Dr. Michael Ruscio, DC is a clinician, Naturopathic Practitioner, clinical researcher, author, and adjunct professor at the University of Bridgeport. His work has been published in peer-reviewed medical journals and he speaks at conferences around the globe.
Clinical research has revealed an association between indoor tanning and several health risks, including the subsequent occurrence of melanoma and nonmelanoma skin cancers, the development of psychological dependence, and a tendency toward other high-risk health behaviors.
Short-term daily intermittent fasting may be a safe, tolerable, dietary intervention in type 2 diabetes patients that may improve key outcomes including body weight, fasting glucose and postprandial (after a meal) variability.
These findings should be viewed as exploratory, and a larger, longer study is necessary to corroborate these findings.
The preferred meal to skip was breakfast
Intermittent fasting led to an overall spontaneous decrease in caloric intake as measured by food photography
Conclusion: Combinations of multistrain probiotic bacteria showed promise in preventing the incidence of infection following colorectal surgery. However, the efficacy of one or two strains of probiotics remains undetermined.
Perhaps you have multi-antimicrobial compounds released when you use a multi-strain probiotic
Current evidence suggests that several environmental factors including vaccination, maternal smoking, thimerosal exposure, and most likely assisted reproductive technologies are unrelated to risk of ASD. On the contrary, advanced parental age is associated with higher risk of ASD
Birth complications that are associated with trauma or ischemia and hypoxia have also shown strong links to ASD, whereas other pregnancy-related factors such as maternal obesity, maternal diabetes, and cesarean section have shown a less strong (but significant) association with risk of ASD.
The studies on toxic elements have been largely limited by their design, but there is enough evidence for the association between some heavy metals (most important inorganic mercury and lead) and ASD that warrants further investigation.
Coffee consumption seems to increase the risk of developing rheumatoid arthritis (RA) and type 1 diabetes mellitus (T1DM)
By contrast, coffee consumption may exert a protective role against multiple sclerosis, primary sclerosing cholangitis, and ulcerative colitis.
In other studies, coffee consumption was shown to influence disease course and management options. Coffee intake led to a decrease in insulin sensitivity in T1DM, in methotrexate efficacy in RA, and in levothyroxine absorption in Hashimoto’s disease
Further, coffee consumption was associated with cross reactivity with gliadin antibodies in celiac patients – caution here, we already clarified this here.
This study provides further evidence that living in a farming environment during childhood is protective of asthma incidence in adolescence and adulthood and this finding provides further support for the hygiene hypothesis
Of 800 studies identified through the literature search, 15 were finally included. The studies comprised a total of 957 subjects.
The effect sizes were small – it was significant from a numeric statistic but it was not clinically meaningful
In This Episode
Episode Intro … 00:00:40 Fecal Microbiota Transplantation … 00:01:18 H. Pylori Eradication Therapies … 00:03:55 Tanning Beds … 00:06:46 Healthy Gut Healthy You Book … 00:09:05 Effects of Intermittent Fasting … 00:10:36 Vitamin D to Prevent Acute Respiratory Tract Infections … 00:15:46 Excessive Iodine Intake and TSH … 00:17:17 Iodine Status & Thyroid Function in Children … 00:20:55 Probiotics for the Prevention of Necrotizing Enterocolitis … 00:22:53 Benefits of Levothyroxine Replacement Therapy … 00:24:00 Probiotics Reduce Postoperative Infections … 00:27:45 Environmental Risk Factors for Autism … 00:29:55 Coffee and Autoimmunity … 00:31:55 Significantly Higher Fecal Counts of the Yeasts Candida … 00:35:00 Hygiene Factors Associated with Childhood Food Allergy … 00:39:08 Association of Living in a Farming Environment with Asthma … 00:40:06 Fungal Dysbiosis Associated w/ Visceral Hypersensitivity … 00:41:30 Effects of Probiotics on Body Weight, Body Mass Index, Fat Mass … 00:46:30 Episode Wrap-up … 00:48:45
Dr. Michael Ruscio: Hey, everyone. Welcome to Dr. Ruscio Radio. This is Dr. Ruscio. And let’s jump into another edition of health news updates where we provide you with a short summary of a number of recently published studies that are noteworthy. Today, we’ll be talking about, amongst other things, H. pylori treatment updates, tanning beds, intermittent fasting, vitamin D supplementation, iodine and thyroid, coffee and autoimmunity, intestinal yeast and more.
Now, what the title tells you that may be important to understand is some of the more traditional recommendations, if I can even use the term traditional because FMT is so new or its clinical application becoming more widely accepted is so new. But traditionally, the recommendation is it may be best to wait to undergo an FMT until one is asymptomatic, meaning if you have ulcerative colitis or Crohn’s in this case. It may be better to wait until you are not in a flare or you’re in remission. Wait until that point before having the FMT.
However, this study shows that it may be a suitable treatment, like steroids may be, to help induce remission when someone is having a flare. So the results. After FMT, 70% of the patients showed clinical response and 43% of the patients achieved clinical and endoscopic remission at the 12-week mark. 30% of the patients were nonresponders at the end of the 12 weeks. The donor did not matter.
There is currently debate regarding should there be one donor or multiple donors and do the characteristics of a donor make a difference. And there seems to be some data showing yes. In this case, there’s some data showing it does not matter. No adverse events were observed in the majority of patients; however, about 24% experienced mild adverse events such as nausea, vomiting, abdominal pain, diarrhea, and the like after FMT.
So their conclusion: “FMT could be considered as a promising rescue treatment modality before surgery in patients with refractory”—meaning nonresponsive—“ulcerative colitis.” And you may have heard me say before I think one of the next treatments or the next treatment that will receive FDA approval for FMT would be inflammatory bowel disease. The data there is just mounting. And as this study shows, it’s continuing to show promise.
H. Pylori Eradication Therapies
Ok. The next study, “Optimization Strategies Aimed to Increase the Efficacy of H. Pylori Eradication Therapies.” I just want to read two quotes from this paper. “The efficacy of triple therapies in the presence of resistance can be significantly improved by the addition of bismuth salts”—which we talked about with Dr. Paul Anderson in biofilms on a recent podcast—“which offer an additive effect in combination with antibiotics.” They continue, “Overall, probiotics seem to reduce antibiotic side effects, but the increase in eradication rate is not so evident. Therefore, they”—meaning probiotics—“cannot be generally recommended for clinical practice yet.”
So I actually disagree because we do have fairly compelling data, meaning more than one, I believe, meta-analysis showing that probiotics have a synergistic effect and make antibiotics more effective. There does seem to be, for reasons I don’t fully understand, that conventional medicine is quite resistant to the use of probiotics. There’s mounting data, good data, showing that probiotics can be effective. Perhaps, because it’s something very foreign to what’s discussed in medical school that this seems to be outside of the comfort zone. Maybe once a big pharmaceutical house comes out with their patented probiotic more people will get on board. But we already kind of have that through VSL#3 which has been used in a number of clinical trials.
And the high-dose version of that is prescription-only. VSL#3, if you think about the three-category system of probiotics that I talk about in the book, that would be a category one probiotic. A mixture of predominantly Lactobacillus and Bifidobacterium blends. But for whatever reason, there seems to be this resistance amongst many in conventional medicine to probiotics, even though there’s pretty compelling data.
And the other thing that’s important to mention here is probiotics show almost no adverse events and at very best they show extremely mild adverse events. They’re inexpensive, and they tend to have other secondary health benefits. So the reason for the resistance to probiotics being accepted is beyond me. I think it’s unfortunate. It shows an unfortunate bias.
And also, regarding strategies for H. pylori, synergistic interventions to help with the eradication of H. pylori, remember that there is one study that showed that n-acetylcysteine when administered with antibiotics almost doubled or maybe even slightly higher than doubled the eradication rate of H. pylori.
Ok. “Tanning Beds’ Impact on Health and Recent Regulations.” I’ll quote for you from this paper. “As the use of indoor tanning beds gained popularity in the decades after their appearance in the market in the early 1970s, concerns arose regarding their use.” Important right here. “The clinical research has revealed an association between indoor tanning and several health risks, including the subsequent occurrence of melanoma and non-melanoma skin cancers, the development of physiological dependence, and a tendency toward high-risk health behaviors.” That’s very important.
Continuing, “In the face of mounting evidence, legislation has been passed which includes the restriction of access to tanning beds by minors in 42 states and the District of Columbia and the recent reclassification by the Food and Drug Administration, which now categorizes tanning beds as a class 2 device and worthy of restrictions and oversight.” My thoughts. I lean toward agreement with this statement, definitely.
There’s not much data regarding tanning beds specifically. There’s a fair amount of data showing an association—or healthful association between sun exposure and various outcomes. But the question has been asked, well, would a tanning bed be something that could be used for a substitute when people don’t have access to sun in the wintery months and what have you?
And there’s not a lot of data to answer that question. But the data that is available does seem to show detriment. However, there was a recent criticism paper published of a paper detailing some of the detriments of tanning beds. And in the next edition or one of the next editions of our Future of Functional Medicine Review monthly clinical newsletter, I’m going to provide you with a summary of the initial paper and then the critical appraisal of that paper to see if perhaps some of the criticisms of tanning beds have been overinflated, which I could very well see being the case because there’s certainly a dogma attached to tanning beds.
And I don’t really have a dog in the fight one way or the other, but I would like to know what the truth is. And so, we’ll be providing you with a breakdown on that in the clinical newsletter soon. Alrighty.
Healthy Gut Healthy You Book
Healthy Gut, Healthy You, the book. Have you read it? It’s been out for a number of weeks now which actually at this point probably about two to three months. And so far, I’ve gotten some great feedback from you guys. So thank you so much for the feedback, for the Amazon reviews, for the notes that you’ve been sending over social media, or what have you. But if you’ve enjoyed it and if it’s helped you, if you would please take a moment to write a review on Amazon, that would be hugely helpful. And your reviews are really critical in helping the book reach more people.
Some authors come into this already having had written a book and having had developed a big marketing budget for a book. I do not have that. I have put all of my resources into developing the website, the research team, and to providing you the best, most high-quality data I can on a weekly basis. I haven’t been saving stuff away to really pay for exposure for the book to have a big marketing campaign. It’d be great if I did, but I don’t.
What I do have, hopefully, is a good relationship with you and you will do me a huge favor in taking a moment to review this book on Amazon that does help us climb higher in the charts which has a kind of exponential benefit. And also sharing it with family and friends and with people that you think it can help. So hopefully you’ve read it and you’ve benefited from it. And if so, please help me out. If not, check it out. So far the results and the feedback we’ve got have been pretty promising.
Effects of Intermittent Fasting
“Effects of Intermittent Fasting on Health Markers in Those with Type 2 Diabetes: A Pilot Study.” Conclusion: “The results from this pilot study indicate that short-term, daily, intermittent fasting may be a safe, tolerable dietary intervention in type 2 diabetes that may improve key outcomes, including body weight, fasting glucose, and post-prandial”—that just means after a meal—“variability. These findings should be viewed as exploratory, and a larger, longer study is needed to corroborate these findings. Although, not a study requirement”—and this is interesting—“all participants preferred choosing eating hours starting in the mid-afternoon.” Meaning, people preferred to skip breakfast. “And the continued intermittent fasting led to an overall spontaneous decrease in caloric intake as measured by food photography.”
So a few interesting things here. One, not probably shocking is that intermittent fasting can help with diabetes and some of the other markers associated with diabetes. Also, probably not shocking is that the preferred meal to skip was breakfast, and the preferred time to start eating food was in the midafternoon. What else is interesting here and may be a bit more new and noteworthy is that intermittent fasting led to an overall spontaneous decrease in caloric consumption.
And I think what is likely happening here is people have damaged their satiation apparatus, the feedback between the gut and the brain that tells them that they’re full and to stop eating. And this can happen, in my opinion, with stress, with poor food choices, probably those two being the biggest. And underneath poor food choices, you can have hyper-palatable foods. You can have artificial sweeteners. You can have excess sugars. But in any case, I think what happens in part when people intermittent fast is they help to reset their satiation apparatus and they end up eating a little bit less which can definitely be a health-promoting thing.
However, I have another suspicion which is in healthier populations, intermittent fasting can lead to an unhealthy reduction in calories. And I’ve experienced this personally, and I’ve seen enough patients where this has happened in the clinic where I feel comfortable making a note of this observation on the podcast here which is some people are fasting their way to health problems. So we have to be careful with intermittent fasting. And I think what ends up happening is you have someone who is fasting too much. They’re really getting jazzed about their early morning coffee, and they put all these neurotropics in it and MCT. And they’re not eating all morning and they’re jacked up on catecholamines and stimulants and stimulation. And that feels good, but after a while, they really start running into a detrimental level caloric deficit. And they start exhibiting signs of burnout.
So just keep your eyes open for that. If you’re having fatigue, if you’re having brain fog, if you’re having insomnia, if you’re having irritability, and you’re intermittent fasting, then you may want to scale back the degree of your intermittent fasting. And also, remember to keep in mind the broader context: the more stress you’re under the more you should be cautious with intermittent fasting. So keep that in mind. Definitely something that can be helpful, but we want to make sure not to overdo it with intermittent fasting also.
Hey, everyone. I just wanted to say thank you to Biocidin, who has helped make this podcast possible. If you’re not familiar with Biocidin, they have a quality line of products, including anti-microbials, a soil-based probiotic, and a gut detox formula, amongst other things.
And how I came to learn about Biocidin was actually after a few patients of mine—who had been reacting to all other forms of anti-microbials—went out, did some experimentation, and actually found the only anti-microbial formula that they did not negatively react to was Biocidin. So this got me to open my eyes and give them a further look.
And they have a few products I think are worth mentioning. One is their anti-microbial Biocidin, which comes in a few different forms. They also have Proflora®4R, which is one of the few soil-based probiotics that I recommend. And also they have Dentalcidin, which is their Biocidin in the toothpaste form. And this may actually help with the removal of oral biofilms.
Now, if you go to Biocidin.com and you use the code RUSCIO, they will give you free shipping and a free bottle of Dentalcidin when you purchase their comprehensive cleansing program. They do have wholesale pricing available for licensed healthcare practitioners if you email [email protected]
So Biocidin definitely has some helpful products for improving your gut health. And I would definitely recommend checking out Biocidin for more information on a few of these tools that can help you in optimizing your gut health.
Vitamin D to Prevent Acute Respiratory Tract Infections
So the fact that those who were very vitamin D deficient doesn’t really surprise me. But it’s more noteworthy to mention that it may be better to have a somewhat physiological dosing of vitamin D, meaning you take a daily dose rather than having one pill per week of 100,000 IU or potentially even higher than that in a monthly dose. So that does make sense physiologically, because if we think about the primary method through which we obtain vitamin D, it’s through the sun. And most likely, you’re not going to be obtaining one huge dose of sun exposure per week. We’ve already talked about how dangerous that is. But you would be experiencing multiple bouts of shorter-duration sun exposure throughout the week. So having your vitamin D supplementation reflect that makes complete sense.
Excessive Iodine Intake and TSH
So let’s talk a little bit about iodine, two studies here on iodine. “Excessive Iodine Intake in TSH Reference Interval.” Data from the Korean National Health and Nutrition Examination Survey. A total of 6564 patients were examined. The median urinary iodine concentration was 299 mcg/L. So 299 was the median value, and the range goes from 158 to 699. And they continued that this suggests there’s more than adequate iodine intake in Korea.
Now, come back to that for a moment. The median range was 299. The reference range for the lab is 158 to 699. Now, some may say, “Well, isn’t it better to be at the highest end of the range?” And I think that’s a mistake to just assume that it’s better to be at the higher level of intake for a given vitamin. And as I continue, you’ll see why. “With high iodine intake in all age groups and in both females and males, the TSH reference interval in the Korean reference population was shifted right.” Meaning, the higher the iodine intake the higher the TSH became. So it shifted from 0.6 to 6.8 when you went to the highest group of iodine intake.
Continuing, “The prevalence of overt and subclinical hypothyroidism in Korea according to this reference interval was 0.7% and 3.12%.” With this higher iodine intake induced changes, you saw a 0.7% occurrence of overt hypothyroidism and an essentially 3.0% incidence of subclinical hypothyroidism. And they continue, “This was significantly associated with nutritional iodine status.”
Conclusion: “This first nationwide survey demonstrates more than adequate intake and a right-shifted distribution of serum TSH in the Korean general population.” So again, saying that more simply, as iodine intake went up, TSH levels also went up and 0.7% incidence of overt hypothyroidism and a 3.0% incidence of subclinical hypothyroidism.
This is why I am cautious with iodine. I do think there is some evidence showing that iodine could help with subclinical hypothyroidism. But unfortunately, it does appear that iodine, as long as you’re getting an adequate daily intake most of the time, and this puts you around roughly 1100 mcg per day, a sweet spot may be 450 mcg per day. As long as you’re getting that in, you should be ok. And there’s definitely a fair amount of evidence showing that higher intake can be problematic.
Now, that’s not to say you couldn’t run a short experiment for a few months on a higher intake of iodine, maybe 1 mg per day. I wouldn’t go much higher than that. That’d be, I think, reasonable. You could go a little higher. I just don’t think it’d be necessary, but in any case. And you could try TSH and see how someone does. But high dosing, especially when you get up into the multi, multi milligrams, I think that can be problematic, especially when that’s done for a very long period of time but with no real justification for continuing.
Iodine Status and Thyroid Function in Spanish School Children
Now, here’s another study though that’s really the counterpoint to this. “Iodine Status in Thyroid Function Among Spanish School Children Aged 6-7.” “Iodine intake was adequate in Spanish school children; however, no correlation was found between TSH and median urinary iodine in any geographic location.” So one study in adults, one study in children. The study in adults showing a deleterious effect with higher—deleterious may be a bit strong, but semi-deleterious effect from high iodine intake. And another study in children showing no association between high—and when I say high, that’s high in the normal range—iodine intake in thyroid function.
So the data here are mixed. And that’s what can be challenging is because you can find a study to support a pro-high-iodine intake or an anti-high-iodine intake position. However, as you’ve hopefully caught from the podcast, it’s important not to make decisions based upon one study but rather look at the body of evidence at large and see where the trend in the data lies because one study can be extraordinarily misleading. So it’s important to look and average the data here.
While I do think you can make a case for iodine supplementation in the shorter term, there is also a fair amount of risk associated with high iodine intake. So quite simply, just making sure that you have an adequate daily intake for most people is going to be a good place to start. And without getting too far into that, we’ve spoken quite a bit in the past about iodine. We did a three-part podcast series. If you go to our homepage and type in the search box, I believe it was entitled something along the lines of “Iodine: Getting to the Truth” or something like that. You’ll see a three-part podcast series that comes up where we really go through this in detail with all our references. All right. Moving on.
Probiotics for the Prevention of Necrotizing Enterocolitis
“Probiotics for the Prevention of Necrotizing Enterocolitis”—say that three times fast—“in Very Low Birth Weight Infants: A Meta-Analysis and Systematic Review.” Conclusion: “Overall, probiotics led to a significant reduction in necrotizing enterocolitis incidence and mortality in very low birth weight infants. Differences in probiotic agents and the influence of prenatal steroids and feeding regimes may explain the difference in outcomes between studies.” So they’re saying there’s some variance in outcome, but other factors may be influencing that variance.
But the main thing I want to showcase with this study is even in very low birth weight infants, probiotics seem to have a benefit. I know for parents, sometimes they’re not sure if probiotics should or should not be used. I talk about in the book that there is fairly compelling evidence that probiotics offer benefit even for infants, even pre-term and very low birth weight infants as we talked about in this study. So definitely something to consider for children and seems to be very safe.
So let’s look at what the study found. T4 helped those with a significantly elevated TSH but did not help those with a mildly elevated TSH. Now, they defined significant elevations of TSH as a TSH over 10.0. And they defined a mild elevation as between 4.2 and 10.0 in a TSH. This is very important to keep in mind because sometimes you hear people commenting on the thyroid, saying things like, “I’d like to see thyroid between 0.5 and 2.5.” But they don’t clarify that those guidelines are meant for people who are diagnosed hypothyroid, and you’re trying to steer the dose of the medication. It’s not for Susie Smith who has a normal thyroid and is trying to be proactive. What that recommendation does is it stresses people out.
When someone is otherwise healthy and they have a TSH of 6.8 and a free T4 in the normal range and you tell them that there’s something wrong with their thyroid, that’s detrimental to the patient. I would tread very lightly on that conversation because the data shows that subclinical hypothyroidism, meaning you have that TSH of 6.8 and a normal free T4, doesn’t necessarily mean that there’s a problem.
In fact, many cases of subclinical hypothyroidism, that mildly elevated TSH, will revert back to normal in time with no intervention at all. Also, the subclinical hypothyroidism is often not connected to any negative outcome. But there are some factors that are important to evaluate contextually. So the older someone is, if they have an elevation of TSH, the less problematic that elevation of TSH likely is. Or said differently, if someone is young, 20s, 30s, 40s, and they have this elevation, well, the younger they are, the more concerning an elevation it is.
Also, the degree of elevation of the TSH is important, as was found in this study from essentially 4.0 to 10.0 for TSH, they did not show any benefit from using thyroid hormone replacement medication. However, above 10.0 did. So when you look at these factors collectively, you can better steer the decision-making process when someone comes in with high TSH and normal free T4. So how high is TSH? Is it above or below 10.0 and how old are they? Are they older or younger?
And I don’t believe a definitive line has been drawn for what constitutes older or younger in this case, but 60-65 may be a reasonable cut off—and this is just my speculation—wherein you see a TSH above 10.0 in someone who’s over 65, then that may not require action. And there are some studies to back that up. But if you see a TSH above 10.0 in someone who is under 65 and especially if they’re significantly under 65, 40s, 30s, 20s, then they may benefit from a trial on thyroid medication.
Now, there’s some debate in, I guess you could say, probiotic clinical research. Some would have you believe that we have to go through this exhaustive evidence-based review for every condition in which we want to use a probiotic, and we have to pair the right one or two strains of a probiotic for the condition that has been most well studied. And I appreciate the evidence-based nature of that and the desire to be discriminating. I also think on the other hand that is far too reductionistic, and I do not think that probiotics can be used in that precise of a way.
I rather thing it’s better to look at the probiotics according to the category system I outlined earlier. And oftentimes, you see multi-strain formulas, especially for category one—Lactobacillus and Bifidobacterium blends—to show the most benefit. And this may be because probiotics, as we’ve discussed, have perhaps one of the larger in my opinion mechanisms through which probiotics vector benefit is through the secretion of antimicrobial compounds.
So perhaps, you have multi-antimicrobial compounds released when you use a multi-strain probiotic. I don’t have anything definitive to back that up, but this may be part of the reason why we see multiple-strain probiotics tending to out-perform single-strand probiotics, at least for the category one.
Environmental Risk Factors for Autism
“Environmental Risk Factors for Autism: An Evidence-Based Review of Systematic Reviews and Meta-Analyses.” Findings: “Current evidence suggests that several environmental factors including vaccination, maternal smoking, thimerosal exposure, and most likely assisted reproductive technologies are unrelated to the risk of autism. On the contrary, advanced prenatal age is associated with higher risk of autism. Birth complications that are associated with trauma or ischemic and hypoxia”—meaning lack of oxygen or blood flow—“have also shown strong links to autism. Whereas other pregnancy-related factors such as maternal obesity, maternal diabetes, Cesarean section have shown less strong but significant associations with autism.”
“The reviews on nutritional elements have been inconclusive about the detrimental effects of deficiency in folic acid and omega-3, but vitamin D does seem to be deficient in patients with autism. The studies on toxic elements have been largely limited by their design, but there is enough evidence for the association between some heavy metals, most importantly inorganic mercury and lead, and autism that warrants further investigation.”
So there’s a lot there, but essentially they’re suggesting that there may be some factors that have not been as appreciated that may be responsible for a significant association to autism and other factors that may have experienced more attention that may be less responsible, like heavy metals. But they’re also admitting that more data would be important to have.
We talked about previously acetaminophen has been proposed by another group of researchers as something that may also contribute to risk. And I did not see that mentioned here. I have not read this full study; I’m just providing you with a summary of the abstract. But if this is something that is near and dear to your heart—hopefully it’s not, but if it is—this paper may provide some insights.
Coffee and Autoimmunity
All right. “Coffee and Autoimmunity: More Than a Hot Beverage.” And we’ve spoken about this study also in a previous edition in the Future of Functional Medicine Review, and we gave you kind of a full breakdown. But I just wanted to touch on this briefly here and give you a couple tidbits.
“While some studies report conflicting results, general trends have been identified. Coffee consumption seems to increase the risk of developing rheumatoid arthritis and type 1 diabetes. By contrast, coffee consumption may exert a protective role against multiple sclerosis, primary sclerosing cholangitis, and ulcerative colitis.” Some of these words I don’t pronounce very often, and they really throw you a nice challenge. Ok.
“Concerning other autoimmune diseases such as systemic lupus, psoriasis, primary biliary disease, Crohn’s disease, there was no significant association found.” Good news there. “In other studies, coffee consumption was shown to influence disease course in management options. Coffee intake led to a decrease in insulin sensitivity in type 1 diabetes and methotrexate efficacy in rheumatoid arthritis and in levothyroxine absorption in Hashimoto’s disease. Further, coffee consumption was associated with cross-reactivity with gliadin antibodies in celiac patients.”
But I’m going to add this in here. Caution, because we’ve already I don’t want to say debunked but clarified that that finding was in one study and it was only found in instant coffee. Essentially what was found was instant coffee was often found to be contaminated with gluten. So it wasn’t truly cross-reaction. There was gluten contamination, and that is where the problem with gluten reactivity in coffee came from. And unfortunately, that seems to have been conflated to coffee at large, and the data does not seem to support that. And we did perform a review of the literature on that.
And again, the only data to support any reaction between coffee and gluten was instant coffees that were contaminated with gluten. But unfortunately, I think some of the autoimmune crusaders got a little bit too excited about that and there’s the erroneous belief circulating that all coffee could cross-react with gluten. And unfortunately, this is causing people with autoimmune conditions who are already kind of fear-factored into eating somewhat restrictively to avoid even more foods that they may not actually need to. So I am all for trying to manage and optimize autoimmunity with diet, but we also don’t want to have someone undergo the rigors of a dietary restriction that does not seem to be indicated nor helpful. So coffee and autoimmunity.
Significantly Higher Fecal Counts of the Yeasts Candida and Saccharomyces
So what we see here is there’s a higher predilection to have fungal overgrowth in those with celiac. And there was not a difference in parasites. This is important for two reasons. One, it’s important to understand that in those who have celiac and who are not fully responding to diet, dysbiosis may be one of the factors contributing the lack of responsiveness to a gluten-free diet.
And we’ve discussed and this is also detailed in the book, there have been a number of studies but one most notable that has examined why patients with celiac who go gluten-free don’t respond. And in this one study in particular I’m thinking of, 13 patients were assessed. Ten had SIBO. One had Giardia, one had Blasto, and one had a worm, I believe is the way the other three broke down. They were all treated with antibiotic therapy, and they all saw an amelioration of their symptoms, meaning they all became non-symptomatic after treating dysbiosis of different forms. But they improved after treating dysbiosis.
Here’s a study showing Candida and yeast may fall under that umbrella of dysbiosis in those with celiac. Does this also apply to non-celiac gluten sensitivity? I think to a degree, yes. And there’s some evidence to support that. The other important thing from this study is that parasites were not different, and I do find parasites in some patients in the clinic.
However, I think natural medicine was blaming parasites for everything 20 years ago. Now that we have more sophisticated testing, we’re realizing that more often it’s likely dysbiosis of bacteria and fungus, oftentimes the bacteria and fungus that belong there like yeasts and like SIBO that are causing problems that we used to attribute to parasites. And now that we have more advanced methods of analysis, we’re able to piece that together.
Also, some of it may not be anything wrong with the flora, with the bacteria and the fungus. It may have to do with an immune system that is just hyperreactive. And the terrain is somewhat normal, but the immune system is hyperreactive even to that normal terrain. So anyway. This study is showing that fungus and yeast may be a consideration also in those with celiac, and parasites I do think have a time and a place for evaluation but are probably much less of something to be considered within the management of people who have gone gluten-free and have been somewhat nonresponsive to that dietary intervention.
Dr. Ruscio Resources
Hey, everyone, this is Dr. Ruscio. I quickly wanted to fill you in on the three main resources that are available to you in case you need help or would like to learn more. Of course, I see patients both via telemedicine, via Skype, and also at my physical practice in Walnut Creek, California.
There is of course my book, Healthy Gut Healthy You, which gives you what I think is one of the best self-help protocols for optimizing you gut health and of course understanding why your gut is so important and so massively impactful on your overall health.
And then finally, if you are a clinician trying to learn more about my functional medicine approach, there is The Future of Functional Medicine Review, which is a monthly newsletter. Which is a training tool to help sharpen clinical skills. All of the information for all three of these is available at the URL drruscio.com/resources. And in case you are on the go, that link is available in the description on all of your podcast players. Okay, back to the show.
Hygiene Factors Associated with Childhood Food Allergy
Ok. “Hygiene Factors Associated with Childhood Food Allergy and Asthma.” “Our findings support the accumulating evidence of an association between skin infections and eczema with food allergy.” But they also caution, “Because these results could be subject to recall bias, additional prospective studies are needed to substantiate these findings.”
So nothing hopefully overly surprising here to see that food allergy and skin conditions tend to trend together. That makes perfect sense. And this probably comes down to in part early life factors for the development of their microbiota in their gut which also influences their immune system systemically and that will impact things like environmental allergy, skin infection, skin conditions, and also food allergy.
Association of Living in a Farming Environment with Asthma
And along those same lines, “Association of Living in a Farm Environment with Asthma Incidence in Canadian Children.” “This cohort study provides further evidence that living in a farming environment during childhood is protective of asthma incidence in adolescents and adulthood. And this finding provides further support for the hygiene hypothesis. The 14-year cumulative incidence of asthma among children living in farming environments was 10%, which was significantly lower than that observed for children in rural non-farming areas 13%, in non-rural environments 16%.”
Ok. So we do see—again, it’s something we talked about before—a protective effect for living in a farming environment. But the effect I wouldn’t say is huge. It’s significant, clearly, to jump from 10% to 13% to 16%. But sometimes I think it may be easy to fall into the thinking of, I didn’t raise my child in the ideal environment. Now, they have 100% chance of developing X, Y, or Z immune-mediated reaction.
So give yourself a little bit of a break if you’re a parent. Worst-case scenario, they may have seen a 6% increase which is definitely something but maybe not as much as sometimes it’s exaggerated or inflated to be. Ok.
Now, we’ve talked about small intestinal fungal overgrowth in previous podcasts. And just a moment ago, we talked about essentially fungal or yeast dysbiosis in IBS. And we’ve also had Dr. Rao on the podcast again who talked about small intestinal fungal overgrowth and has found treatment with—his drug of choice is fluconazole. I like using herbal medications for this. But this is an important thing to keep in mind.
I think this is most notable to help counterbalance some of the SIBO hysteria that’s occurring. I do think we’ve gotten to the point now where SIBO has gotten ahead of itself, where people are starting to blame SIBO for everything. And trust me, I am empathetic to the SIBO situation. It’s something I see quite a bit of in my clinic, but people are starting to blame it for everything. They’re starting to only eat regarding SIBO, only think regarding SIBO. And your gut is not that simple.
There’s much more going on in your gut than just SIBO. And there’s much more going on in your gut than just Candida. But these studies are showing that—for example, for someone who tests negative for SIBO but still has symptoms, people could go down a whole crazy whirlwind. They could try to track down hydrogen sulfide SIBO. They could say, “Well, I need to first treat for biofilms and then re-test.” It could get crazy. They could think that they have small intestinal fungal overgrowth, which they very well could have.
But the point I’m trying to make here is it’s important not to have your heart set on one diagnosis just because you are jazzed coming off of a summit which I think are great educational tools, but it’s important not to lose sight of the bigger picture of your gut. Now, they say something here’s that’s important which is “visceral hypersensitivity.” There are some people who will have no SIBO. They will not have overgrowth. But they will be hypersensitive to normal levels of gas pressure.
So sometimes an intervention that is needed is to essentially reduce gas to a subnormal level as the low FODMAP diet may do. And thus, improve someone’s symptoms. But it’s important not to think about that only through the lens of SIBO because someone may say, “Well, I heard that if someone has SIBO they should go on a low FODMAP diet. Or because I don’t have SIBO shouldn’t I or don’t I not have to worry about following a low FODMAP diet?” Well, that’s not always the case.
Again, that’s being a bit too reductionistic because we know the low FODMAP diet does work for people who do not have SIBO, likely because of hypersensitivity to gas pressure. So it’s reducing—the low FODMAP diet is reducing the gas pressure or it may also be through the mechanisms of reducing inflammation via reducing cytokines or reducing histamine or via the low FODMAP diet’s ability to help with motility and the, I guess, resurrection to more of normal levels of serotonin cells and PYY cells in the gut. And those cells modulate motility. Inflammation may damage those cells and cause problems with motility.
So the point I’m making here is there’s a lot going on in the gut. And the more that you learn, the more that you realize it’s not good practice to consolidate all of your thinking, recommendations, and interventions around what the most in-vogue issue in the gut is right now. At the moment, it’s SIBO. And I’m glad that that attention is there, but we also want to be careful not to overextend and allow a culture to develop that will have people looking at SIBO like the next adrenal fatigue diagnosis which is something that I think got way ahead of itself and then really detracted from the credibility and the degree of how seriously other people took the condition because it was being overexploited at every turn. And therefore, almost ended up like a little boy who cried wolf where no one started to believe any of the recommendations or the claims because it was just way overinflated to begin with.
Effects of Probiotics on Body Weight, Body Mass Index, Fat Mass
“The studies comprised a total of 957 subjects. Duration of the interventions ranged from three to 12 weeks. And administration of probiotics resulted in a significantly larger reduction in body weight, BMI, body fat all compared to placebo.” However, the devil is in the details. “0.6 kg were lost”—of weight—“0.27 in BMI, 0.6 in body fat,” which is why they continue, “the effect sizes were small.”
So it’s important to understand there’s a difference between statistically significant and clinically meaningful. In this case, they were statistically significant, but they were not clinically meaningful. It’s another important thing that unfortunately is done to mislead the healthcare consumer into buying a test or into buying a treatment is showing that, yes, this has been shown effective because the effect was shown not to be a chance, meaning it wasn’t a statistical outlier; it was significant from a numeric perspective. But you also have to tie that to a clinically meaningful change or what you can end up with is an intervention that you feel did not work for you.
If you went on a probiotic and you lost 0.6 kg, you could say, “Well, the probiotic worked, technically.” Your weight loss was statistically significant. But you’ll say, “Yeah, but I don’t feel like I lost any weight.” Yeah, because you really didn’t lose a clinically meaningful amount of weight. So just a couple of details there that are important to keep in mind.
All right, guys. That is this podcast. Hopefully, you got a lot out of that. Also, remember, if you’ve read the book and you liked it, please leave a review on Amazon. That does so much to help the book reach more people. And share with your friends and family and drop me a note and let me know what kind of results that you’ve had. All right, guys. We’ll talk to you next time. Bye.
I care about answering your questions and sharing my knowledge with you. Leave a comment or connect with me on social media asking any health question you may have and I just might incorporate it into our next listener questions podcast episode just for you!
Transform your health
Every product is science-based, validated by real-world use, and personally vetted by Dr. Ruscio, DC.