolism is slowing down makes you gain more weight, but it has already been proven that fat people have a higher basal metabolism[1].
■Japanese Sumo wrestlers are famous for eating a lot of rice and being fat, but I believe that, to put it in extreme terms, they will gain weight because of a mix of (A) and (B).
Although it looks like they eat more and are gaining weight, the mechanism should be the same as that of people who try dieting, but in the end, they gain more weight than before due to the rebound effect.
References：
[1] Dr. Jason Fung, The Obesity Code, 2016, Pages 62.
2016.03.03
The Set-Point Weight; The Precondition Regarding the Rebound Effect
-
Contents
-
- Each person has the ability to maintain their present condition
- Encounter with the set-point theory
1. Each person has the ability to maintain their present condition
First of all, I want to explain the most important point. It's the assumption that each person has the ability to maintain their present condition, also known as preserving current stasis in the body.
I recognize that this is the precondition of everyone regarding weight control.
For example, there are three women:
(A) 48kg･･･who can't gain weight even if she eats a lot.
(B) 58kg･･･who can easily gain two kilos if she lets her guard down and eats a little more.
(C) 85kg･･･ 〃
All through the year, we get thinner when we are busy, and we gain a little fat when we aren’t active and eat a lot. Although everyone repeats the same pattern, even if we don't calculate calories strictly, the body shape of person won't change so easily. Fat people are fat and thin people are thin.
In other words, I believe that each person has a stable weight based on their body's homeostatic functions, which I initially defined as their "base weight."
[Base weight] = The stable weight one returns to after spending 3-5 days relaxing without excessive exercise or work, while consuming calories based on their daily energy needs.
However, despite the lack of official proof or definition, some researchers have already used the concepts of 'set-point weight.' Additionally, my "base weight" can be confused with "baseline weight," which is used in some studies. Therefore, I will use 'set-point weight' or ‘set-point’ for body weight going forward."
In this example, Person A's set-point weight is forty-eight kilograms. However, for Persons B and C, the weights they quickly revert to when they let their guard down and eat a lot—sixty kilograms and eighty-seven kilograms, respectively—can be considered their actual set-point weight. This means that their homeostatic functions are working to maintain those weights.
So, it’s difficult to assume a person’s body and weight condition only with caloric intake.
Consider the example above, that if A continues an intake of 100kcal over her recommended daily caloric intake every day for several months or years, the assumption is that it will accumulate into fat and she will eventually gain weight up to the eighty-kilogram level. This is wrong (She might gain weight but that is a different mechanism).
In general, people who are overweight are more likely to be restricting calories and eating modestly, so their current weight is often lower than their set-point weight. On the other hand, thin people don't have caloric restrictions, so their current weight and their set-point weight are often close. (Temporary overeating may lead to further weight gain beyond the body’s set-point, but I believe this weight gain is temporary and does not alter one’s set- point weight.）
Therefore, ‘thin A’ won't gain weight even if she eats a lot, and B and C will gain weight immediately as soon as they eat a lot.
▽Example of Hozumi Hasegawa, the professional boxer who defended his title ten times as the twenty-sixth Champion of WBC World bantamweight class.
The Bantamweight limit is fifty-three-point-five kilograms(53.5kg). As his body got older, losing weight became harder. For a defending match, he had to lose more than ten kilograms in a month.
But, as soon as the match was over and he started to eat, his weight increased ten kilograms in a few days. The rate of going back to his set-point weight was fast. Those who have tried diets and eat less than usual might have experienced this. Often, it's called the rebound effect.
2. Encounter with the set-point theory
Most of us do not consciously adjust our daily energy intake and expenditure. Nevertheless, an individual's body weight remains relatively stable.
Individual body weight variance is typically only 0.5% over periods of 6 to 10 weeks[1,2] (Khosha and Billewicz 1964). According to cross-sectional data, weight changes over longer periods of time are still modest, and even diabetic individuals display coefficients of body weight variation of only 3.7– 4.6% over a period of five years[1,3] (Goodner and Oglive 1974).
With the global increase in obesity since the 1970’s, these coefficients of body weight variation may no longer be as accurate. However, many people still stay lean (especially in Asia), and, in fact, even those who are overweight or obese manage to maintain their weight, heavy as they may be, for many years[4].
In other words, despite some fluctuations in weight in daily life, there must be an internal regulatory mechanism that works to keep weight and fat within a certain range over the long haul.
■In recent years, the role of homeostatic regulation has been acknowledged, and there is growing evidence that the body employs physiological mechanisms to control energy balance and maintain body weight at a genetically and environmentally determined "set-point."[5]
When a person loses weight, the body substantially lowers energy expenditure, often more than expected based on changes in body composition or the thermic effect of food.
Additionally, it triggers hormonal changes that increase appetite and modifies food preferences through behavioral adaptations, aiming to restore body weight to its set-point range[6].
This feedback mechanism is known to apply not only to weight loss but also to temporary overeating[7].
When I started writing this blog, I had no knowledge of the theory about the body's "set-point," but it almost aligned with what I had always believed. I now believe that understanding the set-point theory is crucial in preventing the spread of obesity and proposing effective weight loss methods.
In particular, to explain the global rise in obesity since the 1970’s, I believe it is essential to understand how (I) genetic and biological factors, and (II) environmental and behavioral factors combine to increase the body’s set-point for weight. I believe my intestinal starvation theory can contribute to this understanding.
For more details, please refer to the articles below.
[Related article]
The Increasingly Important "Set-Point" Theory of Body Weight
References：
[1]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.
[2]KHOSLA T, BILLEWICZ WZ. MEASUREMENT OF CHANGE IN BODY-WEIGHT. Br J Nutr. 1964;18:227-39.
[3]Goodner CJ, Ogilvie JT. Homeostasis of body weight in a diabetes clinic population. Diabetes 1974 Apr;23(4):318-26.
[4] Gary Taubes. 2011. Why we get fat. New York: Anchor books, Page 59.
[5]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.
[6]Ganipisetti VM, Bollimunta P. Obesity and Set-Point Theory. 2023 Apr 25. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2024 Jan–. PMID: 37276312.
[7]Bray GA.The pain of weight gain: self-experimentation with overfeeding. Am J Clin Nutr. 2020 Jan 1;111(1):17-20.