Health News Reviews: Updates on Low FODMAP Diets, Fasting, Gene-Tailored Diets, Leaky Gut, Parasites, and Paleo Versus Mediterranean Diet

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Health News Reviews: Updates on Low FODMAP Diets, Fasting, Gene-Tailored Diets, Leaky Gut, Parasites, and Paleo Versus Mediterranean Diet

Episode Intro

Dr. Michael Ruscio: Hey everyone. Welcome to Dr. Ruscio Radio. This is Dr. Ruscio. And let’s jump into another episode of health news reviews – updates on some of the latest research that’s been published, why it’s important, and what it means for you.

But before we do that, I’m happy to announce that there is finally a finalized plan in place for the book, which has been a long time coming. I apologize for some of the back and forth. As you may have remembered me mentioning, I was pretty much about to sign on board with a publisher, and that turned out not to be a great fit. It kind of forced me to change the plan, and we’ve found a good plan, and we have a hard launch date for the book. Either February 1^st or February 15^th. That small detail is to be determined soon. But within the first two weeks of February, the book will be available, which I’m incredibly excited about. There will be a presale campaign for the book some time starting in mid-December, so you’ll see a number of announcements for that. But we’ll definitely put a presale out to our audience before anybody else has an opportunity to buy.

I can’t tell you, again, how excited I am for this. The book took a lot of work. It’s challenging to tell a story that is scientifically advanced and true to science and factual and correct, but also has an interesting storyline. And this book was literally a distillation, not only of my clinical experience, but of about 300 pages of research. And just under 1000 references of high quality reference-type clinical trials and above, usually. So clinical trials, systematic reviews, and/or meta-analyses are what comprised the majority of the references.

To put that into an interesting storyline is challenging, and that took a lot of frustrating days. And the thing that’s probably most salient to you guys outside of that aspect is how everything that you’ll learn in the book is codified at the end of the book into a personalized step-by-step plan. You’ve probably heard me mention this before, that for people who have more severe ailments, they’ll probably need to undergo more of the steps. And for people with more mild ailments, they’ll be able to do less of the steps. And at the end of every step, there’s a self-assessment that directs you where to go next. So it truly lives up to the promise I try to always be espousing, which is cost-effective and efficient functional medicine.

So in this case—again, if you need more, you can do more, and that will make it efficient for you. But if you need less, you will only have to do less. And that will make it faster and more cost-effective for you. So I’m very excited about that. More details to be announced as they’re available. But I wanted to put that out there, because I’m sure people were starting to think, “Did you write a book? What the heck is going on with that, because it’s been a while.” So, that’s some updates on the book. Let’s now jump into some studies.

Duodenal Enteroendocrine Cells, IBS, and the Low FODMAP Diet

A very interesting study entitled “Changes in Duodenal Enteroendocrine Cells in Patients with Irritable Bowel Syndrome Following Dietary Guidance”. Now, essentially what this study found was that when they put patients with IBS on a low FODMAP diet, there was a changing in the densities of certain cells in the intestines known as enteroendocrine cells. Let me just read you the conclusion.

“In conclusion, the densities of several duodenal enteroendocrine cells in IBS patients changed toward the values measured in controls following dietary guidance.”

So essentially what that means is, they took patients with IBS, and they took patient with control. They did samples of their intestinal tissues, and they measured the density of cells known as enteroendocrine cells. And they looked at what happened to the IBS patients after a low FODMAP diet. They found that after the low FODMAP diet, the density of the enteroendocrine cells became more like that of healthy controls. I’ll give you another quote here.

“The changes in serotonin and somatostatin cell densities may have contributed to the improvements in IBS symptoms, particularly pain and diarrhea.”

So what this study is finding is something that I think is very important. And I will be outlining this and expanding upon this at my presentation at the 2017 Ancestral Health Symposium, that video should be available on the internet afterward if you can’t make it there in person. They may have live streaming, I’m not sure.

But the point is this: we are very tuned into changes in bacteria. But what if other things are changing that may be more important? In this case, what if some of the intestinal endocrine system, the cells that secrete things like serotonin, are changing in a healthy way when going on a low FODMAP diet? This hints to something; and I’ll actually present some other studies at the AHS presentation that support one of my posits, which is there may be other changes from the low FODMAP diet that are healthy outside of bacteria. And this is showing endocrine changes, and there’s also so evidence showing immune system changes, because the low FODMAP diet can actually lower histamine.

So, you’ve probably heard me say that I’ve regrettably observed that care in gut health may have gotten worse over the past few years with the boom of interest in the microbiota, because there’s a lot of academic information that’s pre-clinical that’s distracting people from what the clinical science actually says. So this would be an example of that. If someone is afraid to go on a low FODMAP diet, or doesn’t try it because they think it’s going to cause negative changes in bacteria in their gut, they may be operating in a bacterial centric manner, which is skewed by the bacterial centric research, which is ignoring the fact that clearly this diet has impressive documentation to help clinically.

Now, it’s a different story in terms of you need to be fanatically strict to a very low FODMAP diet forever. No. That’s probably not what’s supported. So we shouldn’t take the extreme, and conflict that with long-term recommendations. But certainly I think there are improvements that are attained from the low FODMAP diet that go way beyond that of just bacteria.

Gut Microbiota Profiles in Active and Sedentary Women

And more on the gut, here’s a second study. “Difference in Gut Microbiota Profile Between Women with Active Lifestyle and Sedentary Women.” Essentially, they assessed via quantitative PCR analysis. So, DNA testing. They mapped the microbiota, which I’ve said is not something that’s clinically relevant at this point, but is used for research. Here’s some of the research. What they showed was, let me read a quote.

“Body fat percentage, muscular mass and physical activity significantly correlated with several bacterial populations. In summary, we provide the first demonstration of interdependence between some bacterial genera and sedentary behavior parameters, and show that not only does the dose and type of exercise influence the composition of gut microbiota, but also the breaking of sedentary behavior.”

So essentially what they’re finding and showcasing is that being healthy, or being fit, or having a healthy body composition, or exercising, all these things positively impact your microbiota. In fact, breaking sedentary behavior and beginning exercise was also shown to cause improvements in the microbiota.

So you’ve probably heard me say, and I’ve been saying for years, that we shouldn’t be looking at the gut microbiota as this one-way street where if we can just force it to become more diverse, we will see a healthy change to the host. We have to remember that in many cases, the health of the host is what dictates the health of the microbiota.

So, this is most egregiously and erroneously showcased by those that try to test the microbiota via microbiota mapping and then recommend personalized probiotic recommendations to try to increase diversity to try to quell disease or increase the health of the host. You can certainly use prebiotic supplements; I don’t have a problem with that. But doing it under the guise of treating a test result as a way to help somebody really has no science to support it.

This is one of many studies that are surfacing that are starting to show that the health of the host is a major dictate of the health of the microbiota. So we shouldn’t be looking at this as a one-way street. It is bidirectional. And the best way, in my opinion, to improve the health of the gut are not these highly tailored manipulate-your-microbiota assays, but rather clinical fundamentals: identify inflammatory burdens, identify infectious or dysbiotic burdens, things like SIBO, Candida, inflammatory bowel disease, elimination/reintroduction diets, low FODMAP diets. And that’s really where you going to get the brunt of the improvement from the gut perspective. And then leverage that with healthy lifestyle changes, like exercise, and you have yourself a pretty winning combination.

Non-Thyroidal Illness Syndrome Treated with Triiodothyronine

All right, next study. “Non-Thyroidal Illness Syndrome in Patients Exposed to Indoor Air Dampness Microbiota Treated Successfully with Triiodothyronine.” Essentially, this study wanted to see if patients who were exposed to essentially indoor mold would benefit from the addition of T3. And they did. They showed benefit. And they argued that perhaps one of the reasons why they showed benefit was because of a downregulation of conversion of T4 to T3. I’m certainly open to that.

This is one study that showcases that. And the ideal solution may be a combination, or ultimately getting to the source of the mold or air contaminants. But for some patients, that may not be possible. And this is where I think a trial of the T3 could be helpful.

Now, they may have reported; I didn’t dig deeply enough to uncover this. They may have reported that the ratio of free T3 to reverse T3 had a bearing. I’m actually really curious. If anybody wants to pull this study, and see if the ratio of free T3 to reverse T3 before starting T3 dictated if someone would respond or not respond, I’d be very curious to see that.

My inkling is that there would be little to no predictive value, meaning the lab test didn’t tell you if someone would respond better or not to therapy, because I don’t think the lab values are that precise with thyroid. And we’ve seen that in some of the studies that I’ve simply put patients on different forms of hormone, and noted a subset of the population prefers T4, a subset prefers T3.

Now, you may argue that that comes down to the lab testing. My hunch from having had ordered the expanded assays for a few years is that it’s not quite that simple. But again, if anybody wanted to pull that paper, dig into those details, and let us know in the comment section, I would be grateful. And I would probably send you a free copy of the book. Or a T-shirt, once we make T-shirts. That’s another project we’re working on. But anyway, if anybody wanted to do that, I’d be curious to see what that shows.

Meal Frequency, Food Intake, and Weight

Okay, moving on. “Effects of Meal Frequency on Weight Loss and Body Composition: a Meta-Analysis.” “A total of 15 studies were identified that investigated meal frequency in accordance with the criteria outlined.” To quote. “Feeding frequency was positively associated with reductions in fat mass and body fat percentage as well as an increase in fat-free mass.”

So that’s something that’s encouraging. Another quote here, “In conclusion, although the initial results of this meta-analysis suggest a potential benefit of increased feeding frequencies for enhancing body composition, these findings need to be interpreted with circumspection.”

And that may be because some of the quality of the studies here was not that high. And there may have been one study that skewed the results, because one study showed an inordinately positive finding. So when you look at some other studies—this next one here. “Eating Frequency, Food Intake, and Weight: A Systematic Review of Human and Animal Experimental Studies.” Out of the 13 studies reporting on consumption, 61% found no significant effect of eating frequency on weight. And 64% found no significant impact on other anthropometric measures.

2 Large Meals vs. 6 Small Meals for Diabetics

However, there’s another study here. “Eating Two Larger Meals a Day (Breakfast and Lunch) Is More Effective Than Six Smaller Meals in a Reduced-Energy Regimen for Patients with Type 2 Diabetes: A Randomised Crossover Study.” They actually did show that eating only breakfast and lunch reduced body weight, high fasting glucose, and C-peptide and glucagon. So they did show that in patients with type 2 diabetes, I’ll quote. “These results suggest that, for type 2 diabetic patients on a hypoenergetic diet­­” —low-calorie diet—“eating larger breakfasts and lunches may be more beneficial than six smaller meals during the day.”

So this kind of hints at something that we’ve discussed in the past. Well firstly, a foundational concept we’ve discussed, which is if you look at all the data on a topic, you rarely have a super strong opinion, because you will see, very quickly, contradictory results just like this. And that’s why one of my strongest indicators for someone I do not want to learn from or listen to is someone who has a very strong opinion, because they are almost always ignorant of the contradictory information, which means they have a narrow view, which means they are narrowly educated, which means that you do not want to learn from them.

However, if we look at this data, we of course do see that reinforced. But we see an important takeaway, which is, while there does tend be disagreement, there also tends to be trends in terms of who may or may not benefit. So type 2 diabetics, people who have metabolic conditions of excess, or are showcasing the inability to manage energy appropriately. And when I say energy, I just mean dietary calories. They may do better from a fasting intervention, whereas someone who might be stressed, at a more normal body weight, they exhibit a lot of signs of burnout, or high allostatic load, or even the term that I hate, adrenal fatigue. Or if you want to call it HPA dysfunction; guys, put it simply, people who seem like they’re over-burdened. They don’t sleep well. They’re tired during the day. They like caffeine. They get ‘hangry’ if they don’t eat. Right? These people may not do as well on two meals per day, or intermittent fasting, and they may do better with small, frequent meals.

Speculating there a little bit, but certainly I think it seems reasonable to suggest that people that have things like overweight, high cholesterol, high blood sugar, diabetes, are kind of a bullseye for the highest probably of a positive response to something like intermittent fasting. Whereas those who are exhibiting signs of burnout or stress or high allostatic load or adrenal fatigue, whatever you want to call it, they may have the highest likelihood of a negative reaction. And patients with digestive ailments and maladies probably fall somewhere in between.

And that’s a little bit harder to discern, because there are cases where digestion may benefit, but then metabolism may not benefit. So these are people who report, “Yeah, I feel less bloated when I don’t eat. But I also get hangry and irritable.” So you have to kind of balance that out. I think these patients may be ones that do well with modified fasts. Using something like an elemental diet solution, or a master’s cleanse type solution can be helpful there.

Diet and the Apolipoprotein E Genotype

So, moving on. “The Effect of Apolipoprotein E Genotype on Response to Personalized Dietary Advice Intervention: Findings from the Food4Me Randomized Controlled Trial.” So essentially, they wanted to see if they gave patients a gene tailored APOE diet—and this was a diet that was lower in saturated fat. They wanted to see if that would have a higher benefit for improving their blood lipid panels. And essentially what they found is that whether or not someone had the APOE genotype did not predict whether or not they would respond better or worse to the genotype based diet.

Now, this is one of those studies where, gosh, you ask yourself, “Where did these authors learn how to communicate?” Because the sentence structure and the clarity of the way they write could not be more ambiguous or more difficult to discern.

So reading this study was one of those studies that makes me want to jump off the roof of my complex. Because it’s just terrible. But I did read it begrudgingly, and dig through the details. And we will be doing a more detailed write up to give you some of the finer points in an edition of The Future of Functional Medicine Review clinical newsletter. So that’s coming there in the future.

Long story short, the gene testing that then gave you the gene-tailored diet was no more effective than being just a regular person going on a diet. And why I think that’s important is because I do think that the utility of gene testing and gene treatment has been way overstated. And I will change my mind as soon as some compelling research is presented that refutes that.

Unfortunately, what I’ve seen is more often than not, you do not see consistency in any benefit shown from following these gene recommendations. And I think we talked previously about the large Chinese study that gave patients with MTHFR folic acid, not folate, folic acid. And showed a reduced stroke risk. So again, if everything we’ve heard about the MTHFR genotype is true, then folic acid is like poison for them. Yet how do they reduce stroke by giving a Chinese population folic acid?

And there’s I think another study I’ll come to in a moment that further corroborates that. But here they found that the gene testing didn’t seem to have a huge impact. Although they did show that people were more prone to follow the dietary recommendations if they were told it was based upon their genetics. So there may be some utility there in compliance. But unfortunately, the treatment was no more effective.

Paleolithic & Mediterranean Diet on Mortality

“Paleolithic and Mediterranean Diet Pattern Scores Are Inversely Associated with All-Cause and Cause-Specific Mortality in Adults.” So to quote: “We investigated associations of 2 diet pattern scores, the Paleolithic and the Mediterranean, with all-cause and cause-specific mortality.” A total of 2513 patients died during the median follow-up of 6.25 years.

So essentially what they showed was the hazard ratio for all-cause mortality, cancer mortality, and cardiovascular disease mortality. They were essentially 0.7 and 0.6 respectively for the Paleo diet and the Mediterranean diet. What that means is, anything below 1 is going to be considered positive, 1 is going to be considered neutral, and above 1 is going to be considered deleterious or dangerous, or risk increasing. So below 1 reduces risk, above 1 increases risk.

And they showed that both the Paleo diet and the Mediterranean diet decreased your risk of having all-cause mortality, cancer mortality, and cardiovascular disease mortality. Although there was a slight favor toward the Mediterranean diet here. I’m not sure if it would be considered significant. I wasn’t able to pick that out, if the difference between Paleo and Mediterranean was considered significant. But they both decreased all-cause mortality.

And I think this is important. Because you’ve probably heard me say that we’ve seen trials showing improved markers of cardiovascular disease and also body weight and BMI and things like that when we look at the Paleo diet, and low-carbs diets, compared to other diets. This is probably more important data, because it shows outcome.

So it’s important that we balance that opinion of the Paleo and low-carb diets potentially having a slight edge, because this study showed about equivalent, and potentially even a slight edge for a more important outcome, which was death from any cause, death from cancer, and death from cardiovascular disease. But also important to remember, both these diets produced a protective effect. So a good study there.

Paleolithic & Mediterranean Diet and Risk of Colorectal Adenomas

“Paleolithic and Mediterranean Diet Scores and Risk of Incident, Sporadic Colorectal Adenomas.” So essentially—I’ll just read you the conclusion here. “These findings suggest that greater adherence to the Paleolithic diet pattern and greater adherence to the Mediterranean diet pattern may be similarly associated with lower risk of incident, sporadic colorectal adenomas.”

So again, another study here looking at Paleo versus Mediterranean, and both showing the ability to reduce risk. Now, another important issue I should mention here is for those that tell you that meat causes cancer, that’s really, in my opinion, cherry-picking of data showing that a society that has increased consumption of probably sugar, processed foods, and processed meats has an increased incidence of cancer. And what is extrapolated from that is, “Look! Increased meat equaled increased cancer.”

But of course, taking an unhealthy diet and sucking out one macronutrient from that entire unhealthy diet, and blaming that one macronutrient is just disgustingly ignorant. And how that happens, by any of these doctors you see in documentaries wearing the white coat, pretending to know what they’re talking about, is disgusting and it makes me want to punch the television. So when you look objectively at information like this, you clearly become irritated at how anyone could make such ignorant, dogmatic recommendations.

Now, I’m certainly not saying that I have all the answers. But I know enough not to make a statement that is totally refuted by any decent science. And here we have two studies that we just went through; both with a fairly decent sample size. This last study had about 564 cases, and the one before that had a few thousand. And so we’re seeing a reducing in all-cause mortality, including cancer. So, to say that meat causes cancer or disease is really kind of throwing the baby out with the bathwater.

And I would be inclined to think that if we took a study that looked at increased consumption of canned vegetables, and we showed an increased predilection of potentially, I don’t know, sodium-induced high blood pressure for those who are sodium sensitive, or some other type of disease. Potentially gastric cancer, because of some of the preservatives used in the linings of the cans. Then we can make an argument saying that vegetables cause cancer, which would be stupid. So hopefully that helps you, if you’re trying to grapple with the recent documentary, which I will not name, but you’ve probably heard of, that was just an abomination because it was so scientifically inaccurate and fraught with non-scientific claims posing as science.

Persistence of Non-Celiac Wheat Sensitivity

Okay, next study. “Persistence of Nonceliac Wheat Sensitivity, Based on Long-Term Follow-Up.” “We investigated how many patients with a diagnosis of non-celiac wheat sensitivity still experienced wheat sensitivity after a median follow-up time of 99 months. We collected data from 200 participants….” In total, 88% of patients improved after a diagnosis of non-celiac wheat sensitivity, 98% who strictly adhered to a gluten-free diet had reduced symptoms, whereas only 58% who did not adhere to a gluten-free diet had continued improvement of their symptoms. Of the 22 patients who are able to perform a double-blind, placebo-controlled challenge, reintroduction of gluten, 20% reacted to wheat. So this led the authors to conclude: “We conclude that nonceliac wheat sensitivity is a persistent condition.”

So this is something that just provides some scientific validity to what I think many of us have seen. There is definitely a subset of patients who are not celiac who are sensitive to gluten. So, important to be aware of this information. It’s a good reference if you’re a clinician and you’re trying to defend your position. But also remember, I think you have a much more defendable position if you don’t make this a, “you have to practice gluten avoidance to the level of a celiac patient,” even if you don’t see that to be true in your own experience. I think it’s very important to be practical, have patients perform an elimination, and then try a reintroduction and see how they feel.

Now, you may want to make a recommendation, if they have a family history of autoimmunity, and say, “You may never want to make gluten a staple. But hopefully you’ll be able to get away with it on occasion without too much repercussion. Why don’t you go ahead and try a little bit here and there, see how you feel, and practice a level of avoidance that’s correspondent with the reaction that you have.” That’s a much more defendable position because you’re personalizing their level of avoidance to their level of reaction.

Postprandial Serum Endotoxin Modulated by Dietary Fat

“Postprandial Serum Endotoxin in Healthy Humans Is Modulated by Dietary Fat in A Randomized, Controlled, Cross-Over Study.” “Meal fatty acid composition modulates postprandial serum endotoxin concentration in healthy adults. However, postprandial endotoxin was not associated with systemic inflammation.”

So, essentially what they’re saying here is the amount of fat you eat affects endotoxin, which is essentially a way of measuring leaky gut. The ability of bacterial cell wall fragments to get through the gut membrane into the blood stream. So fat increases leaky gut, and I hate even saying that. But more importantly, it was not associated with systemic inflammation.

Now, what’s interesting is that if fat was causing a pathogenic leaky gut, I would think you would see much higher levels of negative outcomes in these studies. Like these Paleo diet studies, which are, of course, going to be relatively higher in fat than a Mediterranean diet, than you do. You don’t see a high incidence, for example, of digestive upset when patients go on higher fat diets. In fact, you could probably make the argument that the majority of studies in patients, especially with digestive symptoms that go on a lower-carb, higher fat diet, actually have improvements.

Now, remember… actually I shouldn’t say remember because I don’t think we’ve talked about this before. But I will be presenting on this at AHS. One study did show that a low FODMAP diet reduced leaky gut. So it may not all be about fat. And the reason why you may see fat increase leaky gut is there may be more of these endotoxin particles in fats to be transferred across the gut lumen. So it may not be that the diet is driving that, it just may be that there’s more endotoxin in a high fat meal than there is in a non-high fat meal.

So, getting way out of the weeds, getting out of the details, I don’t buy the fact that fat increases leaky gut. Because if that were true, we would probably see much more negative outcomes in patients on higher fat diets. So this is a reason why we shouldn’t fret over mechanism when we have outcome data. And I can provide a counter-mechanism, which is a low FODMAP diet can show a reduction in leaky gut. So who wins? Well, that’s where we go to the outcome data. What do the clinical trials show? Both low FODMAP and low carb work well for people. But they don’t work well for all people. So do some dietary experimentation and use the diet that works best for the person sitting in front of you, or if you’re doing the experiment yourself, whichever one you feel best on.

Carbohydrate Intake, Verbal Memory, and the APOE Genotype

Next study, “Increased Carbohydrate Intake is Associated with Poorer Performance in Verbal Memory and Attention in an APOE Genotype-Dependent Manner.” To quote, “These results provide support to the idea that decreasing carbohydrate intake may offer neurocognitive benefits, with specific cognitive domains affected in an APOE genotype-dependent manner.”

Now, what becomes confusing about this is you’ve probably heard others say that those with the APOE, especially APOE-4 genotype, should be eating a low fat diet. And I’ll put a quote in notes here by Dr. Maria Cirillo, there seems to be some disagreement on this. And what I think the most practical recommendation is is to have someone experiment with different diets.

• Maria Carillo, the Director of Medical and Scientific Relations at the Alzheimer’s Association in Chicago, made clear the connection between the brain and the heart by citing how, in many trials, those lifestyle recommendations for diet and exercise have proven to be beneficial for brain health. In other words, the body is more integrated than doctors once believed. What affects one vital organ also affects another, and the bottom line is that you can affect how those organs perform and age based on your lifestyle choices. If you have two ApoE4 genes, you may have a greater risk of developing Alzheimer’s, but only if you “turn on” that gene with a high-fat diet
  • http://www.huffingtonpost.com/dr-suzanne-steinbaum/heart-brain-health_b_4210231.html

I like starting with the Paleo diet that’s moderate or lower in carbs. That does not mean a ketogenic diet. It just means having someone eat mostly healthy meats, vegetables, some fruits. Really somewhat limited on grains and starchy carbs, at least for a little while, and then see how they do. And a lot of people feel better on that, but some people clearly report, “I just need some rice. I need some quinoa. I need more potatoes.” Then we kind of personalize the diet to them. And it’s not super hard to figure out if you just listen to your body a little bit.

And my inkling, I know this is not super scientific for the quantified-self crowd out there, but the diet that you feel best on is probably going to be the best diet for you. You can use some basic lab testing to try to assist you in making that connection. Look at your blood sugar, look at some of your lipids and cholesterol. But I don’t think we’re there quite yet with the gene testing being able to predict exactly what diet is going to be the best for you.

So, I remain open on all this. But I think we really haven’t sorted this out, because I see conflicting findings fairly often. And usually conflicting findings mean that we don’t really know what we’re talking about just yet. So we should take a pause and focus on the data that we have more solidly bore out before trying to make things more exotic. Because exotic and wrong is not as good as non-exotic, or simple and right.

Here, we’ve gone over one study showing that APOE-4 should eat low-fat, another study showing that APOE-4 should eat low-carb. So until we get this sorted out, I would not place a ton of stock in the gene testing. I am not a gene expert, so there may be things here that I’m missing. But from what I’ve seen, I’ve not seen agreement. I’ve seen contradiction, which makes me take pause and be a little bit reticent about the utility of this testing.

Dr. Ruscio Resources

Hey, everyone, in case you’re someone who is in need of help or would like to learn more, I just wanted to take a moment to let you know what resources are available. For those who would like to become a patient, you can find all that information at drruscio.com/gethelp.

For those who are looking for more of a self-help approach and/or to learn more about the gut and the microbiota, you can request to be notified when my print book becomes available at drruscio.com/gutbook. You can also get a copy of my free 25-page gut health eBook there.

And finally, if you’re a healthcare practitioner looking to learn more about my functional medicine approach, you can visit drruscio.com/review. All of these pages are at the drruscio.com URL, which is D-R-R-U-S-C-I-O dot com, then slash either ‘gethelp,’ ‘gutbook,’ or ‘review.’ Okay, back to the show.

Self-treatment with Helminths

OK, next study. “Practices and Outcomes of Self-Treatment with Helminths Based on Physicians’ Observations.” So, this study essentially examined the effect, or lack of effect, of people who were self-treating with helminths, or worms. And just to provide some background context, there’s kind of this underground movement of people who have non-responsive or somewhat debilitating inflammatory and autoimmune conditions who are seeking aid from helminths, which is the medical term for worms.

So a few findings here. “Five physicians monitoring more than 700 self-treating patients were interviewed. The results strongly support previous indications that helminth therapy can effectively treat a wide range of allergies, autoimmune conditions, and neuropsychiatric disorders, such as major depression and anxiety…. Approximately 57% of the self-treating patients observed by physicians in the study had autism.”

There does seem to be a fairly strong contingent of those with autism who are turning to this therapy, and considering having one doctor who has been doing quite a bit with this on the podcast to expand. I also wanted to mention that the two most popular organisms currently used by self-treaters were what’s abbreviated as HTC, and Trichuris suis. So these are kind of hard to say, so I’ll leave them there in the notes. But we’re going to be doing a little more on helminths in the future. I’m curious about this. I think there could be some utility, but I think selecting for the right patient subset is going to be important. So something definitely to keep our eyes out for. And we’ll be having one, if not two, helminth-minded physicians on the podcast to talk a little bit more.

Distribution of Parasites Detected in Stool Samples

And while we’re talking about helminths, let’s talk about another study on parasites. “Distribution of Parasites Detected in Stool Samples of Patients Admitted to Our Parasitology Laboratory During a Three-Year Period Between 2012 and 2014.” In total, 6757 stool samples in Turkey, and this is where parasites are more common than in the United States, were assessed. “Parasites were detected in 3.7% of the samples, while no parasites were detected in 96% of the samples. The distribution of intestinal parasites was as follows: Blastocystis hominis (63%), Giardia intestinalis (26%), Taenia sp. (4.8%), Entamoeba histolytica (1.6%), and Enterobius vermicularis (2.4%).” I haven’t even heard of that one before.

So what I wanted to illustrate with this study is the incidence of parasites is actually not very common. Blasto—do we consider blasto a parasite or not? It’s kind of in the gray area. I like the Mayo Clinic’s position on this, which is treat it in patients who have symptoms. And in patients who are asymptomatic, they may be asymptomatic carriers because it does not seem to confer damage to all hosts.

But when I look at this, outside of Blasto, you don’t see a ton of parasites. So sometimes you get patients who have been reading a lot on the internet about the parasite is the cause of all diseases, and sometimes these patients can be challenging in the clinic, because they’re so convinced that a parasite is the problem. And I wish they could see through my eyes how oftentimes it’s not necessarily a parasite, but it could be something like dysbiosis. Or overzealous immune activation in the gut. And these things don’t require more and more treatment of parasites. In fact, I would argue that parasites are fairly easy to treat with the exception maybe of Amoeba histolytica. Parasites can be fairly easy to get rid of.

It’s these conditions that are more so dependent upon your body maintaining a healthy ecosystem, and preventing dysbiosis. That may be dependent upon motility or your immune system. Or even where it’s not dependent upon your body to maintain a healthy microflora, but rather that your immune system is not well-calibrated to get along with your microflora. And you’re having this chronic immune response to the actual healthy commensal bacteria in your gut.

These are the cases that can be more challenging to manage. And can have this relapsing, remitting, relapsing, remitting type cycling that people sometimes think are the lifecycle of parasites. But really in my opinion are not. And it’s based upon looking at studies like this. And then running a full comprehensive parasitology on most patients, and just seeing that they’re not that common. So anyway, that’s a study on parasites.

Metronidazole, Probiotics, and Bacterial Vaginosis

Another study here, “Effects of Metronidazole Combined Probiotics Over Metronidazole Alone for the Treatment of Bacterial Vaginosis: a Meta-Analysis of Randomized Clinical Trials.” And to quote. “The result has showed”—I think their English is a little off here—“an overall little significance for the efficacy of metronidazole combined probiotics over metronidazole alone for the treatment of bacterial vaginosis.” Boy, that’s bad English. This must have been a study published in another country that was translated.

So essentially, they showed that probiotics combined with metronidazole did not provide any benefit with metronidazole alone. However, we’ve talked about other trials that have shown that probiotics may be helpful. And I believe it was via a meta-analysis for bacterial vaginosis. So perhaps that benefit is masked when it’s combined with the use of metronidazole.

Also, remember that in women who have bacterial vaginosis and/or UTIs, there is some evidence showing that hormones, female hormones, have an impact on the pH in the vagina, and that has an impact on the predilection or predisposition toward vaginal dysbiosis. So don’t forget. If a woman is exhibiting signs of female hormone imbalances, that can be a relatively easy fix to help with the microbiota in the vagina and in the gut, as we talked about with Dr. Rao a little while back, how there is that progesterone receptor in the colon that can be affected by female hormones. And I’ve definitely seen that in my practice.

If you’re a female patient of mine, you may have heard me comment that the co-presentation of a woman exhibiting female hormone imbalances and digestive ailments is fairly common. And they tend to respond very well when treated together.

Levothyroxine and Subclinical Hypothyroidism

Ok, a few more studies here. Levothyroxine Shows No Benefit in Elderly Patients with Subclinical Hypothyroidism, Trial Finds. So subclinical hypothyroidism is when you have high TSH and normal T4 according to the conventional ranges. This study did not show any benefit in those who are elderly.

You may have remembered me mentioning that the data seems to show that the population that will have the least benefit from treating subclinical hypothyroidism with thyroid hormone is elderly because there is this likely age-associated increase in TSH that’s normal. So a mild elevation of TSH in someone who is elderly is probably somewhat normal. Therefore, treating that is not going to have much of an effect. And this is why we see some of the studies showing this.

Escherichia Coli Nissle 1917 and Ulcerative Colitis Remission

“Role and Mechanisms of Action of Escherichia Coli Nissle 1917 in the Maintenance of Remission in Ulcerative Colitis Patients: An Update.” To quote, “It is the only probiotic recommended in ECCO guidelines as effective alternative to mesalazine in maintenance of remission in UC patients.”

So, you may have heard me say that it’s a shame that we don’t have this probiotic available in the states. Because there is some impressive research, especially in it regarding inflammatory bowel disease, and more specifically in ulcerative colitis. Here’s one of the studies that supports that.

Probiotic Consumption on Gastrointestinal Transit

Ok, just a couple more studies here. “Contemporary Meta-Analysis of Short-Term Probiotic Consumption on Gastrointestinal Transit.” So, essentially they looked at 15 clinical trials and they show that probiotics, yes, can shorten intestinal transit. Meaning if you have slow intestinal transit, probiotics can assist with that. And they found that the most effect, meaning a medium to large treatment effect, were for Bifidobacterium lactis HN019 and Bifidobacterium lactis DN173010. And they commented that other probiotic strains yielded negligible reductions in intestinal transit time.

So this is certainly interesting. I’ve linked here to another study showing similar results. And I believe these were similar results with other probiotics. I’m not positive on this second reference I’ve put in here. But essentially what I’m trying to illustrate is that probiotics can help with intestinal transit. I’m not sold that any probiotic effect is super-strain specific. I remain 1000% open. But every time I’ve looked to see, for example, with constipation: was there a miracle probiotic? No, because I can find other studies that show different strains also positively impact constipation or SIBO.

So after seeing enough studies showing different strains can cause the same benefit, I’m inclined to think that the benefit from probiotics is not highly strain specific. There may be a small number of exceptions to that rule. But I think at large most of the benefit of probiotics are probably not super-strain specific. And when you think about the complexity of the microbiota, how a given probiotic affects the microbiota, and how it affects someone immune system, I think it’s likely that you’re not going to see highly strain specific effects. That’s my speculation. But I think we’ll see that continue to be reflected by the research studies.

Saturated Fat, Sugar, and Coronary Heart Disease

And last study here. Last two studies. “The Evidence for Saturated Fat and for Sugar Related to Coronary Heart Disease.” Essentially, this study is just telling us something that I think many of us have known, which is that dietary guidelines should shift focus away from reducing saturated fat and from replacing saturated fat with carbohydrates, specifically when these carbohydrates are refined. So essentially saying that sugar, especially refined carbs, is likely more dangerous than saturated fat and we should try to balance out our recommendation not to vilify saturated fat so much. Because it sometimes pushes people to eat too much carb. And this can be dangerous, especially if they’re refined carbs.

Vitamin B12 & Folic Acid on Depressive Symptoms

And last study. “Effects of Two-Year Vitamin B12 and Folic Acid Supplementation on Depressive Symptoms and Quality of Life in Older Adults with Elevated Homocysteine Concentrations: Additional Results from the B-PROOF Study, an RCT.” I’ll just quote you. “In conclusion, two-year supplementation with vitamin B12 and folic acid in older adults with hyperhomocysteinemia”—high homocysteine—“showed that lowering homocysteine concentrations does not reduce depressive symptoms, but it may have a small positive effect on health-related quality of life.”

Episode Wrap-up

So that takes us through another edition of health news reviews. Thank you guys so much for all of your support. I just want to again say that the iTunes reviews are going up nicely, and that’s really helping us to climb the chart and to reaching to help more people, so I really appreciate you guys taking a moment out to leave a review for the show. I will talk to you next time. Thanks, bye.

What do you think? I would like to hear your thoughts or experience with this.

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Dr. Ruscio is your leading functional and integrative doctor specializing in gut related disorders such as SIBO, leaky gut, Celiac, IBS and in thyroid disorders such as hypothyroid and hyperthyroid. For more information on how to become a patient, please contact our office. Serving the San Francisco bay area and distance patients via phone and Skype.