One hundred trillion cells make up the human body, but only a tenth of those are actually human cells.1 Thus, for all intents and purposes, humanity is just a mule train for the bacteria, viruses, and other microorganisms that comprise the remaining nine-tenths of our bodies’ cells. Not only that, scientists have learned that these little critters affect mood, perception, and other types of cognitive function that influence your health, relationships, job, and last but not least, your boyish or girlish figure.2 Our gut bacteria are the most important and most studied of these microorganisms.
Trillions of gut bacteria begin colonizing the human colon the minute we are born, forming what scientists call a commensal relationship.3 This means a relationship involving two organisms where one of them profits, and the other receives no benefit, but suffers no harm. Understanding the difference between commensalisms, mutualisms, and parasitic relationships is important to this discussion. Like a healthy marriage, in mutualism both organisms benefit from their relationship. In a parasitic relationship, one organism benefits from the relationship. However, unlike the commensal relationship the other party incurs harm. While, most scientists believe our relationship with the bacteria in our intestines is commensal, some argue that it is mutualistic. I wonder if the relationships between some people and some of the gut bacteria they host are all three, depending on the time and terms of engagement.
This matters because gut bacteria create an environment that influences our physiology, metabolism, and psychology.3 This “bacterial hood” concerns obesity and metabolic disorders because of the tremendous numbers, varieties, and abilities of these little guys to secrete bioactive compounds that ferment carbohydrates and affect fat absorption.4,5 It matters whether you are in a relationship where: 1) you’re not really getting anything out of it, but not getting hurt, or 2) you are getting something and giving something, or 3) you are being used like a low-interest credit card. Likewise, the nature of a person’s relationship with his or her intestinal bacteriaalso matters.
I do not believe there is any way the relationship between a person, and the bacteria that he or she hosts, is commensal. It is a relationship. Show me a relationship where one side gets nothing out of it and yet there is no harm, and I will show you a lost episode of the Twilight Zone. Of course, our bacterial relationships are mutualistic. Hello—they live in our bodies—can we say free rent? Plus, my bacteria are getting free rent at the beach in LA. However, in return they help me digest my food, absorb nutrients,6,7 and affect my Central Nervous System,8 mood, and cognitive function.2 So how is that relationship commensal? That sounds mutualistic to me; so count me in the dissenting mutualistic-relationship camp.
Lab experiments have shown that intestinal bacteria prompt a wide variety of responses in the intestinal lining of mice, subsequently controlling the gut barrier and endocrine functions.9-13 In addition, our little tummy critters affect systemic inflammation and impact cellular metabolism in the liver and fat tissue, and influence balance in glucose and lipid levels.14 Thus, they matter as much as using a good grade of oil matters to a car engine. When scientists transferred gut bacteria from thin mice to fat mice, the latter subsequently became thin,7,15 suggesting that the kind of intestinal bacterial environment and its behavior predisposes animals to obesity, or to being thin. That puts another nail in the coffin of obesity being a character flaw.
If differences in my little intestinal critters is the reason I can sell shade space at parades, the possibilities of medications and nutrition strategies is very exciting. However, developing a comprehensive understanding of the functional influences and individual differences will be like looking for a contact lens at a Metallica concert. Even though microbiologists knew different diets created different types of bacterial hoods in the intestines before Metallica could spell Heavy Metal, they had only studied it in mice, so how that translated to humans was unclear.
A study recently published in Nature discovered that what you eat rapidly changes what little critters are living in the bacterial neighborhoods of your intestines.3 For the 78 million obese Americans, this is a FedEx truck at the door - filled with hope.
But, wait, what’s the catch? As always, with human biology, it goes back to the ancients and being adaptive. They were hunters and gathers. Hunters and gatherers ate what they could find. They might eat nuts for weeks, and then suddenly catch a fish. Having rapidly changing gut bacteria increased nutrients because gut bacteria affect nutrient fermentation and absorption.6,16 Dominos Pizza did not deliver to the Fertile Crescent or the Serengeti. So, it makes perfect sense.
However, that was then and this is now. How does this easily influenced gut bacteria work for modern humans who are not hunters and gatherers but rather supermarket shoppers, restaurant patrons, and food-delivery recipients? Especially since human evolutionary biology is the same while the Fertile Crescent is now a strip mall and the Serengeti basically a theme park. Also, most processed foods are drugs, not food.17,18 How do our little tummy critters like all the white-flour, processed sugars, and those polysyllabic chemicals? The answer is simple. We have no idea. Now if we could just accept that and move on, there would be no problem. Regrettably, that is not an option because the more research we do, the more we learn about the extensive effects of the gut bacteria on virtually all realms of human existence.
For example, take the work of Dr. Emeran Mayer, Director of The Oppenheimer Family Center for the Neurobiology of Stress at UCLA. Mayer, one of the pioneers in studying the bidirectional relationship between gut bacteria and the brain,19 has implicated connections between gut bacteria and mood, decision-making, and pain perception.2 Mayer’s Ingestive Behaviors and Obesity Program, led by Dr. Claudia Sanmiguel, is looking at changes in the tummy bacteria in bariatric populations that could one day replace bariatric surgery with nutritional intervention. Can you imagine?
John Lennon said, “Imagine there’s no…” Well, thanks to what we are learning about our little tummy critters, I can imagine there’s no obesity, no strokes, no diabetic blindness, no crippled minds, no deconstructed lives, no mourning child, or grieving spouse left behind. Yes, I can imagine. Remain Fabulous and Phenomenal
3. David LA, Maurice CF, Carmody RN, et al. Diet rapidly and reproducibly alters the human gut microbiome. Nature. Jan 23;505(7484):559-63.
4. Ley RE, Turnbaugh PJ, Klein S, Gordon JI. Microbial ecology: human gut microbes associated with obesity. Nature. 2006 Dec 21;444(7122):1022-3.
5. Turnbaugh PJ, Hamady M, Yatsunenko T, et al. A core gut microbiome in obese and lean twins. Nature. 2009 Jan 22;457(7228):480-4.
6. Hehemann JH, Correc G, Barbeyron T, Helbert W, Czjzek M, Michel G. Transfer of carbohydrate-active enzymes from marine bacteria to Japanese gut microbiota. Nature. Apr 8;464(7290):908-12.
7. Tremaroli V, Backhed F. Functional interactions between the gut microbiota and host metabolism. Nature. Sep 13;489(7415):242-9.
8. Tillisch K. The effects of gut microbiota on CNS function in humans. Gut Microbes. May 16;5(3).
9. Olszak T, Neves JF, Dowds CM, et al. Protective mucosal immunity mediated by epithelial CD1d and IL-10. Nature. May 22;509(7501):497-502.
10. Arpaia N, Campbell C, Fan X, et al. Metabolites produced by commensal bacteria promote peripheral regulatory T-cell generation. Nature. Dec 19;504(7480):451-5.
11. Diehl GE, Longman RS, Zhang JX, et al. Microbiota restricts trafficking of bacteria to mesenteric lymph nodes by CX(3)CR1(hi) cells. Nature. Feb 7;494(7435):116-20.
12. Fritz JH, Rojas OL, Simard N, et al. Acquisition of a multifunctional IgA+ plasma cell phenotype in the gut. Nature. Jan 12;481(7380):199-203.
13. Mulder IE, Schmidt B, Stokes CR, et al. Environmentally-acquired bacteria influence microbial diversity and natural innate immune responses at gut surfaces. BMC Biol. 2009;7:79.
14. Maloy KJ, Powrie F. Intestinal homeostasis and its breakdown in inflammatory bowel disease. Nature. Jun 16;474(7351):298-306.
15. Turnbaugh PJ, Ley RE, Mahowald MA, Magrini V, Mardis ER, Gordon JI. An obesity-associated gut microbiome with increased capacity for energy harvest. Nature. 2006 Dec 21;444(7122):1027-31.
16. Ochman H, Worobey M, Kuo CH, et al. Evolutionary relationships of wild hominids recapitulated by gut microbial communities. PLoS Biol.8(11):e1000546.
17. Davis C, Levitan RD, Kaplan AS, Kennedy JL, Carter JC. Food cravings, appetite, and snack-food consumption in response to a psychomotor stimulant drug: the moderating effect of "food-addiction". Front Psychol.5:403.
18. Gearhardt AN, Davis C, Kuschner R, Brownell KD. The addiction potential of hyperpalatable foods. Curr Drug Abuse Rev. Sep;4(3):140-5.
19. Times LA. Dr. Emeran Mayer: Second Brain <http://www.latimesmagazine.com/the-california-cure-emeran-mayer-second-brain.html>. Accessed. Los Angeles Times.