by Rachel Stuck, RDN
You might be familiar with “calories in, calories out” (or CICO) as an approach to losing weight or maintaining a healthy weight. The idea is that if you eat less food than your body needs you will lose weight, and if you eat more food then your body needs you’ll gain weight. Seems simple enough, right? In reality, simply calculating your daily calories and filling your diet with foods that fit the calorie recommendations might not be the best approach. Is a calorie just a calorie, or does the type of food make a difference? The answer is complicated—thanks to the bacteria living in our gut.
While some evidence supports putting your body in a calorie deficit to cause weight loss, there’s more to the story. Cravings, hunger regulation, and how the body breaks down food to turn it into energy all have bigger roles in weight loss than the number of calories listed on nutrition labels. (1) When we eat, the enzymes in our mouths and digestive tracts break food down into smaller pieces. Only the smallest pieces are absorbed and utilized for energy. The undigested food is removed from the body. How our food interacts with our gut bacteria after a meal is the complicated part.
Gut bacteria play a role in the food we eat, and therefore how well we are able to maintain a healthy body weight. They might be involved in our cravings and the feeling of satisfaction we experiece from eating certain foods, especially those with added fat and sugar. While the exact mechanism is still not understood, experts hypothesize that the variety and diversity of bacteria in the gut influence how the host reacts to certain foods. A particular food may be more satisfying or impact cravings for certain foods between meals. (2) Unfortunately, this is most commonly caused by the “bad bacteria,” which may create stronger cravings for and satisfaction from poor food choices like sweetened beverages and fried food. (2) As if cravings aren’t already difficult to ignore, our gut bacteria add a megaphone to their cries for that afternoon cookie you have been trying to break up with.
Gut bacteria are also involved in how food is digested and the utilization and creation of certain nutrients. It is well known by researchers that intestinal gut bacteria synthesize vitamin B12 and vitamin K2 in the body, but their role in carbohydrate, fat, and protein utilization is showing to be just as important. (3,4)
Because our bodies naturally lack the ability to break down complex fiber, some carbohydrates are hard for us to digest. This is why a cow is able to survive on a diet of grass, but humans are not. Cows have the necessary enzymes, not to mention several stomachs, to aid in the breakdown of complex fibers in grass. For humans, foods like whole grains and vegetable fibers are similar to grass because they contain indigestible fibers that the human digestive system cannot fully process. Although these fibers are indigestible to our enzymes, bacteria in the gut can break down complex fibers for further utilization. As bacteria break down fibers, they produce gases and something called short-chain fatty acids (SCFAs).
Short-chain fatty acids may reduce the risk of disease, and are important for maintaining the intestinal lining of the colon and stimulating leptin production. (5,6,7) Leptin is a hunger hormone that sends a “stop eating” signal to the brain when the stomach is full. This signal, if working properly, will help you avoid that uncomfortable overstuffed feeling. But, when there is an imbalance or a lack of good bacteria in the gut, leptin might not be able to do its job, leading to overeating—and eventually weight gain.
Although it’s not as well researched as carbohydrates, there is also an association between gut bacteria and protein synthesis and fat metabolism. Researchers found that gut bacteria affect protein metabolism by initiating the breakdown of proteins, as well as producing essential amino acids (the building blocks of protein). (8,9) While this doesn’t mean that we need to undermine the importance of dietary protein, it might mean that we need to focus on the health of our gut bacteria to ensure we are getting the most out of our post-workout protein shake.
Similar to protein, the association with gut bacteria and fat is not fully understood. A 2012 study found that the presence of certain microbes, specifically Firmicutes, in the gut stimulates the absorption of fat in zebrafish. (10) While this is not a human study, it does offer insight into how bacteria in the gut affect fat absorption, especially because levels of Firmicutes (in humans) have been found to increase with body mass index (BMI).
The relationship between weight gain and the bacteria in the gut is similar to the chicken and the egg debate. Is weight gain and obesity to blame for an unhealthy gut microbiome, or does our gut microbiome contribute to how quickly we gain weight? The simple answer is that they both affect each other. If the diet disrupts the gut microbiome, the gut microbiome will suffer and therefore be unable to help the body digest and metabolize properly. There is also a possibility that a damaged gut microbiome (due to illness, stress, intolerance, and medications like antibiotics) can weaken the population of gut bacteria and create imbalances, leading to disrupted hunger cues and poor nutrient utilization. (11)
Several mouse studies have reported that transferring the gut bacteria from an obese subject to a lean subject can cause weight gain in the lean subject. (12) Although human studies replicating the methods in these mouse studies have not been conducted, researchers have been able to differentiate between the microbe composition of obese individuals and that of lean individuals. This might mean that if obese individuals work to change the composition of their gut microbiomes, they may also be able to alter their ability to break down fiber-rich foods and be more aware of their fullness and hunger cues. (13)
As you can see, there is still a lot to learn about the relationship and various jobs of bacteria related to metabolism and utilizing foods. But what is unquestionable is the importance of maintaining a lifestyle to support the health and stability of our gut bacteria when setting weight-loss goals or starting a new health plan.
by Lucia Weiler, RD, PHEc
Scientists are discovering more about how our gut health impacts everything from skin conditions to mental health. It’s no surprise that many experts believe that minding our gut health will become an increasingly important health priority in the future.
The good news is that a few simple changes to what you eat and how active you are can help improve your gut health.
Three simple tips to take care of your gut are:
Fluids aid healthy digestion. Drink fluids throughout the day to keep you well hydrated. On average, most people get about 80% of their fluid intake form drinking water and other beverages, and the other 20% from foods.
General recommendations are to aim for:
Moving your body helps keep the food moving through your gut. Be active for healthy digestion.
US HHS physical activity guidelines recommend adults engage in at least 150 minutes of physical activity a week.
There is evidence to show that a few brisk 10-minute walks each day bring health benefits. Consider taking short walks during the day and use the stairs instead of the elevator to stay active.
By Lillian So Chan
Intestinal permeability, also known as “leaky gut,” has been linked to many inflammatory and autoimmune diseases. Why is a healthy gut barrier important in protecting against these diseases?
All body surfaces, such as skin and the gut wall, are lined by layers of protective epithelial cells, which are connected by cell-cell junctions. These junctions serve three main purposes:
Healthy barrier function is crucial in maintaining a balanced state of homeostasis. Breaking or even slightly disturbing these barrier layers can lead to serious health consequences, including inflammation and infection.
Our gut wall epithelial layers are constantly challenged by foreign substances that pass through the intestine, such as food and drink, drugs, microorganisms, pathogens, and toxins.
A healthy gut environment is preserved because the tight junctions in the mucus gut wall effectively and selectively control what passes through the epithelial layers, keeping pathogens and toxins out while allowing nutrients to pass through.
The gut epithelial barrier can become permeable as a result of genetic predisposition, gut pathogens, and hyperglycemia (high blood glucose concentration). For example, IBD (inflammatory bowel disease, such as Crohn’s) involves both environmental factors (smoking, diet, exposure to pollutants) and a genetic predisposition involving mutations in about 100 genes associated with epithelial cells, barrier functions, and immunity.
A recent study of experimental depletion of one IBD susceptibility gene has led to decreased gut barrier function and promoted gut inflammation and IBD.
In another study, researchers demonstrated how pathogenic bacteria can induce gut barrier defects, translocate to lymph nodes and liver via blood circulation, and trigger systemic autoimmune disease lupus erythematosus.
Chronic high blood glucose concentration, which is common in obesity, diabetes, and other metabolic syndromes, also disrupts the gut barrier, leading to gut and system inflammation and infections.
Researchers reported that chronic hyperglycemia affects barrier functions through metabolic and gene transcriptional reprogramming in the gut epithelial cells, which is regulated by a glucose transporter. This results in increased translocation of pathogenic bacteria and bacterial parts, causing inflammation in the gut and other parts of the body.
Unrestricted passage of pathogens and cells across the epithelial layers occurs when the integrity of the cell-cell junctions is disrupted. By allowing the passing of antigens and pathogens into epithelial layers and blood circulation, defective and “leaky gut” barrier can both initiate and maintain inflammation and spread infection.
Buckley, A. and Turner, J R, “Cell Biology of Tight Junction Barrier Regulation and Mucosal Disease,” Cold Spring Harbor Perspective in Biology, U.S. National Library of Medicine, 2 Jan. 2018, https://www.ncbi.nlm.nih.gov/pubmed/28507021.
Citi, S. “Intestinal barriers protect against disease,” Science, 9 March 2018, https://science.sciencemag.org/content/359/6380/1097.
Manfredo Vieira, S, et al. “Translocation of a gut pathobiont drives autoimmunity in mice and humans,” Science, 09 Mar 2018, https://science.sciencemag.org/content/359/6380/1156.
Mohanan, V, et al. “C1orf106 is a colitis risk gene that regulates stability of epithelial adherens junctions.” Science, U.S. National Library of Medicine, 9 Mar. 2018, https://www.ncbi.nlm.nih.gov/pubmed/29420262.
Thaiss C A, et al. “Hyperglycemia drives intestinal barrier dysfunction and risk for enteric infection,” Science, 23 Mar. 2018, https://science.sciencemag.org/content/359/6382/1376.
Luissint A C, et al. “Inflammation and the Intestinal Barrier: Leukocyte-Epithelial Cell Interactions, Cell Junction Remodeling, and Mucosal Repair,” Gastroenterology, U.S. National Library of Medicine, Oct. 2016, https://www.ncbi.nlm.nih.gov/pubmed/27436072.
Khor, B, et al. “Genetics and pathogenesis of inflammatory bowel disease,” Nature, U.S. National Library of Medicine, 15 June 2011, https://www.ncbi.nlm.nih.gov/pubmed/21677747.
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