Previously I discussed the relation of the human microbiome to malnutrition. Furthermore, in the previously discussed study, the twin that developed kwashiorkor had an underdeveloped microbiome for their age (3 years). Microbiomes, like many parts of our body, continue to grow and develop as we age. So, how does this developmental process of the microbiome? Well, although babies are born with personal assortment of microbes recieved from their mom, it takes a couple of years for the micrbiome to fully form. A recent study suggests that the immune system of babies are actively suppressed in order to further develop this microbiome (Elahi, et al, 2013). Previously, the lack of immune defense in infants has believed to have been related to immature immune cells. Nevertheless, this particular study found another possible explanation. Researchers discovered that blood cells found in infant umbilical cords (called CD71 cells) actually act as an immunosuppressive. Researchers hypothesized that perhaps the purpose of CD71 cells is to combat the natural inflammation that would occur upon abrupt colonization of bacteria. Furthermore, by suppressing the immune system, babies could catch good microbes (along with the cold-inducing microbes) (Elahi, et al, 2013). However, this study did not investigate the amount of time babies have a suppressed immune system; but it's speculated that the immune system would strike a balance a couple of years after birth.
Who knew being sick had its benefits?
Reference:
Elahi, S., Shaaban, A. F., Kinder, J. M., Ertelt, J. M., Way, S. S., Kalfa, T. A., et al. (2013). Immunosuppressive CD71+ erythroid cells compromise neonatal host defence against infection. Nature, 504(7478), 158-162. Retrieved May 16, 2014, from http://dx.doi.org/10.1038/nature12675
I've previously discussed how gut bacteria can effect the metabolism as well as the immune system; but could gut bacteria be related to malnutrition? Kwashiorkor is a form of deadly malnutrition that occurs when there is a lack of protein in the diet. However, the mystery is that children who suffer from kwashiorkor can can still get this disease despite having the exact same diet as children who remain unaffected.
A study investigating this mystery researched 300 pairs of twins (both monozogtic and dizygotic) from Malawi, a country in southern Africa where kwashiorkor is fairly common. The researchers continued to study the 300 pairs of twins through the first three years of life. It was observed that although none of the twins were malnourished to begin with, often times one twin out of the pair would develop kwashiorkor and the other would remain healthy. Researchers studied the feces of the infected children before and after a therapeutic food intervention in order to see what sort of microbes the children had in their gut. It was discovered that children who suffered from kwashiorkor had abnormal communities of microbes which only improved temporarily with treatment (Smith, et al, 2013).
Researchers then transplanted gut bacteria from three pairs of twins into special mice who completely lacked a microbe community due to being raised in a sterile environment. After receiving a diet similar to that of what children have in Malawi, mice who received the microbes from the ill children started loosing weight. This suggests that perhaps gut bacteria play an important role in malnutrition, and that malnutrition could potentially be treated with strains of probiotics in the future. Nevertheless, questions still remain about how these children are being cared for at home and why generally one out of each pair become malnourished (Smith, et al, 2013).
Reference
Smith, M. I., Knight, R., Concannon, P., Rich, S. S., Kau, A. L., Cheng, J., et al. (2013). Gut Microbiomes of Malawian Twin Pairs Discordant for Kwashiorkor. Science, 339(6119), 548-554.
Today I'm going to discuss a study that challenges what scientists (and consumers) believe about the human metabolism. This study doesn't directly discuss effects of gut bacteria, but instead hormones secreted in the gut (which are regulated by gut bacteria). Nevertheless, I found this study extremely interesting and believe it highlights an important concept; the power of the mind and its communication with the gut. It's widely accepted that the nutritional facts of our food item of choice, whether it be a slice of pizza or a bowl of salad, will effect our bodies in predictable ways as labeled on the side of the box or bag. Metabolic science asserts that the degree in which you metabolite food is directly related to the amount of calories being consumed. Grhelin (regulated by Helicobacter pylori) is a hormone secreted in the gut that tells your brain you are hungry and slows your metabolism. If you chose to eat a low-calorie meal (such as a salad), grhelin levels only drop a little and as a result, the metabolism only increases marginally. On the other hand, if you chose to indulge in a high- calorie meal (like a whole box of meat-lover's pizza), grhelin levels drop more and metabolic activity is increased significantly.
A study investigating the power of food labels over human physiology discovered that metabolism may be influenced by the brain. Could food labels act as placebo pills and alter the rate of metabolism in the human body? Could reading the icecream's nutrition facts actually effect your waistline?
In this particular study, 2 groups of people were given the same milkshake which contained about 300 calories. The catch? Each group received differently labeled milkshakes. One group received a milkshake that was labeled "Low-Calorie, Sensishake, 0% Fat, No Added Sugar, Only 140 Calories". The second group received the same milkshake, only labeled as "Indulgence, 620 Calories". It was discovered that grhelin levels dropped about three times more when the participant believed he/she was indulging in a high-calorie shake in comparison to the "Sensishake" group (Crum et al, 2011). This means that despite both groups drinking the exact same milkshake, one group had a different metabolic response.
This is an astounding study, as it suggests that our beliefs about our food matter in the metabolism of it.
Reference:
Crum, A. J., Corbin, W. R., Brownell, K. D., & Salovey, P. (2011). Mind over milkshakes: Mindsets, not just nutrients, determine ghrelin response.. Health Psychology, 30(4), 424-429.
Last week I discussed the effects gut bacteria have on the central nervous system and as well as their influence on behaviors observed in mice. These findings suggest that perhaps gut flora manipulation would prove to be an effective treatment of psychological disorders. To elaborate on this idea, I found a study that measured psychological changes under the treatment of probiotics. This study investigated the effects of probiotics on depression, hostility, and anxiety-yielding promising results for potential future treatment methods. A probiotic formulation of Lactobacillus helveticus R0052 and Bifidobacterium longum R0175 was given to a general population. Using the Hopkins symptoms checklist-90, the researchers found that people who received the probiotics significantly improved over a 30 day period with a decrease in anxiety and depression, as well as sub-areas such as obsessive compulsion and paranoid-ideation (Messaoudi et al., 2011). One possible explanation for these findings is that probiotics reduce brain inflammation. The probiotics used in this research decrease the amount of inflammatory-inducing cytokines (proteins that signal other cells) found in the gut (Messaoudi et al., 2011). It's speculated that the signals from the cytokines travel via the vagus nerve to the brain (although there are other hypothesis about how these signals travel as well). Brain inflammation has been linked to depression and anxiety; thus priobiotics' ability to reduce inflammation signaling may be linked to the study's findings. However, researchers concluded that not only can probiotics assist in behavioral abnormalities, but in general well being. Moreover, it is believed that chronic stress could disrupt the delicate balance of gut bacteria and thus potentially lead to diseases. However, the researchers speculate that taking probiotics could keep the gut in good health and prevent such unbalance in the future if/when stress arises (Messaoudi et al., 2011).
Reference:
Messaoudi, M., Violle, N., Bisson, J., Desor, D., Javelot, H., & Rougeot, C. (2011). Beneficial psychological effects of a probiotic formulation (Lactobacillus helveticus R0052 and Bifidobacterium longum R0175) in healthy human volunteers. Gut Microbes, 2(4), 256-261.
This week I'll begin discussing how microbiota of the gut can effect your brain! Believe it or not, the bacteria you host in your gut may play an important role in brain chemistry and behavior.
One study I found particularly interesting investigated whether or not anxiety could be linked to gut flora. Researchers took 'fearless' mice and 'anxious' mice and swapped their gut bacteria; so the fearless mouse now had the anxious mouse's microbiota (and vice versa). By altering the microbes of the gut, the anxious mice became bold while the fearless mice became timid. Additionally, the researches investigated the effects of diet, probiotics, and antibiotics on a group of aggressive mice. Due to various alterations of microbes, the aggressive mice appeared to become more docile (Collins, et al., 2013).
You might be asking yourself, 'how could this be possible?!' Well, by measuring the brain chemistry of mice with altered gut microbiota, researchers discovered chemical changes in areas of the brain dealing with emotion/mood as well as an increase in a chemical known as brain-derived neurtrophic factor. Moreover, brain-derived neurtrophic was found to be increased in the hippocampus region of the brain, and is believed to influence both learning and memory (Bercik, et al., 2011).
Because this is a relatively new area of study, there are still many unknowns. However, researchers are hopeful that eventually alteration of gut flora could become an effective treatment for various disorders of the central nervous system, including psychiatric disorders (Collins, et al., 2013).
I found this short video really informative (and fun). It explains gut flora across the human body and discusses why gut microbiota are so important. Although it does not discuss the effects of microbiota on the brain, I still thought it might help some of you grasp the idea of the human microbiome. Enjoy!
(Gudenkauf, 2013).
References:
Bercik, P., Verdu, E. F., Denou, E., Collins, S. M., Mccoy, K. D., Macri, J., et al. (2011). The Intestinal Microbiota Affect Central Levels of Brain-Derived Neurotropic Factor and Behavior in Mice.Gastroenterology, 141(2), 599-609.e3.
Collins, S. M., Kassam, Z., & Bercik, P. (2013). The adoptive transfer of behavioral phenotype via the intestinal microbiota: experimental evidence and clinical implications. Current Opinion in Microbiology, 16(3), 240-245.
Gudenkauf, A. (Producer). (2013). The Invisible Universe of the Human Microbiome. United States: NPR.
I previously discussed how an unhealthy gut can cause tissue inflammation and ultimately lead to obesity. Nevertheless, gut microbiota have further reaching effects than just weight gain. According to recent studies, the biological makeup of your gut could play a significant role in the onset of both type 1 and type 2 diabetes. The cause of type 1 and 2 diabetes is not explicitly known. Type 1 diabetes is not preventable and often runs in families, but isn't related to lifestyle choices (such as diet and exercise). Type 2 diabetes is preventable and closely related to genetics, high blood pressure, and obesity. However, research suggests that another factor in diabetes could be related to the health and biological makeup of your gastrointestinal tract. In the development of type 1 diabetes, there are three crucial factors relating to gut health that interact closely with one another. The microbiota found in the gut (specifically those that trigger inflammation) play an important role in the formation of autoimmune diabetes. Moreover, it is believed that the interaction of gut bacteria and the mucosal immune system in postnatal development may have long-term effects and implication for the formation of type 1 diabetes later in life (Vaarala, et al. 2008). Another factor is the degree of permeability of the intestinal wall. Those suffering from type 1 diabetes have a more permeable gut than those without the disease. Low levels of a special tight junction protein known as "claudin" cause an increased permeability in intestines of individuals with type 1 diabetes. This extreme permeability not only leads to increase exposure to sugar, but to other dietary antigens that trigger an immune response. Furthermore, an altered mucosal immune system could be a significant factor in failure for the body to form tolerance which consequently lead to autoimmune responses (Vaarala, et al. 2008).
A study investigating the relationship between gut flora and the development of type 2 diabetes discovered that gut flora may play a role in increasing the permeability of the intestinal walls. Mice fed a high fat diet which induced type 2 diabetes showed an increase in adherence of bacteria to the membrane of the intestines. Ultimately, these bacteria are able to move through the membrane and into the adipose tissue (stored fat) as well as the blood (Amar, et al. 2011). However, with a probiotic treatment (Bifidobacterium animalis subsp. lactis 420), membrane adherence diminished along with the translocation of bacteria to fat cells and blood. Utilizing such probiotics may prove helpful in controlling diet induced diabetes, as inflammation was reversed in this particular study (Amar, et al. 2011). References: Amar, J., Chabo, C., Waget, A., Klopp, P., Vachoux, C., Bermúdez-Humarán, L. G., Smirnova, N., Bergé, M., Sulpice, T., Lahtinen, S., Ouwehand, A., Langella, P., Rautonen, N., Sansonetti, P. J. and Burcelin, R. (2011), Intestinal mucosal adherence and translocation of commensal bacteria at the early onset of type 2 diabetes: molecular mechanisms and probiotic treatment. EMBO Mol Med, 3: 559–572. doi: 10.1002/emmm.201100159
Vaarala, O., Atkinson, M. A., & Neu, J. (2008). The "Perfect Storm" for Type 1 Diabetes: The Complex Interplay Between Intestinal Microbiota, Gut Permeability, and Mucosal Immunity.Diabetes, 57(10), 2555-2562.
In my previous post I briefly discussed the many different
ways in which gut flora contribute to our health and wellbeing. Today I will be
discussing how gut flora relate to a major health risk that effects countless individuals
across a wide array of demographics. With easy access to cheap and fattening foods,
little time to exercise, and in some cases, unfavourable genetics; many industrialized
and developing countries suffer from high obesity rates. However, despite
common belief, obesity is not simply related to diet and lifestyle choices.
Environmental factors, genetics, and systemic and adipose tissue inflammation
also contribute to weight gain (Kotzampassi, et al. 2014).
The 100 trillion cells of microbiota found in the human gut
play an important role in energy harvest and body weight. This concoction of
bacteria is extremely diverse amongst humans; although, Firmicutes and
Bacteroidetes (Actinobacteria) are dominant types. In fact, studies suggest
that a gut composition including more Firmicutes and less Bacteroidetes (and
overall less microbiota diversity) is linked to slower metabolic pathways and
increased fat storage (Kotzampassi, et al. 2014). Furthermore, Bifidobacterium
spp. of the phylum Actinobacteria, may have anti-inflammatory effects leading
to a leaner host. Nevertheless, the
bacteria falling under the phylum Firmicutes, Staphylococcus aureus, may lead
to inflammatory effects, increasing the risk of obesity. In summary, such
findings suggest that manipulation of gut bacteria could be a fundamental
practice in preventing the onset of obesity (Kotzampassi, et al. 2014).
Reference:
Katerina Kotzampassi, Evangelos J. Giamarellos-Bourboulis,
and George Stavrou, “Obesity as a Consequence of Gut Bacteria and Diet
Interactions,” ISRN Obesity, vol. 2014, Article ID 651895, 8 pages, 2014.
doi:10.1155/2014/651895
