A relatively effective strategy of gut bacteria is to disrupt the regulatory systems by which our bodies regulate hunger and satiety. 

Our bodily reactions cause us to eat something when our blood sugar drops and our energy reserves dwindle. 

At the same time, our bodily systems stop our desire to eat before we overeat. 

This control of hunger and satiety occurs through a combination of receptors in the stomach, a series of hormones such as leptin and ghrelin, and other peptide messengers. 

And it is precisely these satiety and hunger messengers that many gut microbes target! 

In fact, several scientific studies have shown that many of our gut microbes can produce their own peptides, which are similar to the body's own satiety or hunger messengers.

This allows them to attach themselves to the corresponding receptors and make us believe, for example, that we are far from satiated and full.

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A study by French researchers demonstrated the tremendous and far-reaching influence of gut flora in this area. 

They found that gut bacteria of the species Escherichia coli significantly change their behavior when we eat a meal!

At first, they eagerly devour the nutrients we give them, and they multiply rapidly. 

But after about 20 minutes, these particular bacteria suddenly stop their production of cellular degrading agents. And they suddenly start producing specific messenger substances that our bodies usually use to indicate satiety and feeling full. 

At first glance, this seems counterproductive, doesn't it? Why would gut bacteria voluntarily cut off their supply of nutrients by signaling a feeling of satiety? 

Well, this can be explained by survival instincts and maintaining balance in the gut.

French researchers found that this may have benefits for certain types of bacteria in our gut. 

Once these bacteria have established themselves in our guts, it is best for them if the balance between species remains as stable as possible. Therefore, it is not advantageous should an unwelcome competitor suddenly gain the upper hand. 

In other words, the intestinal bacteria Escherichia coli ensures that it receives sufficient nutrients and avoids nutritional excesses that would only benefit its competitors (other gut bacteria).

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Our desire for sweetness could also be related to the intestinal germ Escherichia coli. 

This gut bacterium produces sugar compounds in its cell wall (so-called lipopolysaccharides or LPS) that decrease our cravings for sweet foods!

Research with mice found that these sugar compounds appear to have a far-reaching influence on our desire for sweets. 

When the researchers administered the mice a strong dose of the bacterial lipopolysaccharides, their organisms responded promptly.

After about fifteen hours, the scientists detected increased levels of the satiety hormone leptin in the rodents' blood. 

And within a week, the number of taste receptors on the tongue responding to sweetness had also decreased. 

So, as a result, the mice simply had less appetite for sweet foods. 

It is unclear why the cell wall sugars of Escherichia coli have this effect. 

One explanation here could also be competitive avoidance. In fact, this gut bacteria may require less sugar than other gut bacteria. 

Inhibiting cravings for sweet foods ensures that sugar-hungry competitors (other gut bacteria) receive less supply of sugar and thus thrive less.

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An estimated 50% of the happiness and addiction hormone dopamine comes not from the brain but from our gut. 

The substance dopamine is produced there by various intestinal bacteria such as Escherichia coli, Bacillus cereus, Proteus vulgaris, and even by the pathogenic germ Staphylococcus aureus.

The concentrations of dopamine in cultures of these types of gut bacteria are 10 to 100 times higher than the concentrations of dopamine in human blood.

The neurotransmitter dopamine plays a crucial role in our reward system and in possible addictions:

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About 95% of the human body's serotonin (a happiness hormone) is located in the gastrointestinal tract, and the rest (5%) is in the brain. 

In other words, virtually all the serotonin in the blood comes from our gut and digestive system.

Our intestinal bacteria are thus highly involved in producing the happiness hormone serotonin.

For example, the lactic acid bacterium Bacillus infantis produces the serotonin precursor tryptophan, a substance also found in happiness-inducing chocolate. 

Good to know: Various bacteria stimulate the intestinal wall cells to produce serotonin. And serotonin is released from the gut when the enteric nerves are stimulated.

Conclusion: When our gut bacteria are absent, reduced in number, or if there is an imbalance (called dysbiosis), our serotonin levels in our body drop, and we feel less happy and a bit depressed. 

This then prompts us to eat comfort foods like chocolate or other sweets.

So healthy and balanced gut flora is crucial to feeling happy and not depressed!

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Our gut microbes can also influence our feelings of anxiety, as experiments with mice have shown.

Research showed that calm mice implanted with the gut flora of particularly anxious mice also exhibited more anxious behavior. 

Conversely, fearful, anxious animals could also be made braver via transplantation of gut flora from calm mice without anxiety symptoms. 

Certain lactic acid bacteria dampened the release of stress hormones and made their hosts braver.

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In more extreme cases, the bacteria of our digestive tract do not shy away from provoking pain either!

Several scientific studies show that crying children who cry a lot in the first few months and often suffer from colic show typical changes in their gut flora. 

These studies have shown that the inconsolable crying of newborns with colic is associated with changes in the gut microbiota, including:

It was also noted that colic in infants leads to increased administration of nutrition (milk) which can result in accelerated weight gain.

The researchers speculate that the influential power of our gut flora thus also plays a role in colic in newborns. 

A baby who cries sends a clear signal to the parents, who then pay more care and attention to the baby and will most likely also feed it more.

Put another way, colic of the intestines in newborns can be triggered by our gut bacteria to increase the administration of nutrition. 

This gives the baby more nutrition. These nutrients then provide the gut with the bacteria they so desperately desire.

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Communication between our brain and our gut happens through the vagus nerve. 

This tenth cranial nerve connects the approximately 100 million nerve cells in the digestive system to the base of our brain. Thus, it is a central communication link between our brain and the gastrointestinal system. 

Our digestive tract uses this vagus nerve to signal, among other things, when the stomach is full and we are satiated.

In addition, our internal organs also receive specific instructions from this vagus nerve.

Good to know: Studies on mice have shown that blockage of the vagus nerve leads to a loss of appetite and drastic weight loss.

By the way, the reverse is also possible! Research on rats showed that the vagus nerve can stimulate appetite and cause one to keep eating even when the stomach is already full. 

This is the case when the vagus nerve is stimulated by certain signaling substances, such as the substance noradrenaline.

Our gut bacteria have the power to affect communication between our brain and nervous system.

This is because the nerve cells of the digestive tract, which are connected to the vagus nerve, are also in contact with our intestinal system through numerous receptors on the cell surface. 

These contact points respond, for example, to signaling substances produced during digestion but also to the presence of certain bacteria and their waste products in the intestines. 

In other words, gut bacteria can disrupt vagus nerve signals (and eating behavior).

Numerous commensal and pathogenic bacteria in our intestinal system produce peptides strikingly similar to leptin, ghrelin, peptide YY, and neuropeptide Y. These are mammalian hormones that regulate the sense of satiety and hunger.

For example, certain studies show that some gut bacteria produce messenger substances that activate the vagus nerve and thus induce more desire for food.

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