Skip to main content

Verified by Psychology Today

Billi Gordon Ph.D.

A Hijacked Brain and a Tongue Held Hostage

The micro-thugs that own us

Micro-Thug Life: It’s a Jungle

Only one-tenth of the trillions of cells in our bodies are human cells, Nine-tenths are bacteria, viruses, and other microorganisms.2 Since we host these little guys, their nutrient supply is dependent on what we eat.3 Thus, survival pressures force them to influence our eating behaviors to serve their nutritional needs, which are not always concordant with our best interests.4 Therefore, in essence, gut organisms are really just microscopic thugs that hijack our bodies and behaviors for personal gain, by 1) creating cravings in us for foods that serve their nutritional needs, not ours,5 or by 2) manipulating our moods so we turn to comfort foods that serve their purposes, not ours.6-8 Humans may host these micro-gangsters, but if gut bacteria controls our food cravings and moods, to serve their agenda - who really holds the deed to this house we call self? 

Enteric Turf Wars

The world’s 2.4 billion obese and their gut gangsters are already there. Like the large gangs, such as the MS 13, or the Crips,10 the larger groups of gut bacteria have more resources to allocate to various processes.11-14 Hence, they have a greater ability to influence ingestive behaviors and moods. The fewer varieties of gut bacteria we have, the greater chance we have for sub optimal ingestive behavior. 8,14For example, Prevotella15 flourishes on carbohydrates, whereas some gut bacteria specifically require sugar and chocolate. Bacteroidetes 11 like fats, so my Bacteroidetes loved that saturated fat fest I had for lunch. Just look around you, and find someone in a fudge coma and you can bet their micro-thug bacteria is waiting for those nutrients like a ruthless pimp waiting on "his" money.   

The Gut Thugs' Gats

Like a dissatisfied thug becomes toxic, when our gut gangsters don’t get their nutrients they release toxins that affect our moods,6-8 because negative moods result in increased eating. Where there is mood, there is dopamine and serotonin.22 Dopamine is the brain’s happy dance drug, and serotonin is the brain’s “don’t dance too long” drug. 21-23

"The hypothesis that microorganism in our intestine have somehow managed to hack into our reward system, enabling them to make us crave for foods that are good for them is intriguing,” says Dr. Emeran Mayer, Director of the Oppenheimer Family Center for the Neurobiology of Stress in the David Geffen School of Medicine at UCLA. Mayer, who was one of the early pioneers of brain-gut communication, is one of an elite group of authorities on this matter. Mayer also says,  “If this concept turns out to be correct, one could speculate that as a by-product of this food-seeking strategy, alterations in mood may be a consequence, as dopamine plays a role in depression as well."

Mayer’s Ingestive Behaviors and Obesity Program continually conduct compelling research. For example, Dr. Claudia Sanmiguel is investigating an association between successful weight-loss maintenance after bariatric surgery and changes in gut bacteria and functional brain activity. Her colleague, Dr. Arpana Gupta, says, “Sex and racial differences in gut bacteria are not well defined in the U.S. but increasingly data suggests they may communicate with the Central Nervous System via neural, endocrine and immune pathways that possibly influence brain function and behavior, in a sex and race-specific manner.” Naturally, she’s on that like traffic on an LA Freeway.

At the end of the day, it is scary to think that our cravings, moods, and even our brain’s reward system is being hijacked by little turf-warring gut micro-thugs for their own needs. On another note, it is extremely exciting, because animal studies have shown that these little thugs are very vulnerable to pre-biotics, pro-biotics, and fecal transplants. For me, and many like me, that translates into time. Better times, and more time, with my family, friends, and Godchildren. Remain Fabulous and phenomenal.  

Click here to receive notices of new post via email

Click here to visit me at UCLA Center for the Neurobiology of Stress

Click here to like Obesely-Speaking of FaceBook

Click her to visit me on The Huffington Post

Click here for the Billi Club (Billi Gordon Fan Page)

Click here to follow me on Twitter

Click here and find something surprising

Click here to visit Dr. Gordon Online

Click here for Google Plus 


 1. Organization WH. WHO Data and Statistics <;. Accessed. WHO, 2014.

2. Stein R. Finally, A Map Of All The Microbes On Your Body <…;. Accessed. National Public Radio, 2012.

3. Devkota S, Chang EB. Nutrition, microbiomes, and intestinal inflammation. Curr Opin Gastroenterol.  Nov;29(6):603-7.

4. Rhee SH, Pothoulakis C, Mayer EA. Principles and clinical implications of the brain-gut-enteric microbiota axis. Nat Rev Gastroenterol Hepatol. 2009 May;6(5):306-14.

5. Norris V, Molina F, Gewirtz AT. Hypothesis: bacteria control host appetites. J Bacteriol.  Feb;195(3):411-6.

6. Tillisch K. The effects of gut microbiota on CNS function in humans. Gut Microbes.  May 16;5(3).

7. Cryan JF, Dinan TG. Mind-altering microorganisms: the impact of the gut microbiota on brain and behaviour. Nat Rev Neurosci.  Oct;13(10):701-12.

8. Forsythe P, Sudo N, Dinan T, Taylor VH, Bienenstock J. Mood and gut feelings. Brain Behav Immun.  Jan;24(1):9-16.

9. Gonzalez-Rodriguez I, Ruiz L, Gueimonde M, Margolles A, Sanchez B. Factors involved in the colonization and survival of bifidobacteria in the gastrointestinal tract. FEMS Microbiol Lett.  Mar;340(1):1-10.

10. Center FNGi. National Gang Threat Assessment: Federal Bureau of Investigation 2011.

11. Xu J, Mahowald MA, Ley RE, et al. Evolution of symbiotic bacteria in the distal human intestine. PLoS Biol. 2007 Jul;5(7):e156.

12. Schloissnig S, Arumugam M, Sunagawa S, et al. Genomic variation landscape of the human gut microbiome. Nature.  Jan 3;493(7430):45-50.

13. O'Connor EM, O'Herlihy EA, O'Toole PW. Gut microbiota in older subjects: variation, health consequences and dietary intervention prospects. Proc Nutr Soc.  May 13:1-11.

14. Le Chatelier E, Nielsen T, Qin J, et al. Richness of human gut microbiome correlates with metabolic markers. Nature.  Aug 29;500(7464):541-6.

15. Shah HN, Gharbia SE. Ecophysiology and taxonomy of Bacteroides and related taxa. Clin Infect Dis. 1993 Jun;16 Suppl 4:S160-7.

16. Baba S, Osakabe N, Yasuda A, et al. Bioavailability of (-)-epicatechin upon intake of chocolate and cocoa in human volunteers. Free Radic Res. 2000 Nov;33(5):635-41.

17. Rios LY, Gonthier MP, Remesy C, et al. Chocolate intake increases urinary excretion of polyphenol-derived phenolic acids in healthy human subjects. Am J Clin Nutr. 2003 Apr;77(4):912-8.

18. Duca FA, Sakar Y, Covasa M. The modulatory role of high fat feeding on gastrointestinal signals in obesity. J Nutr Biochem.  Oct;24(10):1663-77.

19. Shibata R, Kameishi M, Kondoh T, Torii K. Bilateral dopaminergic lesions in the ventral tegmental area of rats influence sucrose intake, but not umami and amino acid intake. Physiol Behav. 2009 Mar 23;96(4-5):667-74.

20. Yamamoto T. Central mechanisms of roles of taste in reward and eating. Acta Physiol Hung. 2008 Jun;95(2):165-86.

21. Hoebel BG, Hernandez L, McClelland RC, Schwartz D. Dexfenfluramine and feeding reward. Clin Neuropharmacol. 1988;11 Suppl 1:S72-85.

22. Mayer EA, Chang L, Lembo T. Brain-gut interactions: implications for newer therapy. Eur J Surg Suppl. 1998(582):50-5.

23. Bray GA. Drug treatment of obesity. Baillieres Best Pract Res Clin Endocrinol Metab. 1999 Apr;13(1):131-48.



All photos purchased from Shutterstock by UCLA CNS Permission to use an alter granted to Dr. Gordon