Here we go with Health News Updates – Episode 2. Today we will discuss: the thyroid-SIBO connection, probiotics and H. Pylori, vitamin D and fatigue, iodine and thyroid autoimmunity, CoQ10 and fatigue, viruses and hypothyroid, and more…
In This Episode
Episode Intro … 00:00:42
Vitamin D on Polycystic Ovarian Syndrome … 00:02:12
Mode of Delivery and Risk of Celiac Disease … 00:03:30
Impact of Sleeping with Reduced Glycogen Stores in Triathletes … 00:05:05
Vitamin D3 on Self-Perceived Fatigue … 00:08:06
Urinary Iodine in Early Pregnancy … 00:09:46
Autoimmune Thyroiditis in Children … 00:13:12
Thyroid Status on Glycated Hemoglobin … 00:14:48
Hypovitaminosis D and Uterine Fibroids … 00:18:04
Capsule Endoscopy in Celiac Disease … 00:19:51
Psoriasis and Risk of Celiac Disease … 00:21:16
Human Gut Colonisation … 00:24:32
High Androgen Levels and Hypothyroidism … 00:26:08
Resistant Starch Lowers Glucose and Leptin … 00:28:10
Abdominal Massage on Constipation … 00:31:50
Coenzyme Q10 on Liver Enzymes … 00:33:22
Probiotics on Gut Microbiota … 00:34:35
Epstein-Barr Virus and Thyroid Diseases … 00:36:21
Parasitic Infections in Children … 00:40:09
Multistrain Probiotic Supplementation … 00:41:47
Levothyroxine Therapy and SIBO … 00:43:25
Episode Wrap-up … 00:47:38
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Dr. Michael Ruscio: Hey, everyone. Welcome to Dr. Ruscio Radio. This is Dr. Ruscio. Man! I’m just getting back from Chicago, the Integrative SIBO Conference out there. And that was just fantastic, great lineup of speakers—Dr. Leonard Weinstock, Dr. Allison Siebecker, Dr. Steven Sandberg-Lewis, Dr. Scarpignato, the Italian pharmacist who’s super smart, Dr. Nirala Jacobi—just a few new people who I didn’t know of before who I was really impressed with—Dr. Paul Anderson also. Great cast.
And I have to admit. I was nervous, not about the academic information I was presenting, but the ability to be as funny as some of the other speakers, namely Dr. Weinstock—just hilarious as I’m getting to know him and listening to him more. He is really funny and obviously very smart.
But great event. And I’m sure they have that available as a webinar to purchase. So you may want to check that out. There was really some good information. I presented on biofilms and some of our biofilm research and also on advanced methods for treating methane.
Today, let’s do episode 2 of, hopefully, what you guys are liking of these health news highlights. And we can just jump in and hope this is not a complete disaster. Okay. Here we go.
Vitamin D on Polycystic Ovarian Syndrome
First study—“Effect of Vitamin D Supplementation on Polycystic Ovarian Syndrome: A Systematic Review and Meta-Analysis of Randomized Controlled Trials.” (https://www.ncbi.nlm.nih.gov/pubmed/28107851). So again, this is our highest level of scientific evidence. And to quote, “Evidence from available RCT [which is randomized controlled trials, which are what are summarized in meta-analyses] suggest vitamin D supplementation may be beneficial for follicular development and menstrual cycle regulation in patients with PCOS.”
So this is very interesting, essentially showing that vitamin D may help with PCOS. Why may that be? Potentially because of vitamin D’s anti-inflammatory and immunoregulatory action. If there is some inflammation and/or autoimmunity that underlies PCOS, then that may help.
There’s some evidence that suggests vitamin D may also help with blood sugar regulation. And of course, that’s one of the underlying pathophysiologies of PCOS, or drivers of PCOS—it can be high blood sugar.
So interesting study there—very high level scientific documentation that vitamin D may be beneficial for those with PCOS.
Mode of Delivery and Risk of Celiac Disease
Okay, another study. “Mode of Delivery and Risk of Celiac Disease: Risk of Celiac Disease and Age at Gluten Introduction Cohort Study.” (https://www.ncbi.nlm.nih.gov/pubmed/28196682) So essentially, the conclusion here, “In this cohort of children genetically predisposed to celiac disease, the mode of delivery did not influence the risk of developing celiac disease.”
So, this is reassuring maybe mainly to help people not feel—I don’t want to say guilty, but I think sometimes when we look back at decisions we made potentially as parents—not that I am a parent, but from what I’ve gathered from speaking with parents, they feel a little bit guilty about decisions that they made that they wouldn’t make now if they had the same level of understanding.
However, I think it’s important to illustrate that just because there’s some evidence showing that Cesarean section birth or not breastfeeding may increase the incidence of certain autoimmune conditions doesn’t mean that that’s a guarantee for autoimmune conditions. And there’s not even necessarily consensus that that will increase the risk of a given autoimmune condition.
So there is certainly evidence that counters this, but it’s an interesting study that’s showing that, at least in this cohort of children who were at genetic risk for celiac disease, the method of delivery (meaning vaginal birth compared to Cesarean section birth) did not have an impact. Okay.
Impact of Sleeping with Reduced Glycogen Stores in Triathletes
Here’s an interesting one. “The Impact of Sleeping with Reduced Glycogen Stores on Immunity and Sleep in Triathletes.” (https://www.ncbi.nlm.nih.gov/pubmed/27491620) “Sleeping and training the next morning regularly with reduced glycogen availability has minimal effects on skeletal markers of immunity and the incidence of upper respiratory tract infections and sleeping patterns in trained athletes.”
So essentially, what this is saying is going a little bit low carb and trying to deplete some of your glycogen stores, at least in this group of athletes, didn’t have an impact on respiratory infections and sleep. Now, if someone is really burnt out, then this may be a problem.
And what’s interesting here, to give the opposite side of this, is sometimes we have this belief that we shouldn’t eat carbs before bed. And sometimes, you hear this thinking that you should have your largest meal for breakfast. That should be your biggest meal.
What do they say? Eat breakfast like a king, lunch like a piper, and dinner like a peasant—or something like that—which may be true. And I’m sure there’s some evidence to support that.
But there’s also a large amount of evidence showing that things like intermittent fasting, wherein people usually have no breakfast and have a larger lunch and dinner, are beneficial for metabolism.
And there are even some studies showing that things like carb back loading, meaning that you eat low carb most of the day and then have most of your carbs at nighttime, can be beneficial for metabolism.
This is an approach I gravitate toward. I know Robb Wolf has mentioned he gravitates toward this also. And I definitely notice that I feel a little bit better when I eat that way.
And also, I sleep a little bit better. I tend to sleep a little bit better, I think. It’s not a glaring association, but I may sleep a little bit better when I partition my carbs to the later half of the day. And it makes sense, potentially because my training is usually later in the day.
So this study showed the opposite of that, but it may be that athletes can get away with a little bit more. So anyway, just keep in mind that even though we have one study showing one thing, there are other studies showing the opposite.
And maybe a nice takeaway for this, both for patients and providers, is you have to find your own truth with a lot of this stuff. And I was just commenting to someone the other day. A big part of what I do in the clinic with my patients is just reflect back to my patients the experience that they’re having and help them have the confidence and trusting their own observations.
And I can do that because I look at both sides of the evidence on a lot of these things. And when you do, you see that there’s no one-size-fits-all. And so a lot of my addition, or my aid to the process for someone trying to regain their health is simply, in part, helping them listen to their own experience, especially when it comes to these things that are highly individual like diet. Okay.
Vitamin D3 on Self-Perceived Fatigue
Another one—“Effect of Vitamin D3 on Self-Perceived Fatigue: A Double-Blind Randomized Placebo-Controlled Trial.” (https://www.ncbi.nlm.nih.gov/pubmed/28033244) Conclusion, essentially, “Vitamin D treatment significantly improves fatigue in otherwise healthy persons with vitamin D deficiency.”
Why this is important in my mind, amongst other things, is the double-blind, placebo-controlled nature of this trial. To give someone vitamin D and telling them that we want to see if vitamin D will increase your energy and then seeing them report an increase in energy—ugh. A lot of that could suffer from placebo effect. 43% has been shown to be the average placebo impact in randomized, controlled trials.
So to say, “My patients get better from X,” that’s not always a great barometer because oftentimes, much of that is the placebo effect, which I would estimate if they’re going to see a doctor and they respect and trust that doctor and the doctor says, “We’re going to do X to help with Y,” they’re going to have a pretty high level of expectation to see that improvement.
So this is nice because we have a placebo-controlled trial showing that vitamin D may help with fatigue. So it may not change recommendations hugely.
I think most people should be on at least a minimal dose of vitamin D through the winter months and then hopefully in the summer months obtain vitamin D exposure via the sun. But nonetheless, there’s some nice evidence here supporting vitamin D for fatigue. Okay.
Urinary Iodine in Early Pregnancy
*Note: Dr. Ruscio mis-spoke in the video which has been corrected in the transcript below. With regard to dosage, milligrams should be used as the unit of measure instead of grams.
“Urinary Iodine in Early Pregnancy Is Associated with Subclinical Hypothyroidism in Tianjin, China: An Observational Study.” (https://www.ncbi.nlm.nih.gov/pubmed/28212640) So essentially, they found that women in early pregnancy with subclinical hypothyroid were iodine sufficient but still at risk of iodine deficiency as the pregnancy progressed. So as the pregnancy uses up nutrients, the risk of iodine deficiency became higher.
Now, this study got me thinking about a couple things. The population of thyroid patients that may do the best with iodine supplementation may be those with subclinical hypothyroid, meaning their TSH is high and their T4 is normal, and who are also negative for thyroid autoimmunity.
So they may be some of the best candidates, because this subclinical hypothyroidism may be happening, because the thyroid is lacking some of the nutrients needed to make thyroid hormone. However, this is not very common. Thyroid autoimmunity is the leading cause of hypothyroidism in Western countries. And iodine deficiency is not incredibly common.
Now, regarding that, from a dietary perspective, 450 mcg a day might be the sweet spot. I really wouldn’t recommend becoming that anal so as to try to map this out to 450 mcg a day from a dietary intake perspective.
But that’s what the literature suggests, if you remember back to the podcast from—gosh!—now, probably about a year and a half ago where we detailed this. And I will put the links to those podcasts. They were entitled, “Thyroid [& Iodine]: Getting to the Truth, Part 1 and 2.”
Now, additionally, supplementing with iodine, you can probably get away with up to 15 milligrams a day, but I would recommend going on the lower end of that spectrum, to 1 to 2 milligrams a day max, which would equate to 1000 to 2000 mcg a day to prevent any confounding results, which could be actually making the subclinical hypothyroidism worse.
Iodine deficiency can cause subclinical hypothyroid or hypothyroid, but iodine excess can also cause subclinical hypothyroid or hypothyroid. So the “more is better” definitely does not apply to iodine in my opinion. But that’s based upon a pretty extensive and exhaustive review of the literature.
So again, those with subclinical hypothyroidism, which is high TSH, normal T4 according to conventional ranges and are negative for thyroid autoimmunity, may be one of the prime candidates for iodine supplementation—450 mcg up to about 1100 mcg daily dietarily or 1 to 2 milligrams a day, not to exceed 15 milligrams a day.
Autoimmune Thyroiditis in Children
“Improving Iodine Nutritional Status and Increasing Prevalence of Autoimmune Thyroiditis in Children”—so another study on iodine and thyroid. (https://www.ncbi.nlm.nih.gov/pubmed/28217504) “The levels of urinary iodine were significantly higher in children with autoimmune thyroiditis as compared with controls.” So there was a positive correlation between urinary iodine excretion and thyroid antibodies.
So again, there’s just so much evidence showing that high intake of iodine provocates thyroid autoimmunity. I have a really hard time with some of the camps that are die hard iodine for hypothyroidism. Can you justify a reasonable supplementation with iodine like we just outlined? Yeah, but once you start getting up into 6, 10 milligrams a day, I really think that’s a misguided approach.
And again, this is looking at both sides of the evidence, coming into the review of the evidence on this issue a few years ago totally open and maybe even leaning a little bit more toward the pro-iodine side, and then looking at what the evidence shows and saying, “Geez, I don’t know how some of these die hard iodine circles exist on the internet.” Well, I do know. It’s because of not looking at both sides of the evidence.
So, open to iodine, and there may be a small number of people who do really well with very high doses. But again, I think for thyroid autoimmunity, we have to be careful. Okay.
Thyroid Status on Glycated Hemoglobin
“Effect of Thyroid Status on Glycated Hemoglobin” (or hemoglobin A1c). (https://www.ncbi.nlm.nih.gov/pubmed/28217494) So let me step back. Hemoglobin A1c is essentially a 60 to 90 day average of blood sugar, and it’s indexed to the glycation, or like the rusting, of red blood cells.
So the more oxidation or inflammation, to use these terms loosely, you have in your body, the more quickly your red blood cells will acquire this glycation or this rust or this oxidation and the higher the level of your hemoglobin A1c will go.
Now, high blood sugar is a main driver of this internal inflammation, or oxidation or glycation or rusting, whatever you want to term it, so hemoglobin A1c is often used as a marker of the last two to three months of your average of your blood sugar.
However, there’s a little twist here. “Baseline hemoglobin A1c levels were found to be significantly higher in hypothyroid patients which reduced significantly after achievement of euthyroidism,” meaning normalization of thyroid hormone levels, “without any change in glucose levels.”
So again, what they found was those with hypothyroid that was untreated had a misleadingly elevated hemoglobin A1c that returned to normal once these patients were put on thyroid medication without any change in glucose levels.
So, what this tells you is potentially being hypothyroid allows excess oxidation or glycation. And that can falsely elevate hemoglobin A1c. When I say ‘falsely,’ I mean it may falsely lead one to think that they have high blood sugar when they actually don’t.
This is important to keep in mind, because it’s not terribly uncommon in the clinic for hemoglobin A1c to be a couple points high, yet a patient’s fasting blood glucose and a patient’s fasting insulin are normal. And then patients get concerned, “Oh my god! I read on the internet that my hemoglobin A1c should be below X, Y, or Z.”
Again, this is a very important issue to manage appropriately in terms of the conversation. And my response is typically, “Since we haven’t seen any of these other markers of blood sugar abnormal, I’m more inclined to think this is a false positive. There are other things in the body that can cause inflammation, that can falsely elevate hemoglobin A1c.
“We’ll keep an eye on it. But I’m not overly concerned about your blood sugar at this time. Let’s continue forward with our process of focusing on these fundamental factors, whatever they are, that should hopefully reduce your inflammation and reduce this hemoglobin A1c.”
It’s important that we do that and not falsely tell people they need to diet harder or what have you if it doesn’t seem to be well supported.
Remember, one marker elevated or depressed in isolation is not always highly diagnostically significant. Oftentimes, you want to be looking for a family of markers that function together to really substantiate that. Okay.
So again, remember. In someone with hypothyroid, especially that’s untreated, hemoglobin A1c may be falsely positive.
Hypovitaminosis D and Uterine Fibroids
“Hypovitaminosis D and ‘Small Burden’ Uterine Fibroids: Opportunity for a Vitamin D Supplementation.” (https://www.ncbi.nlm.nih.gov/pubmed/28033263) So essentially, this study looked at the association between vitamin D and uterine fibroids.
They found that there was no correlation between baseline levels of vitamin D and fibroids. However, after 12 months of supplementation with vitamin D, there was a lower rate of surgical or medical treatment due to the progression of the fibroids in the treatment group compared to the control.
So only 13% of the treatment group required medical intervention, whereas 30% of the controls required medical intervention. So that’s important to note.
So essentially, the conclusion, “Supplementation with vitamin D restores normal vitamin D in women with small burden fibroids. And it may be a viable therapy for these women.”
So again, it seems like some of these conditions that are loosely associated with either inflammation or potentially autoimmunity, which we could loosely maybe put these uterine fibroids and maybe even PCOS in the inflammatory/autoimmune bucket very vaguely and very broadly, may improve from vitamin D supplementation.
Capsule Endoscopy in Suspected Celiac Disease
“Role of Capsule Endoscopy in Suspected Celiac Disease: A European Multi-Centre Study.” Conclusion: “Capsule endoscopy has a high diagnostic yield in cases of suspicion of celiac disease and leads to changes in the clinical course of the disease.” (https://www.ncbi.nlm.nih.gov/pubmed/28216978) Essentially, what I think is noteworthy from this study is the capsule endoscopy, I think, is a much more attractive option for patients in terms of an assessment.
And for some patients that are apprehensive about a traditional endoscopy, you may want to speak with your gastroenterologist about a capsule endoscopy, because they’re not as invasive and they seem to give fairly good information.
Now, I am not a gastroenterologist. I do not run traditional endoscopy and also run capsule endoscopy and am able to give you my firsthand clinical experience.
But there does appear to be an emerging role for these things in the research literature and rightfully so. As technology advances, hopefully, people will need less traditional endoscopy, which is fairly invasive, and we can rely more heavily on these capsule endoscopies.
So if there’s a condition that your gastroenterologist has suggested endoscopy for, yet you’re apprehensive about doing that, then ask about capsule endoscopy. Okay.
Psoriasis and Risk of Celiac Disease
“Psoriasis and Risk of Celiac Disease: A Systematic Review and Meta-Analysis.” (https://www.ncbi.nlm.nih.gov/pubmed/28216724) So again, our high level scientific evidence. “Our meta-analysis demonstrated an approximately threefold increased risk of celiac disease among patients with psoriasis.”
So if you have psoriasis, there’s a threefold increase of celiac disease. So how important is this? Well, it’s certainly nothing new. I think most people know that if you have one autoimmune condition, you’re at higher risk for another autoimmune condition.
But there are also some important caveats here, which are we don’t want to fear people. Or if we’re a patient, we don’t want to be afraid that because we have one autoimmune condition, we’re like this ticking time bomb.
Yes, we want to do everything we can do to improve our health just as if we had a different condition like diabetes or IBS, because if you have a condition and you don’t do anything about that condition, naturally, there’s oftentimes an increased risk for another condition.
But the other part of this argument that’s often left out—or the other part of this conversation that’s often overlooked is how much of an impact or increased risk is someone really at.
Now, a loose prevalence in terms of percentage of psoriasis, it’s about 4%. So when you have a threefold increase, you go from 4% to about 12%. So that’s certainly something.
But it’s just important to realize that sometimes when we say a threefold increase, that may make someone think that they have an 80% chance of having a condition. But in this case, your max might be around 12-ish percent.
So it’s just important to understand that just because you have a doubling of the risk or even, in this case, a tripling of the risk, it doesn’t mean you’re all of a sudden going to be at a relatively high risk for a given condition.
We still want to do everything we can and should do to be optimally healthy, but I don’t think it’s in good interest to be overly hard driving, if you’re a patient or if you’re a doctor, to try to quell autoimmunity if it makes you stressed out.
Yes, eat healthy. Investigate your gut health. Use probiotics, vitamin D—all these things that we’ve talked about that are good for general gut health and also have some influence on autoimmunity. Do those things.
But you get to a point where, after you’ve done some of those basics, you get on the negative side of the diminishing returns curve. You have the law of diminishing returns, which is like an inverted U.
As you first start putting time and energy into your health, you have a tremendous, positive return on your investments. But then if you keep putting more time and energy into your health, you actually go into a negative return on your investment.
So it’s important to keep that in mind. And I just wanted to use this study as a way to showcase that point. Okay.
Human Gut Colonisation
“Human Gut Colonisation May Be Initiated in Utero by Distinct Microbial Communities in the Placenta and Amniotic Fluid.” (https://www.ncbi.nlm.nih.gov/pubmed/27001291) Conclusion: “Based on these data, we propose that the stepwise microbial gut colonization process may be”—key words here—“initiated already prenatally by a distinct microbiota in the placenta and amniotic fluid.”
What does this mean? Put quite simply—while mom is pregnant, she’s already colonizing the microbiota of her infant. And if you remember way back, we talked about studies showing that pregnant mothers that had exposure to farm animals while they were pregnant—that was more beneficial from an immune perspective for the child compared to if the child had exposure to these farm animals when they were 3 months, 6 months, a year, two years, what have you.
So the earlier the exposure, including while the child is inside mom, the more protective, likely because mom’s environment is already responsible for colonizing the developing fetus before they’re even birthed.
So this is just an example that shows part of the mechanism which is placentally and through the amniotic fluid.
High Androgen Levels and Hypothyroidism
Really interesting one here—“High Androgen Levels Protect Against Hypothyroidism.” (https://www.ncbi.nlm.nih.gov/pubmed/27861716) “Hypothyroidism was less frequently seen in women with PCOS,” which causes high testosterone or similar male-type hormones, “and in men when compared with the general population. Androgen seemed to protect against hypothyroidism.”
So this may account for part of the reason why there are more autoimmune conditions, generally speaking, in women than there are men. And part of the reason for this—again, loosely speaking—may be because testosterone can be a bit immunosuppressive.
One of the things I’ve often wondered about is, could testosterone replacement therapy for women be a viable treatment for autoimmunity? But the challenge there is that treatment is going to create other side effects like acne, increasing facial hair growth, and scalp hair loss.
So is that treatment a viable treatment for women? Probably not. Is this study interesting nonetheless? I think so. And it illustrates that, again, androgens may be protective against autoimmunity.
Now, what this may mean, being very speculative here, is that for the right case under the right supervision, an anti-aging approach where a woman optimizes her androgens into the normal range for a female potentially could have some benefit on autoimmune conditions. And that may also increase a woman’s sex drive and what have you.
So if a woman is androgen deficient, getting her into the sufficient range may be helpful. It’s just if you go too high, then you’re going to start having some of these negative side effects that women don’t want, like facial hair growth, male pattern baldness, acne, and what have you. Okay.
Resistant Starch Lowers Glucose and Leptin
“Resistant Starch Lowers Postprandial Glucose and Leptin in Overweight Adults Consuming a Moderate-to-High-Fat Diet: A Randomized-Controlled Trial.” (https://www.ncbi.nlm.nih.gov/pubmed/28222742) So I don’t want to go into too much detail about this, but essentially, resistant starch, type 2, 30 grams a day over six weeks caused an improvement in glucose, homeostasis, leptin, and PYY. But there was no impact on body composition. Here’s the key thing here. There was no significant difference observed between the treatment group and the control group.
So I just mention that because it’s easy to take a piece of these findings and miscontextualize them or misrepresent them and try to make a case of resistant starch. Resistant starch, prebiotics, and fiber can have a beneficial effect on blood glucose, and I outline this in my coming print book.
Prebiotics probably have the best evidence for them, and they can have a sizeable impact on blood glucose. The challenge is the dose has been so high in some of these studies, I believe over 20 grams a day, that the incidence of gastrointestinal side effects is going to be pretty high.
So I’m open to the resistant starch. I do have some patients use it. For some patients, it tends to be very beneficial, but I really think it was way overhyped.
And when I looked into some of the studies that were supporting people’s arguments for resistant starch on the internet when it was really coming into vogue a few years ago, I was shocked at the lack of any kind of human trials and how much of the fanfare was fueled by mouse model studies, mechanism studies.
And that was one of the key observations that really helped me hone in on the fact that you can be extremely misled if you look at lower level type science, because I looked at that information. I said, “Geez. There’s a lot of fanfare here, but the supportive information is not very strong.”
However, we do have a number of trials showing people with gastrointestinal problems like IBS and IBD may actually do worse or be at higher risk for negative reactions from things like prebiotics and resistant starch.
So I was very suspicious that we were going to see after some of the fanfare cooled a lot of people coming forward and saying, “This actually made me worse.”
And I remember Robb Wolf was one of the first people that mentioned that he thought he felt better on resistant starch for a couple weeks, and then he felt like he really regressed.
And I’ve seen that in the clinic many a time, enough times to where I don’t usually start with any type of resistant starch or prebiotic in anyone that has significant GI conditions. If someone is fairly healthy and just needs a little bit of a gut tune up, then you can usually get away with these things.
And I’ve said this before. Usually the healthier someone is, the higher the chance they’ll respond positively to fiber, prebiotics, and resistant starch. The more symptomatic they are, especially digestively, the higher the chance for a negative reaction.
So this study just shows you have to be careful, because you could misinterpret this reference as being highly supportive, but when you actually look at their results, they weren’t significant, and they certainly weren’t clinically meaningful.
Abdominal Massage on Constipation
“The Effect of Abdominal Massage on Constipation and Quality of Life.” (https://www.ncbi.nlm.nih.gov/pubmed/26825564) To quote, “These findings indicate that abdominal massage applied to patients diagnosed with postoperative constipation reduced symptoms of constipation, decreased time intervals between defecation, and increased quality of life.”
So, not incredibly surprising that post-surgically someone may want to undergo massage for their abdomen to help prevent scar tissue formation and potentially bowel obstruction.
And this reinforces in a loose way therapies like the Clear Passage Therapy, where we had Larry and Belinda Wurn on the podcast talking about how they’ve had nice results with certain patients with bowel obstructions or abdominal and pelvic adhesions.
So something to keep on your radar screen if you’re a patient suffering and can’t really seem to figure your gut out, so to speak, or a practitioner advising someone, then this might be something, after you’ve gone through some of the initial phase therapies to consider.
And when I say ‘this,’ I mean some sort of abdominal-pelvic massage, but a therapeutic massage that’s geared at breaking down scar tissue and applied very therapeutically. I wouldn’t say go see just a general massage therapist for a relaxation-type massage. This would have to be someone who’s trained in this type of massage or therapy specifically.
Coenzyme Q10 on Liver Enzymes
“Functions of Coenzyme Q10 Supplementation on Liver Enzymes, Markers of Systemic Inflammation, and Adipokines in Patients Affected by Nonalcoholic Fatty Liver Disease: A Double-Blind, Placebo-Controlled, Randomized Clinical Trial.” (https://www.ncbi.nlm.nih.gov/pubmed/26156412) Whew! That’s a mouthful.
So essentially here, taking 100 mg of CoQ-10 supplementation daily resulted in a significant decrease in liver enzymes, AST, GGT, also CRP (C-reactive protein), and tumor necrosis factor alpha, and the grades of nonalcoholic fatty liver disease in the treatment group compared to the control.
So this is interesting, essentially showing that CoQ-10 may help to lower liver enzymes and improve liver function. And CoQ-10 is something I’m definitely looking at increasingly more favorably when we see trials showing it can help with energy, trials showing it can help with liver function, even some trials showing that it may help with your skin in terms of euthanizing the skin appearance. So it’s definitely something that I think is a pretty attractive supplement.
Probiotics on Gut Microbiota
“The Effect of Probiotics on Gut Microbiota during the Helicobacter pylori Eradication: Randomized Controlled Trial.” (https://www.ncbi.nlm.nih.gov/pubmed/26395781) So essentially, what they showed and what they did was they treated two groups of patients with antibiotics for H. pylori.
And what they found was there were fewer changes in things like Firmicutes, Bacteroidetes, and Proteobacter—fewer changes in those in the group on the probiotic at the same time as the antibiotic. So the probiotics protected against microbiota changes induced by antibiotics. And also, there was less antibiotic-resistant bacteria seen in the group also using the probiotics.
Remember, there have also been other studies—in fact, we go as high as systematic reviews with meta-analyses showing that co-administration of probiotics with antibiotics enhances the clearance rate of H. pylori.
And it also reduces some of the side effects from the antibiotics, probably because it helps preserve your resident microbiota and decreases anti-microbial resistant genes.
So this is an important study. And it just, again, shows why probiotics can be a very effective therapeutic tool and why you should not avoid taking probiotics while taking antibiotics because you think that the antibiotics are going to kill them. That’s understandably so, in terms of the inference, but it’s really not well advised. So if you’re taking an antibiotic, really consider taking a probiotic at the same time.
Epstein-Barr Virus and Thyroid Diseases
“The Role of Epstein-Barr Virus Infection in the Development of Autoimmune Thyroid Diseases.” (https://www.ncbi.nlm.nih.gov/pubmed/25931043) To quote, “We assume that high prevalence of Epstein-Barr virus infection in cases of Hashimoto’s and Graves’ disease imply a potential etiological”—or causative—“role of Epstein-Barr virus in autoimmune thyroiditis.”
Now, essentially, they’re saying that Epstein-Barr virus may be one of the factors that causes and drives Hashimoto’s. The thing that I’m a little less clear on is, does treatment of the Epstein-Barr virus have an effect on the course of the Hashimoto’s? It may.
And we’ve certainly seen that in some studies, specifically in H. pylori models and in one Blastocystis hominis case report study, that the treatment of gut infections or gut imbalances can improve thyroid.
Now, whether or not treatment of viruses follow that same course, it’s hard to say. I’m definitely open to it. I wish we had a little bit better data, because I haven’t seen much in the way of symptomatic improvement in patients I have done courses of anti-viral treatment with.
So I’m definitely open to it. But after you see enough cases where you see Epstein-Barr virus that would be considered truly positive according to the lab work and then you treat with antivirals and you see minimal to no symptomatic improvement, then I’m a bit more reserved, although I did have a chronic fatigue patient last week who did see one of his symptoms, which was post-exercise fatigue, improve after a course of antivirals.
Some of his other symptoms, like brain fog, didn’t improve. But one of maybe five of his symptoms did improve after the antiviral. So I’m certainly open to it, and its role in terms of those with autoimmune thyroid, I think, is yet to be determined.
I would recommend addressing other things first and then circling back and looking to see how the lab work looks. Remember, the early antigen fraction of Epstein-Barr virus is probably the most indicative of the clinical course of Epstein-Barr.
So if you’re seeing that drop greatly—let’s say someone comes back positive. You treat them for SIBO. And then you retest the early antigen and that has dropped tremendously. You may want to wait a while and monitor the early antigen fraction, because if that continues to stay low and/or continues to decrease, you may not need to move to antivirals.
But if it goes back up or if it doesn’t really budge much after the gut treatment, then you may want to consider circling back to it.
What is considered a ‘normal?’ I don’t know. I see some patients that go from very, very high in terms of relative to the reference range, drop down maybe by half or even drop by a factor of three, but they’re still positive.
But what does that mean? You really have to weigh the patient in front of you, how they’re feeling, and the Epstein-Barr serology, and also look at that in context of the thyroid autoimmune markers. Remember that we’ve talked about 100-300, even below 500 for the TPO antibodies is probably okay.
So if someone comes in with a TPO of 275 and their Epstein-Barr virus is reactivated and they’re generally healthy, do you have to treat it? Maybe not. So it’s just something to think about. Okay.
Parasitic Infections in Children
“Parasitic Infections in Children with Chronic Spontaneous Urticaria.” (https://www.ncbi.nlm.nih.gov/pubmed/27907915) So essentially, this study looked at 211 children with chronic, spontaneous urticarial, and they detected parasites in 10% of these patients. Blastocystis hominis was the most common.
After treatment, the urticaria continued in five, was reduced in six, and disappeared in ten patients. Why is this? It may be the impact of something like Blasto in the gut and how that affects histamine or just the general immune status in the gut, which is also tied in with histamine.
I should mention that gastrointestinal complaints were significantly more frequent in these patients with parasitic infections that also had urticaria than those without. So that’s something to piece together.
It’s not to say that everyone that has a parasite will have gastrointestinal symptoms, but certainly, if they do have gastrointestinal symptoms, that’s a red flag that you may want to look into that more closely.
And I believe we reported—gosh!—I believe it was with David maybe a year and a half ago now. We did a case review with him. And I want to say he had Blasto. He may have had SIBO in addition, but he did pretty darn well after anti-microbial therapy and his urticaria. Okay.
Multistrain Probiotic Supplementation
“Effects of Multistrain Probiotic Supplementation on Glycemic and Inflammatory Indices in Patients with Nonalcoholic Fatty Liver Disease: A Double-Blind Randomized Clinical Trial.” (https://www.ncbi.nlm.nih.gov/pubmed/26430826) In the probiotic group, insulin, insulin resistance, an inflammatory marker—tumor necrosis factor alpha, and another one—interleukin 6 all decreased significantly at the end of the study compared to the beginning of the study.
Conclusion: “Considering the effects of probiotic supplementation on the reduction of glycemic and inflammatory indices in patients with nonalcoholic fatty liver disease, consumption of probiotics is recommended as a complementary therapy in these patients.”
Why is this? Why do probiotics both reduce inflammation and seem to especially help this group with nonalcoholic fatty liver disease?
It may be, first of all, because of the anti-inflammatory effect of probiotics, probably via modulating the gut immune system and helping repair the gut barrier, but also because messes in the gut are cleaned up by the liver. Everything in the gut drains to the liver via a vein called the portal vein.
So the more problems you have in the gut, the more work the liver has to do to clean all that up. So it’s probably no surprise, seeing that things that improve gut health also improve liver health. In this case, probiotics reduced inflammation in those with preexisting nonalcoholic fatty liver disease. Okay.
Whew! This is a workout mentally!
Levothyroxine Therapy and SIBO
All right. Last one. This is the best for last maybe. “Levothyroxine Therapy and Impaired Clearance Are the Strongest Contributors to Small Intestinal Bacterial Overgrowth: Results of a Retrospective Cohort Study.” (https://www.ncbi.nlm.nih.gov/pubmed/28223728)
In 1809 patients, they were assessed for SIBO and for other co-accompanying conditions. The main results—“Levothyroxine use or being hypothyroid significantly increased the risk that someone would have SIBO. This was even more impactful than if someone had had prior intestinal surgery or immunosuppressive drug use.”
So again, this is how this played out. If you had been using immunosuppressive drugs or had intestinal surgery, that increased your risk of SIBO.
Your risk was even more increased if you were hypothyroid and untreated and, paradoxically, the most increased if you were on Levothyroxine (so you are being treated for they hypothyroidism), which suggests there’s a mechanism associated with hypothyroid in addition to the actual hypothyroidism of the hormones, because people are hypothyroid and untreated had some risk, but people who were hypothyroid but treated (so they were in the normal ranges) had the most risk.
So this tells us that there’s probably another component of having thyroid autoimmunity that puts one at risk for SIBO. And what it may simply mean is that those who have more severe hypothyroidism and, therefore, have it detected earlier and then, therefore, go on treatment earlier—they have a more severe case of thyroid disease, which also, through mechanisms that we don’t quite understand yet, has an impact on gut and increases risk for SIBO independent of levels of thyroid hormone.
So why this is so important in my mind is because there’s an overwhelming number of people that I see—albeit I have a biased perspective, because people oftentimes see me because of the focus on the gut—but an astonishing number of patients come in, thinking that they have a thyroid problem, meaning they’re already on thyroid hormone, and their levels are generally normal.
And they come in wanting to go deeper into the thyroid. They want to try to tweak their T3 to reverse T3 ratio or drive further down their antibodies or what have you.
And they’re coming in with these symptoms that they think are being driven by their thyroid, like insomnia, depression, weight gain, constipation, but the actual problem is in the gut. And when we improve their gut health, all the thyroid-like symptoms go away.
So very important. If you’ve gone through some of the broad strokes for your thyroid, you really may want to consider a good gut evaluation because, as this study suggests loosely and as my clinical experience definitely supports, if you’ve tried one or two thyroid medications, if you’ve tried a T4 and then you’ve tried a T4 with T3 and you’re not seeing a noticeable improvement, then I wouldn’t go any further down the thyroid road.
I’d go to the gut road, because it might ultimately be a problem in the gut that’s causing you to continue to have the symptoms that you think are being driven by thyroid but are actually being driven by, in this case, what might be SIBO.
And this will appear in the Future of Functional Medicine Review clinical newsletter. We’ll do a more in depth write up and give clinicians a, “Here’s what we should do with this clinically” kind of thing. But I think you have some of the salient broad strokes on that.
So, boy! That’s another review. And gosh! There are more studies than I can even keep up with. So we’ll do another one of these soon. Feedback so far on this type of episode has been very favorable. So please continue to let me know what you think, especially if you don’t like this, because if no one tells me things that they don’t like, I’m never going to know.
So anyway, that’s episode 2 of health news recap and highlights. Hopefully, you enjoyed it. And we will talk to you guys next time. Okay. Thanks! Bye-bye.