Yup, another early morning class. Well, it’s not all so bad – my nutrition professor is going to discuss which foods we should be eating to maximize our performance during physical activity (verdict: we don’t know… But it’s probably not a bad idea to eat your greens!). Pretty interesting topic right?
I zoned out, AGAIN. Just once I’d like to get through one full lecture with full concentration. Anyways, as I was wandering the recesses of my mind, I stumbled upon a terrific blog idea: How does physical activity impact our gut bacteria and vice-versa?
As mentioned in previous blogs, the gut microbiota plays a crucial role in human health; it prevents the survival of pathogenic bacteria (these critters harm you and can even kill you), stimulates the proliferation of epithelial cells (i.e. the cells that line your intestines and are thus in direct contact with the bacteria living there. Proliferation is a good thing – it allows the lining of the intestines to replenished frequently and remain rejuvenated) (1) and helps to digest certain nutrients that we can’t digest on our own. It’s a love-hate relationship, really; while we require the gut flora to keep us alive and well, an altered gut bacteria has been associated with many diseases such as obesity, heart failures, cancer, and diabetes (see previous blogs).
Now, is there a correlation between physical activity and a healthy gut microbiota?
Many studies have shown that physical activity is associated with a healthy microflora. Studies by Dr. Matsumoto and his colleagues have successfully demonstrated that rats following a rigorous running regimen harbor a different gut microbiome composition than control rats whom refrained from running. This showed that rats who did running exercises had a different microbial composition in the gut (2).
So what? Matsumoto investigated his findings deeper, and found that this exercise-induced microbiome produced high levels of an infamous compound known as “butyrate”. Butyrate has been well characterized as a potent suppressor of both colon cancer and inflammatory bowel disease (2, 3)
A revealing study by CC Evans in 2014 built on Matsumoto’s work. Evans and his colleagues demonstrated (through an elegant set of experiments) that mice were able to counter the obesity-inducing effects of a high-fat diet through exercise alone. “But you already knew that !”
The real interesting finding made by Evans was that as the mice ran for greater distances, the lower their Firmicutes:Bacteroides ratio became in the gut (4). If you’re familiar with our previous blog, then you may remember that a lower ratio correlates with weight loss. Essentially, they showed that exercise played a role in preventing obesity by favoring a bacterial composition that is similar to those in lean mice regardless of the diet.
Although, these studies have shown some promising results, you might be wondering if this applies to human beings.
A study on the “fecal microbiota of individuals with different fitness levels” (5) following similar diets showed that people with a higher cardiorespiratory fitness had a greater microbial diversity in their gut. This study by Estaki et al. demonstrated that people who were more physically active had an increase in gut microbial diversity irrespective of the diet, and that diversity is a potent driver of optimal gut health. Additionally, similar to the study in mice, fit individuals showed an increase in butyrate producing bacteria
How does doing exercise change the microbial diversity in the gut?
Further studies are required to fully comprehend the mechanism by which exercise changes the composition of gut bacteria. Nevertheless, one possible theory is that exercise causes lactic acid to be produced in the body, which could be converted by certain bacteria in the gut to butyrate (6).
So if you didn’t already have enough reasons to get to the gym, here’s one more: these studies demonstrate the potential of exercise to be used as a treatment to restore a healthy gut microbiota. We can, quite literally, run our way to a better microbiome.
1. S. Rakoff-Nahoum, J. Paglino, F. Eslami-Varzaneh, S. Edberg, and R. Medzhitov, “Recognition of commensal microflora by toll-like receptors is required for intestinal homeostasis,” Cell, vol. 118, no. 2, pp. 229–241, 2004.
2. M. Matsumoto, R. Inoue, T. Tsukahara et al., “Voluntary running exercise alters microbiota composition and increases n-butyrate concentration in the rat cecum,” Bioscience, Biotechnology, and Biochemistry, vol. 72, no. 2, pp. 572–576, 2008.
3. Tan, Hwee Tong, Sandra Tan, Qingsong Lin, Teck Kwang Lim, Choy Leong Hew, and Maxey C. M. Chung. "Quantitative and Temporal Proteome Analysis of Butyrate-treated Colorectal Cancer Cells." Molecular & Cellular Proteomics 7.6 (2008): 1174-185. Web.
4. C. C. Evans, K. J. LePard, J. W. Kwak et al., “Exercise prevents weight gain and alters the gut microbiota in a mouse model of high fat diet-induced obesity,” PLoS ONE, vol. 9, no. 3, Article ID e92193, 2014.
5. M. Estaki, J. Pither, P. Baumeister et al., “Cardiorespiratory fitness as a predictor of intestinal microbial diversity and distinct metagenomic functions,” The FASEB Journal, vol. 30, no. 1, pp. 1027–1035, 2016.
6. S. H. Duncan, P. Louis, and H. J. Flint, “Lactate-utilizing bacteria, isolated from human feces, that produce butyrate as a major fermentation product,” Applied and Environmental Microbiology, vol. 70, no. 10, pp. 5810–5817, 2004.
Did you know that cardiovascular disease is the second leading cause of death in Canada after cancer? In fact, every 7 minutes, in Canada, someone dies from cardiovascular disease, that’s 206 people dying from heart disease every day (1)!
Several factors contribute to cardiovascular disease such as smoking, the amounts of fats and cholesterol in the blood, high blood pressure, the amount of sugar in the blood and blood vessel inflammation (when blood vessels become inflamed, they may become weakened, stretch, and either increase in size or become narrow -- even to the point of closing entirely) (2).
These are all factors that you might have heard previously. But have you heard of the very important link between your gut bacteria and heart disease?
As described in many of our previous blogs, we greatly benefit from microbial activities in our gut. In fact, bacteria in our gut are essential for the production of vitamins (such as vitamin B and vitamin K), digestion of carbohydrates and production of short chain fatty acids among others. Short chain fatty acids are produced when our gut bacteria ferment the fiber we intake and they play an important role in health and disease. Despite these beneficial effects, studies in the past 10 years have shown that the gut microbiota (bacteria harboring our gut) is associated with several diseases such as obesity, type 2 diabetes and cardiovascular disease among others.
As a matter of fact, gut bacteria produce a chemical that increases clotting in the arteries (meaning that it creates a blockage in a blood vessel linked to the heart). Studies show that when this chemical called TMAO (trimethylamine oxide) is added to human platelets, which are tiny blood cells that help your body form clots to stop bleeding, the formation of artery-blocking clots was much faster (4). TMAO is made in the body as a waste product of gut microbes. Furthermore, when researchers increased blood TMAO levels in mice by feeding them a diet rich in choline, which is a TMAO precursor, they found that the animals formed clots faster than those with lower TMAO levels. These results were not seen in mice that lacked gut microbes. When intestinal microbes from mice that produced high levels of TMAO were transplanted into mice with no gut bacteria, the recipients’ clotting risk increased (4). Moreover, TMAO levels were found to be higher in patients with heart failure compared with those without heart failure.
As mentioned above, choline is a precursor of TMAO and this can be found in high amounts in foods rich in cholesterol and fats such as:
Nevertheless, it is still important to take choline nutrients in moderate amount since choline deficiency can cause neurologic impairment. L-carnithine is another common dietary nutrient ingested that produces TMAO (4). In contrast to choline, L-carnithine is not required in our diet since our body is still able to generate it on its own. Studies show that vegetarians and vegans have a reduced capacity to make TMAO compared to omnivores (person that eats food of both plant and animal origin). Basically, this shows that there is a shift in the population of gut bacteria in omnivores that prefer L-carnitine which enhances the potential to produce TMAO (4).
Nutrients rich in L-carnitine are:
Interestingly, the Dr. Oz show recommended a few years ago to take supplements of L-carnitine claiming that it could increase energy, speed up weight loss and improve athletic performance. After seeing the new research about L-carnitine, he is saying to NOT take these supplements as it has been shown to increase the risk of cardiovascular disease (http://blog.doctoroz.com/dr-oz-blog/why-we-were-wrong-l-carnitine).
Now, my recommendation to you is to reduce as much as possible the consumption of red meat as it has been to shown to be very rich in both L-carnitine and choline, which are precursors of TMAO.
Finally, results of this study show how much of an impact the gut bacteria has on our overall health. The gut microbiota represents a new target for therapeutic manipulation and targeting for the treatment and prevention of cardiovascular diseases.
1.”Facts about Heart Disease." Facts about Heart Disease | The Heart Research Institute - Heart Research Institute. Heart Research Institute, n.d. Web. 25 June 2017.
2. "What Causes Heart Disease?" National Heart Lung and Blood Institute. U.S. Department of Health and Human Services, 21 Apr. 2014. Web. 25 June 2017.
3. Jonsson, Annika Lindskog, and Fredrik Bâckhed. "Role of Gut Microbiota in Atherosclerosis." Nature Reviews Cardiology 14.2 (2016): 79-87.
4. Tang, W.h. Wilson, and Stanley L. Hazen. "The Contributory Role of Gut Microbiota in Cardiovascular Disease." Journal of Clinical Investigation 124.10 (2014): 4204-211.
I’m always on the lookout for new ways to improve my health, whether it be through diet, exercise or — the all-too-often neglected third member of the U.S. Army’s Performance Triad — sleep. And while some health trends border the edge of insanity (Tapeworms, anyone?), others have a fair share of scientific literature backing up their claims.
One such trend that has slowly but surely began to establish its niche in pop culture is intermittent fasting (IF). If it sounds familiar, you may have seen this video circulating on your Facebook newsfeed. While there are a handful of IF variations that exist (and you can read all about those here), they are all usually adapted to serve one common purpose — to encourage weight-loss by moderately decreasing our calorie intake by 500-1000 calories per day.
Sounds crazy, right?
Well, maybe not.
The National Institute of Health (that’s the largest biomedical research institution in the world!) concluded that low-calorie diets can lower total body weight by an average of 8% in the short term (3-12 months), and that these low-calorie diets maintain significant weight loss over a 5-year period (1) (and that’s important, because “yo-yo dieting”, or the failure to maintain weight-loss, correlates with increased body fat (2)).
But the effects of caloric restriction, at least in mice, seem to extend far beyond weight loss to include more subtle health-promoting advantages. First suggested 82 years ago by C.M. McCay (3), a research team headed by J.D. Han recently found that mice following a low-calorie diet (defined as 30% less calories than usual) were healthier and lived 20-25% longer than mice following a “normal”-calorie diet. Not only that, but these mice exhibited the lowest and most stable body weight and fat content, as well as the best metabolism (4).
Despite these exciting findings, researchers couldn't figure out why low-calorie diets increased overall health — until 2013, when Liping Zhao and his research group studied the gut bacteria in mice that followed a low-calorie diet their entire lives. Zhao and his colleagues demonstrated that calorie restriction selected for certain gut bacteria, such as Lactobacillus, whose presence in our gut correlates with longer lifespan, while also reducing the amount of gut bacteria that are associated with decreased lifespan (5). In other words, it seems that reducing our daily calorie intake promotes the growth of “good” bacteria that prevent aging, while at the same time inhibiting the growth of “bad” bacteria that makes us age quicker.
But how can gut bacteria influence our lifespan? While the answer to this question isn’t obvious, we still have a pretty good idea of what is likely happening, and it involves the process of inflammation. We’ve all seen inflammation in action — when you get a paper cut, you’ll notice your skin becoming red, warm and painful. This is the result of immune cells (and blood) rushing to the site of the cut to kill the bacteria that are trying to enter your body. This kind of inflammation doesn’t last long (a few hours to a few days), and the bacteria are promptly killed (that’s a good thing!).
Here’s the problem: something different — and more destructive — can happen inside our bodies. Our gut is littered with bacteria, and while most of them aren’t recognized by our immune system, some of them are, and this kind of inflammation can last an abnormally long time. That’s dangerous: long-term (or “chronic”) inflammation is known to speed-up the deterioration of the cardiovascular system (6), as well as increase the incidence of stroke and cognitive loss at younger ages (7). In other words, chronic inflammation shortens our lifespan.
And guess what — meals high in calories have been associated with increases in chronic, lifespan-crippling inflammation (8).
That’s why eating less calories seems to increase lifespan in mice. Zhao found that a low-calorie diet encouraged the growth of anti-inflammatory gut bacteria while simultaneously inhibiting the growth of pro-inflammatory bacteria (5). That means that by eating less (~500 fewer calories per day), we can potentially decrease chronic inflammation, thereby living longer, healthier lives.
1. Strychar, I. 2006. Diet in the management of weight loss. CMAJ 174: 56-63.
2. Mackie, G. M., D. Samocha-Bonet, and C. S. Tam. 2017. Does weight cycling promote obesity and metabolic risk factors? Obes. Res. Clin. Pract. 11: 131-139.
3. McCay, C. M., M. F. Crowell, and L. A. Maynard. 1989. The effect of retarded growth upon the length of life span and upon the ultimate body size. 1935. Nutrition 5: 155-171; discussion 172.
4. Zhou, B., L. Yang, S. Li, J. Huang, H. Chen, L. Hou, J. Wang, C. D. Green, Z. Yan, X. Huang, M. Kaeberlein, L. Zhu, H. Xiao, Y. Liu, and J. D. Han. 2012. Midlife gene expressions identify modulators of aging through dietary interventions. Proc. Natl. Acad. Sci. U. S. A. 109: E1201-1209.
5. Zhang, C., S. Li, L. Yang, P. Huang, W. Li, S. Wang, G. Zhao, M. Zhang, X. Pang, Z. Yan, Y. Liu, and L. Zhao. 2013. Structural modulation of gut microbiota in life-long calorie-restricted mice. Nature communications 4: 2163.
6. Danesh, J., P. Whincup, M. Walker, L. Lennon, A. Thomson, P. Appleby, J. R. Gallimore, and M. B. Pepys. 2000. Low grade inflammation and coronary heart disease: prospective study and updated meta-analyses. BMJ 321: 199-204.
7. Wilson, C. J., C. E. Finch, and H. J. Cohen. 2002. Cytokines and cognition--the case for a head-to-toe inflammatory paradigm. J. Am. Geriatr. Soc. 50: 2041-2056.
8. Blackburn, P., M. Cote, B. Lamarche, C. Couillard, A. Pascot, A. Tremblay, J. Bergeron, I. Lemieux, and J. P. Despres. 2003. Impact of postprandial variation in triglyceridemia on low-density lipoprotein particle size. Metabolism 52: 1379-1386.
Vegetable and fruit juice based diets are growing in popularity among busy people who don’t have the time to get in their daily fruits and veggies. Fruits and vegetables are sources of many biologically active things that help health and decrease the risk of disease.  For example fruits and veggies have molecules called polyphenols.
Polyphenols have a variety effects that have been proven in the lab such as being antioxidants, immune system stimulating, and killing bacteria.  Polyphenols are not well absorbed by the body and often continue to the colon where they can be digested by bacteria in the gut. These bacteria break down polyphenols into smaller molecules which also become food to other bacteria. Fruits and vegetables are also high in fermentable fibers which have prebiotic activities. Prebiotics are compounds that bacteria living in us, can use as food to grow. High fiber intake has many positive effects like lowered risks of cardiovascular disease, type 2 diabetes, and some cancers. 
The gut microbes play a role in our everyday health. One of these roles is that the gut microbiota has been shown to affect the development of obesity and obesity-related disease.  The two types of bacteria which are found in humans in greatest numbers are the Firmicutes and Bacteriodetes.  Studies have shown that supplementing diets with more polyphenols shows a decreased amount of Firmicutes and more Bacteriodetes. This is interesting because lowered Firmicutes levels and higher Bacteriodetes is also associated with leaner individuals, while obese people have opposite proportions.  A scientific study followed a 3-day juice-based diet of 6 blends of fruit/vegetable juices. The results showed that people lost significant amounts of weight and kept it off for two weeks. People on this diet showed increased amounts of Bacteroides bacteria which can degrade plant fibers and complex polysaccharides. 
What fruits/veggies are high in polyphenols?
The break down: Research shows that leaner people have the same gut bacteria, that the juice diet promotes. Although this may not mean instant weight loss, studies are showing that the juice diet has definite benefits to the body. Why not add more juice to your diet?
Rule of thumb: Choose fruits and veggies that are richly hued when juicing. For example, red and purple fruits often are excellent sources of polyphenols. However, don’t be afraid to stray to other colours. All fruits and veggies have nutrients and vitamins that are good for your bodies.
1. Tome-Carneiro, J. & Visioli, F. Polyphenol-based nutraceuticals for the prevention and treatment of cardiovascular disease: Review of human evidence. Phytomedicine: international journal of phytotherapy and phytopharmacology, doi:10.1016/j.phymed.2015.10.018 (2015).
2. Li AN, et al. Resources and biological activities of natural polyphenols. Nutrients. 2014;6:6020–6047. doi: 10.3390/nu6126020.
3. Dahl, W. J. et al. Health Benefits of Fiber Fermentation. Journal of the American College of Nutrition 1–10, doi:10.1080/07315724.2016.1188737 (2017).
4. Korpela K, et al. Gut microbiota signatures predict host and microbiota responses to dietary interventions in obese individuals. PloS one. 2014;9:e90702. doi: 10.1371/journal.pone.0090702.
5. Million M, Lagier JC, Yahav D, Paul M. Gut bacterial microbiota and obesity. Clinical microbiology and infection: the official publication of the European Society of Clinical Microbiology and Infectious Diseases. 2013;19:305–313. doi: 10.1111/1469-0691.12172.
6. Stenman, L. K., Burcelin, R. & Lahtinen, S. Establishing a causal link between gut microbes, body weight gain and glucose metabolism in humans - towards treatment with probiotics. Beneficial microbes 1–12, doi:10.3920/BM2015.0069 (2015).
7. Flint HJ, Scott KP, Duncan SH, Louis P, Forano E. Microbial degradation of complex carbohydrates in the gut. Gut microbes. 2012;3:289–306. doi: 10.4161/gmic.19897.
8. Henning, S. M., et al. (2017). "Health benefit of vegetable/fruit juice-based diet: Role of microbiome." Sci Rep 7(1): 2167.
In our most recent blog post, we discussed the importance of vitamins such as vitamin K2. Another crucial vitamin for healthy gut functions is vitamin D. Vitamin D represents a group of fat-soluble vitamins which are required for increasing intestinal absorption of calcium, iron, magnesium, phosphate, zinc (1). The most important in humans are vitamins D2 and D3. While this vitamin is often associated with the skin, it can be acquired from food intake just as well as from sunlight.
A study recently showed that a deficiency in vitamin D changes the intestinal microbiome and reduces vitamin B production in the gut. This means that there is a change in the type of bacteria living in our gut when we do not have enough vitamin D in our system (2). Furthermore, this lack of vitamin B leads to negative changes in our immune system. Our bodies suffer from increased inflammation and this can lead to autoimmunity – meaning our immune system is attacking healthy tissues and cells.
Finally, low levels of vitamin D have been linked with an increased risk of depression. Not only is this vitamin important for a healthy gut and a strong immune system, but also our mental health (3). It really is a molecule with several, diverse effects. Others include bone health, cancer, cardiovascular disease, cognition/dementia, pregnancy, and weight loss as well.
Therefore, it is very important to maintain normal levels of vitamin D in our blood.
What can you do?
1. Holick, Michael F. "High Prevalence of Vitamin D Inadequacy and Implications for Health." Mayo Clinic. Mayo Clinic Proceedings, Mar. 2006. Web.
2. Gominak, S. C. "Vitamin D Deficiency Changes the Intestinal Microbiome Reducing B Vitamin Production in the Gut. The Resulting Lack of Pantothenic Acid Adversely Affects the Immune System, Producing a "pro-inflammatory" State Associated with Atherosclerosis and Autoimmunity." Medical Hypotheses. U.S. National Library of Medicine, Sept. 2016. Web.
3. Black, L. J., P. Jacoby, K. L. Allen, G. S. Trapp, P. H. Hart, S. M. Byrne, T. A. Mori, L. J. Beilin, and W. H. Oddy. "Low Vitamin D Levels Are Associated with Symptoms of Depression in Young Adult Males." The Australian and New Zealand Journal of Psychiatry. U.S. National Library of Medicine, May 2014. Web.
4. Jakobsen, Jette, and Pia Knuthsen. "Stability of Vitamin D in Foodstuffs during Cooking." Stability of Vitamin D in Foodstuffs during Cooking. Food Chemistry, 1 Apr. 2014. Web.
Vitamins are essential micronutrients needed in small quantities to sustain life. We need to take vitamins from food because the human body either does not produce enough of them or none at all. There are currently 13 recognized vitamins which are either fat-soluble (stored in the fatty tissues of the body and the liver) or water-soluble (do not get stored in the body for long - they soon get excreted in urine) (1).
As you might have learned from previous blogs, the human gastrointestinal tract (GIT) is colonized by a vast array of microorganisms known as the gut microbiota. The intestinal microbiota (microbes that harbours our gut) plays a pivotal role in food digestion and energy recovery, while it can also act as an important supplier of vitamins. In humans it has been shown that members of the gut microbiota are able to synthesize vitamin K as well as most of the water-soluble B vitamins (2).
Some subtypes of Vitamin K2 can only be supplied to the host through bacteria in the gut such as Ruminococcaceae, Bacteroides, Prevotella, Alistipes, Oscillibacter, Bilophila, Odoribacter and Barnesiella species. Moreover, it seems that the Bacteroides and Prevotella species are the most prevalent in generating different subtypes of vitamin K2 (6).
The current research on Vitamin K2 and health is extremely promising. It could have life saving implications for a lot of people. Unfortunately, the average intake of this important nutrient is incredibly low in the modern diet.
What can you do?
1. Leblanc, Jean Guy, Christian Milani, Graciela Savoy De Giori, Fernando Sesma, Douwe Van Sinderen, and Marco Ventura. "Bacteria as Vitamin Suppliers to Their Host: A Gut Microbiota Perspective." Current Opinion in Biotechnology 24.2 (2013): 160-68
2. Hill, M. J. "Intestinal Flora and Endogenous Vitamin Synthesis." European Journal of Cancer Prevention 6 (1997): n. pag.
3. Marques, Tatiana Milena, Rebecca Wall, R. Paul Ross, Gerald F. Fitzgerald, C. Anthony Ryan, and Catherine Stanton. "Programming Infant Gut Microbiota: Influence of Dietary and Environmental Factors." Current Opinion in Biotechnology 21.2 (2010): 149-56.
4. Mizuta, Toshihiko, Iwata Ozaki, Yuichiro Eguchi, Tsutomu Yasutake, Seiji Kawazoe, Kazuma Fujimoto, and Kyosuke Yamamoto. "The Effect of Menatetrenone, a Vitamin K2 Analog, on Disease Recurrence and Survival in Patients with Hepatocellular Carcinoma after Curative Treatment." Cancer 106.4 (2006): 867-72.
5. Kubota, K., T. Sawada, J. Kita, M. Shimoda, and M. Kato. "6594 POSTER Effect of Menatetrenone, a Vitamin K2 Analog, on Recurrence of Hepatocellular Carcinoma After Surgical Resection â€“ Final Results of Randomized Controlled Study." European Journal of Cancer 47 (2011): n. pag.
6. Karl, J. P., X. Fu, X. Wang, Y. Zhao, J. Shen, C. Zhang, B. E. Wolfe, E. Saltzman, L. Zhao, and S. L. Booth. "Fecal Menaquinone Profiles of Overweight Adults Are Associated with Gut Microbiota Composition during a Gut Microbiota-targeted Dietary Intervention." American Journal of Clinical Nutrition 102.1 (2015): 84-93.
7. Kidd, P. M. "Vitamins D and K as Pleiotropic Nutrients: Clinical Importance to the Skeletal and Cardiovascular Systems and Preliminary Evidence for Synergy." Alternative Medicine Review : A Journal of Clinical Therapeutic. U.S. National Library of Medicine, Sept. 2010.
8. Filippis, Francesca De, Nicoletta Pellegrini, Luca Laghi, Marco Gobbetti, and Danilo Ercolini. "Unusual Sub-genus Associations of Faecal Prevotella and Bacteroides with Specific Dietary Patterns." Microbiome 4.1 (2016): n. pag.