Tag Archives: symbiont

Stress, Microbiome, Inflammation and the Pancreas & Liver

flow chart stress intestinal function inflammation

Sometimes things happen that seem to come out of nowhere. It happens to all of us, usually when we least expect it because we are busy taking care of others or life in general. So here’s a scenario: Imagine that one day your blood sugar suddenly skyrockets and your Medical physician informs you that your liver and pancreas are not functioning properly. What could cause this? Well, many things could, but the one thing in common is inflammation. If the pancreas is inflamed, the Islets of Langerhans sometimes stop producing insulin and blood sugar doesn’t get stored, so it jumps up. If the inflammation is early in life, the immune system may go to the point of forming antibodies to the Islets, destroying them and causing Type 1 diabetes. If the body becomes inflamed later in life, cells may not respond to insulin anymore, causing Type 2 diabetes. But if the pancreas is inflamed, it doesn’t work properly. The liver can be implicated too, as it stores extra energy (glucose) reserves for when you need them. Liver inflammation can also cause diabetes. While these changes are all known to occur in people that are obese and have an unhealthy diet, how is it possible for it to happen this quickly, and in someone who isn’t obese? The answer lies in the fact that the immune system is mostly controlled by our gut bacteria and GALT, or gut-associated lymphoid tissue, dendritic nerve endings, and other points of information exchange between the microbiome and the host immune system.

Research has shown that exposure to short-term social/emotional stress causes alteration of the gut microbiome. This altered microbiome in turn does not control the immune system approriately, resulting in increased systemic inflammation (which can make the social stress worse, as both the inflammation and the altered microbiome affect brain function and mood). See the illustration above, which is from my book The Symbiont Factor.

Another factor that can alter the microbiome and trigger widespread inflammation is short term dietary change, to a less beneficial diet. In research terminology, a diet that causes microbiome demise, inflammation and disease is called a Western Diet. It is used to produce a sick lab animal to study, and mimics what the average American consumer eats every day.

Sleep is absolutely necessary for a healthy microbiome, and disruptions of our circadian rhythms and sleep cycles has been shown to disrupt our microbiome and cause inflammation.

Exposure to air affects our microbiome too! Air is actually replete will huge numbers of human skin cells and bacteria from other people in the vicinity. The longer we are in a space with other people, the more we inhale parts of their microbiome combined with the microbiome of the space. These organisms then influence our own microbiome, so if the exposure was to unhealthy microbiomes, the result can be…inflammation once more.

Sometimes the scenario can revive imbalances and infections we’ve had before, such as chronic viral infections (shingles, for example, or herpes) or chronic bacterial infections such as Lyme disease-where the organism was in a dormant state due to good immune function-waiting for an opportunity.

Ok, so…can we picture a scenario where all of the above are combined? Stress, bad food, interrupted sleep with no real dark/light cycles, and lots of sick people/bad bacteria? Bingo-it’s the place where we send people to get well: a hospital.

What should we do to recover from this systemic inflammation?

  1. Regular sleep, hitting the bed and waking same time every day, preferably in a multiple of 90 minutes. So, 6 hours, 7.5 hours, 9 hours so that we don’t interrupt a sleep cycle. No lights, no devices at night. No bright little blue “charging” LEDs.
  2. Healthy food, and preferably some of it fermented. There is a great fermented oatmeal recipe earlier on this blog, and many areas have private individuals making fantastic fermented vegetables. Here in coastal Maine, “A Stone’s Throw to Health” is one such business, with handcrafted ferments by Sheila Perloff-Eddison.
  3. Avoid deep fried food, hydrogenated fats, sweets, gluten. Even if you’re not gluten sensitive, eating it when you’re inflamed raises the odds of you becoming gluten sensitive. No fast food. Real meat, vegetable, greens, fruit.
  4. Probiotic Bifidobacteria, in double the normal doses. Add prebiotic inulin, pectin, FOS, GOS supplements to help feed the newly introduced organisms.
  5. Curcumin is hugely effective for reducing inflammation, improving insulin sensitivity, healing liver and pancreas. Not turmeric, which is 5% curcumin, but 95% curcumin-the real stuff. I take 6-8 capsules a day, minimum, if I’m injured or inflamed. It works better than drugs-check out the Ghosh study in the bibliography below.
  6. Some other products, such as jerusalem artichokes/sunchokes, jicama, artichokes, asparagus, pomegranate, rhubarb, ginger have been shown to have fantastic prebiotic and anti-inflammatory benefits.
  7. Make a point of, several times per day, praying or meditating on peaceful/optimistic and loving thoughts while breathing deeply. The physiologic effects improve autonomic tone and gut function, helping to recolonize healthy bacteria while healing gut membranes.

 

Sources:

Fermented Vegetables: http://www.astonesthrowtohealth.com/

Curcumin: http://progressivelabs.com/product.php?productid=17110&cat=0&page=1

Inulin: http://www.amazon.com/Prebiotin-Prebiotic-Fiber-8-5-Powder/dp/B001RVFSFS/ref=sr_1_2_a_it?ie=UTF8&qid=1459361720&sr=8-2&keywords=prebiotic

For more info: http://www.amazon.com/Symbiont-Factor-Microbiome-Redefines-Humanity/dp/1500553948/

Fermented oatmeal recipe: https://thesymbiontfactorblog.com/2016/01/26/super-synbiotic-breakfast-improved/

 

Bibliography:

Rhubarb extract prevents hepatic inflammation induced by acute alcohol intake, an effect related to the modulation of the gut microbiota.

Neyrinck AM, Etxeberria U, Taminiau B, Daube G, Van Hul M, Everard A, Cani PD, Bindels LB, Delzenne NM.

Mol Nutr Food Res. 2016 Mar 18. doi: 10.1002/mnfr.201500899. [Epub ahead of print]

PMID:26990039

Combination with Red ginseng and Polygoni Multiflori ameliorates highfructose diet induced metabolic syndrome.

Kho MC, Lee YJ, Park JH, Cha JD, Choi KM, Kang DG, Lee HS.

BMC Complement Altern Med. 2016 Mar 9;16(1):98. doi: 10.1186/s12906-016-1063-7.

PMID:26961224

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Chronic Psychological Stress Disrupted the Composition of the Murine Colonic Microbiota and Accelerated a Murine Model of Inflammatory Bowel Disease.

Watanabe Y, Arase S, Nagaoka N, Kawai M, Matsumoto S.

PLoS One. 2016 Mar 7;11(3):e0150559. doi: 10.1371/journal.pone.0150559. eCollection 2016.

PMID:26950850

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Early Alterations in Glycemic Control and Pancreatic Endocrine Function in Nondiabetic Patients With Chronic Pancreatitis.

Lundberg R, Beilman GJ, Dunn TB, Pruett TL, Freeman ML, Ptacek PE, Berry KL, Robertson RP, Moran A, Bellin MD.

Pancreas. 2016 Apr;45(4):565-71. doi: 10.1097/MPA.0000000000000491.

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Hepatoprotective Effect and Synergism of Bisdemethoycurcumin against MCD Diet-Induced Nonalcoholic Fatty Liver Disease in Mice.

Kim SB, Kang OH, Lee YS, Han SH, Ahn YS, Cha SW, Seo YS, Kong R, Kwon DY.

PLoS One. 2016 Feb 16;11(2):e0147745. doi: 10.1371/journal.pone.0147745. eCollection 2016.

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Protective Role of Dietary Curcumin in the Prevention of the Oxidative Stress Induced by Chronic Alcohol with respect to Hepatic Injury and Antiatherogenic Markers.

Varatharajalu R, Garige M, Leckey LC, Reyes-Gordillo K, Shah R, Lakshman MR.

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Maithilikarpagaselvi N, Sridhar MG, Swaminathan RP, Sripradha R.

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Curcumin Attenuates Oxidative Stress and Activation of Redox-Sensitive Kinases in High Fructose- and High-Fat-Fed Male Wistar Rats.

Maithili Karpaga Selvi N, Sridhar MG, Swaminathan RP, Sripradha R.

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Maithilikarpagaselvi N, Sridhar MG, Swaminathan RP, Zachariah B.

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Abarikwu SO, Durojaiye M, Alabi A, Asonye B, Akiri O.

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Liu Z, Dou W, Zheng Y, Wen Q, Qin M, Wang X, Tang H, Zhang R, Lv D, Wang J, Zhao S.

Mol Med Rep. 2016 Feb;13(2):1717-24. doi: 10.3892/mmr.2015.4690. Epub 2015 Dec 17.

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Morrone Mda S, Schnorr CE, Behr GA, Gasparotto J, Bortolin RC, da Boit Martinello K, Saldanha Henkin B, Rabello TK, Zanotto-Filho A, Gelain DP, Moreira JC.

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Int J Clin Exp Pathol. 2015 Sep 1;8(9):11503-9. eCollection 2015.

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Curcumin attenuates chronic ethanol-induced liver injury by inhibition of oxidative stress via mitogen-activated protein kinase/nuclear factor E2-related factor 2 pathway in mice.

Xiong ZE, Dong WG, Wang BY, Tong QY, Li ZY.

Pharmacogn Mag. 2015 Oct-Dec;11(44):707-15. doi: 10.4103/0973-1296.165556.

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High Fat High Cholesterol Diet (Western Diet) Aggravates Atherosclerosis, Hyperglycemia and Renal Failure in Nephrectomized LDL Receptor Knockout Mice: Role of Intestine Derived Lipopolysaccharide.

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PLoS One. 2015 Nov 18;10(11):e0141109. doi: 10.1371/journal.pone.0141109. eCollection 2015.

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T-Helper Cell-Mediated Islet Inflammation Contributes to β-Cell Dysfunction in Chronic Pancreatitis.

Talukdar R, Sasikala M, Pavan Kumar P, Rao GV, Pradeep R, Reddy DN.

Pancreas. 2016 Mar;45(3):434-42. doi: 10.1097/MPA.0000000000000479.

PMID:26474432

Curcumin Induces Pancreatic Adenocarcinoma Cell Death Via Reduction of the Inhibitors of Apoptosis.

Díaz Osterman CJ, Gonda A, Stiff T, Sigaran U, Valenzuela MM, Ferguson Bennit HR, Moyron RB, Khan S, Wall NR.

Pancreas. 2016 Jan;45(1):101-9. doi: 10.1097/MPA.0000000000000411.

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Curcumin inhibits lung cancer invasion and metastasis by attenuating GLUT1/MT1-MMP/MMP2 pathway.

Liao H, Wang Z, Deng Z, Ren H, Li X.

Int J Clin Exp Med. 2015 Jun 15;8(6):8948-57. eCollection 2015.

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Curcumin attenuates ethanol-induced hepatic steatosis through modulating Nrf2/FXR signaling in hepatocytes.

Lu C, Zhang F, Xu W, Wu X, Lian N, Jin H, Chen Q, Chen L, Shao J, Wu L, Lu Y, Zheng S.

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Naijil G, Anju TR, Jayanarayanan S, Paulose CS.

Nutr Res. 2015 Sep;35(9):823-33. doi: 10.1016/j.nutres.2015.06.011. Epub 2015 Jul 2.

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Pancreatic β-Cells Limit Autoimmune Diabetes via an Immunoregulatory Antimicrobial Peptide Expressed under the Influence of the Gut Microbiota.

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Immunity. 2015 Aug 18;43(2):304-17. doi: 10.1016/j.immuni.2015.07.013. Epub 2015 Aug 4.

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Transl Res. 2016 Jan;167(1):214-27. doi: 10.1016/j.trsl.2015.04.011. Epub 2015 Apr 29. Review.

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Kostic AD, Gevers D, Siljander H, Vatanen T, Hyötyläinen T, Hämäläinen AM, Peet A, Tillmann V, Pöhö P, Mattila I, Lähdesmäki H, Franzosa EA, Vaarala O, de Goffau M, Harmsen H, Ilonen J, Virtanen SM, Clish CB, Orešič M, Huttenhower C, Knip M; DIABIMMUNE Study Group, Xavier RJ.

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Curcumin ameliorates streptozotocin-induced liver damage through modulation of endoplasmic reticulum stress-mediated apoptosis in diabetic rats.

Afrin R, Arumugam S, Soetikno V, Thandavarayan RA, Pitchaimani V, Karuppagounder V, Sreedhar R, Harima M, Suzuki H, Miyashita S, Nomoto M, Suzuki K, Watanabe K.

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Rashid K, Sil PC.

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Greiner TU, Hyötyläinen T, Knip M, Bäckhed F, Orešič M.

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Bifidobacterium breve in premature infants…Really no benefit?

2baby newborn b

It’s early morning on the Maine coast, and as I do my usual “thing” and look at my social media feeds I see a pattern on Twitter: dozens of people have either written about or retweeted references to a Lancet study showing “no benefit for Bifidobacterium breve in premature infants”. Well, that sounded unlikely to me, so I started to drill deeper into the information. First, it is important to state that several prior studies have found that Bifido does indeed help; a review of the studies by Baucells had the same conclusion. There is a very obvious major problem with the logic behind the study saying there is no benefit, and I’m going to point it out in a moment. Let’s look at a bit of background for anyone not familiar with the issues discussed.

Our bodies are colonized by trillions of symbiotic bacteria, and they help to build our immune system and keep our gut healthy (along with many other critical functions). Premature infants face several challenges, including necrotizing enterocolitis-an inflammatory infection of the intestines that is often fatal. The colonization of the intestines with symbiotic bacteria begins prior to birth, but really progresses after normal birth because of ingestion of a starter culture of vaginal bacteria and breastfeeding, which provides needed prebiotics (substances that feed beneficial bacteria) present in breast milk. Not breastfeeding is a risk factor for an abnormal gut bacterial population, as is birth by c-section, as both rob the infant of the mother’s bacteria. Premature infants often face both challenges.

The research study in question examined the use of a strain of Bifidobacterium breve in premature infants to reduce the incidence of necrotizing enterocolitis. The probiotic was added to dilute elemental infant formula, with the control group receiving only the formula. There was no benefit found to the introduction of B. breve in this manner. This finding has been trumpeted across the Twitterverse since the study was published, usually with the title just saying there is no benefit.

The first issue is that infant formula has already been shown to be inferior to human breast milk for the prevention of necrotizing enterocolitis (Hay). Why use infant formula instead of human breast milk? Apparently this is quite common, which astounds me. With the hundreds of thousands of dollars in equipment and training involved in premature infant care, human breast milk is not routinely used although it reduces fatal infections?  I was actually a little shocked by this, but considering the anti-breastfeeding bias that still exists for some reason, it may not be so surprising. Corporate influence on the birth process has long promoted formula over breast, against all scientific logic.

The second issue is related to the first. One of the basic foundation concepts of probiotic interventions that is familiar to any health practitioner versed in symbiont-based health strategies is “Seed and Feed”. Adding beneficial organisms and then not feeding them does not work as well as nourishing them after their introduction. Sounds simple enough, right? Studies have already been done showing that formula and breast milk are quite different in their effect on symbiont organisms (Liu) with breastmilk being superior. Another study (Repa) showed that probiotics prevented necrotizing enterocolitis in infants fed breastmilk but not in those fed formula. Another study (Yao) found that adding Oligosaccharides (a prebiotic) to infant formula raised Bifidobacterium levels in those infants.

So, in summary, this study found that the introduction of Bifidobacterium probiotic to a premature baby receiving formula of no nutritional benefit to the organism was of no benefit. And this is somehow considered newsworthy? The concepts behind “seed and feed” are not revolutionary, complex nor undiscovered. It isn’t rocket science; if you don’t feed the organisms they do not survive. Yet, the articles referring to the study simply state “Bifidobacterium of no use in premature infants”…..which is simply not true, even if it is “on the Interwebs”.

References:

The Symbiont Factor: http://tinyurl.com/h2m5lq8

1.

Bifidobacterium breve BBG-001 in very preterm infants: a randomised controlled phase 3 trial.

Costeloe K, Hardy P, Juszczak E, Wilks M, Millar MR; Probiotics in Preterm Infants Study Collaborative Group.

Lancet. 2015 Nov 25. doi:pii: S0140-6736(15)01027-2. 10.1016/S0140-6736(15)01027-2. [Epub ahead of print]

 
2.

[Probiotic associations in the prevention of necrotising enterocolitis and the reduction of late-onset sepsis and neonatal mortality in preterm infants under 1,500g: A systematic review].

Baucells BJ, Mercadal Hally M, Álvarez Sánchez AT, Figueras Aloy J.

An Pediatr (Barc). 2015 Nov 20. doi:pii: S1695-4033(15). 10.1016/j.anpedi.2015.07.038. [Epub ahead of print] Spanish.

PubMed [citation]
3.

Effects of term infant formulas containing high sn-2 palmitate with and without oligofructose on stool composition, stool characteristics, and bifidogenicity.

Yao M, Lien EL, Capeding MR, Fitzgerald M, Ramanujam K, Yuhas R, Northington R, Lebumfacil J, Wang L, DeRusso PA.

J Pediatr Gastroenterol Nutr. 2014 Oct;59(4):440-8. doi: 10.1097/MPG.0000000000000443.

 
4.

Probiotics (Lactobacillus acidophilus and Bifidobacterium bifidum) prevent NEC in VLBW infants fed breast milk but not formula.

Repa A, Thanhaeuser M, Endress D, Weber M, Kreissl A, Binder C, Berger A, Haiden N.

Pediatr Res. 2015 Feb;77(2):381-8. doi: 10.1038/pr.2014.192. Epub 2014 Nov 25.

5.

Human Breast Milk and Infant Formulas Differentially Modify the Intestinal Microbiota in Human Infants and Host Physiology in Rats.

Liu Z, Roy NC, Guo Y, Jia H, Ryan L, Samuelsson L, Thomas A, Plowman J, Clerens S, Day L, Young W.

J Nutr. 2015 Dec 16. doi:pii: jn223552. [Epub ahead of print]

 
6.

Strategies for Feeding the Preterm Infant.

Hay WW Jr.

Neonatology. 2008/01/01 00:00; 94(4): 245-254

PMC [article]

 

 

 

The Microbiome as an Ecosystem. What’s in common between wolves and our microbiome?

tick_deer

The microbiome is often described as an ecosystem, but what does that mean really? To understand this, we really have to use a bigger analogy, one that applies to an ecosystem that we can see. A video about the wolves of Yellowstone National Park has been making the rounds on Facebook (https://www.youtube.com/watch?v=ysa5OBhXz-Q), and it does a great job of illustrating how things really work. Most of us are led to believe that biological systems are inherently stable, but that is simply not true-they are truly quite dynamic and always in a state of flux. In the Yellowstone example, the reintroduction of a few wolves after a 70 year absence caused a cascade effect greatly out of perceived proportion to the introduction of a few animals. The wolves chased the elk out of the valleys and river basins, where they had been overgrazing. This resulted in increased grass, shrub and tree growth, which reduced river erosion and altered the whole terrain. The effect was compounded by bears descending to the valleys to eat from the newly grown berries, chasing more elk away. Beavers returned, since they eat the bark of the young trees. Their activities changed the topography even further! Many other species end up returning, bringing stability to the ecosystem. That is a recurrent theme: ecosystem diversity increases function and systemic stability.

When we consider our internal ecosystem, a similar effect happens. When the microbiome is healthy and diverse, its effects can be seen in skin, immune, brain, hormone function along with practically everything else directly or indirectly. The person is healthier, happier and better functioning physically, mentally and emotionally. Isn’t that the goal when we want to become “healthy?”

In contrast is the unhealthy microbiome, often resulting from poor diet or antibiotics in food or as medicine, and function is lost throughout the body. As I’m working on a short book on Lyme disease, I am constantly reminded of this. The tremendous loss of diversity in gut bacteria (one patient’s uBiome results showed her to be in the “0 percentile” compared to other women for gut bacterial diversity) results in immune dysfunction. Examples include a loss of Interleukin-10 production, important because it protects brain cells from bacterial infection as occurs in neuroborreliosis. IL-10 also inhibits inflammatory IL-17 production triggered by the Lyme spirochete, thereby restoring the integrity of the blood-brain barrier and joint capsule membranes, making it harder for the spirochete to evade phagocytic immune cells sent to kill it. Another classic example is microbiome production of alpha-galactosylceramide, which activates invariant Natural Killer T-cells. These iNKT cells are necessary for several of the body’s immune reactions to Borrelia burgdorferi, the Lyme bug. So, through antibiotic treatment to kill Borrelia, the body’s microbiome is decimated-taking with it much of the immune response needed to prevent reinfection or relapse. Why is this important, and what can we do about it? well…stay tuned to find out!

 

 

 

 

 

 

New Study shows a Bacterial Colony communicates like a Brain!

Human intelligence brain medical symbol represented by a close up of active neurons and organ cell activity related to neurotransmitters showing intelligence with memory and healthy cognitive thinking activity.

A new study published recently has shown that bacterial colonies have an additional channel of communication than previously thought-they can communicate through ionic channels between cells. This allows bacteria in a colony to exchange data through electrical impulses; electrically charges particles (ions) in a manner remarkably similar to how a brain’s neurons communicate with one another!

This new study is fascinating to me, as one of the principal concepts in The Symbiont Factor was that a bacterial colony acts more like a multicellular organism than a group of single celled organisms. Professor Eshel Ben-Jacob had shown this communication ability through his many research studies, and was the first (as far as I know) to profess that colonies functioned in a logical intelligent manner. In my book, I show how gut bacteria influence the host organism to facilitate their continued survival and reproduction (traits normally attributed to far more complex organisms) by altering our metabolism, gut function, appetite for different items, brain function and many other variables.

This new study should make the health of your symbiont bacterial colony even more of a priority!

http://ucsdnews.ucsd.edu/pressrelease/biologists_discover_bacteria_communicate_like_neurons_in_the_brain

http://www.sciencedaily.com/releases/2013/05/130528180900.htm

http://www.ncbi.nlm.nih.gov/pubmed/26200335

http://www.ncbi.nlm.nih.gov/pubmed/18298829

http://www.ncbi.nlm.nih.gov/pubmed/25968641

From the Zombie Files: Ampulex dementor, obesity, and brains. What’s the connection?

One of the central concepts of The Symbiont Factor is that there are times in nature that organisms can take control of another organism’s nervous system, rendering it “a zombie”. This isn’t a zombie in the Hollywood sense, just a host organism that no longer is singularly in control of itself due to the effects of other organisms that “hijack” its nervous system.

In this case, a new organism has been discovered, a fearsome looking wasp in Thailand. This wasp hunts cockroaches, and injects a neurotoxin into them. This makes the cockroach lose active control of its legs so that it cannot escape, and the wasp can eat it slowly while it is still alive. Nature really has some gruesome stories, doesn’t it?

In our own bodies, we have a colony of trillions of bacteria. The late Prof Eshel Ben-Jacob performed experiments and wrote articles documenting how large bacterial colonies were able to act with logic, more as multicellular  organisms. Like multicellular organisms, their activities have a goal: survival. In the case of our microbiome, it is beginning to appear that their ability to alter our nervous system function and our brain activity is not randomized. There is a bi-directional influence at work: as an example, the bacteria that thrive on a fatty diet make us crave fatty foods, and those that thrive on sweets make us crave sweets. If we eat the fatty foods or sweets, it of course preferentially benefits the organisms that thrive on it. This is why there seems to be a “tipping point” in gaining weight such that our energy level drops and our appetite changes, facilitating weight gain. The actual organisms that help us lose weight and stay lean have been identified (Akkermansia mucinophilia is one example), as have those that make us gain weight. Their effect is significant enough that they have been called “obesogens”. It isn’t a single organism but a pattern of demographic shift-more of these/less of those-that results in weight gain or loss.

The changes to brain function, sensory sensitivity (ie what smells tasty to you), mood and behavior shift (a stress microbiome!) make us just a little like a zombie too in some cases. Certainly our behavior and our function is the result of the activity of trillions of symbiont organisms as well as our own decision-making. In effect “we” are composed of many organisms!

Relevant links (many are in the bibliography of The Symbiont Factor: http://tinyurl.com/p3b9o9d):

http://www.treehugger.com/natural-sciences/terrifying-new-dementor-wasp-species-named-evil-spirits-harry-potter.html

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3995701/

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4380304/

http://www.ncbi.nlm.nih.gov/pubmed/26047662

http://www.ncbi.nlm.nih.gov/pubmed/24430437

http://www.ncbi.nlm.nih.gov/pubmed/25968641

http://www.ncbi.nlm.nih.gov/pubmed/25401094

http://iopscience.iop.org/1478-3975/11/5/053009/pdf/1478-3975_11_5_053009.pdf

The Brain as a Puppet: Gut Bacterial Control of Human Development and Behavior

Human intelligence brain medical symbol represented by a close up of active neurons and organ cell activity related to neurotransmitters showing intelligence with memory and healthy cognitive thinking activity.

Human intelligence brain medical symbol represented by a close up of active neurons and organ cell activity related to neurotransmitters showing intelligence with memory and healthy cognitive thinking activity.

One of the most fascinating discoveries of the last decade is the extent of influence that our bacterial microbiome has on our brain. We are really quite used to thinking of “ourselves” as a singular identity and yet our very mind may be more of a chorus than a solo. Trillions of bacteria all compete to have their needs met and their voice heard, and all of them have the ability to alter the very function of our brain at the most fundamental level. Several research papers have documented this (see references below in case you feel I’m off my rocker for saying some of the things I’m going to say 🙂

Today’s researchers are examining the many ways that gut bacteria can communicate with the human brain, and have found many pathways. The symbionts can alter the sensitivity of our neurotransmitter receptors, can release molecules that mimic neurotransmitters, produce neurotransmitters and release them into blood circulation, inflict pain or stimulate pleasure. What is the motive and why would they do this? How did bacteria learn Pavlovian training and use it to manipulate our mood, behavior and activity? The answer goes back quite far, but comes down to one thing: survival. From the beginning of evolution, bacteria have influenced the development of the multicellular organism. In many ways, you could look at bacteria as the most basic unit of life although this is generally a title attributed to the cell. Cells themselves are composed of structures that may have originated as bacteria that learned/evolved cooperative relationships. Today’s robotics researchers are studying spontaneous collective functioning as well, a parallel interest of mine. We now are fairly certain that gut bacterial symbionts not only guide the development of the human brain after birth, but influence its development before birth as well. To take that thought a step further, previous generations of symbionts have guided and facilitated the evolution of the human brain itself. Their genetic reservoir of DNA “data” is orders of magnitude greater than that of the human host, and has the ability to evolve and adapt on-the-fly during a lifetime. This gives the potential for intragenerational evolution as well as intergenerational, allowing us to evolve a bit during our lifetime and then pass this on to our children (unless they are born by caesarian section or blasted with antibiotics and vaccinations at a young age, but…that is the subject of other posts!) During our lifetime, from our earliest moments, our symbiont organisms are constantly tweaking our behavior and senses to suit their needs. In a way, we are the machine that permits them to live as a multicellular organism in a far more advanced manner, and in a world that many of them cannot survive in without us. It’s as if we built a gigantic robot that could house the entire human population (except, well, there are more gut bacteria in one human than there are humans on the planet) and used this robot to live in places that we normally could not survive in. We would certainly guide the robot to find foods that we can benefit from and do things that aid our survival. Gut bacteria do exactly that, and very elegantly. It isn’t coincidence that obligate anaerobes cause us to be stressed, which makes us breathe shallowly, tense up our muscles so they burn up oxygen, and even begin to develop apnea during the daytime and at night. What is the result? less oxygen in the gut, and that is what an obligate anaerobe benefits from. Our eating behavior is controlled by gut symbionts, to the point that some can inflict pain directly if we don’t eat something they need or trigger euphoric feeling when we give in and eat what they need. This is the reason that “diets” are so challenging, and particularly so for the obese individual-we are Pavlov’s dog, and the trainer has a cattle prod in one hand and a direct brain pleasure stimulation in the other. What will be your choice today? Yes, we can overcome that and eat a diet of “our” choosing, but only successfully after that diet and behavior changes result in changes to the microbiome. You see, once the microbiome is fed a certain way, the organisms that survive on that diet are the ones that become dominant. You can “starve out” harmful/nonbeneficial organisms, but it isn’t easy or pleasant. During a recent podcast interview with the entertaining and brilliant Clint Paddison (The Paddison Program for Rheumatoid Arthritis) he explained to me that fasting is a primary step in recovery/healing from RA. So, you see, we are as much the puppet as the master-it’s a two way street and while the host influences the symbionts, it works both ways. Symbionts can change our very perception of our world, altering our senses to guide our behavior to their benefit.

Ok, so with these thoughts in “mind” consider what the true effect of our diet is. Every single thing you eat and drink or even breathe alters symbiont bacteria to favor those that thrive on the substances in question. Eat a lot of fast “food”? You’ve selectively feeding the organisms that thrive on that. The problem is that apparently most of them are not beneficial to host health! We should also consider that all of these changes to gut bacteria as a result of our eating/drinking/breathing have consequences to our mental function. Everything from mental clarity, intelligence, emotional stability, personality-our very potential as human beings-is influenced by the bacteria that live in our gut. So which do you want to feed, the ones that may make you feel ill mentally and physically or the ones that could help you reach your true potential and live as long and healthy a life as possible?

If you’re intrigued by this discussion even a bit, you should consider reading the reference articles below. If you’d like to understand the subject better but want to read it in English and not research-ese, then please read my book, The Symbiont Factor. You can find it on Amazon as an e-book or paperback at the following link: http://tinyurl.com/p7mx6hh

References:

http://www.ncbi.nlm.nih.gov/pubmed/25401092

http://www.ncbi.nlm.nih.gov/pubmed/25772005

http://www.ncbi.nlm.nih.gov/pubmed/25103109

http://www.ncbi.nlm.nih.gov/pubmed/25974299

Top Ten Reasons that the Microbiome Matters:

As I’ve been busily shutting down one clinic to open another, I’ve logged many miles of driving-which has given me time to think about the microbiome as well (really!) Why would the microbiome matter? Here’s my top ten list, as a microbial tribute to David Letterman’s years of late night entertainment:

10. It guides the development of the human brain early in life

9. It influences our moods, desires, behaviors throughout life

8. The microbiome helps develop and guide the immune system

7. Our HPA axis (Hypothalamus, Pituitary, Adrenal) is heavily influenced by the microbiome early in life, which determines our response to stress…

6. The human microbiome can alter the way our brain’s receptors respond to neurotransmitters, changing it significantly.

5. If our microbiome becomes imbalanced (dysbiosis) it can cause inflammation, brain dysfunction, immune dysfunction, changes in appetite, obesity, depression…and many other problems

4. The microbiome is extremely vulnerable to antibiotics from doctors or in (non-organic) meat that we consume. Once species die off and diversity is lost, dysbiosis results

3. Glyphosate, the most commonly used herbicide on the planet, is toxic to gut bacteria (and also mitochondria that supply our cells with energy)

2. Gut bacteria are true symbiont organisms; they aren’t “hitching a ride” but are indeed a part of us that functions more like a vital organ. They are part of why we are alive; death of the microbiome causes disease and aging!

1. The only source of energy that fuels this planet is sunlight, and only plants (true plants, algae, cyanobacteria) can process sunlight into biomass. After that, only bacteria can digest plants to produce energy…so everything from termites to cattle including us can only digest plants because of our gut bacteria. No gut bacteria? very very bad news!

So, get out your copy of my book, The Symbiont Factor, and read up on the microbiome, okay? Oh, you don’t have it yet? Be good to your bugs and buy a copy then!

http://tinyurl.com/kh4g8nm