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.

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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.