How Bacteria Influence Food Cravings and Weight.
By Renata Trister DO
Studies on the gut-brain axis suggest that the bacteria in your gut could strongly influence your food choices.
97 percent of women and 68 percent of men report having cravings for foods they are trying to avoid. Cravings are thought to be a combination of psychological and physiological factors and are a major barrier to weight loss and health.
Recent evidence suggests that gut microbes might play a significant role in influencing cravings. Given that microbes evolved with us and depend on the foods we eat for survival, it follows that these organisms influence our eating preferences to improve their own chances of survival.
The enteric nervous system (found in the gut) is connected to the central nervous system (the brain and spinal cord) via the gut-brain axis. This term is more of a description of the interrelationship between the intestines and the brain. The two are connected by the circulatory system and the lymphatic system.
The enteric nervous system is also connected directly to the brainstem via the vagus nerve. The vagus nerve acts as a superhighway for communication between the gut and the brain and is the longest nerve cell in the autonomic (unconsciously controlled) nervous system. Studies on the vagus nerve found that vagal blockade can lead to marked weight loss, while vagal stimulation triggers excessive eating in rats.
Different microbes have different food preferences. Bacteroidetes have a preference for particular fats; Prevotella likes carbohydrates; Bifidobacteria prefer dietary fiber.
All of these microbes require these foods to grow and reproduce. Studies have shown that a low concentration of nutrients triggers increased virulence in many microbes as a survival mechanism. Virulence is the ability of a particular microbe to cause damage to the host. For many human-associated microbes, the production of virulence toxins is altered by the detection of simple sugars and other nutrients.
When bacteria metabolize foods, they produce various metabolites. Microbial metabolites include many neuroactive agents that are small enough to penetrate the blood-brain barrier. Studies on chocolate cravings have found that even when eating identical diets, people who crave chocolate have different microbial breakdown products in their urine than people who do not crave chocolate.
Short-chain fatty acids (SCFAs), metabolites produced from the fermentation of dietary fiber in the GI tract, are able to modify the expression of genes in cells throughout the body, including brain cells.
Other microbially derived molecules are able to mimic hunger or satiety hormones. Your body normally secretes hormones like ghrelin (to stimulate your appetite) and peptide YY (to signal that you are full). Many gut bacteria are able to manufacture small peptides that mimic these hormones. Helicobacter pylori is a great example. Eradication of Helicobacter pylori is accompanied by an array of metabolic and hormonal changes in the host. Weight gain following H. pylori eradication is a poorly understood phenomenon and probably results from an interaction between multiple factors. Ghrelin, a peptide hormone secreted by the stomach, is involved in the regulation of food intake and appetite and may account for some of these changes. Studies have demonstrated that H. pylori infection suppresses circulating ghrelin levels. Gastric expression of ghrelin, also suppressed by H. pylori, clearly increases following eradication. Weight gain following H. pylori eradication may be attributable to changes in plasma and gastric ghrelin. As wide use of antibiotics continues, many people now no longer have Helicobacter pylori present in their microbiome.
Microbes therefore can interfere with human appetite by either directly mimicking satiety and hunger hormones or indirectly inducing this autoimmune response.
Bacteria also produce neurotransmitters. More than 50 percent of your body’s dopamine and 90 percent of your body’s serotonin are produced in your gut, along with about 30 other neurotransmitters. These molecules are critical for signaling between cells of the nervous system. Dopamine and serotonin are involved in the regulation of eating behaviors.
An increasing number of studies are showing connections between the gut microbiota with stress, depression and anxiety. In 2004, an experiment showed that mice raised in sterile conditions with no gut microbes had an exaggerated hypothalamic–pituitary–adrenal (HPA) axis response to stress. The effect was reversed by colonization with Bifidobacterium species. Furthermore, a study published in 2012 found that germ-free mice prefer sweets and have a greater number of sweet taste receptors.
Microbial diversity may determine how easily host behavior can be changed. Obese individuals tend to have lower microbial diversity than individuals of a healthy weight. This may partially explain why people who are overweight tend to have difficulty with cravings.
To support your microbiome you may try the following:
Several strains of Bifidobacterium and Lactobacillus have been shown to improve anxiety- and depression-like eating behaviors.
Prebiotics are foods that selectively feed certain beneficial microbes. Try fermentable fiber found in foods like plantains, onions, garlic, and sweet potatoes. Supplementing with inulin or resistant starch is also an option.
Eating a clean diet rich in green vegetables, healthy proteins and fats supports the health of both your body and the microbiome.