My Dr diagnosed my with sibo (Small intestinal bacterial overgrowth)

defined as the presence of excessive bacteria in the small intestine.

anybody have experience with this?

advice is mixed online; some say more pro biotics, some say they will add to the problem.

I am already taking bio - kult 2xday when not on abx.

My doctor's approach was to take antimicrobial herbs in the morning and evening (berberine, black walnut, artemesinin, olive leaf, wormwood) and in the afternoon take high-quality probiotics and consume healthy fermented foods and beverages. No sugar or gluten. (If you have mast cell activation issues, then cut out the fermented stuff, and make sure your probiotics are low-histamine strains.) I didn't have symptoms from my SIBO and gut dysbiosis until I started treating them, so keep in mind you might rock the boat a little at first. Go slowly. I started with one drop each of the herbs, and worked up gradually. I lost 25 pounds in the first month - yikes! Good luck.

Probiotics are generally out for SIBO. Generally you'll get Xifaxin and sometimes Neomycin depending if it's hydrogen or methane dominant. Also avoid fiber.

IMO, almost everyone with Lyme Disease has SIBO or a degree of it. Correcting this would most likely correct their problems. This is a lot easier said than done because of the vast diversity of the problems that can exist. If your immune response is competent, you won't get Lyme unless it is a very virulent strain. SIBO reduces your ability to fight other infections because most of your immune system is required to contain SIBO. Add multiple pathogens to the equation and it gets very difficult because your immune system is fighting on so many fronts.

I think fiber is a waste to be honest. I don't think we need it. There's a book called The Fiber Myth but I haven't read it. But it just passes through you undigested. I think it causes more problems than it fixes, especially with impaired digestion/gut issues. But it's a controversial opinion to have.

I agree with jb1994 - fiber is a total waste - look up the miracle recovery from Lyme(without any abx) on a fiber free diet: http://meatheals.com/2018/02/04/charlene-andersen/

The main problem with fiber is that SCFA are highly immunosuppressive - good for symptoms management but bad for eventual recovery.

Here are the actual research of what SCFAs are doing with out immune systems.

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3257741
Regulation of Inflammation by Short Chain Fatty Acids
The ability of leukocytes to migrate to the foci of inflammation and to destroy microbial pathogens also seems to be affected by the SCFAs. In this review, the latest research that describes how SCFAs regulate the inflammatory process is presented. The effects of these fatty acids on isolated cells (leukocytes, endothelial and intestinal epithelial cells) and, particularly, on the recruitment and activation of leukocytes are discussed. Therapeutic application of these fatty acids for the treatment of inflammatory pathologies is also highlighted.

https://www.ncbi.nlm.nih.gov/pubmed/2295846
Short-chain fatty acids produced by anaerobic bacteria inhibit phagocytosis by human lung phagocytes
The effect of short-chain fatty acids on the phagocytic activity of human alveolar macrophages and neutrophils was investigated. These acids, butyric, propionic, and succinic, are produced by anaerobic bacteria. The results indicate that phagocytosis of Staphylococcus aureus by human lung phagocytes is strongly inhibited by the end products of anaerobic catabolism and support the hypothesis that the antiphagocytic activity present in the supernatants of anaerobic cultures may be dependent on the presence of short-chain fatty acids.

All of the short-chain fatty acids tested induced an inhibition of phagocytosis both in absolute numbers of ingested bacteria and in rates of engulfment, which were already significant at 15 min (P < .001;figure IA right).

In the presence of short-chain fatty acids (15:1 bacteria-to PMNL ratio), a proportional decrease in the mean number of ingested bacteria (from 8 ± 0.9 to 4.1 ± 1.4) and of the metabolic activation (from 42.0 ± 2.5 fmol 02/PMNL to 27.1 ± 1.9 fmol 02/PMNL) was observed.

O2 consumption per ingested bacteria in the presence of short-chain fatty acids was not significantly different from a matched control with the same number of phagocytosed bacteria (6.58 ± 0.47 fmol OiPMNLIbacterium with short-chain fatty acids and 6.50 ± 0.52 fmol 02/PMNLIbacterium in the control). These data indicate that short-chain fatty acids did not inhibit PMNL metabolic activation and that the decreased heat effect could be accounted for by the inhibition of the phagocytosis.

Short-chain fatty acid impairment of S. aureus phagocytosis by alveolar macrophages, besides representing a good experimental model in vitro, acquires particular significance in terms of pathogenesis of mixed anaerobic lung infections, from which S. aureusis frequently retrieved . The induced suppression of alveolar macrophage defense could account for the infection by S. aureus, which is normally eliminated by the resident phagocytic population without PMNL recruitment and influx of exudate . From a wider infectivologic point of view, the available evidence indicates that short-chain fatty acids are important virulence factors that inhibit host phagocytic defenses as diverse as PMNLs and macrophages and may contribute to the pathogenesis of anaerobic infections.

Suppressive effect of short-chain fatty acids on production of proinflammatory mediators by neutrophils
https://www.ncbi.nlm.nih.gov/pubmed/21167700/

Time and Concentration Dependent Effects of Short Chain Fatty Acids on Lipopolysaccharide- or Tumor Necrosis Factor α-Induced Endothelial Activation
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5867315/

Anti-inflammatory properties of the short-chain fatty acids acetate and propionate: A study with relevance to inflammatory bowel disease
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4395634/

SCFAs suppress LPS-induced release of TNFα from neutrophils

Protein levels of TNFα and IL-8, released from lipopolysaccaride (LPS)-stimulated (1 μg/mL) human neutrophils, were determined with ELISA (Figure ​(Figure1).1). Acetate, propionate and butyrate (all 30 mmol/L) decreased LPS-stimulated TNFα release to the culture medium from 24 ± 1 pg/mL to 16 ± 0.1 pg/mL (P < 0.01), 8 ± 0.2 pg/mL (P < 0.01) and 6 ± 0.2 (P < 0.01), respectively (Figure ​(Figure1;1; upper panel, bars). The LPS-stimulated increase in IL-8 protein levels from 190 ± 21 pg/mL to 3753 ± 152 pg/mL was not affected by SCFAs (Figure ​(Figure1;1; lower panel).

jb1994 said...
Thanks Dmitry.

I know I'm not wrong because our ancestors didn't have nearly as much fiber as we do now. .

This is perhaps the most incorrect statement I've ever read on this board.

I'll address Dmitry's post when I have more time. You guys aren't seeing the forest for the trees.

Also, as for the Carnivore/Zero-Carb folks cited, those are anecdotal reports of just a few people.

Regarding Alison Lyons, I'm not sure I'd call her a success story. In her post -- which is four years old with no follow-up -- she reported some symptom relief, but she also revealed lots of food reactions and taking lots of supplements.

And, the person I've seen cited most frequently, Charlene Andersen, is also an anecdotal story. She alleges that she and her husband Joe have only eaten fatty ribeyes and water for 20 years. Is she healthy? We have no idea, as she has never posted any lab results -- whether Lyme-/infection-related or standard blood labs.

I have no reason to disbelieve either/any of these folks. That's not the point. The point is it's all self-reported and there's nothing that I've seen that tracks data over time. Aside from Charlene and Joe's purported 20-years of meat-and-water-only diet (with no health markers), this is a relatively new diet for most of the people who have adopted it. Following it for two months, six months, or a year is, basically, meaningless.

I've already seen this with Paleo, Primal, Low-Carb, Ketogenic, etc.

Perhaps this will turn out to be "THE" diet for everyone, but I think it will take a while for the impact to be revealed. Of course, there will not be any randomized clinical trials on it. No one will fund such studies.

Lastly, I certainly don't discount the positive impacts that people are reporting. As previously stated, I don't believe these people are being deceitful. I'm just skeptical of the short duration, the uncertainty of the mechanisms of action, the lack of monitoring and tracking biomarkers, and what may happen over the long term, among other things. It's not about being right or wrong, it's about the truth -- whatever it may be.

But butyrate acetate and propionate suppress our immune systems which are already suppressed by abx to a huge degree - look up my links posted above they even drop phagocytosis which is critical for a host defense against borrelia. Maybe Charlene Andersen got the most value just from the fiber(and its metabolites) drop first.

And stop being an animal protein deficient second:


Protein energy malnutrition increases arginase activity in monocytes and macrophages
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4228191/

Protein energy malnutrition is commonly associated with immune dysfunctions and is a major factor in susceptibility to infectious diseases.
In this study, we evaluated the impact of protein energy malnutrition on the capacity of monocytes and macrophages to upregulate arginase, an enzyme associated with immunosuppression and increased pathogen replication.

Our results show that monocytes and macrophages are significantly increased in the bone marrow and blood of mice fed on a protein low diet. No alteration in the capacity of bone marrow derived macrophages isolated from malnourished mice to phagocytose particles, to produce the microbicidal molecule nitric oxide and to kill intracellular Leishmania parasites was detected. However, macrophages and monocytes from malnourished mice express significantly more arginase both in vitro and in vivo.

Using an experimental model of visceral leishmaniasis, we show that following protein energy malnutrition, the increased parasite burden measured in the spleen of these mice coincided with increased arginase activity and that macrophages provide a more permissive environment for parasite growth.

Protein energy malnutrition (PEM) is thought to be one of the major causes of immunodeficiency. PEM and infection have always been closely associated, as PEM is a common cause of susceptibility to infections. Undernutrition in children negatively impacts on thymic development, therefore compromising immune responses . In malnourished patients, both innate and acquired immunity are affected [4, 5] and common immune defects are an imbalance in the ratio of CD4/CD8+ T cells [6], low expression levels of CD69 on lymphocytes [7], biased T helper cell responses [8], reduced antibody responses [6]; impaired phagocytosis by macrophages [9, 10], lower nitrite/nitrate concentrations in wound fluid [11] and decreased NF-kappa B activation by macrophages [12] have also been shown in experimental models of PEM(Protein energy malnutrition).

Impact of malnutrition on disease development in Leishmania infantum-infected mice

We have previously showed that increased arginase correlates with increased parasite replication and that competitive inhibition of arginase resulted in reduced parasite growth [26, 30]. Here we determined whether the increased arginase activities observed in mice fed with a low protein diet did coincide with increased parasite load. Seven days after the start of the diets, mice were infected i.v. with Leishmania (L). infantum and 8 days later, parasite load and arginase activities were measured in the spleen. As shown in Figure 5A, the increased parasite load in the spleen of MN mice (p =0.0286) coincided with increased arginase activity (p =0.0286, Figure 5B).

In macrophages, efficient parasite replication is controlled at least in part by arginase: catabolism of L-arginine by arginase results in the production of polyamines that the parasites use for their replication; competitive inhibition of arginase reduced the production of polyamines in BMMΦ activated with IL-4 and thereby clearly reduced parasite replication [26]. Since BMMΦ derived from MN mice express more arginase, we assessed whether this provides a more permissive environment for parasite growth; we activated BMMΦ with IL-4 and infected them with L. infantum and measured their growth as well as arginase activity; unstimulated macrophages as well as macrophages stimulated with IFN-γ and TNF-α were used as controls. As shown in Figure 5C, L. infantum grew significantly better in IL-4-stimulated BMMΦ derived from MN mice (p =0.0286), and this increase in parasite burden coincided with increased arginase activity (p =0.0286, Figure 5D). As shown previously [26], no parasites could be detected in BMMΦ activated with IFN-γ and TNF-α; no significant difference was observed in parasite growth in unstimulated BMMΦ derived from MN and control mice (p =0.6857, Figure 5C).
The results presented in Figure 5 show that L. infantum-infected mice on a low protein diet have a significantly higher parasite burden paralleled by significantly increased arginase activity, which provides a more permissive environment in host macrophages for parasite growth.

PEM is one of the major causes of immunosuppression, modifying both innate and adaptive immunity. It is highly prevalent in low-income countries, particularly in children . In the developed world, PEM is also a serious health concern, mainly seen in the elderly, with up to 10% of older people undernourished in nursing homes and up to 50% of older people undernourished when discharged from hospital [34]. Malnutrition is associated with a plethora of problems, such as fatigue, anaemia, cognitive abnormalities, immune dysfunctions and increased susceptibility to infections [34]. Monocytes and macrophages play a major role in the elimination of pathogens. Here we show that the frequency of monocytes is increased in the bone marrow and PBMCs of MN mice, suggesting a dysregulation in the haematopoiesis in these mice. This is in agreement with a study by Borelli et al. [35] that showed a 2.5-fold increase in the number of peripheral blood monocytes. Whereas macrophages and monocytes can be instructed to kill intracellular pathogens, they can also act as “safe target”. Indeed, in Leishmania major infected nonhealing mice, macrophage-granulocytes precursor cells were shown to be dramatically increased during infection, thereby offering a large number of host cells for the parasites to infect [36, 37]. Since these cells have not yet developed their full microbicidal potential [37], the parasites cannot be killed efficiently and the myeloid cells represent therefore a more permissive environment for the parasites to survive. We also showed an increase in the frequency of F4/80 + Ly6C + inflammatory macrophages in the blood of MN mice; these macrophages have been shown to be rapidly recruited to sites of inflammation. Since malnutrition has been associated with chronic inflammation [38], this might explain the increased frequency of these macrophages during PEM.

I see some potential problems with zero carb diet. Also there is a lot of pseudoscience and misinformation around it.

Keto Diet Problem #1: Keto diet followers continually claim that infants are in ketosis during breastfeeding.

Amber O'Hearn, a very prominent keto diet figure, who applied ketogenic dieting to herself about 9 years ago to manage obesity, OCD, depression(in other words, to control inflammation) makes this affirm over and over again, ex:

http://foodmed.net/2017/10/l-amber-ohearn-carnivore-meat-keto-lchf/
...I noticed that even textbooks about newborn infants acknowledge that babies are in ketosis when breastfeeding...

I tried to find the actual scientific confirmation.
Instead what I've found is this:

http://www.foodsmartsnutrition.com/blog/2017/10/20/weekly-q-a-babies-ketosis-and-misinformation
Myth: Babies are in ketosis and eat keto throughout infancy, until they transition to a solid-food diet.
Fact: Babes are NOT in ketosis and are not eating keto during infancy if they are consuming breastmilk or standard infant formula. The only time that babies are maintained in ketosis is during a medically-supervised ketogenic feeding intervention, with special, prescription formula.

Fats/Carbs/Proteins macros for the ideal infant food(breast milk):
https://static1.squarespace.com/static/58de9ff0c534a502b3a6cc20/t/59eabd5d4c326de32f2e72a8/1508556135001/Keto+infographic.png?format=1000w

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Keto Diet Problem #2: suppression of NLRP3 inflammasome pathway:

Ketosis, NLRP3, and Arthritis
https://crownmd.net/ketosis-nlrp3-and-arthritis/
– The NLRP3 inflammasome pathway is fundamental in the development of arthritis
– The ketone body, beta-hydroxybutyrate (BHB) inhibits the NLRP3 inflammasome
– ketosis may be a powerful tool in the toolbox for reducing arthritic burden.
...
Ketones block the NLRP3 Pathway
The research supports that the dysregulation of the NLRP3 inflammasome is a primary driver in the development of osteoarthritis, DDD, rheumatoid arthritis, and gout. It has also been demonstrated that there are therapeutic benefits from blocking this pathway. Pharmaceutical companies are working on NLRP3 blocking medications.

Activation of NLRP3 inflammasome in human neutrophils by Helicobacter pylori infection
https://journals.sagepub.com/doi/abs/10.1177/1753425915619475

Development of tissue inflammation accompanied by NLRP3 inflammasome activation in rabbits infected with Treponema pallidum strain Nichols
https://bmcinfectdis.biomedcentral.com/articles/10.1186/s12879-018-2993-0

NLRP3 Inflammasome and Host Protection against Bacterial Infection
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3792593/

NLRP3 Is a Critical Regulator of Inflammation and Innate Immune Cell Response during Mycoplasma pneumoniae Infection.
https://www.ncbi.nlm.nih.gov/pubmed/29061706

^ There is also a very high possibility that NLRP3 is required to control b.b. infection too (just not researched yet) and with chronic, ketosis induced, NLRP3 suppression a theoretical possibility exists that people in ketosis are immune suppressed against infections and just slowly moving towards eventual relapse.

I still think though that the healthy diet should mainly consist of animal products(fatty cheese, fatty meats) with minimum vegs(fiber) and some oxalates-free starch like white rice to avoid dropping into ketosis(easy checked with blood ketone checker like FreeStyle Ketone meter) with no proteins overload(since excessive proteins are always converted into glucose there is no logical reason to go hard with them).

I've been in healthcare for 26 years and never seen a protein deficient person. I would bet 99.9% of physicians never see a protein deficient person. It just doesn't happen in the U.S. unless someone is confined and food is held from them.

There is quite a bit of research linking animal protein intake to cancer. When I say a lot, I mean a lot. There is also a lot of research showing elevated fiber intake reducing your chances of cancer. It starts at 25 grams of fiber per day but the more fiber you eat, the more protective it is against cancer.

The WHO has processed meat classified as the same level of carcinogen as thallium. That is a Class I carcinogen which means it is known to cause cancer in humans. So processed meat is the same as a radioactive substance when it comes to cancer causing potential.

I wouldn't recommend white rice when brown rice has been shown to decrease insulin spikes and reduce body fat.

There are multiple issues with animal protein. The majority of the research focuses on ingestion of saturated fats that accompany the protein and it can cause cardiovascular disease. I also heard a prominent physician say that the saturated fats directed effected the tight junctions in the GI tract. That would be huge for a Lyme patient because the translocation of bacteria would be a major concern. Then there is the issue of excessive nitrogen intake when the ornithine pathway is compromised by a protozoan through ornithine decarboxylase or ornithine acetyltransferase. This will greatly increase oxidative stress and alter the microbiome through pH changes in the GI tract.

Georgia Hunter said...
I've been in healthcare for 26 years and never seen a protein deficient person. I would bet 99.9% of physicians never see a protein deficient person."...................................................." It just doesn't happen in the U.S. unless someone is confined and food is held from them.

Maybe it’s something new for you to learn about.

I am one and there are others.

At least in your opinion, .1% of Drs have seen this.! Not many, but some. Prob a little more though.

Low globulin protein and low total protein are not completely unheard of, Ive been to Drs who have seen this, Immunologists. Im fit , have muscle and protien is still low on blood serum testing per the basic comprehensive metabolic panel. Even with three different testing laboratories. Ive looked into it. Maybe I just use it up? It’s not in my urin. The other , albumin, Im good with.

I spent one whole Saturday goggling this, seen others, no explanation though.

There will always be people who don’t fit a regular health lab mold. Remember, per some professional opinions, "chronic lyme" doesn't exist either. ............wait a minute....what? Oh, they just dont know yet..

Post Edited (astroman) : 3/22/2019 5:32:14 PM (GMT-6)

Hard to believe this quote of a quote still does not work correctly on this forum.
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Irishlymie - prob got a little more info than you wanted. Back to your post- my sibo got under control with what I mentioned- avoiding the fodmap foods. You dont need to avoid all fiber. I was eating to much of the fodmaps. Goggle it. Many cant digest the fodmap sugar, so then bacteria does in the small intestine. This is starting to get more known in the sibo crowd. So common that a gastro Dr said to try it. Easy to try. I did use some digestive enzymes and anti-candida marketed herbs to speed things.

I eat fodmap foods again, just not as much.

No gas, no bloating, back to normal. No sibo.

No Rx needed so far in my case.