In this article, I will discuss the central theme of this blog: why a state I call “intestinal starvation” can lead to weight gain. This idea is based on my own personal experience, which I have organized and interpreted from a physiological perspective and presented here as a hypothesis. 

When I entered university, my body weight had dropped into the 30-kilogram range. Even when I increased my food intake, my weight barely increased.

However, at one point, despite eating relatively little, my body weight suddenly increased by about five kilograms over the course of four to five days. This increase involved not only body fat but also muscle mass. Because I was underweight at the time, I strongly felt that this rapid weight gain was not a coincidence but rather the result of a distinct physiological change.

　　　
The idea presented in this article may seem counterintuitive to many readers. Nevertheless, for those who feel that weight gain cannot be fully explained by calorie balance alone, I hope this perspective offers a useful way of thinking. 

The idea that humans have evolved to store fat more efficiently in preparation for temporary food shortages or famine is one that most researchers studying obesity have likely considered at least once. However, this simple hypothesis has historically been treated with caution—or even skepticism—within the scientific community[1].

Underlying this skepticism is the common observation that people with obesity tend to have a higher energy intake, whereas individuals experiencing severe famine, such as refugees in parts of Africa, are markedly underweight due to malnutrition. From this perspective , some may raise the following counterargument: 

“If hunger leads to weight gain, then refugees in Africa should be overweight.”　

This condition can be regarded as a modern form of hunger that began to emerge primarily in developed countries around the 1970s and has since been spreading to many parts of the world.

In developed countries, diets have increasingly shifted toward the routine consumption of high-calorie, highly processed foods. In particular, when a diet is consistently dominated by rapidly digestible refined carbohydrates and (ultra-)processed foods, undigested matter does not remain in the intestinal tract for extended periods, which may create conditions that make intestinal starvation more likely to occur. 

　　　
In fact, obesity has become a serious problem even among some low-income populations worldwide[2]. What is commonly observed in these settings is not simply excessive caloric intake or high sugar consumption, but rather a poorly balanced diet heavily reliant on inexpensive refined carbohydrates and highly processed foods. 

I propose that one of the fundamental problems underlying obesity is that the body-weight set point is elevated. I further suggest that this upward shift in the set point may involve adaptive responses that are triggered when the body, in some form, perceives a state of starvation. 

In this section, I will explain the concept of intestinal starvation—one form of perceived starvation—and the process by which it may lead to weight gain, using an analogy from plant biology. (Note that the discussion here is limited to intestinal starvation and does not attempt to explain other known or unknown mechanisms involved in weight gain.)

Having said that, it should be emphasized that this does not imply that the protrusions on the intestinal folds—the villi—physically elongate. What I am proposing is not a change in the intestinal structure or function itself, but rather more superficial changes that influence absorptive efficiency.

As a result, the surface area available for contact with nutrients increases, and the effective absorptive efficiency may rise in a way that is not merely transient  but can persist thereafter.

If such a change in absorptive efficiency occurs, regardless of whether the weight gain is 0.3 kg or 3 kg, the body may transition to a state of energy homeostasis at a higher body weight within a relatively short period of time. Unlike weight gain caused by overeating, this would imply an upward shift in the body-weight set point itself.

This hypothesis may help explain, at least in part, why individuals with obesity—despite having substantial energy stores in the form of body fat—can exhibit metabolic resistance to caloric restriction[3].

【Related articles】The Increasingly Important "Set-Point" Theory of Body Weight

     
    
Taken together, I propose that one fundamental difference between obese and lean individuals may lie in how efficiently ingested food is digested and absorbed.

In Japan, people with obesity sometimes describe themselves as “having a body that gains weight even from drinking water.” Of course, drinking water alone does not lead to weight gain. However, this expression may intuitively reflect a state in which nutrient absorption efficiency is elevated in individuals with obesity.

Weight gain reflecting an elevation of the body-weight set point means, from the perspective of energy homeostasis, that the balance point at which energy intake and expenditure are matched has shifted to a higher level. In other words, a more positive energy balance becomes easier to maintain, making weight loss increasingly difficult.

Even if body weight temporarily decreases through caloric restriction, it is highly likely to rebound once the original diet is resumed.

Moreover, repeated cycles of dietary restriction may raise concerns about a gradual increase in body weight over the long term. With extreme dietary restriction, prolonged periods of hunger are common, which may make intestinal starvation more likely to occur during this process and, in turn, further elevate the set point for body weight.
       

However, these findings are primarily observational and do not demonstrate that the increase in body fat itself—or the associated increase in body weight load—directly stimulates muscle growth. 

In this hypothesis, increases in muscle mass are not attributed to mechanical loading from higher body weight. Rather, they are considered to occur alongside increases in body fat to some extent as a secondary change associated with alterations in nutritional status and the metabolic environment.
          

An increase in overall nutrient uptake shifts the body toward a more positive energy balance, while simultaneously allowing the following phenomena to occur. Since digestive enzymes and many hormones are composed of proteins (amino acids), improvements in nutritional status may lead to changes in digestive function and appetite regulation mechanisms.

In contrast, in an excessively lean state, reduced absorptive efficiency may limit the body’s ability to effectively utilize ingested nutrients, such as protein. As a result, decreases in the muscle mass that supports internal organs, together with reduced secretion of digestive enzymes, can further impair the capacity to digest and absorb food efficiently.

This creates a vicious cycle in which a negative energy balance is more easily maintained. Consequently, even when caloric intake is increased, body weight may not increase easily.

【Related articles】
After Gaining Weight, We Eat Too Much and Do Less Exercise

References

[1]Speakman JR, Elmquist JK. Obesity: an evolutionary context. Life Metab. 2022 Apr 29;1(1):10-24. 

[2]Gary Taubes. Why We Get Fat. New York: Anchor Books. 2011. Pages 15-32.

[3]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.

[4]Kyle UG et al. Fat-free and fat mass percentiles in 5225 healthy subjects aged 15 to 98 years. Nutrition. 2001 Jul-Aug;17(7-8):534-41. 

[5]Heymsfield SB et al. Human body composition: advances in models and methods. Annu Rev Nutr. 1997;17:527-58. 

[6] Janssen I et al. Skeletal muscle mass and distribution in 468 men and women aged 18-88 yr. J Appl Physiol (1985). 2000 Jul;89(1):81-8. 

[7]Fornari R et al. Lean mass in obese adult subjects correlates with higher levels of vitamin D, insulin sensitivity and lower inflammation. J Endocrinol Invest. 2015 Mar;38(3):367-72. 
        

This time, I would like to discuss three key factors－plus one additional factor－that may contribute to the occurrence of what I call “intestinal starvation."

【Related article】

In addition to these, many other factors may also be indirectly involved in the recent increase in obesity. However, it is not always clear how multiple factors combine to drive weight gain across the population as a whole.

I propose that one possible explanation involves a mechanism I refer to as “intestinal starvation.”

This condition is unlikely to occur due to a single factor alone, but is more likely to arise when the three factors (+1) described below overlap at the same time. For this reason, it may help explain how everyday eating habits and lifestyle patterns—when considered together—can lead to weight gain.

This idea is consistent with the view that consuming low-GI (glycemic index) foods and minimally processed foods help prevent obesity.

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 small amounts.

Eating speed, how well you chew, and how much fluid you drink during meals may also influence this factor.

【Related article】
The Dilution Effect/ Pushing Out Effect of Carbohydrates

Eating Fat/Oil Can be a Deterrent to Gaining Weight (3 Perspectives Regarding Fat)

Many people report gaining weight due to lifestyle changes such as skipping breakfast or eating dinner late at night. Behind this type of weight gain caused by irregular daily routines lies the issue of long gaps between meals—in other words, enduring hunger for extended periods of time.

Eating late at night does not always lead to weight gain by itself. If dinner has to be late, having a small snack in the early evening—such as nuts, milk, or a sandwich—can help prevent intestinal starvation by avoiding prolonged hunger.

Even when eating the same meals, people with strong stomachs and high digestive capacity may be more likely to experience intestinal starvation than those whose digestion is slower. In today’s society, where energy-dense foods are common, the ability to digest protein and fat may have a particularly strong influence on whether intestinal starvation occurs.

On the other hand, people with sensitive stomachs or conditions such as gastroptosis may find it difficult to fully digest all ingested food in the first place.

If genetic factors contribute to obesity, then the secretion of enzymes and hormones that affect digestive capacity and appetite, as well as the sensitivity of their receptors, is likely to play a major role. Of course, these factors can also change due to environmental and lifestyle influences.
      

In addition to the three factors, I added one more important element as “+1,” which can be explained by “continuity.”

What this means is that not only the meal you have just finished, but also your previous meal and the meals before that can influence whether intestinal starvation occurs or not. 

The reason is that the intestines are very long—about 7 to 8 meters in total (with the small intestine alone being about 6 meters)—and it takes, on average, more than ten hours for food to pass through the entire intestinal tract. Because intestinal starvation is judged across the whole intestine (or possibly only the small intestine), it is influenced not only by a single meal, but also by your previous meal and the meals before that.

This is also the flip side of why eating well-balanced meals three times a day is thought to help prevent obesity: it helps ensure that the intestines are continuously exposed to food of adequate quality, reducing the chance that the body interprets the situation as “starvation.” 

From an evolutionary biology perspective, humans and many other animals are thought to have developed mechanisms to cope with intermittent food shortages over long periods of evolution. Because periods of abundant food were limited, the ability to store energy in the liver, skeletal muscles, and adipose tissue was likely favored by natural selection.

From this perspective, obesity can be understood not merely as a consequence of overeating, but as a state that arises as a result of adaptive physiological responses, in which the body attempts to store energy when it perceives a risk of starvation.

　
The concept of “intestinal starvation” adds a new perspective to the discussion of how our bodies perceive a lack of food, moving beyond the traditional focus on energy intake alone.

【Related articles】
Why Does the Body Perceive That It Is More Starved than in the Past?

Note 1: It is unclear whether intestinal starvation is sensed throughout the entire gut or only in the small intestine, which is sometimes referred to as the "second brain."

Note 2: Because dietary fats generally require more time for digestion and gastric emptying, they may, in some individuals, help prevent the onset of intestinal starvation. However, there is substantial individual variability in the capacity to digest fats, and when fats are consumed together with refined carbohydrates, this suppressive effect may not be sufficiently achieved.

【Related articles】Eating Fat/Oil Can be a Deterrent to Gaining Weight

Even if you consume a large amount of food, a diet composed mostly of refined carbohydrates and other easily digestible items (including certain protein sources and small amounts of fat)—combined with long gaps between meals, such as eating only twice a day—can induce an intestinal starvation state or a condition very close to it.

Even when overall food intake is small, a diet composed mainly of easily digestible foods such as refined carbohydrates and certain protein sources (e.g., ultra-processed foods such as simple burgers or sandwiches, or instant noodles) may still trigger intestinal starvation. 

Due to recent dieting trends, many people try to keep breakfast or lunch light in an effort to lose weight, but this approach may end up being counterproductive in the long run.

In contrast, when you eat a balanced diet including fiber-rich vegetables, and minimally processed foods three times a day, some fraction of undigested matter remains in the intestinal tract continuously throughout the day, making it less likely for intestinal starvation to be induced.

Since human genes are unlikely to change dramatically over just a few decades, changes in lifestyle and food environments since the 1970s are likely to have had a substantial impact on the recent global rise in obesity[3].

Strictly speaking, four factors (see Note 3) need to overlap for intestinal starvation to be triggered, which may explain why obesity is more likely to occur at the intersection of multiple factors, including genetic, environmental, and physiological factors.

Note3: The four factors are “what you eat,” duration of hunger, digestive ability, and continuity.

Genetic traits related to intestinal starvation include the secretion capacity and receptor sensitivity of enzymes and hormones that regulate digestion and appetite. In particular, differences in genetic background—reflecting both population-level and individual variability—that enable more rapid digestion of proteins and fats may influence the occurrence of intestinal starvation.

Of course, these biological traits may also change as a result of acquired conditions, such as obesity or gastric reduction surgery performed for weight loss.

Since the 1970s, one of the most notable environmental changes, I believe, has not merely been the increase in energy-dense foods, but rather the rise in easily digestible foods resulting from industrialized food production. Examples include refined carbohydrates, certain protein sources, and ultra-processed foods.

In vegetables and grains, the less digestible parts have been removed (e.g. refined grains), and some are now mashed or strained (e.g. mashed potatoes and potage soups). Meat and fish are often minced or ground, making them easier to digest.

<Lifestyle>

Intestinal starvation is related not only to what people eat but also to "how they eat."

Since the 1970s, changes in lifestyle have been accompanied by dramatic shifts in eating habits. In Japan, for example, the traditional rice-based breakfast has gradually been replaced by a Western-style breakfast consisting of toast, coffee, and fried (or boiled) eggs, etc.

    
In addition, many people now tend to eat light breakfasts and lunches, while consuming the majority of their daily calories at dinner. Such eating patterns may promote intestinal starvation, because our intestines are about seven to eight meters long, and all ingested food may be completely digested while traveling through the intestinal tract. 

Intestinal starvation represents an adaptive physiological response related to intestinal processing and hormonal secretion, and may prove that people who eat a balanced diet every day are likely to be less prone to weight gain. 

Although intestinal starvation may not be directly associated with the gut microbiota, the types of foods consumed have a significant impact on the intestinal environment.

Individuals who eat a wide variety of foods in a well-balanced manner are less likely to induce intestinal starvation, which may indirectly suggest a relationship that those with a healthier gut microbiota are less susceptible to obesity.

<References>

[1]Flores-Dorantes MT, Díaz-López YE, Gutiérrez-Aguilar R. Environment and Gene Association With Obesity and Their Impact on Neurodegenerative and Neurodevelopmental Diseases. Front Neurosci. 2020 Aug 28;14:863. 

[2]Khan MJ et al. Role of Gut Microbiota in the Aetiology of Obesity: Proposed Mechanisms and Review of the Literature. J Obes. 2016;2016:7353642. 

[3] Jason Fung. The Obesity Code. Greystone Books, 2016, Page 21-2.