Consuming Less Calories Than Spending Them. Is That The Whole Story?

This article explores the notion that the simple equation of eating fewer calories than the amount you spend each day is the only determinant when it comes to weight loss or gain.

If you’ve ever read a popular fitness article that has talked about how to lose or gain weight, then there’s a good chance you’ve stumbled across a pretty common-sense idea that the amount of calories which you take in should be lower than the amount of calories you spend each day. This means that, for example, if you consume around 2000 calories and spend 2200 calories, you should be maintaining or slightly losing your weight.

This idea has been (and is being) promoted by a great deal of internet fitness and health gurus. However, there’s another side to this story that is being increasingly acknowledged as an important factor. And no, neither genetics nor environment are the icing on the cake about to be mentioned. While both represent a vital aspect that can’t be neglected, it’s food digestion and our microbiota that also play a key role in obesity and determining how you will react to the food you are eating.

A word or two about genetics

Before I continue, I have to clear up two things about genetics. Some people actually seem to be more susceptible to being in a higher weight range and thus becoming overweight and obese, as studies have observed a heritability estimate between 40 to 70% [1]. However, this does not in any way imply genetic determinism, as some people might smugly conclude.

Explained in layman’s terms – if you have been brought up in a family that has always been overweight or obese that doesn’t necessarily mean that you will be like that as well. It does, however, raise the probability of you becoming overweight/obese. Moreover, newer studies explored the relationship between specific genetic components and measures of body composition (e.g. amount of fat tissue), they’ve observed that genetics explain only a low proportion of the differences found in BMI.

Let’s rephrase this in a different way. You are the researcher and take a random group of people from a certain environment and calculate their BMIs and use that as your measure for obesity (which isn’t necessarily the best way of measuring obesity to be honest). Then you take their genetic data and test to what extent do the differences in their genetic data account for differences in their BMIs. Using this procedure only a low percentage of BMI differences would be explained by differences in the genetic makeup of people [2].

Sorry for the digression. I wanted to make it clear that while genetics do affect your chances of becoming obese and play a role in this story, they are by far not the only factor to take in account for.

As mentioned before, however, the microbiome found in your gut is a novice in this field, relatively to genetics and other factors, and greatly affects how the food you consumed gets digested. Human evidence so far is somewhat sparse (compared to animal trials) as of yet. On the other hand, more and more knowledge from this field seems to indicate that we have been jumping to quick conclusions in the past when talking about the lean = calories in < calories out equation. 

How important is the gut, anyway?

After we eat food it immediately starts breaking down. Certain nutrients already get broken down while food is being chewed. Food digestion is rather complex topic and still a topic of ongoing research. Having said that, we must be aware that between ten trillion to 100 trillion (10˘14) microorganisms populate adult intestines. The majority of these organisms can be found in our colon. Furthermore, most of these living creatures are bacteria necessary for food to be digested properly. Two major bacterial phyla in humans are the Firmicutes (60-80%) and the Bacteroidetes (20-40%) [3].

Naming these two phyla is important because they seem to be differently present in obese people compared to lean people [3]. An increase in the Firmicutes and decrease in the Bacteroidetes phylum seems to be more prevalent in people who are obese [3]. Moreover, people with low bacterial richness seem to have a higher prevalence of insulin resistance, more inflammation responses, are more likely to be obese, and have an increased amount of cholesterol, not that there is anything necessarily wrong with the latter [4]. They also tend to be associated with a better absorption rate of calories, which means that someone would actually receive more calories from the same meal than someone else, solely due to their microbiota. Moreover, a change in how these calories are actually used up in the body can also be present when certain conditions in the microbiota are satisfied [4]. With some even proposing shifts in the microbiome as a possible cause for obesity [5].

To talk about the mechanisms in detail would be a whole story for itself. Dotted down shortly;

How the food is being digested is changed in the presence of certain phyla of bacteria, or by suppression of a certain biochemical factor, which through a chain of events, leads to an increased deposition of triglycerides in fat cells.

Studies on mice

This field of research seems to be home to some interesting studies, at least compared to traditional nutritional studies. One study used mice without a microbiota. These mice had much less fat compared to normal mice, despite the former eating more. In a later step of this study, microbiota from obese mice fed with a western diet were transferred to the microbiota-free mice. The latter then observed a significant increase in obesity, compared to mice with microbiota transplants from lean mice who were fed with a lean low-fat diet, where these differences weren’t nearly as high. It also has to be pointed out that both groups were receiving the same amount of food with the same starting weight. The only difference in this study were the previously mentioned microbiotas. And while it is true that these were only mice and that our digestive system is probably quite different, it does pose a question, how this would play out in humans studies, were it to be used [6].

In another study, researchers transferred human feces into mice and then fed them with either the Western diet or a low-fat and plant-rich diet for two weeks. After this protocol, they transferred the acquired microbiota from these mice in microbiota-free mice. The poor guys from this new group who received the microbiota from mice which ate in line with a typical Western diet, gained weight much quicker compared to the other group. All of this happened after only two weeks. [7]

Finally, there was another interesting study where mice were put in a co-housing setting. This study showed that the microbiota of lean mice (one group of mice was lean and the other was obese) was more invasive than those of obese mice. Their procedure involved infecting mice without microbiota with either microbiota of obese or lean mice. Following this step, the mice without microbiota either lost (lean microbiota) or gained (obese microbiota) weight. When these mice were co-housed, the newly obese mice (obese microbiota) didn’t gain any new weight due to invaders from the microbiota of the newly lean mice (lean microbiota). This basically tells us that certain members of the Bacteroidetes family seem to be more aggressive when compared to different members of the microbiota of obese mice. [8]

Your diet in general is one of the most relevant key players that shapes the microbial diversity of your gut [9, 10, 11]. Thus, the prevalence of certain kinds of bacteria in our microbiota greatly alters with a change in food patterns. This doesn’t come as a particular surprise. Changes in the gut microbiota could reflect a distant evolutionary past where selective pressures urged into existence a community of bacteria in our microbiota that could rapidly adapt to changes in eating patterns, considering food scarcity, meat availability, and other factors. [12]

Some human evidence

One interesting aspect when talking about the gut is that newborns acquire their first microbiota from their mothers. This happens at the moment of birth and as such it is not surprising that newly born babies share a similar gut microbiome, especially when we consider their main food source for the next couple of months.

Having acquired their mother’s microbiota, babies (and people later in life) will have them changed.  Namely, the microbiota is highly variable with different factors such as age, sex, family, diet, and even geography, affecting it [13]. Furthermore, we can modulate it with either prebiotics, probiotics, and antibiotics as well.

The latter three represent a group of different products that will probably become increasingly popular in the future and will be used for different purposes, compared to their current usage and level of popularity. Prebiotics are food ingredients that stimulate the growth of a limited number of microbial species in our gut. Some mice studies have shown promising applications where the administration of oligofructose to mice, which were fed a diet very high in fat, normalized the inflammatory response which is usually associated with a high-fat diet. Continuing this line of thought, antibiotics (e.g. glycopeptide and penicillin) have been used for more than 60 years to induce weight gain in animals. According to one study, newborn children exposed to antibiotics during the first six months of their lives actually exhibited a higher body mass consistently throughout this period [15]. This relationship, however, hasn’t been completely researched after this time period as of yet.

Concluding remarks

Strong experimental evidence about the effects of the microbiome in animal studies where rodents (mice in this case) are being used, cannot serve as a point of reference for causality of the human gut. This should be obvious. In order for us to be able to say this, we would need actual evidence from human studies with similar levels of the conclusiveness of their results. Namely, dramatic differences in genetic susceptibility can sometimes exist in different animals (e.g. mice), which, when translated to human studies, only exhibit minor or no differences [14].

About Author

Sebastijan Veselic

BSc in Psychology, currently doing a MSc in Cognitive science. Pursuing and interested in many academic and scientific disciplines and topics, as well as some less so. These include, but are not limited to, cute cats on the internet.

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