Friday, July 27, 2018

Emotional Attacks....It's not about you

Emotional Attacks are not about you unless you are the attacker, then I would really urge you to take a good look inside...

I have tried many times to explain to others that an emotional response to someone's words is not about them but all about you and your own triggers and belief or insecurities. It is a time to reflect on that which you may need to address and clear within yourself.

I could not have said it better than this article by Madison Taylor.


You cannot control other people's emotions, but you can control your own.
Hurtful confrontations often leave us feeling drained and confused. When someone attacks us emotionally, we may wonder what we did to rouse their anger, and we take their actions personally. We may ask ourselves what we could have done to compel them to behave or speak that way toward us. It's important to remember that there are no real targets in an emotional attack and that it is usually a way for the attacker to redirect their uncomfortable feelings away from themselves. When people are overcome by strong emotions, like hurt or anguish, they may see themselves as victims and lash out at others as a means of protection or to make themselves feel better. You may be able to shield yourself from an emotional attack by not taking the behavior personally. First, however, it is good to cultivate a state of detachment that can provide you with some protection from the person who is attacking you. This will allow you to feel compassion for this person and remember that their behavior isn't as much about you as it is about their need to vent their emotions.

If you have difficulty remaining unaffected by someone's behavior, take a moment to breathe deeply and remind yourself that you didn't do anything wrong, and you aren't responsible for people's feelings. If you can see that this person is indirectly expressing a need to you--whether they are reaching out for help or wanting to be heard--you may be able to diffuse the attack by getting them to talk about what is really bothering them.

You cannot control other people's emotions, but you can control your own. If you sense yourself responding to their negativity, try not to let yourself. Keep your heart open to them, and they may let go of their defensiveness and yield to your compassion and openness.

Monday, July 23, 2018

Fish oils and Increased bleeding risk...fact or fiction?

Fish Oil Consumption Does Not Increase Bleeding Risk

by Lewis Chang, PhD

Fish oil is rich in omega-3 fatty acids EPA and DHA. Increased intake of EPA and DHA is beneficial for cardiovascular health, cognitive function, mental health, maternal and child health, immunity and inflammation. EPA and DHA supplements are becoming more and more popular across a wide diversity of people; from healthy individuals to vulnerable populations with impaired health.
Higher omega-3 concentrations may compete with fatty acids such as arachidonic acid for metabolizing enzymes. The interaction results in a decreased production of compounds that induce platelet aggregation and an increased production of compounds with anti-platelet properties, hence the anticoagulation benefits of omega-3. However, for patients who are under antithrombotic therapy (either with platelet aggregation inhibitors such as aspirin or anticoagulant drugs such as warfarin), the potential risk of bleeding due to the concurrent use of omega-3 fatty acids has been a concern by many clinicians, particularly surgeons.1,2
Multiple clinical studies have been conducted to investigate whether omega-3 fatty acids pose a clinically significant bleeding risk. So far, the findings have been consistent:
  • A 2004 Cochrane review of 48 randomized controlled trials and 41 epidemiological analyses concludes that 0.4-7 g/day omega-3 fatty acids do not result in any change in clinical bleeding manifestations3
  • A 2007 review of 19 clinical studies involving nearly 4400 surgical patients concludes that the risk for clinically significant bleeding was virtually nonexistent with the use of 1.4-21 g/day of omega-3 fatty acid supplements, even with the concurrent use of antiplatelet or antithrombotic medications4
  • A 2013 systematic review of 10 randomized trials involving nearly 1000 adults 60 years or older concludes that there is no difference in total adverse event rates between daily use of placebo or 0.03-1.86 g EPA and/or DHA for 6-52 weeks5
  • A 2014 review of 7 randomized controlled trials and 3 epidemiological studies concludes that omega-3 fatty acid treatment has no effect on the risk of clinically significant bleeding in either monotherapy or combination therapy settings and there is no support for discontinuing the use of omega-3 fatty acid treatment before invasive procedures6
  • A 2017 systematic review based on 32 publications on healthy subjects and 20 publications on patients undergoing surgery finds that fish oil supplements reduce platelet aggregation in healthy subjects and do not increase intra- or post-operative bleedings in patients, and concludes that discontinuation of fish oils supplements prior to surgery is not recommended7
Despite the accumulating evidence demonstrating the safety of fish oil, the worry seems to persist, especially when at risk patients are involved.
Most recently, researchers from Danone Food Safety Centre (Palaiseau, France) and Nutricia Research (Utrecht, the Netherlands) evaluated the safety data from 8 clinical intervention studies involving over 600 patients, including oncology patients, HIV patients, ICU patients, and patients with Alzheimer’s disease.8 The levels of omega-3 fatty acids received by these patients (either via oral consumption or tube feeding) ranged from 1.5-10.2 g/day with a duration of 8 days to 52 weeks. The outcomes included bleeding-related adverse events, prothrombin time, and partial thromboplastin time. In the end, the researchers found no evidence of increased risk of bleeding with the use of omega-3 fatty acid products in these patients, with or without concomitant use of antithrombotic medications.
In summary, the legitimate concern of increased bleeding as a result of omega-3 fatty acid intake has not been supported by numerous randomized controlled trials and epidemiological studies involving a wide range or participants, from healthy young folks to surgical patients to very vulnerable older patients.

Why is this Clinically Relevant?
  • Fish oil or EPA/DHA products are associated with a variety of benefits, from cardiovascular health to cognitive function to anti-inflammation
  • The concern of increased risks of bleeding associated with these ingredients has not been validated by a large number of clinical studies and systemic reviews
  • Clinicians should inform patients of the safety of omega-3 fatty acids for the vast majority of the population, and there is no scientific evidence supporting the discontinuation of omega-3 products prior to surgery

  1. Bays HE. Safety considerations with omega-3 fatty acid therapy. Am J Cardiol. 2007;99(6A):35C-43C.
  2. Braga M, Ljungqvist O, Soeters P, et al. ESPEN Guidelines on Parenteral Nutrition: surgery. Clin Nutr. 2009;28(4):378-386.
  3. Hooper L, Thompson RL, Harrison RA, et al. Omega 3 fatty acids for prevention and treatment of cardiovascular disease. Cochrane Database Syst Rev. 2004(4):CD003177.
  4. Harris WS. Expert opinion: omega-3 fatty acids and bleeding-cause for concern? Am J Cardiol. 2007;99(6A):44C-46C.
  5. Villani AM, Crotty M, Cleland LG, et al. Fish oil administration in older adults: is there potential for adverse events? A systematic review of the literature. BMC Geriatr. 2013;13:41.
  6. Wachira JK, Larson MK, Harris WS. n-3 Fatty acids affect haemostasis but do not increase the risk of bleeding: clinical observations and mechanistic insights. Br J Nutr. 2014;111(9):1652-1662.
  7. Begtrup KM, Krag AE, Hvas AM. No impact of fish oil supplements on bleeding risk: a systematic review. Dan Med J. 2017;64(5).
  8. Jeansen S, Witkamp RF, Garthoff JA, van Helvoort A, Calder PC. Fish oil LC-PUFAs do not affect blood coagulation parameters and bleeding manifestations: Analysis of 8 clinical studies with selected patient groups on omega-3-enriched medical nutrition. Clin Nutr. 2018;37(3):948-957. you truly have it?

Integrity has been a huge learning curve for me and really defining what it, is the key. There are many of us that do not know or practice true integrity and the reason may be that we do not know ourselves or really pay attention to our word and the creations that come from that.

Even the definition of Integrity in the dictionary does not cover the true scope of it.

Here's what I have learned and continue to practice about integrity. It is a matter of your word. Nothing more and nothing less......
(the teachings at Landmark and my Body and Brain yoga practice has really helped me integrate this fully)

There are tow aspects of Integrity - Keeping your word and honoring your word.

Keeping your word consists of the following:

  • Doing what you know to do...That is taking responsibility for your self and doing your job, or tasks to the best of your ability. Attending meetings and games and events you committed to.
  • Being on time and respecting the time of others.
  • Doing what you said you would do...on time and joyfully.
  • Doing what others would expect you to do even if you haven't said you would do in a marriage...sharing the chores, taking out the trash, changing diapers, doing the dishes or cleaning your space. In relationships....treating the other person with respect and being honest, taking responsibility for your own emotions and being on time for plans together. When attending courses or continuing education...doing your work, paying attention and treating the presenters/lecturers with respect, and being on time.
  • Doing complete work with whatever you do.....don't half ass it and expect other to pick up the slack or expect them to accept it.
  • Doing what you do as it was meant to be done.
  • Being your word...fulfilling on your commitments, on time and whole heartedly, and when not possible honoring your word.
Honoring your word is:

Whenever you will not be keeping your word and you become aware of the fact (including not keeping your word on time) sharing the following with everyone impacted:

  1. That you will not be keeping your word and how you will keep your word in future and by when and how...or that you will not be keeping your word at all.
  2. And what you will do to deal with the impact the failure to keep your word (or keeping it on time) has on others.
And when not keeping your word you can restore Integrity by acknowledging your promise or agreement/commitment that you broke and letting them know that you understand the impact that had on the situation or circumstance. Then express what it is that you will do in future to prevent yourself from breaking another promise or agreement/commitment.

These actions will ensure trust and accountability with you and towards you in all your future endeavors and relationships.

The world is lacking in Integrity and it affects how well things work and how well a business, organization and country runs. It affects relationships, and the workability thereof, it basically affects everything and everyone in life.

Some may even define Integrity as sincerity...being sincere in how you present and walk through the world. Be the person who you know you and everyone can always count on because you are your word and you honor your word. Be sincere in your expression and creation in life.

Phytosterols and Inflammation...

Phytosterols and Inflammation: What’s the Story?

by Ashley Jordan Ferira, PhD, RDN

Obesity and cardiometabolic disease are metabolic perturbations associated with inflammation chronicity. The Western diet is typified by a surplus of calories, low nutritional quality, and high pro-inflammatory potential, thereby fueling excess adiposity, which further leads to inflammation. To break this obesity-inflammation cycle, adopting a healthful dietary pattern and incorporating regular physical activity is critical. Furthermore, identifying foods and nutritional bioactives that can reduce or counteract inflammation is important for the development of targeted nutrition therapies. This blog focuses on a class of plant lipids: phytosterols.

Phytosterols are known for their cholesterol-lowering ability
Phytosterols, which encompass plant sterols and stanols, are the plant kingdom’s analog of cholesterol (found in the animal kingdom). A large, robust body of research supports the established role of phytosterol supplementation in cholesterol reduction and by extension, cardiovascular disease risk reduction.1-3 By competing with cholesterol absorption in the gut and increasing biliary cholesterol excretion in the feces, daily phytosterol supplementation (in the range of 1.8-3g/day on average) induces LDL-cholesterol reductions in the range of 5-15%, a clinically meaningful magnitude.1

The Western diet creates a “phytosterol gap”
A typical Western diet only provides ~300 mg/day of phytosterols and 30 mg/day of phytostanols on average.2 Unrefined vegetable oils, whole grains, nuts, and legumes are natural sources of phytosterols, albeit in trivial amounts relative to the amount of phytosterols you would actually need to consume (along with the caloric price you would pay) to impact serum cholesterol levels.3

Exploring the potential, anti-inflammatory role of phytosterols
Phytosterols have more recently been investigated for their hypothesized role in diminishing inflammation, although the body of research is relatively small and equivocal at best. The potential anti-inflammatory role of phytosterols has been explored in preclinical4-9 and clinical10 studies. The in vitro cell culture4-7 and in vivo animal8-9 studies have suggested anti-inflammatory properties for phytosterols via their modulation of inflammatory activity of immune cells (macrophages and neutrophils). In contrast, the clinical evidence from a meta-analysis of randomized controlled trials utilizing phytosterol-fortified foods found no effect on C-reactive protein (CRP), a biomarker for chronic, low-grade inflammation.10
Genetic disorders often shed light on underlying physiological mechanisms. Sitosterolemia, also known as phytosterolemia, is a rare autosomal recessive genetic disease caused by homozygous or heterozygous mutations in specific genes: either/or ABCG5, ABCG8.11 Individuals with this mutation have increased absorption of dietary phytosterols in the gut and decreased biliary excretion; they consequently accumulate phytosterols in the blood at 30-100x higher than normal.12 Cholesterol (from animal products) levels can also be mildly to moderately elevated in these patients, some of whom experience hypercholesterolemia and premature atherosclerosis.11-12

Phytosterol and inflammation research: what’s new?
A recent 2018 study13 sought to expound upon the potential mitigating role of phytosterols on inflammatory cytokines in obesity and metabolic disease models in humans and animals. First, the observational clinical study looked at cross-sectional relationships between phytosterol levels in the blood and inflammatory biomarkers in Japanese adults with and without diabetes.13 Distinct, inverse correlations were observed: higher serum sitosterol levels were associated with lower serum IL-6 and TNF-α (pro-inflammatory cytokines) levels in the diabetic and healthy individuals, and with lower PAI-1 in the healthy individuals only.13 No significant associations were seen for CRP and serum sterol levels.13 After controlling for a slew of potential confounders, the relationship between sitosterol levels, IL-6 and TNF-α persisted.13 Sitosterol is the predominant phytosterol in plant oils.2-3
Next, a well-designed animal model of sitosterolemia, obesity, and chronic inflammation assessed the effects of high circulating phytosterols (by deleting genes ABCG5/8) on body weight, glucose metabolism, and inflammatory cytokines in mice fed a high-fat diet.13 Compared to ABCG5/8 heterozygote (G+/-) control mice, the ABCG5/8 knockout (KO) (G-/-) mice had significantly higher plasma phytosterol levels, while plasma cholesterol levels were similar between groups.13 The control and KO mice had similar food intake, but the KO mice had significantly less body weight gain and adipose tissue expansion, as well as suppressed fatty liver changes.13 Furthermore, KO mice had lower IL-6 and TNF-α levels in plasma and tissues, in addition to lower expression of inflammation-related genes in the liver (for TNF-α and PAI-1) and adipose (for IL-6, TNF-α, and MCP-1).13 Although animal study results cannot be generalized to humans, the results of this study suggest that a mechanism may exist such that sitosterol suppresses obesity-related chronic inflammation and attenuates metabolic dysfunction.13

What’s the upshot?
Chronic inflammation is thought to play a major role in metabolic disease development. Phytosterols, “famous” for their clinical utility in cholesterol-lowering,1-2 may also be involved in suppressing obesity-related chronic inflammation according to recent research, albeit in its early stages.13 While underlying mechanisms require further exploration, the potential role of phytosterols in mitigating inflammation is definitely worth discovery, particularly via human intervention studies.

  1. Fumeron F et al. Interindividual variability in the cholesterol-lowering effect of supplementation with plant sterols or stanols. Nutr Rev. 2017;75(2):134-145.
  2. Gylling H et al. Phytosterols, phytostanols, and lipoprotein metabolism. Nutrients. 2015;7(9):7965-7977.
  3. Linus Pauling Institute. Micronutrient Research Center. Phytosterols. Accessed June 18, 2018.
  4. Awad AB et al. Phytosterols decrease prostaglandin release in cultured P388D1/MAB macrophages. Prostaglandins Leukot Essent Fatty Acids. 2004;70(6):511-520.
  5. Navarro A et al. Anti-inflammatory and immunomodulating properties of a sterol fraction from Sideritis foetens Clem. Biol Pharm Bull. 2001;24(5):470-473.
  6. Kurano M et al. Plant sterols increased IL-6 and TNF-α secretion from macrophages, but to a lesser extent than cholesterol. J Atheroscler Thromb. 2011;18(5):373-383.
  7. Valerio M et al. β-sitosterol down-regulates some pro-inflammatory signal transduction pathways by increasing the activity of tyrosine phosphatase SHP-1 in J774A.1 murine macrophages. Int Immunopharmacol. 2011;11(8):1012-1017.
  8. Plat J et al. Protective role of plant sterol and stanol esters in liver inflammation: insights from mice and humans. PLoS One. 2014;9(10):e110758.
  9. Hu Q et al. Phytosterols improve immunity and exert anti-inflammatory activity in weaned piglets. J Sci Food Agric. 2017;97(12):4103-4109.
  10. Rocha VZ et al. Effects of phytosterols on markers of inflammation: a systematic review and meta-analysis. Atherosclerosis. 2016;248:76-83.
  11. Berge KE et al. Accumulation of dietary cholesterol in sitosterolemia caused by mutations in adjacent ABC transporters. Science. 2000;290(5497):1771-1775.
  12. U.S. National Library of Medicine. Genetics Home Reference. Sitosterolemia. Accessed June 19, 2018.
  13. Kurano M et al. Sitosterol prevents obesity-related chronic inflammation. Biochim Biophys Acta. 2018;1863(2):191-198.

Ashley Jordan Ferira, PhD, RDN

Dr. Ashley Jordan Ferira is Manager of Medical Affairs and the Metagenics Institute, where she specializes in nutrition and medical communications and education. Dr. Ferira’s previous industry and consulting experiences span nutrition product development, education, communications, and corporate wellness. Ashley completed her bachelor’s degree at the University of Pennsylvania and PhD in Foods & Nutrition at The University of Georgia, where she researched the role of vitamin D in pediatric cardiometabolic disease risk. Dr. Ferira is a Registered Dietitian Nutritionist (RDN) and has served in leadership roles across local and statewide dietetics, academic, industry, and nonprofit sectors.

Blood type diet...yes or no?

Health Benefits of Blood-Type Diet Found to be Unrelated to Individual’s Blood Type

by Lewis Chang, PhD
Based on the theory that each blood type (i.e., O, A, B, and AB type) represents distinct genetic traits and ancestral dietary habits, the popular “blood-type diet” advocates eating according to one’s blood type to achieve optimal health. For example, individuals who are type O (“the hunter”) would benefit most from a high-animal protein diet with avoidance of grains, legumes and dairy products; type A (“the agrarian”) are best with a vegetarian diet; type B (“the nomad”) are encouraged to eat dairy products while avoiding chicken, corn, wheat, lentils and tomatoes; and type AB (“the enigma”) should follow a dietary pattern between type A and B. However, the rationale and the proposed health claims of the blood-type diet have not been validated scientifically.
Researchers from the Department of Nutritional Sciences at the University of Toronto (Ontario, Canada) recently conducted a study to examine the validity of the blood-type diet.1 The study included 973 adults who participated in the Toronto Healthy Diet Study—a 6-month study that assessed the effect of dietary advice, food provision, or both on body weight and cardiovascular disease risk factors. Their mean age was 44.6 years and mean BMI was 32.5 kg/m2. A 196-item food-frequency questionnaire was used to assess the participant’s dietary intake at baseline and after 6 months. Then, the diet adherence scores were calculated to determine an individual’s relative adherence to each of the 4 blood-type diets.
The investigators found that following the blood-type diet was associated with improvements in cardiometabolic risk factors such as BMI and waist circumference. However, the beneficial effects were similar between those who matched the diet with the corresponding blood type and those who did not.1 For example, the type A diet was not only beneficial for type A individuals, but also equally beneficial for those with other blood types. This suggests that the benefit of a blood-type diet, which may simply represent a healthy eating pattern, is independent of a person’s blood type.
Although these results provide evidence against the blood-type-specific health claims made by advocates of the blood-type diet, the dietary patterns recommended by the blood-type diet are characterized by healthy, whole foods with avoidance of refined carbohydrates and processed products. Thus, those switching from the typical unhealthy Western diet to any blood-type diet likely will experience improvements in overall health. This may explain why many people have great confidence in this diet.
The study was supported by the Canadian Institutes of Health Research, and the results have been published in Journal of Nutrition.
Why is this Clinically Relevant?
  • Individuals with higher adherence to the blood-type diet experienced improvements in cardiometabolic risk profile, but this effect was irrespective/independent of their blood type
  • The health claims made by the blood-type diet remain unsupported by scientific evidence. However, the blood-type dietary pattern is rich in healthy foods and recommends avoidance of refined carbohydrates and processed foods
  • Following recommendations from any of the blood-type diets will be an improvement from the typical, unhealthy Western diet. Therefore, those who follow the blood-type diet are likely to benefit from it.
  1. Wang J, Jamnik J, Garcia-Bailo B, Nielsen DE, Jenkins DJA, El-Sohemy A. ABO genotype does not modify the association between the “blood-type” diet and biomarkers of cardiometabolic disease in overweight adults. J Nutr. 2018;148(4):518-525.

The SIBO dilemma

The SIBO Dilemma: How the Optimistic “Magic Bullet” Falls Short for Most Patients

by Vincent Pedre, MD
Small intestinal bacterial overgrowth (SIBO) is a controversial diagnosis that can masquerade behind a variety of symptoms, not all of which involve the characteristic bloating, gas and abdominal pain. SIBO also manifests as rosacea,1 diarrhea, constipation, anxiety,2 depression, fatigue, and iron deficiency. The astute clinician needs to hold a high degree of suspicion because a patient with SIBO may not present with the classic symptoms. For example, a recent severe case I saw presented only with diarrhea.
First of all, a few definitions are in order. SIBO is a chronic, excessive bacterial colonization of the small bowel. This means the patient with SIBO may have an overgrowth of the commensal microbiota in the small intestine, normally averaging between 103—10CFUs (colony-forming units)/mL, or backwards migration through the ileocecal valve into the small intestine of the normal bacterial flora from the large intestine, where the average is 1012-13 CFUs/mL.3 Once established, the organisms produce hydrogen or methane gas or a combination of the two in excess and consume vital nutrients before the person has a chance to absorb them, leading to malnutrition and fatigue. Hydrogen is produced by bacteria, but methane is produced by another group of organisms known as “archaea,” which fall under a different kingdom. This becomes relevant when considering treatment. The typical complaint is bloating after meals, with the timing thereof ranging from minutes to an hour later depending on the location of the SIBO.
Factors that put someone at risk for SIBO include:3
  • Hypochlorhydria (low production of hydrochloric acid in the digestive track)
  • Chronic antacid therapy (especially with PPIs or H2-blockers)
  • Gastroparesis (secondary to diabetes type I or II); motility of the stomach is abnormal or absent
  • Gallbladder/bile dysfunction
  • Pancreatic enzyme deficiency
  • Slow-transit constipation
  • Disruption of the migrating motor complex (MMC), as may be caused by radiation
  • History of bulimia
  • Multiple courses of antibiotics
  • Ileocecal valve incompetence
  • Diet rich in sugars and simple carbohydrates
  • Heavy alcohol use
Testing for SIBO is done either via a jejunal aspirate, which is the gold standard, or most often through a less invasive breath test that detects both methane (CH4) and hydrogen sulfide (H2S) gases, using one of two sugars (glucose or lactulose) to induce the gas production. Since CH4 and H2S are not produced as metabolic byproducts of human cells, the expired gas during a three-hour breath test is generated by bacterial fermentation as the provoking solution travels through the gut. It takes about 120 minutes to reach the end of the ileum and another hour to complete transit through the colon. Taking into account a patient’s clinical picture is important in order to interpret the results of the testing. Based on a spike in hydrogen and/or methane gas as described below, a positive test is confirmed within the 120-minute mark.
SIBO breath testing is considered positive when:
  • H2S production rises by 20 parts per million (ppm) or greater over the lowest preceding value within 120 minutes after ingesting the solution
  • Methane production rises by 12ppm or greater over the lowest preceding value within 120 minutes after the testing solution
  • A combined sum of H2S and CH4 production rises 15ppm or greater above the lowest preceding value within 120 minutes
Rifaximin arrived as the perfect solution to treating SIBO. The controversy with typical antibiotics is that they would be absorbed before they reached their target in the small bowel, especially for distal SIBO.4 Rifaximin, unlike other antibiotics, is not absorbed; staying in the intraluminal space where the antibiotic is needed to reduce the bacterial overgrowth back to normal.  Unfortunately, because of its apparent resistance to conventional treatment, SIBO is a source of great frustration for patients and clinicians alike. SIBO often recurs in the same patient within several months of treatment. It will usually respond to repeat treatment with rifaximin; however, we know that this remedy is only at most 40-80 percent effective in IBS without constipation.5-6
Frequency of SIBO among those suffering from IBS, is between 4-78%7particularly the diarrhea-predominant type. However, methane-predominant SIBO, which is often characterized by constipation, does not respond well to rifaximin therapy alone. In these cases, neomycin is often added to rifaximin,8 but it has a high risk of ototoxicity, making it a less desirable adjunct to treatment. Therefore, what remain are natural, herbal antimicrobials that can be quite effective without the risks of toxicity. The difference is that this treatment must be of longer duration to resolve SIBO.
My Recommendations for Therapy
The herbal remedies that I have found to be effective, either in combination with themselves or post-antibiotic therapy include ingredients like peppermint oil, berberine, and oregano oil.
For symptom relief:
  • A combination of peppermint oil with calming lavender oil and chamomile extract
To address bacterial overgrowth (very likely accompanied with yeast overgrowth) the following may be taken together, or in an alternating two week cycle:
  • A blend of concentrated aromatic essential oils, including thyme and oregano, that help support intestinal microbial balance
  • A concentrated berberine formula makes a great adjunct to SIBO treatment, including after rifaximin therapy for 2—3 months to prevent a recurrence
For improving the digestion and absorption of nutrients:
  • An extra-strength, pancreatic-derived enzyme complex with protease, lipase and amylase
For promoting a healthy gastric environment:
  • A zinc-carnosine complex, which helps improve gastric mucosal integrity and function
The key to successful SIBO treatment is to understand that remedies work best in combination, and the patient must also follow a SIBO-specific diet until you are sure that the SIBO is totally resolved.  I usually wait until after the first month of therapy before adding a probiotic, because early on a probiotic can aggravate SIBO symptoms of gas and bloating. The best protocol for adding probiotics post-SIBO treatment is to “start low and go slow”, making sure the patient is tolerating the probiotic without worsening symptoms. A good probiotic to start with has a lower concentration of live organisms per capsule, for example 4 billion live organisms per capsule, so the dose can be titrated as tolerated.
A repeat SIBO breath test is useful in gauging progress post-treatment, and helps guide the duration and intensity of therapy. SIBO patients require close monitoring, so I recommend meeting with them twice in the first month of therapy, then monthly for another 2 – 5 months to ensure complete resolution.
There are no magic bullets for the treatment of SIBO.  Each individual patient has unique needs; therefore, a combination of treatments and ongoing monitoring is recommended for SIBO.
  1. Parodi A, Paolino S, Gerco A, et al. Small intestinal bacterial overgrowth in rosacea: clinical effectiveness of its eradication. Clinical Gastroenterology Hepatology. 2008;6(7):759-764.
  2. Addolorato G, Mirijello A, D’Angelo C, et al. State and trait anxiety and depression in patients affected by gastrointestinal diseases: psychometric evaluation of 1641 patients referred to an internal medicine outpatient setting. Int J Clin Pract2008;62(7):1063-1069.
  3. Dukowicz AC, Lacy BE, Levine GM. Small intestinal bacterial overgrowth: a comprehensive review. Gastroenterol Hepatol. 2007;3(2):112-122.
  4. Di Stefano M, Malservisi S, Veneto G, Ferrieri A, Corazza GR. Rifaximin versus chlortetracycline in the short-term treatment of small intestinal bacterial overgrowth. Aliment Pharmacol Ther. 2000;14(5):551-556.
  5. Pimental M, Lembo A, Chey WD, et al. Rifaximin therapy for patients with irritable bowel syndrome without constipation. N Engl J Med. 2011;364(1):22-32.
  6. Scarpellini E, Gabrielli M, Lauritano CE, et al. High dosage rifaximin for the treatment of small intestinal bacterial overgrowth. Alimentary Pharm. and Ther. 2007;25(7):781-786.
  7. Ghoshal UC, Shukla R, Ghoshal J. Small intestinal bacterial overgrowth and irritable bowel syndrome: a bridge between functional organic dichotomy. Gut liver. 2017;11(2):196-208.
  8. Low K, Hwang L, Hua J, Zhu A, Morales W, Pimentel M. A combination of rifaximin and neomycin is most effective in treating irritable bowel syndrome patients with methane on lactulose breath test. J Clin Gastroenterol. 2010;44(8):547-550.

    Vincent Pedre, MD
    Dr. Vincent M. Pedre is Medical Director of Pedre Integrative Health and President of Dr. Pedre Wellness. He is a board-certified internist and Functional Medicine certified practitioner in private practice in New York City. His philosophy and clinical practices blend Western and Eastern medical traditions, defined by an integrative, functional, and systems-based approach to well-being. Dr. Pedre is a Clinical Instructor at the Mount Sinai School of Medicine, as well as certified in yoga and Medical Acupuncture.