Branched Chain Amino Acids, BCAA’s, are a common addition to the diet for bodybuilders and athletes. Here’s a new research study, published this month, that shows BCAA’s help change your gut bacteria. Specifically, the encourage more Bifidobacteria (which boosts immune function but lowers inflammation) and Akkermansia (which helps build lean muscle mass and reduce fat). As there is much research now connecting aging with inflammation, even calling it “inflammaging”, these are both great things. It’s also somewhat of a departure from the thought of usng probiotics and prebiotics to modulate the gut bacteria, adding amino acids to our microbiome toolbox!
Most of us should be familiar with the disease known as Parkinson’s Disease, which ruins countless lives by creating a movement disorder characterized by shaking type of movements. It leads to difficulty moving at all, and in late stages the most common treatments lead to dyskinesthia which is a type of writhing uncontrolled movement. Without detailing the actual nerve pathways, part of the problem is neurodegeneration in a part of the brain called the basal ganglia, in an area known as the Substantia Nigra. When this area is overtaxed and inflamed, a process known as oxidative stress occurs, damaging neurons and created neurofibrous “tangles” known as α-synuclein aggregations.
There is a great deal of research that has been done to detail some natural ingredients that can be used to either prevent, or help treat Parkinson’s. These can sometimes reduce the amount of medication needed, and postpone the onset of dyskinesthia. In some cases successful treatment has occurred and symptoms are gone. The major “theme” of treatment with natural products is to reduce inflammation, block oxidative stress, and promote healthy metabolism in those neuronal cells.
Curcumin is an extract of turmeric, and contains 95% curcuminoids-the active ingredient. This makes it 19 times stronger than turmeric, which only contains 5%. Curcumin has been found to block inflammation, reduce oxidative stress, rescue nerve cells that have been affected, and even to reverse the accumulation of α-synuclein in the brain. I’ve attached a little over two dozen peer-reviewed studies about curcumin and Parkinson’s in the Bibliography. Curcumin is best taken before a meal, and with a tablespoon of coconut oil which boosts absorption and is good for the brain as well.
Another useful herb is Skullcap, Scuttelaria baikalensis, which contains the ingredient Baicalein. This has also been extensively studied for use in treating and reversing some of the effects of Parkinson’s, and is a very promising herb. Note that there aren’t any studies that look at what would happen if you use this AND curcumin, but you can imagine that it should work even better as they do not function through the same mechanisms.
The last strategy I’d like to mention is gut bacteria optimization. As I wrote an entire book about gut bacteria (The Symbiont Factor) I’ll try to be brief. Our gut bacteria wield a big influence on brain and immune function, helping to both tone and control immune function and regulate both the production of neurotransmitters and the sensitivity of neurotransmitter receptor sites in the brain. An imbalance of gut bacteria, which can be assessed with a uBiome.com gut bacteria census, can create functional changes that make the brain less efficient and more inflamed. This sets the stage for Parkinson’s, as neuroinflammation is a required building block of this disease.
Now, you might ask yourselves why this information is not more well known in the Parkinson’s world…it doesn’t actually even appear on the National Parkinson’s Foundation website although many less effective interventions are mentioned. This is because, simply, much of the research is done in search of new drugs to create by copying the action of useful herbs and natural processes. This is one way that companies explore for new drugs that can be patented. The real question is why we would wait for that, when the research shows these natural substances to be quite effective in lab and animal models. Of course, double-blind trials on humans will not be performed until drug candidates are created…so don’t look for the final proof of natural substances, because these trials are very expensive and are only carried out when a candidate drug ($$$) is being evaluated. In other words, follow the money!
The Symbiont Factor: http://tinyurl.com/z5568ct
Hu Q, Uversky VN, Huang M, Kang H, Xu F, Liu X, Lian L, Liang Q, Jiang H, Liu A, Zhang C, Zhu S.
Biochim Biophys Acta. 2016 Jul 14. pii: S0925-4439(16)30168-5. doi: 10.1016/j.bbadis.2016.07.008. [Epub ahead of print]
Gao L, Li C, Yang RY, Lian WW, Fang JS, Pang XC, Qin XM, Liu AL, Du GH.
Pharmacol Biochem Behav. 2015 Jun;133:155-63. doi: 10.1016/j.pbb.2015.04.004. Epub 2015 Apr 18.
Xue X, Liu H, Qi L, Li X, Guo C, Gong D, Qu H.
Brain Res Bull. 2014 Apr;103:54-9. doi: 10.1016/j.brainresbull.2014.02.004. Epub 2014 Feb 24.
Wang YH, Yu HT, Pu XP, Du GH.
Molecules. 2013 Nov 27;18(12):14726-38. doi: 10.3390/molecules181214726.
Lee E, Park HR, Ji ST, Lee Y, Lee J.
J Neurosci Res. 2014 Jan;92(1):130-9. doi: 10.1002/jnr.23307. Epub 2013 Oct 28.
Zhang Z, Cui W, Li G, Yuan S, Xu D, Hoi MP, Lin Z, Dou J, Han Y, Lee SM.
J Agric Food Chem. 2012 Aug 22;60(33):8171-82. doi: 10.1021/jf301511m. Epub 2012 Aug 9.
Yu X, He G, Du G.
Zhongguo Zhong Yao Za Zhi. 2012 Feb;37(4):421-5. Review. Chinese.
Yu X, He GR, Sun L, Lan X, Shi LL, Xuan ZH, Du GH.
Life Sci. 2012 Jul 26;91(1-2):5-13. doi: 10.1016/j.lfs.2012.05.005. Epub 2012 May 23.
Lu JH, Ardah MT, Durairajan SS, Liu LF, Xie LX, Fong WF, Hasan MY, Huang JD, El-Agnaf OM, Li M.
Chembiochem. 2011 Mar 7;12(4):615-24. doi: 10.1002/cbic.201000604. Epub 2011 Jan 26.
Gasiorowski K, Lamer-Zarawska E, Leszek J, Parvathaneni K, Yendluri BB, Błach-Olszewska Z, Aliev G.
CNS Neurol Disord Drug Targets. 2011 Mar;10(2):184-91. Review.
Hong DP, Fink AL, Uversky VN.
J Mol Biol. 2008 Oct 31;383(1):214-23. doi: 10.1016/j.jmb.2008.08.039. Epub 2008 Aug 23.
Zhu M, Rajamani S, Kaylor J, Han S, Zhou F, Fink AL.
J Biol Chem. 2004 Jun 25;279(26):26846-57. Epub 2004 Apr 19.
van der Merwe C, van Dyk HC, Engelbrecht L, van der Westhuizen FH, Kinnear C, Loos B, Bardien S.
Mol Neurobiol. 2016 Mar 22. [Epub ahead of print]
Song S, Nie Q, Li Z, Du G.
Pathol Res Pract. 2016 Apr;212(4):247-51. doi: 10.1016/j.prp.2015.11.012. Epub 2015 Nov 18.
Cui Q, Li X, Zhu H.
Mol Med Rep. 2016 Feb;13(2):1381-8. doi: 10.3892/mmr.2015.4657. Epub 2015 Dec 8.
Uğuz AC, Öz A, Nazıroğlu M.
J Recept Signal Transduct Res. 2016 Aug;36(4):395-401. doi: 10.3109/10799893.2015.1108337. Epub 2015 Nov 25.
Ganesan P, Ko HM, Kim IS, Choi DK.
Int J Nanomedicine. 2015 Oct 29;10:6757-72. doi: 10.2147/IJN.S93918. eCollection 2015. Review.
Fu W, Zhuang W, Zhou S, Wang X.
Am J Transl Res. 2015 Jul 15;7(7):1189-202. eCollection 2015. Review.
Spinelli KJ, Osterberg VR, Meshul CK, Soumyanath A, Unni VK.
PLoS One. 2015 Jun 2;10(6):e0128510. doi: 10.1371/journal.pone.0128510. eCollection 2015.
Tizabi Y, Hurley LL, Qualls Z, Akinfiresoye L.
Molecules. 2014 Dec 12;19(12):20864-79. doi: 10.3390/molecules191220864. Review.
Phom L, Achumi B, Alone DP, Muralidhara, Yenisetti SC.
Rejuvenation Res. 2014 Dec;17(6):481-9. doi: 10.1089/rej.2014.1591.
Tavassoly O, Kakish J, Nokhrin S, Dmitriev O, Lee JS.
Eur J Med Chem. 2014 Dec 17;88:42-54. doi: 10.1016/j.ejmech.2014.07.090. Epub 2014 Jul 25.
Yang J, Song S, Li J, Liang T.
Pathol Res Pract. 2014 Jun;210(6):357-62. doi: 10.1016/j.prp.2014.02.005. Epub 2014 Feb 23.
Tegenge MA, Rajbhandari L, Shrestha S, Mithal A, Hosmane S, Venkatesan A.
Exp Neurol. 2014 Mar;253:102-10. doi: 10.1016/j.expneurol.2013.12.016. Epub 2013 Dec 29.
Qualls Z, Brown D, Ramlochansingh C, Hurley LL, Tizabi Y.
Neurotox Res. 2014 Jan;25(1):81-9.
Ji HF, Shen L.
CNS Neurol Disord Drug Targets. 2014 Mar;13(2):369-73. Review.
Singh PK, Kotia V, Ghosh D, Mohite GM, Kumar A, Maji SK.
ACS Chem Neurosci. 2013 Mar 20;4(3):393-407. doi: 10.1021/cn3001203. Epub 2012 Dec 17.
Jiang TF, Zhang YJ, Zhou HY, Wang HM, Tian LP, Liu J, Ding JQ, Chen SD.
J Neuroimmune Pharmacol. 2013 Mar;8(1):356-69. doi: 10.1007/s11481-012-9431-7. Epub 2013 Jan 17.
Pan J, Li H, Ma JF, Tan YY, Xiao Q, Ding JQ, Chen SD.
Transl Neurodegener. 2012 Aug 20;1(1):16. doi: 10.1186/2047-9158-1-16.
Agrawal SS, Gullaiya S, Dubey V, Singh V, Kumar A, Nagar A, Tiwari P.
Cardiovasc Psychiatry Neurol. 2012;2012:942981. doi: 10.1155/2012/942981. Epub 2012 Aug
Du XX, Xu HM, Jiang H, Song N, Wang J, Xie JX.
Neurosci Bull. 2012 Jun;28(3):253-8. doi: 10.1007/s12264-012-1238-2.
Ojha RP, Rastogi M, Devi BP, Agrawal A, Dubey GP.
J Neuroimmune Pharmacol. 2012 Sep;7(3):609-18. doi: 10.1007/s11481-012-9363-2. Epub 2012 Apr 21.
Mansouri Z, Sabetkasaei M, Moradi F, Masoudnia F, Ataie A.
J Mol Neurosci. 2012 Jun;47(2):234-42. doi: 10.1007/s12031-012-9727-3. Epub 2012 Mar 15.
Liu Z, Yu Y, Li X, Ross CA, Smith WW.
Pharmacol Res. 2011 May;63(5):439-44. doi: 10.1016/j.phrs.2011.01.004. Epub 2011 Jan 12.
Wang MS, Boddapati S, Emadi S, Sierks MR.
BMC Neurosci. 2010 Apr 30;11:57. doi: 10.1186/1471-2202-11-57.
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?
- 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.
- 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.
- 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.
- Probiotic Bifidobacteria, in double the normal doses. Add prebiotic inulin, pectin, FOS, GOS supplements to help feed the newly introduced organisms.
- 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.
- 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.
- 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.
Fermented Vegetables: http://www.astonesthrowtohealth.com/
Fermented oatmeal recipe: https://thesymbiontfactorblog.com/2016/01/26/super-synbiotic-breakfast-improved/
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]
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.
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.
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.
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.
Varatharajalu R, Garige M, Leckey LC, Reyes-Gordillo K, Shah R, Lakshman MR.
Oxid Med Cell Longev. 2016;2016:5017460. doi: 10.1155/2016/5017460. Epub 2016 Jan 5.
Yarla NS, Bishayee A, Sethi G, Reddanna P, Kalle AM, Dhananjaya BL, Dowluru KS, Chintala R, Duddukuri GR.
Semin Cancer Biol. 2016 Feb 4. pii: S1044-579X(16)30003-7. doi: 10.1016/j.semcancer.2016.02.001. [Epub ahead of print] Review.
Maithilikarpagaselvi N, Sridhar MG, Swaminathan RP, Sripradha R.
J Complement Integr Med. 2016 Feb 4. pii: /j/jcim.ahead-of-print/jcim-2015-0070/jcim-2015-0070.xml. doi: 10.1515/jcim-2015-0070. [Epub ahead of print]
Maithili Karpaga Selvi N, Sridhar MG, Swaminathan RP, Sripradha R.
Sci Pharm. 2014 Nov 4;83(1):159-75. doi: 10.3797/scipharm.1408-16. eCollection 2015.
Dolpady J, Sorini C, Di Pietro C, Cosorich I, Ferrarese R, Saita D, Clementi M, Canducci F, Falcone M.
J Diabetes Res. 2016;2016:7569431. doi: 10.1155/2016/7569431. Epub 2015 Dec 8.
Granados-Castro LF, Rodríguez-Rangel DS, Fernández-Rojas B, León-Contreras JC, Hernández-Pando R, Medina-Campos ON, Eugenio-Pérez D, Pinzón E, Pedraza-Chaverri J.
J Pharm Pharmacol. 2016 Feb;68(2):245-56. doi: 10.1111/jphp.12501. Epub 2016 Jan 15.
Kaakoush NO, Martire SI, Raipuria M, Mitchell HM, Nielsen S, Westbrook RF, Morris MJ.
Mol Nutr Food Res. 2016 Jan 14. doi: 10.1002/mnfr.201500815. [Epub ahead of print]
Tork OM, Khaleel EF, Abdelmaqsoud OM.
Asian Pac J Cancer Prev. 2015;16(18):8271-9.
Maithilikarpagaselvi N, Sridhar MG, Swaminathan RP, Zachariah B.
Chem Biol Interact. 2016 Jan 25;244:187-94. doi: 10.1016/j.cbi.2015.12.012. Epub 2015 Dec 20.
Abarikwu SO, Durojaiye M, Alabi A, Asonye B, Akiri O.
Ren Fail. 2016 Mar;38(2):321-9. doi: 10.3109/0886022X.2015.1127743. Epub 2015 Dec 27.
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.
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.
Oxid Med Cell Longev. 2016;2016:5719291. doi: 10.1155/2016/5719291. Epub 2015 Nov 23.
Perrone D, Ardito F, Giannatempo G, Dioguardi M, Troiano G, Lo Russo L, DE Lillo A, Laino L, Lo Muzio L.
Exp Ther Med. 2015 Nov;10(5):1615-1623. Epub 2015 Sep 17.
Wang L, Lv Y, Yao H, Yin L, Shang J.
Int J Clin Exp Pathol. 2015 Sep 1;8(9):11503-9. eCollection 2015.
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.
Ghosh SS, Righi S, Krieg R, Kang L, Carl D, Wang J, Massey HD, Sica DA, Gehr TW, Ghosh S.
PLoS One. 2015 Nov 18;10(11):e0141109. doi: 10.1371/journal.pone.0141109. eCollection 2015.
Bharwani A, Mian MF, Foster JA, Surette MG, Bienenstock J, Forsythe P.
Psychoneuroendocrinology. 2016 Jan;63:217-27. doi: 10.1016/j.psyneuen.2015.10.001. Epub 2015 Oct 9.
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.
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.
Li Y, Li M, Wu S, Tian Y.
Lipids Health Dis. 2015 Sep 3;14:100. doi: 10.1186/s12944-015-0106-2.
Liao H, Wang Z, Deng Z, Ren H, Li X.
Int J Clin Exp Med. 2015 Jun 15;8(6):8948-57. eCollection 2015.
Lu C, Zhang F, Xu W, Wu X, Lian N, Jin H, Chen Q, Chen L, Shao J, Wu L, Lu Y, Zheng S.
IUBMB Life. 2015 Aug;67(8):645-58. doi: 10.1002/iub.1409. Epub 2015 Aug 25.
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.
Sun J, Furio L, Mecheri R, van der Does AM, Lundeberg E, Saveanu L, Chen Y, van Endert P, Agerberth B, Diana J.
Immunity. 2015 Aug 18;43(2):304-17. doi: 10.1016/j.immuni.2015.07.013. Epub 2015 Aug 4.
Cabrera SM, Henschel AM, Hessner MJ.
Transl Res. 2016 Jan;167(1):214-27. doi: 10.1016/j.trsl.2015.04.011. Epub 2015 Apr 29. Review.
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.
Cell Host Microbe. 2015 Feb 11;17(2):260-73. doi: 10.1016/j.chom.2015.01.001. Epub 2015 Feb 5.
Conlon MA, Bird AR.
Nutrients. 2014 Dec 24;7(1):17-44. doi: 10.3390/nu7010017. Review.
Rashid K, Sil PC.
Toxicol Appl Pharmacol. 2015 Feb 1;282(3):297-310. doi: 10.1016/j.taap.2014.12.003. Epub 2014 Dec 23.
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.
Free Radic Res. 2015 Mar;49(3):279-89. doi: 10.3109/10715762.2014.999674. Epub 2015 Jan 28.
Song Z, Wang H, Zhu L, Han M, Gao Y, Du Y, Wen Y.
Food Funct. 2015 Feb;6(2):461-9. doi: 10.1039/c4fo00608a.
Rashid K, Sil PC.
Biochim Biophys Acta. 2015 Jan;1852(1):70-82. doi: 10.1016/j.bbadis.2014.11.007. Epub 2014 Nov 11.
Greiner TU, Hyötyläinen T, Knip M, Bäckhed F, Orešič M.
PLoS One. 2014 Nov 12;9(11):e110359. doi: 10.1371/journal.pone.0110359. eCollection 2014.
Rouse M, Younès A, Egan JM.
J Endocrinol. 2014 Nov;223(2):107-17. doi: 10.1530/JOE-14-0335.
Galley JD, Nelson MC, Yu Z, Dowd SE, Walter J, Kumar PS, Lyte M, Bailey MT.
BMC Microbiol. 2014 Jul 15;14:189. doi: 10.1186/1471-2180-14-189.
Voigt RM, Forsyth CB, Green SJ, Mutlu E, Engen P, Vitaterna MH, Turek FW, Keshavarzian A.
PLoS One. 2014 May 21;9(5):e97500. doi: 10.1371/journal.pone.0097500. eCollection 2014.
Hansen CH, Krych L, Buschard K, Metzdorff SB, Nellemann C, Hansen LH, Nielsen DS, Frøkiær H, Skov S, Hansen AK.
Diabetes. 2014 Aug;63(8):2821-32. doi: 10.2337/db13-1612. Epub 2014 Apr 2.
Galley JD, Bailey MT.
Gut Microbes. 2014 May-Jun;5(3):390-6. doi: 10.4161/gmic.28683. Epub 2014 Apr 1. Review.
Topol I, Kamyshny A.
Georgian Med News. 2013 Dec;(225):115-22.
Bimonte S, Barbieri A, Palma G, Luciano A, Rea D, Arra C.
Biomed Res Int. 2013;2013:810423. doi: 10.1155/2013/810423. Epub 2013 Nov 10.
Curr Diab Rep. 2013 Oct;13(5):601-7. doi: 10.1007/s11892-013-0409-5. Review.
Um MY, Hwang KH, Ahn J, Ha TY.
Basic Clin Pharmacol Toxicol. 2013 Sep;113(3):152-7. doi: 10.1111/bcpt.12076. Epub 2013 May
Bailey MT, Dowd SE, Galley JD, Hufnagle AR, Allen RG, Lyte M.
Brain Behav Immun. 2011 Mar;25(3):397-407. doi: 10.1016/j.bbi.2010.10.023. Epub 2010 Oct 30.
Wang XD, Soltesz V, Molin G, Andersson R.
Scand J Gastroenterol. 1995 Feb;30(2):180-5.
Johansson ML, Molin G, Jeppsson B, Nobaek S, Ahrné S, Bengmark S.
Appl Environ Microbiol. 1993 Jan;59(1):15-20.
Molin G, Andersson R, Ahrné S, Lönner C, Marklinder I, Johansson ML, Jeppsson B, Bengmark S.
Antonie Van Leeuwenhoek. 1992 Apr;61(3):167-73.
What happens if your microbiome becomes too excessive and colonizes parts of the body where it really shouldn’t set up camp? SIBO, or Small Intestinal Bacterial Overgrowth, is an example of just that! Since this comes up very frequently in discussions with patients, it’s time to share some information about it. This problem is much more common than most would realize, and like many such things can be looked at as a “spectrum” from mild to severe/debilitating. If you feel worse after eating, and feel like taking probiotics makes things worse instead of better, these are some of the symptoms of low stomach acidity.
In the normally functioning digestive tract, the stomach is (relatively) sterile, having a very low pH due to the production of HCl, hydrochloric acid along with enzymes. This means that the stomach is a filter of sorts, killing most bacteria and viruses that might be present on food or beverage you consume. This understanding is validated by the observation that an animal’s stomach acidity is directly related to its place in the food chain. Animals that are pure carrion eaters or predators have the most acidic stomach secretions, while those that eat plants have the least. This serves two purposes: the first is to disinfect food that may even be actively decomposing, while the second is to break the peptide bonds that hold amino acids together to build proteins in meat. Since the stomach is so acidic in meat-eaters, they can eat roadkill and not become ill. A healthy human’s stomach acid inhibits bacterial growth in the stomach and the first part of the small intestine, before it is neutralized by bile secretions. This limits the amount of bacteria that can exist in those areas. This is part of our evolutionary heritage that allowed early Humans to survive on anything from seafood to insects, hunted or trapped meat animals, or stealing the prey of other predators.
Modern lifestyles conspire to reduce this needed acidity. Lack of sleep, too much stimulation, poor breathing dynamics all cause an autonomic imbalance that promotes everything from high blood pressure to poor digestion from low stomach acid. If stomach acid stays abnormally low for too long though, some organisms such as Helicobacter pylori can colonize and take over. This organism will then inhibit stomach acid production, wrecking your health in the process. So, without high stomach acid levels the predator (or human) would get infections and become ill; he also wouldn’t be able to digest the meat he consumes. Humans do not produce quite the stomach acid levels of a cat or dog, but are much closer to that level than a goat or cow.
The first question that brings up is the old debate about whether we are evolved to be vegetarians or meat-eaters. The facts here point squarely toward our physiology being optimized for some of each; definitely a meat-eater but capable of digesting plants too.
It is important to note that in this way, our individual “optimum diet” may be tied to our gastric acid status. If you have low stomach acidity, you’re not likely to digest meat very well, and may find yourself gravitating toward a vegetarian diet. If this choice is made due to low stomach acidity, it’s really running from the problem and still leaving the door open to a dysfunctional disease state. On the other hand, if you’d really like to do well on a Paleo type diet, you should also make sure your autonomics are balanced enough that you can produce adequate stomach acid to break down meat.
The second question is about what would happen if our stomach were not acidic? The obvious answer is bacterial colonization of the stomach and small intestine, with overgrowth compared to the normal condition. This results in a variety of symptoms, from heartburn (think summer roadkill in your stomach…ick) to bloating, allergic sensitization, indigestion, etc. It most definitely results in disruption of the entire microbiome downstream from the stomach also, with many consequences!
Now it gets interesting: What do most people do when presented with those symptoms? Take antacids! I have seen many patients who have been prescribed PPI (protein pump inhibitor; acid-blocking) medications, despite having never undergone any tests to confirm their symptoms indicated excess stomach acid. Stomach acidity declines with age, which is probably because of autonomic imbalance. Our fight-or-flight system (sympathetic system) becomes the dominant system when we’re under stress, fatigued, or if our brain is slowing down. Sound familiar? The parasympathetic system is stimulated by relaxation, deep breathing, less stress, slow relaxed eating, better sleep. Are you getting these things in your life?
To really build a balanced and high-functioning microbiome, it is necessary to start with balanced stomach function, then work downstream from there. Better liver function, small intestine function, large intestine function. One of the reasons many people cannot balance their large intestinal microbiome is that they haven’t managed their stress, breathing, sleep, and eating habits and therefore still have low stomach acid and SIBO to one degree or another.
Lifestyle habits that can help re-balance your autonomic function include deep breathing, yoga, meditation, taking time for yourself to do those things you love, scheduling and planning sleep more effectively, and taking the time to relax and breathe when you eat. There are also very specific functional neurology rehab activities that can aid in this goal. It is also possible to take a supplement that includes HCl and enzymes, to help kill off excess bacteria/H. pylori and begin to heal from SIBO.
So, be nice to your stomach, and your symbionts will thank you!
A while back I wrote about a synbiotic (prebiotic fiber + probiotic bacteria) fermented breakfast, and I’ve improved significantly on it since then so here is an update!
The concept of a synbiotic ferment is to give the beneficial bacteria a headstart before they get introduced into the body by eating them-and then include enough fuel for the journey and any upcoming microbial challenges. With this in mind, a new study was published that verified that prebiotic fibers can selectively benefit specific bacteria down to the species level. That is very useful to know! (Chung) As a note, the best way to read this blog post and many of my others is to right-click on each of the references below and open them in new tabs, take a look at each one, then read the rest of the blog post. Then, you can skip back to the research article when you see something connecting it. The research articles about these ingredients show benefits such as increased testosterone in men, reduced body fat, increased insulin sensitivity/reduced weight gain, prevention of cancer, reduced LDL cholesterol…in other words, fairly profound benefits of letting our microbial friends have their way with the breakfast food before we consume it!
This isn’t a chemical formula, so the proportions can vary a bit and not ruin things. I tend to be someone who cooks by feel and adds a bit of this and a bit of that, so take that into account LOL. I’ll approximate what I usually use and you can adjust accordingly if need be. Note that the picture of adding the grated apple isn’t included, as the day I took these pics I didn’t have an apple! I’ll add it later though. For now, follow the text more than the pictures please 😉
- One cup gluten free oats, uncooked
- 1/4 cup dried cranberries
- 3/4 cup Kefir (I make my own with coconut milk; use what you have!)
- 3 tbsp ground Flaxseed
- 3 tbsp Inulin powder
- One organic apple, peeled and grated
- Enough extra coconut milk to make it totally wet with enough fluid to cover but not make soup (or your fave milk/substitute, but not vanilla or chocolate flavored stuff as the bacteria don’t seem to like that)
Mix all the ingredients in a glass bowl, and place on top of your fridge or other convenient place that isn’t too cold or too warm. Put a saucer under and over the bowl, as it can get frothy and try to escape! Now leave it alone for at least 24 hours, 36 or even 48 if you’re bold. When it’s a bit foamy feeling if stirred, and smells fermented, it’s ready to eat. I take 1/4 to 1/3 of the batch in another bowl, then add a handful of walnuts and some more coconut milk, and sometimes some maple syrup or molasses-just a spoonful-and even a sprinkle of cinnamon. If you heat it, you kill the bacteria so it’s probably much healthier cold. Enjoy!
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”.
The Symbiont Factor: http://tinyurl.com/h2m5lq8
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]
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.
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.
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.
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]
Hay WW Jr.
Neonatology. 2008/01/01 00:00; 94(4): 245-254
For the last month or so, I’ve been hauling boxes and driving a crazy number of miles. I still have another epic trip to make, getting my horse to bring him to Maine. The last trip involved pulling a very heavily loaded 30 foot trailer, and was super stressful and fatiguing. What have I been doing to maintain my brain health and energy level? Many things, actually!
Fermented oatmeal is really versatile stuff. I wrote about it in a previous post, and have been using it extensively. Adding some ground flax seed before fermentation, and walnuts/raisins/coconut milk and maple syrup afterward yields a simple and tasty treat. It’s easy to keep in a cooler while on the road and eat a bit from time to time.
I’ve also been keeping a jar of kimchee in the cooler, and often take a few bites of it during roadside stops (yes, I’ve been traveling alone mostly. On the last run, my two cats didn’t seem to mind the smell-perhaps knowing they had worse in store for me!)
Kefir and yogurt of course help to maintain a low anxiety level and good digestive function during stressful drives. As I follow a Paleo diet pretty closely, I opt for coconut kefir (make my own) and coconut yogurt usually. I’ve also made a point of deep breathing from time to time to keep my autonomic function balanced and prevent constipation or reduced circulation.
Smoked salmon is one of my favorite road foods. I love it on a gluten-free bagel, but will eat it straight out of the wrapper as well (more paleo, right? certainly feels primal eating fish with my fingers as I go down the road…) Get the kind that doesn’t have artificial color and additives if at all possible. I’ve also often eaten sardines at rest areas, as the high omega-3 content of both items should help reduce oxidative stress and inflammation secondary to pushing the brain and body this hard.
Of course, taking a good probiotic/prebiotic with a combination of Lactobacilli and Bifido organisms is a good choice, as both reduce inflammation and anxiety. Snacking on fruit, both fresh and dried, provides some good “road nibbles” while nourishing those beneficial organisms.
Doesn’t this sound like it would help maintain concentration and health while on the road? Compare that with the average person’s choice of fast food and soda while traveling and I think there is quite a contrast!