Tag Archives: inflammation

About those “Turmeric Curcumin” capsules…

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I have been recommending curcumin for years, because of the huge number of research studies demonstrating its power to reduce inflammation, block oxidative stress, and inhibit or kill cancer (and other great benefits!) Lately there has been an explosion of supplements labeled as “turmeric curcumin” or “curcumin complex”. This is about like trying to buy pure cranberry juice. If you see “cranberry juice cocktail” or “cranberry drink” or “cranberry juice beverage”, what does it tell you? Right-it’s mostly apple juice or some other inexpensive juice, with enough of the cranberry juice to flavor it!

The same thing applies to curcumin. I have recommended it to several patients recently, who then tell me a couple weeks later that it didn’t help them. When I ask about the brand and details, it’s one of those labeling bait-and-switch schemes all over. Often the label reads “turmeric curcumin” which really doesn’t mean much, as they are two separate products…which is it? or “turmeric curcumin complex”…

The active, desired ingredient is Curcumin. Turmeric, the spice, is quite inexpensive but only contains typically 5% curcumin. Pure curcumin is most often 95% curcumin, and costs much much more. So, when the label explains that the product contains 450 mg of Turmeric, and 50 mg of curcumin, you can easily see that you’re getting basically ripped off because they’re cutting the good stuff 9:1 with the inexpensive less effective stuff! Then, of course, it doesn’t work as well, because you can’t take enough. I often recommend 6 capsules per day for a very inflamed patient (someone with Lyme disease, for example). That’s 6, 500mg capsules at 95%, or 2850 mg of actual curcumin. If those capsules are 450/50 as in the above example, that’s only 70mg of curcumin in each 500 mg capsule. To get the same effect as 2850 mg of pure curcumin, you’d have to consume over 40 of those capsules, instead of 6 when it’s 95% curcumin!

So, make sure that you get what you’re paying for-real 95% curcumin. There isn’t a “bioavailability problem” as some manufacturers of blends state. It’s a fat soluble substance, so chase your capsules with a spoon of coconut oil. It’s also alcohol soluble…well, I won’t go there just yet!

Stress, Microbiome, Inflammation and the Pancreas & Liver

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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?

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.

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

Free PMC Article

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

Free PMC Article

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.

PMID:26918872

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.

PMID:26881746

Free PMC Article

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.

Oxid Med Cell Longev. 2016;2016:5017460. doi: 10.1155/2016/5017460. Epub 2016 Jan 5.

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Targeting arachidonic acid pathway by natural products for cancer prevention and therapy.

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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.

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Preventive effect of curcumin on inflammation, oxidative stress and insulin resistance in high-fat fed obese rats.

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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Oral Probiotic VSL#3 Prevents Autoimmune Diabetes by Modulating Microbiota and Promoting Indoleamine 2,3-Dioxygenase-Enriched Tolerogenic Intestinal Environment.

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PMID:26779542

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Curcumin prevents paracetamol-induced liver mitochondrial alterations.

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Alternating or continuous exposure to cafeteria diet leads to similar shifts in gut microbiota compared to chow diet.

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Mol Nutr Food Res. 2016 Jan 14. doi: 10.1002/mnfr.201500815. [Epub ahead of print]

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Altered Cell to Cell Communication, Autophagy and Mitochondrial Dysfunction in a Model of Hepatocellular Carcinoma: Potential Protective Effects of Curcumin and Stem Cell Therapy.

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Curcumin prevents inflammatory response, oxidative stress and insulin resistance in high fructose fed male Wistar rats: Potential role of serine kinases.

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.

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Curcumin protects against gallic acid-induced oxidative stress, suppression of glutathione antioxidant defenses, hepatic and renal damage in rats.

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Ren Fail. 2016 Mar;38(2):321-9. doi: 10.3109/0886022X.2015.1127743. Epub 2015 Dec 27.

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Curcumin upregulates Nrf2 nuclear translocation and protects rat hepatic stellate cells against oxidative stress.

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.

PMID:26676408

Curcumin Supplementation Decreases Intestinal Adiposity Accumulation, Serum Cholesterol Alterations, and Oxidative Stress in Ovariectomized Rats.

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.

PMID:26640615

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Biological and therapeutic activities, and anticancer properties of curcumin.

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Exp Ther Med. 2015 Nov;10(5):1615-1623. Epub 2015 Sep 17.

PMID:26640527

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Curcumin prevents the non-alcoholic fatty hepatitis via mitochondria protection and apoptosis reduction.

Wang L, Lv Y, Yao H, Yin L, Shang J.

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

PMID:26617882

Free PMC Article

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.

PMID:26600714

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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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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.

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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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Combination of curcumin and piperine prevents formation of gallstones in C57BL6 mice fed on lithogenic diet: whether NPC1L1/SREBP2 participates in this process?

Li Y, Li M, Wu S, Tian Y.

Lipids Health Dis. 2015 Sep 3;14:100. doi: 10.1186/s12944-015-0106-2.

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

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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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iNKT and MAIT Cell Alterations in Diabetes.

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Front Immunol. 2015 Jul 2;6:341. doi: 10.3389/fimmu.2015.00341. eCollection 2015. Review.

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Super Synbiotic Breakfast, Improved!

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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 😉

Ingredients:

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!

References:

Why does Rheumatoid Arthritis improve during a woman’s period or when pregnant?

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Why does Rheumatoid Arthritis improve during a

woman’s period or when pregnant?

By Richard Matthews DC DACNB

By Richard Matthews DC DACNB

This is an article that I wrote for Clint Paddison, to use for his Paddison Program for Rheumatoid Arthritis. Clint successfully healed himself from RA, and took the extraordinary step of teaching other people how to do it! I’m sharing the article here for my own blog readers.
Rheumatoid Arthritis is a progressive, debilitating autoimmune inflammatory arthritis. The site of actual damage is the synovial membrane of the joint itself, often causing severe angulation deformities of the joint when not controlled. Hands are the most commonly affected area, often in a symmetrical pattern. As it is an inflammatory disorder, the inflammation can also affect the heart, lungs, or other areas of the body. The portions of the immune system that have been identified are the cytokine (inflammatory immune factor) Tumor Necrosis Alpha or TNF-α, Interleukin-6 or IL-6 and Interleukin-17 or IL-17. There are others involved of course but these are the major therapeutic targets for the condition.

hormones-during-pregnancy

It is best to refer to the accompanying drawing to understand the relationship between these factors, as immune function is complex. We have a type of T-cell in our immune system which is called a T-Regulatory cell or Treg. These cells regulate the activity of T-helper cells or Th. The T-helper cells produce cytokines, such as TNF-α, IL-6 and IL-17, which in this case are the prime suspects in this crime!

Our immune system, and the T cells in particular, receive much of their instruction from the microbiome in our gut. Our gut bacteria directly interact with Treg cells, and through that mechanism help to regulate the cytokine system. This interaction has been quite specifically studied down to the genus and species involved.

The species of gut bacteria found to regulate the immune system and reduce inflammation by reducing IL-6, TNF-α and IL-17 include Lactobacillus and Bifidobacterium genus. These organisms have been found to grow well when our gut is reasonably active, a condition that results when we are not in a highly stressed state. They grow well when we have a diet that includes fruits, vegetables and fish. It should not be surprising that this same diet is known to be good for the heart and blood vessels, as atherosclerosis and heart disease are promoted by inflammation.

At least one species, Prevotella copri, is strongly associated with RA. This organism drives the levels of inflammatory IL-17 higher. It thrives in a high-carbohydrate diet, so make sure that your diet includes healthy anti-inflammatory fats and good protein! Also, its growth can be suppressed by seeding and feeding with probiotics, prebiotics, and diet. Another category of organism, segmented filamentous bacteria or SFB, is what initiates the function of the IL-17 cytokine. While getting it started is important, too much SFB can also keep IL-17 levels too high.

Now having identified the immune factors, let’s look at what affects them!
-Progesterone suppresses IL-6 and IL-17
-Estrogen suppresses IL-6 and IL-17
-Microbiome also influences both

Both hormones are elevated around the time of ovulation until the onset of menstruation; essentially during the interval of a woman’s period when she is fertile. Both of these hormones drop off at the onset of menstruation, triggering the sloughing of endometrial lining and blood. Both hormones increase in concentrations during pregnancy, only dropping precipitously at childbirth. It is important to consider that one of the things a woman’s body does in preparation for pregnancy and during pregnancy is to create an increased immune tolerance. If this were not the case, the immune system could treat the developing child as a tumor and attack it, something which actually does happen sometimes and results in miscarriage. It should also be noted that another thing that progesterone does is to reduce inflammation, which is great prior to childbirth, but also may reduce the symptoms of RA during menses or pregnancy—providing a second pathway that explains the relief.

female-cycle

What options does that leave, other than enjoying the brief hormone-induced RA interlude or having another child? Well, progesterone and vitamin D have been used to treat brain inflammation. Certainly a woman should consider using some of the natural and OTC progesterone preparations such as wild yam extract, particularly if evaluation of her existing hormone levels show that there is room for addition of progesterone without levels becoming unnaturally high. Now for the shocker: men also have progesterone, in levels comparable to women during the follicular phase of ovulation. It is converted into testosterone in men, and inhibits the conversion of testosterone into DHT—that nasty little product that causes male pattern baldness and gynecomastia (aka “man-boobs”). Does that mean that men should use low levels of progesterone? Quite possibly! It isn’t the “feminizing hormone” that estrogen is, and its use in men has some precedent already.

Systemic inflammation has the effect of making hormone receptors on the actual cells less functional, so that the hormones do not work as well. Reducing inflammation should therefore also make your existing hormones (progesterone and estrogen in this example) work more effectively. Of course, reducing inflammation helps RA directly as well, since it is an inflammatory condition. Cultivating a diverse and healthy microbiome is at the top of that list, and involves probiotics, prebiotics, diet, lifestyle, stress levels, and avoidance of toxins.

In summary, the sex hormones estrogen and progesterone both inhibit inflammation via inhibition of the IL-6 and IL-17 cytokines. These are the immune molecules that target the actual joint tissue in RA, and they are produced by T-helper cells, which are regulated by T-regulatory cells, which talk to gut bacteria across the intestinal wall to get their instructions. So, healthier gut bacteria means better immune control. Healthier gut bacteria also means better hormone levels and better hormone sensitivity, so it’s a win-win. If getting pregnant is not in your immediate future, and the brief hormone boost afforded by menses is insufficient, supplementation with progesterone may be worth considering in addition to a microbiome-healthy diet with good prebiotics and probiotics. Of course, all of these decisions are best made with the help of some labwork when possible. Identifying your existing microbiome can help to point the direction for improvement whether that means growing more Bifidobacteria or inhibiting the growth of Prevotella copri. In any case, optimize your hormones, and get those symbionts in shape so they can retrain your immune system!
References:
1: Andersson A, Grahnemo L, Engdahl C, Stubelius A, Lagerquist MK, Carlsten H,
Islander U. IL-17-producing γδT cells are regulated by estrogen during
development of experimental arthritis. Clin Immunol. 2015 Sep 28;161(2):324-332.
doi: 10.1016/j.clim.2015.09.014. [Epub ahead of print] PubMed PMID: 26423309.
http://www.ncbi.nlm.nih.gov/pubmed/26423309
2: Kim KW, Kim HR, Kim BM, Cho ML, Lee SH. Th17 Cytokines Regulate
Osteoclastogenesis in Rheumatoid Arthritis. Am J Pathol. 2015 Sep 8. pii:
S0002-9440(15)00445-9. doi: 10.1016/j.ajpath.2015.07.017. [Epub ahead of print]
PubMed PMID: 26362732.
http://www.ncbi.nlm.nih.gov/pubmed/26362732
3: Mortaz E, Adcock IM, Ricciardolo FL, Varahram M, Jamaati H, Velayati AA,
Folkerts G, Garssen J. Anti-Inflammatory Effects of Lactobacillus Rahmnosus and
Bifidobacterium Breve on Cigarette Smoke Activated Human Macrophages. PLoS One.
2015 Aug 28;10(8):e0136455. doi: 10.1371/journal.pone.0136455. eCollection 2015.
PubMed PMID: 26317628; PubMed Central PMCID: PMC4552661.
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4552661/

4: Gluhovschi C, Gluhovschi G, Petrica L, Velciov S, Gluhovschi A. Pregnancy
Associated with Systemic Lupus Erythematosus: Immune Tolerance in Pregnancy and
Its Deficiency in Systemic Lupus Erythematosus–An Immunological Dilemma. J
Immunol Res. 2015;2015:241547. doi: 10.1155/2015/241547. Epub 2015 May 18.
Review. PubMed PMID: 26090485; PubMed Central PMCID: PMC4451247.
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4451247/
5: Tang H, Hua F, Wang J, Yousuf S, Atif F, Sayeed I, Stein DG. Progesterone and
vitamin D combination therapy modulates inflammatory response after traumatic
brain injury. Brain Inj. 2015 Jun 17:1-10. [Epub ahead of print] PubMed PMID:
26083048.
http://www.ncbi.nlm.nih.gov/pubmed/26083048

6: Carasi P, Racedo SM, Jacquot C, Romanin DE, Serradell MA, Urdaci MC. Impact of
kefir derived Lactobacillus kefiri on the mucosal immune response and gut
microbiota. J Immunol Res. 2015;2015:361604. doi: 10.1155/2015/361604. Epub 2015
Feb 24. PubMed PMID: 25811034; PubMed Central PMCID: PMC4355334.
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4355334/

7: Garling RJ, Watts LT, Sprague S, Fletcher L, Jimenez DF, Digicaylioglu M. Does
progesterone show neuroprotective effects on traumatic brain injury through
increasing phosphorylation of Akt in the hippocampus? Neural Regen Res. 2014 Nov
1;9(21):1891-6. doi: 10.4103/1673-5374.145355. PubMed PMID: 25558238; PubMed
Central PMCID: PMC4281427.
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4281427/
8: Moreno J. Prevotella copri and the microbial pathogenesis of rheumatoid
arthritis. Reumatol Clin. 2015 Mar-Apr;11(2):61-3. doi:
10.1016/j.reuma.2014.11.001. Epub 2014 Dec 30. English, Spanish. PubMed PMID:
25555460.
http://www.reumatologiaclinica.org/en/prevotella-copri-microbial-pathogenesis-rheumatoid/articulo/S1699258X1400223X/

9: Furusawa Y, Obata Y, Hase K. Commensal microbiota regulates T cell fate
decision in the gut. Semin Immunopathol. 2015 Jan;37(1):17-25. doi:
10.1007/s00281-014-0455-3. Epub 2014 Oct 15. Review. PubMed PMID: 25315350.
http://www.ncbi.nlm.nih.gov/pubmed/25315350

10: Si D, Li J, Liu J, Wang X, Wei Z, Tian Q, Wang H, Liu G. Progesterone
protects blood-brain barrier function and improves neurological outcome following
traumatic brain injury in rats. Exp Ther Med. 2014 Sep;8(3):1010-1014. Epub 2014
Jul 11. PubMed PMID: 25120639; PubMed Central PMCID: PMC4113529.
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4113529/

11: Sudo N. Microbiome, HPA axis and production of endocrine hormones in the gut.
Adv Exp Med Biol. 2014;817:177-94. doi: 10.1007/978-1-4939-0897-4_8. PubMed PMID:
24997034.
http://www.ncbi.nlm.nih.gov/pubmed/24997034

12: Scher JU, Sczesnak A, Longman RS, Segata N, Ubeda C, Bielski C, Rostron T,
Cerundolo V, Pamer EG, Abramson SB, Huttenhower C, Littman DR. Expansion of
intestinal Prevotella copri correlates with enhanced susceptibility to arthritis.
Elife. 2013 Nov 5;2:e01202. doi: 10.7554/eLife.01202. PubMed PMID: 24192039;
PubMed Central PMCID: PMC3816614.
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3816614/

13: Shapira I, Sultan K, Lee A, Taioli E. Evolving concepts: how diet and the
intestinal microbiome act as modulators of breast malignancy. ISRN Oncol. 2013
Sep 25;2013:693920. doi: 10.1155/2013/693920. Review. PubMed PMID: 24187630;
PubMed Central PMCID: PMC3800670.
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3800670/

14: Tanabe S. The effect of probiotics and gut microbiota on Th17 cells. Int Rev
Immunol. 2013 Oct-Dec;32(5-6):511-25. doi: 10.3109/08830185.2013.839665. Epub
2013 Oct 4. Review. PubMed PMID: 24094077.
http://www.ncbi.nlm.nih.gov/pubmed/24094077
15: Xu L, Dong B, Wang H, Zeng Z, Liu W, Chen N, Chen J, Yang J, Li D, Duan Y.
Progesterone suppresses Th17 cell responses, and enhances the development of
regulatory T cells, through thymic stromal lymphopoietin-dependent mechanisms in
experimental gonococcal genital tract infection. Microbes Infect. 2013
Nov;15(12):796-805. doi: 10.1016/j.micinf.2013.06.012. Epub 2013 Jul 5. PubMed
PMID: 23835188.
http://www.ncbi.nlm.nih.gov/pubmed/23835188

16: Wang HY, Gao WT, He QH, Yang C, Gu W, Yan J, Jiang JX. Endogenous
glucocorticoid increases the basal level of Treg-Th17 balance under early phase
of stress. Chin J Traumatol. 2012;15(6):323-8. PubMed PMID: 23186919.
http://www.ncbi.nlm.nih.gov/pubmed/23186919

17: Ghadimi D, Helwig U, Schrezenmeir J, Heller KJ, de Vrese M. Epigenetic
imprinting by commensal probiotics inhibits the IL-23/IL-17 axis in an in vitro
model of the intestinal mucosal immune system. J Leukoc Biol. 2012
Oct;92(4):895-911. doi: 10.1189/jlb.0611286. Epub 2012 Jun 22. PubMed PMID:
22730546.
http://www.ncbi.nlm.nih.gov/pubmed/22730546

18: Campeau JL, Salim SY, Albert EJ, Hotte N, Madsen KL. Intestinal epithelial
cells modulate antigen-presenting cell responses to bacterial DNA. Infect Immun.
2012 Aug;80(8):2632-44. doi: 10.1128/IAI.00288-12. Epub 2012 May 21. PubMed PMID:
22615241; PubMed Central PMCID: PMC3434593.
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3434593/

19: Ait-Belgnaoui A, Durand H, Cartier C, Chaumaz G, Eutamene H, Ferrier L,
Houdeau E, Fioramonti J, Bueno L, Theodorou V. Prevention of gut leakiness by a
probiotic treatment leads to attenuated HPA response to an acute psychological
stress in rats. Psychoneuroendocrinology. 2012 Nov;37(11):1885-95. doi:
10.1016/j.psyneuen.2012.03.024. Epub 2012 Apr 26. PubMed PMID: 22541937.
http://www.ncbi.nlm.nih.gov/pubmed/22541937

20: Ekmekcioglu C. Are proinflammatory cytokines involved in an increased risk
for depression by unhealthy diets? Med Hypotheses. 2012 Feb;78(2):337-40. doi:
10.1016/j.mehy.2011.11.015. Epub 2011 Dec 6. PubMed PMID: 22153575.
http://www.ncbi.nlm.nih.gov/pubmed/22153575

21: López P, González-Rodríguez I, Gueimonde M, Margolles A, Suárez A. Immune
response to Bifidobacterium bifidum strains support Treg/Th17 plasticity. PLoS
One. 2011;6(9):e24776. doi: 10.1371/journal.pone.0024776. Epub 2011 Sep 22.
PubMed PMID: 21966367; PubMed Central PMCID: PMC3178565.
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3178565/

22: Reading NC, Kasper DL. The starting lineup: key microbial players in
intestinal immunity and homeostasis. Front Microbiol. 2011 Jul 7;2:148. doi:
10.3389/fmicb.2011.00148. eCollection 2011. PubMed PMID: 21779278; PubMed Central
PMCID: PMC3133820.
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3133820/

23: Meyer J, Döring A, Herder C, Roden M, Koenig W, Thorand B. Dietary patterns,
subclinical inflammation, incident coronary heart disease and mortality in
middle-aged men from the MONICA/KORA Augsburg cohort study. Eur J Clin Nutr. 2011
Jul;65(7):800-7. doi: 10.1038/ejcn.2011.37. Epub 2011 Apr 6. PubMed PMID:
21468094.
http://www.ncbi.nlm.nih.gov/pubmed/21468094

24: Weinberg A, Enomoto L, Marcus R, Canniff J. Effect of menstrual cycle
variation in female sex hormones on cellular immunity and regulation. J Reprod
Immunol. 2011 Apr;89(1):70-7. doi: 10.1016/j.jri.2010.11.009. Epub 2011 Mar 22.
PubMed PMID: 21429588.
http://www.ncbi.nlm.nih.gov/pubmed/21429588

25: Srirangan S, Choy EH. The role of interleukin 6 in the pathophysiology of
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26: Yates MA, Li Y, Chlebeck P, Proctor T, Vandenbark AA, Offner H. Progesterone
treatment reduces disease severity and increases IL-10 in experimental autoimmune
encephalomyelitis. J Neuroimmunol. 2010 Mar 30;220(1-2):136-9. doi:
10.1016/j.jneuroim.2010.01.013. Epub 2010 Feb 11. PubMed PMID: 20153059; PubMed
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http://www.ncbi.nlm.nih.gov/pubmed/18039580

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30: http://sbi4u3.weebly.com/endocrine-hormones-basic-mechanisms-and-the-menstrual-cycle.html

31: http://www.medicine.mcgill.ca/physio/vlab/other_exps/endo/reprod_horm.htm

32: https://en.wikipedia.org/wiki/Progesterone

33: http://www.hairloss-research.org/UpdateProgesterone5-08.html

References:

1: Andersson A, Grahnemo L, Engdahl C, Stubelius A, Lagerquist MK, Carlsten H,

Islander U. IL-17-producing γδT cells are regulated by estrogen during

development of experimental arthritis. Clin Immunol. 2015 Sep 28;161(2):324-332.

doi: 10.1016/j.clim.2015.09.014. [Epub ahead of print] PubMed PMID: 26423309.

http://www.ncbi.nlm.nih.gov/pubmed/26423309

2: Kim KW, Kim HR, Kim BM, Cho ML, Lee SH. Th17 Cytokines Regulate

Osteoclastogenesis in Rheumatoid Arthritis. Am J Pathol. 2015 Sep 8. pii:

S0002-9440(15)00445-9. doi: 10.1016/j.ajpath.2015.07.017. [Epub ahead of print]

PubMed PMID: 26362732.

http://www.ncbi.nlm.nih.gov/pubmed/26362732

3: Mortaz E, Adcock IM, Ricciardolo FL, Varahram M, Jamaati H, Velayati AA,

Folkerts G, Garssen J. Anti-Inflammatory Effects of Lactobacillus Rahmnosus and

Bifidobacterium Breve on Cigarette Smoke Activated Human Macrophages. PLoS One.

2015 Aug 28;10(8):e0136455. doi: 10.1371/journal.pone.0136455. eCollection 2015.

PubMed PMID: 26317628; PubMed Central PMCID: PMC4552661.

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4552661/

4: Gluhovschi C, Gluhovschi G, Petrica L, Velciov S, Gluhovschi A. Pregnancy

Associated with Systemic Lupus Erythematosus: Immune Tolerance in Pregnancy and

Its Deficiency in Systemic Lupus Erythematosus–An Immunological Dilemma. J

Immunol Res. 2015;2015:241547. doi: 10.1155/2015/241547. Epub 2015 May 18.

Review. PubMed PMID: 26090485; PubMed Central PMCID: PMC4451247.

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4451247/

5: Tang H, Hua F, Wang J, Yousuf S, Atif F, Sayeed I, Stein DG. Progesterone and

vitamin D combination therapy modulates inflammatory response after traumatic

brain injury. Brain Inj. 2015 Jun 17:1-10. [Epub ahead of print] PubMed PMID:

26083048.

http://www.ncbi.nlm.nih.gov/pubmed/26083048

6: Carasi P, Racedo SM, Jacquot C, Romanin DE, Serradell MA, Urdaci MC. Impact of

kefir derived Lactobacillus kefiri on the mucosal immune response and gut

microbiota. J Immunol Res. 2015;2015:361604. doi: 10.1155/2015/361604. Epub 2015

Feb 24. PubMed PMID: 25811034; PubMed Central PMCID: PMC4355334.

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4355334/

7: Garling RJ, Watts LT, Sprague S, Fletcher L, Jimenez DF, Digicaylioglu M. Does

progesterone show neuroprotective effects on traumatic brain injury through

increasing phosphorylation of Akt in the hippocampus? Neural Regen Res. 2014 Nov

1;9(21):1891-6. doi: 10.4103/1673-5374.145355. PubMed PMID: 25558238; PubMed

Central PMCID: PMC4281427.

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4281427/

8: Moreno J. Prevotella copri and the microbial pathogenesis of rheumatoid

arthritis. Reumatol Clin. 2015 Mar-Apr;11(2):61-3. doi:

10.1016/j.reuma.2014.11.001. Epub 2014 Dec 30. English, Spanish. PubMed PMID:

25555460.

http://www.reumatologiaclinica.org/en/prevotella-copri-microbial-pathogenesis-rheumatoid/articulo/S1699258X1400223X/

9: Furusawa Y, Obata Y, Hase K. Commensal microbiota regulates T cell fate

decision in the gut. Semin Immunopathol. 2015 Jan;37(1):17-25. doi:

10.1007/s00281-014-0455-3. Epub 2014 Oct 15. Review. PubMed PMID: 25315350.

http://www.ncbi.nlm.nih.gov/pubmed/25315350

10: Si D, Li J, Liu J, Wang X, Wei Z, Tian Q, Wang H, Liu G. Progesterone

protects blood-brain barrier function and improves neurological outcome following

traumatic brain injury in rats. Exp Ther Med. 2014 Sep;8(3):1010-1014. Epub 2014

Jul 11. PubMed PMID: 25120639; PubMed Central PMCID: PMC4113529.

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4113529/

11: Sudo N. Microbiome, HPA axis and production of endocrine hormones in the gut.

Adv Exp Med Biol. 2014;817:177-94. doi: 10.1007/978-1-4939-0897-4_8. PubMed PMID:

24997034.

http://www.ncbi.nlm.nih.gov/pubmed/24997034

12: Scher JU, Sczesnak A, Longman RS, Segata N, Ubeda C, Bielski C, Rostron T,

Cerundolo V, Pamer EG, Abramson SB, Huttenhower C, Littman DR. Expansion of

intestinal Prevotella copri correlates with enhanced susceptibility to arthritis.

Elife. 2013 Nov 5;2:e01202. doi: 10.7554/eLife.01202. PubMed PMID: 24192039;

PubMed Central PMCID: PMC3816614.

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3816614/

13: Shapira I, Sultan K, Lee A, Taioli E. Evolving concepts: how diet and the

intestinal microbiome act as modulators of breast malignancy. ISRN Oncol. 2013

Sep 25;2013:693920. doi: 10.1155/2013/693920. Review. PubMed PMID: 24187630;

PubMed Central PMCID: PMC3800670.

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3800670/

14: Tanabe S. The effect of probiotics and gut microbiota on Th17 cells. Int Rev

Immunol. 2013 Oct-Dec;32(5-6):511-25. doi: 10.3109/08830185.2013.839665. Epub

2013 Oct 4. Review. PubMed PMID: 24094077.

http://www.ncbi.nlm.nih.gov/pubmed/24094077

15: Xu L, Dong B, Wang H, Zeng Z, Liu W, Chen N, Chen J, Yang J, Li D, Duan Y.

Progesterone suppresses Th17 cell responses, and enhances the development of

regulatory T cells, through thymic stromal lymphopoietin-dependent mechanisms in

experimental gonococcal genital tract infection. Microbes Infect. 2013

Nov;15(12):796-805. doi: 10.1016/j.micinf.2013.06.012. Epub 2013 Jul 5. PubMed

PMID: 23835188.

http://www.ncbi.nlm.nih.gov/pubmed/23835188

16: Wang HY, Gao WT, He QH, Yang C, Gu W, Yan J, Jiang JX. Endogenous

glucocorticoid increases the basal level of Treg-Th17 balance under early phase

of stress. Chin J Traumatol. 2012;15(6):323-8. PubMed PMID: 23186919.

http://www.ncbi.nlm.nih.gov/pubmed/23186919

17: Ghadimi D, Helwig U, Schrezenmeir J, Heller KJ, de Vrese M. Epigenetic

imprinting by commensal probiotics inhibits the IL-23/IL-17 axis in an in vitro

model of the intestinal mucosal immune system. J Leukoc Biol. 2012

Oct;92(4):895-911. doi: 10.1189/jlb.0611286. Epub 2012 Jun 22. PubMed PMID:

22730546.

http://www.ncbi.nlm.nih.gov/pubmed/22730546

18: Campeau JL, Salim SY, Albert EJ, Hotte N, Madsen KL. Intestinal epithelial

cells modulate antigen-presenting cell responses to bacterial DNA. Infect Immun.

2012 Aug;80(8):2632-44. doi: 10.1128/IAI.00288-12. Epub 2012 May 21. PubMed PMID:

22615241; PubMed Central PMCID: PMC3434593.

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3434593/

19: Ait-Belgnaoui A, Durand H, Cartier C, Chaumaz G, Eutamene H, Ferrier L,

Houdeau E, Fioramonti J, Bueno L, Theodorou V. Prevention of gut leakiness by a

probiotic treatment leads to attenuated HPA response to an acute psychological

stress in rats. Psychoneuroendocrinology. 2012 Nov;37(11):1885-95. doi:

10.1016/j.psyneuen.2012.03.024. Epub 2012 Apr 26. PubMed PMID: 22541937.

http://www.ncbi.nlm.nih.gov/pubmed/22541937

20: Ekmekcioglu C. Are proinflammatory cytokines involved in an increased risk

for depression by unhealthy diets? Med Hypotheses. 2012 Feb;78(2):337-40. doi:

10.1016/j.mehy.2011.11.015. Epub 2011 Dec 6. PubMed PMID: 22153575.

http://www.ncbi.nlm.nih.gov/pubmed/22153575

21: López P, González-Rodríguez I, Gueimonde M, Margolles A, Suárez A. Immune

response to Bifidobacterium bifidum strains support Treg/Th17 plasticity. PLoS

One. 2011;6(9):e24776. doi: 10.1371/journal.pone.0024776. Epub 2011 Sep 22.

PubMed PMID: 21966367; PubMed Central PMCID: PMC3178565.

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3178565/

22: Reading NC, Kasper DL. The starting lineup: key microbial players in

intestinal immunity and homeostasis. Front Microbiol. 2011 Jul 7;2:148. doi:

10.3389/fmicb.2011.00148. eCollection 2011. PubMed PMID: 21779278; PubMed Central

PMCID: PMC3133820.

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3133820/

23: Meyer J, Döring A, Herder C, Roden M, Koenig W, Thorand B. Dietary patterns,

subclinical inflammation, incident coronary heart disease and mortality in

middle-aged men from the MONICA/KORA Augsburg cohort study. Eur J Clin Nutr. 2011

Jul;65(7):800-7. doi: 10.1038/ejcn.2011.37. Epub 2011 Apr 6. PubMed PMID:

21468094.

http://www.ncbi.nlm.nih.gov/pubmed/21468094

24: Weinberg A, Enomoto L, Marcus R, Canniff J. Effect of menstrual cycle

variation in female sex hormones on cellular immunity and regulation. J Reprod

Immunol. 2011 Apr;89(1):70-7. doi: 10.1016/j.jri.2010.11.009. Epub 2011 Mar 22.

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Practical use of fermented and anti-inflammatory foods during stressful times!

Is Organically Grown, Grass-fed Meat Healthier?

ADHD and the Microbiome: Any useful connections?

6 Replies

Life sometimes keeps us quite busy, doesn’t it? I apologize to you, my readers, for the scarce blog posts. I’ve been in the process of pulling off an epic home move of about 1700 miles! So, I write this post while in a campground in Lamoine, Maine USA where I’ve been hunting up a new home for my family and I.

I did quite a bit of research reading about ADHD recently, and thought I would share a few thoughts about it. Most of these thoughts are summarized in the flow chart drawing I created; refer to it when reading this blog post and you’ll see what I mean. What can be learned from a simple uBiome stool sample that can help with ADHD? Well, it turns out that there is quite a bit to look at there! As usual, this isn’t meant to replace your physician’s advice, and it is an example-which may not exactly describe your situation. You should consider using uBiome to run your (or your child’s) sample to see what your particular situation consists of.

The first thing to consider is the imbalance that frequently occurs in a microbiome. You see, it isn’t just about how many species of bacteria live in your gut, it is also about the relative numbers of those species. uBiome, after processing your sample, shows this in the simplest way by clicking on Taxonomy tree. In this format, the larger circles indicate larger populations while the smaller ones indicate, well, smaller. Clicking on each allows one to expand the data down from the phylum level all the way down to the genus level (remember, all life is cataloged by Kingdom, Phylum, Class, Order, Family, Genus, Species. We usually use Genus, Species to identify organisms, such as Homo sapiens or Helicobacter pylori.) When expanding these circles, often there is an obvious imbalance. At this point, I’m going to share some very specific information, and some or all of it may not apply to you or your child. It is an example of how a uBiome analysis can correlate with a condition and symptoms, directing some interventions. One recent patient case was a good example; the only large circles were Firmicutes, which is not such a bad thing. Opening that led to Clostridia being dominant, while Bacilli was minimal. This is meaningful because Bacilli includes Lactobacillus-one of the definite “good guys” that keep things working well. The phylum Actinobacteria was also minimal, significant because it includes another desirable genus, Bifidobacterium. This organism is an initial colonizer of the gut, tames the immune system, and also works with Lactobacillus to produce BDNF.

BDNF stands for Brain Derived Neurotrophic Factor, and it is necessary for the brain to develop new connections and grow/adapt to the life an individual leads. It is needed for plasticity, that ability of the brain to learn and adapt as needed. Low levels of BDNF are associated with ADHD. Your microbiome helps your brain to produce BDNF. Remember that a big part of what your brain learns to do as you grow up is actually blocking things out, not paying attention to more of them. It is a learning process, and in order to concentrate to accomplish tasks we must learn to attenuate non-essential information. This is also necessary for the brain to conserve fuel, because having a neural response to every incoming signal would burn a lot of fuel-in fact, enough to run out in some areas and cause Oxidative Stress.

Oxidative stress can result from depressed levels of antioxidant reserves or from too much stimulation. When nerve cells get overstimulated, they build up waste products and the energy-producing mitochondria become damaged. This is a “cellular death spiral”, because as soon as the mitochondria become damaged, the cell’s capability to metabolize fuel and produce energy is compromised, leading to more oxidative stress and further damage. This has been identified as part of the disease process in Alzheimer’s and Parkinson’s as well as ADHD and Autism. One of the problems that can promote Oxidative Stress is Inflammation.

Inflammation occurs when the immune system become too reactive and begins to attack tissue that is “self” and not “intruder/enemy”. Bifidobacteria are known for helping to dampen the immune inflammatory response, and a deficiency of Bifido contributes to inflammation. Again, inflammation is a key building block of…yes, all the same neurologic diseases. Low levels of Bifidobacteria and Lactobacillus are also significant because these organisms produce a neurotransmitter called Gamma Amino Butyric Acid or GABA.

GABA is an inhibitory neurotransmitter in the brain, and calming drugs or herbs often boost GABA levels. Valerian root or Valium (copycat drug companies, you know?) are good examples as is Kava Kava. Low levels of Lacto and Bifido gut bacteria result in low levels of GABA at the brain. Low levels of GABA at the brain result in less inhibition…ergo, more stimulation! And, the process continues in a positive feedback loop.

It is interesting to note that one intervention that helps elevate GABA and BDNF is exercise. Kids with ADHD are known for often being hyperkinetic, so if you wondered why, it is their brain’s way of balancing the equation to save nerve cells! When kids are reprimanded by teachers and parents are shamed into medicating their children’s “high energy”, it can be detrimental to the developmental process for this reason. This doesn’t mean that doing nothing is better, as a child must be able to focus in order to be able to learn. It just means that medicating their energy level down does not address the root causes of the problem.

So, what would be some natural interventions? First, improved nutrition. Any food that is causing more inflammation needs to be removed from the diet. Often that is sweets (note that Clostridia like sweets) and sometimes specific items such as gluten containing foods. Adding probiotics that contain the Lacto and Bifido organisms (in this patient example) can of course be helpful, but more so if they are also fed the prebiotic fibers that they need to survive (again, ideally this is case-specific). Both can be added to a fruit and vegetable smoothie that is tasty. Neuroprotective supplements such as N-Acetylcysteine will help to minimize the neuronal damage that is occurring. Also DHA/Omega-3 oils are neuroprotective and have been shown to help with ADHD. Curcumin can also reduce the neuroinflammation and is protective as well. It can also help settle gut function and heal the membranes of the intestines if they were inflamed too. Eating less processed food and more fresh (organic as possible) fruits and vegetables helps.

All of these steps are best carried out after having a stool sample analyzed for gut bacteria. Only after seeing the “bacterial census” is it possible to be extremely specific. A different patient’s samples could result in different recommendations! Please contact me for more details should you wish to find out more or schedule an analysis. This does not have to be done locally, as I only need the data from uBiome and a patient questionnaire to determine recommendations. Some of the supplements recommended are not case-specific, such as NAC, DHA/Omega and Curcumin as these will help most types of situations as will a healthier diet. The probiotic formulation is ideally case-specific, as is the prebiotic fibers and these will preferentially feed some categories of organisms more than others.

With proper lab work and specific interventions, it is possible for many individuals with ADHD to control and manage their situation more effectively. For some, it will be more of a cure, with no medication needed. For others, it may mean less medication is needed or the medication works more effectively. It is important to realize that we are all different, and our situations are also different!

Sources for supplements: http://progressivelabs.com/ You’ll have to register to order from them, and it requires specifying who referred you. Please feel free to put my name on that line, and then you will be able to receive your supplements directly from the same manufacturer I use!

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The Symbiont Factor Blog

All About Gut Bacteria, Symbiosis and Human Health!

Tag Archives: inflammation

About those “Turmeric Curcumin” capsules…

Stress, Microbiome, Inflammation and the Pancreas & Liver

Super Synbiotic Breakfast, Improved!

Why does Rheumatoid Arthritis improve during a woman’s period or when pregnant?

Practical use of fermented and anti-inflammatory foods during stressful times!

Is Organically Grown, Grass-fed Meat Healthier?

ADHD and the Microbiome: Any useful connections?

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