Traditional diets are patterns of nutrition and eating inspired by the rich culture and culinary histories of cuisines from around the globe. Emerging research aﬃrms that many of the most well-cherished traditional diets have something to teach us about health and nutrition. While research still debates the evidence of one eating pattern versus another, recommendations are moving towards a whole food-based approach to healthy eating, and one that takes into consideration traditional diets.
The DGA recommended patterns of nutrition and eating continues to reflect white, middle-class Americans and is one more way of saying “we don’t see you” to people of color.
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We have long known that specific brain centers produce and release several substances (like acetylcholine, adrenaline, and cortisol), that modulate gut peristalsis (bowel contractions), vascular tone, bacterial homeostasis, and nutrient absorption in the intestines. But we are now quickly appreciating that our gut microbiota (the collection of bacteria, fungi, yeast, and viruses that live in our intestines), and the substances they make and release, affect nociception by acting directly and indirectly on nerve terminals in the skin, muscles, joints, and deep tissues (1).
But the relationship of the gut microbiota with pain goes beyond modulating the response to noxious signals by peripheral nerve terminals; these bacterial mediators also act on neurons – but also on astrocytes and microglial cells- in the brain and the spinal cord, influencing ‘central’ sensitization and tolerance to pain. Moreover, signals from the gut microbiota also impact on important physiological states like mood, sleep and wake cycles, hunger and satiety, immunity, and hormonal balance. Remarkably, during chronic pain conditions a positive feedback loop – with negative consequences- is often at play, since chronic pain can impair the above processes, and these in turn can further modulate nociception and central pain perception to sustain chronic pain (2, 3, 4).
In a previous blog I discussed how gut bacteria by-products sensitize nociceptors in the gut, leading to chronic pain conditions such as irritable bowel syndrome (IBS) and inflammatory bowel disease (IBD). We’ll now take a look at how the diverse factors released by gut bacteria reach central neurons and influence peripheral and central sensitization, and their role in inflammatory and neuropathic pain.
Gut Microbiota, PAMPs, and Regulation of Pain
Bidirectional communication between gut bacteria and the brain occurs through both neural pathways (vagus nerve terminals in the gastrointestinal tract) and a range of bioactive factors released into the blood. Through these pathways, an abnormal composition of gut bacteria (i.e. gut dysbiosis) can influence both primary hyperalgesia, defined by an increase in the excitability of peripheral nociceptors (afferent sensory endings and fibers), and secondary hyperalgesia (associated with changes in the excitability of neurons in the CNS, including the spinal cord and supra-spinal sites in the brain.
These actions are largely mediated by pathogen-associated molecular patterns (PAMPs), a variety of small molecular motifs conserved within microbe classes, which have shown to contribute to peripheral sensitization under chronic pain conditions, and aggravate several chronic diseases. Gut microbiota-derived PAMPs include bacterial cell wall components, such as LPS, lipoteichoic acid (LTA), peptidoglycan (PGN), and b-glucan, which are transferred into the circulation and bind to pattern recognition receptors (PRR), including Toll-like receptors (TLR 1-9) expressed on immune cells and sensory neurons in the dorsal root ganglia (DRG) of the spinal nerve (5, 6).
A Gut-Brain Superhighway: The Vagus Nerve and Pain
The vagus nerve innervates the digestive tract and senses gut activity through signals from endocrine cells located in the gut epithelia. Digested food (carbs, lipids and proteins) as well as bacterial components and metabolites (notably LPS, or endotoxin, and short-chain fatty acids, or SCFAs) act on enteroendocrine cells (EECs) to modulate their secretion. Notably, EECs were recently found to form synapses with vagal nerve terminals, and transmit information to the brain through both neurotransmitters (serotonin and glutamate) and gut hormones (cholecystokinin, glucagon-like peptide-1, etc.) that regulate a wide range of processes like hunger, mood, stress, and pain.
People with fibromyalgia, a chronic pain condition characterized by central sensitization, were shown to have reduced vagal tone, whereas an abnormal vagal tone was also described in IBS and IBD (7, 8). Whenever vagal activity is depressed, so are its anti-inflammatory effects. This compounds disease symptoms by enhancing regional inflammatory responses in the gut. Moreover, vagal afferent fibers also express a subtype of LPS receptors (TLR4), through which a direct stimulation of brain centers may occur in IBS and IBD due to increased intestinal permeability and transfer of LPS across the gut mucosa (9). Interestingly, research has shown that a much more prevalent burden of daily life, stress, can lower vagal tone and potentiate inflammation. In view of the critical role of this gut-brain neural pathway in health and disease, therapeutic approaches to modulate the activity of the vagus nerve are being actively explored to reduce inflammation associated with various chronic pain conditions (10).
Vagus nerve stimulation (VNS) can be achieved in different ways. Cold exposure, singing, meditation, deep-breathing techniques ( e.g. Bhramari pranayama or “humming breathing”), and cognitive behavioral therapies are just a few strategies to increase vagal tone to help reduce both inflammation and chronic pain. More sophisticated strategies involve the use of implantable or transcutaneous devices that deliver electrical impulses to the vagus nerve; these are sometimes used in treatment-resistant major-depressive syndrome, as well as epilepsy, and were shown to reduce chronic pain in patients with fibromyalgia and arthritis (11, 12).
Bacterial Blood Mediators: Influence on Inflammatory and Neuropathic Pain
While an overt immune response is triggered by acute bacterial infection (bacterial invasion into the blood due to a breach in the skin or gut epithelia), a more subtle mechanism operates during gut dysbiosis, affecting peripheral and central pain sensitization. Neuroinflammation is considered a crucial mechanism underlying central sensitization in chronic pain conditions induced by inflammation or nerve injury. Recent work suggested that not only neurons, but also several other cells in the central nervous system such as endothelial cells, pericytes, microglia, astrocytes, and infiltrating immune cells, react to direct and indirect signals from the gut microbiota that contribute to neuroinflammatory processes (13, 14). Activation of glia (e.g. microglia and astrocytes) can lead to synthesis of proinflammatory cytokines or chemokines, such as TNF-a, IL-1b, and CXCL1, and can elevate and decrease glutamate and GABA levels, respectively, contributing to the development of central sensitization, hyperalgesia (enhanced pain in response to noxious stimuli), and allodynia (pain in response to non-painful stimuli) (5).
A role for gut bacteria in inflammatory pain is mostly supported by animal (preclinical) studies. Several studies have shown that germ-free (GF) mice (raised in a sterile environment from birth) develop visceral hypersensitivity accompanied by overexpression of TLRs and increased levels of cytokines such as interleukin (IL) 6, IL-10, or tumor necrosis factor (TNF)-α in the spinal cord. On the other hand, studies in mice suggest that the presence of commensal gut bacteria may promote hyperalgesia under some conditions. One such study, comparing responses to direct and indirect gut microbiota factors (LPS, carrageenan, TNF-α, IL-1b and CXCL1) in control and germ-free mice showed that inflammatory hypernociception is blunted in the absence of commensal microbiota. This effect was dependent on the availability of IL-10, a main anti-inflammatory cytokine, which was greatly increased in germ-free mice (15). Meanwhile, a recent study showed that vitamin D deficiency in mice induced tactile allodynia associated with neuronal hyperexcitability and reduced microbial diversity, characterized by an increase in Firmicutes and a decrease in Verrucomicrobia and Bacteroidetes (16).
Another type of pain that may be influenced by the bacterial composition in the gut is neuropathic pain. This is characterized by dysaesthesia (abnormal, unpleasant sensations) or allodynia resulting from nerve damage secondary to nerve trauma, chemotherapy drugs, or disease (e.g. diabetes or spinal stenosis) affecting peripheral and central elements of the somatosensory nervous system (17). Chemotherapy-induced peripheral neuropathy (CIPN) is caused by certain anticancer agents (vincristine, paclitaxel, platinum drugs, etc.). Studies in mice showed that commensal gut bacteria were required for optimal tumor-killing activity of oxaliplatin; strikingly, they mediated also mechanical hyperalgesia (enhanced pain) in response to this drug. This effect was reduced in GF mice and in control mice pre-treated with antibiotics, which showed reduced levels of macrophage infiltration and cytokines (IL-6 and TNF-α) in the vicinity of pain-relaying DRG neurons (18). These effects may result from damage of the gut barrier by chemotherapy drugs, which facilitates translocation of PAMPs into the circulation (19).
Neuropathic pain is also common in people with multiple sclerosis (MS), a neurodegenerative disease characterized by loss of myelin, the insulating lipid that ensheaths nerve fibers and ensures proper transmission of the nerve impulse. In addition to current evidence linking gut dysbiosis and MS symptoms, it was reported that gut bacteria can regulate the myelination of nerves, a discovery that opens up promising therapeutic avenues to treat MS (20).
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Targeting the Gut Microbiota to Treat Chronic Pain
Given the important role that gut bacteria play on peripheral and central sensitization associated with chronic pain conditions, several interventions targeting the gut microbiota are being tested in mice and humans with the goal of treating and hopefully eliminating chronic pain. The most simple ones are based on nutrition (healthy diets that include probiotics and prebiotics) and exercise, which contributes to maintain a healthy gut flora and was shown to increase vagal tone and optimize immune responses (5).
Fecal microbiota transplantation (FMT), also called fecal bacteriotherapy, consist in the administration of a solution of fecal matter from a healthy donor into the intestinal tract of a recipient in order to directly change the recipient’s gut microbial composition and confer a health benefit. FMT is used to treat many diseases, including Clostridium difficile infection, IBD, obesity, and insulin resistance. Potential mechanisms underlying the therapeutic effects of FMT on chronic pain include direct competition of pathogenic bacteria with commensal microbiota, protection of the intestinal barrier, restoration of secondary bile acids metabolism, and stimulation of the intestinal immune system. This approach has shown to provide relief for chronic pain conditions such as fibromyalgia, ulcerative colitis, and IBS (21, 22, 23). However, further research is clearly needed, as the efficacy of FMT for IBS has been questioned based on inconsistent results from recent clinical trials. (24, 25).
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21- Thurm, T., Ablin, J., Buskila, D., & Maharshak, N. (2017) Fecal Microbiota Transplantation for Fibromyalgia: A Case Report and Review of the Literature. Open Journal of Gastroenterology 07(04):131-139
22- Tian, Y., Zhou, Y., Huang, S., Li, J., Zhao, K., Li, X., … & Li, X. A. (2019). Fecal microbiota transplantation for ulcerative colitis: a prospective clinical study. BMC gastroenterology, 19(1), 116.
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24- Halkjær, S. I., Christensen, A. H., Lo, B. Z. S., Browne, P. D., Günther, S., Hansen, L. H., & Petersen, A. M. (2018). Faecal microbiota transplantation alters gut microbiota in patients with irritable bowel syndrome: results from a randomised, double-blind placebo-controlled study. Gut, 67(12), 2107-2115.
25- Myneedu, K., Deoker, A., Schmulson, M. J., & Bashashati, M. (2019). Fecal microbiota transplantation in irritable bowel syndrome: A systematic review and meta-analysis. United European gastroenterology journal, 7(8), 1033–1041.
Welcome back to the Healing Pain Podcast with Steven Masley, MD, FAHA, FACN, CNS
We are talking about potentially what is the healthiest diet on the planet. We know that nutrition and diet is a form of personalized medicine. We’re going to talk about one of the most evidence-based and proven diets that can help you with chronic disease and chronic pain. My guest is Dr. Steven Masley. He is a physician, nutritionist, trained chef, bestselling author and creator of the number one all-time health program for public television. His work has been viewed over a million times on PBS, The Discovery Channel and over 700 different media outlets. His book is entitled The Mediterranean Method.
To get started with the Mediterranean diet, I have got a great download for you. You can download this for free. It’s called The Quick Start Guide to Create Your Own Mediterranean Kitchen. To download this, all you have to do is text the word, 167download, to the number 44222 or go to IntegrativePainScienceInstitute.com/167download. I’m excited to talk to Dr. Steven Masley about The Mediterranean Method, his new book, and how the Mediterranean diet can be one of the healthiest diets on the planet. Let’s get started and let’s meet Dr. Steven Masley.
Watch the episode here:
The Healthiest Diet On The Planet With Steven Masley, MD, FAHA, FACN, CNS
Steven, welcome back to the Healing Pain Podcast. It’s great to have you here again.
I’m delighted to be with you.
I’m so excited to talk to you because we are going to go deep on the Mediterranean diet and talk about all the parts and pieces and benefits for people. I’m so excited that someone is publishing a book on the Mediterranean diet and how to do it the right way. Tell us why it was important for you to publish this book at this time.
When you look at diets, there’s so much confusing information and all these things we tell you can’t eat. One of my experiences, they’re hard to follow. A lot of people end up dropping out. Even a well-intended program by 3 to 6 months, they can’t have them anymore. If you look at what’s the easiest diet to follow and which diets have the best health benefits on the planet, by and far, US News & World Report got it right. They ranked it as the number one diet overall and the easiest diet to follow. That’s important that we give some people something that’s realistic to follow and do.
What’s so important about what you said is both in clinical practice and in studies, we need to look at things on a long-term basis. What can people do long-term? There are some studies where people go on very drastic types of diets for 2 to 3 weeks and they may see metabolic improvements as well as other improvements. This diet is the one that people can do long-term. I know this is close to home for you, isn’t it?
It is. I’ve worked in Europe. I’ve worked at as a Sailboat Captain in Southern France. I spent the last seven months sailing from Spain to Turkey. Along with coastline shopping, eating out, studying what is it about the diet in the Mediterranean. They’re different. In Spain, Greece and Italy, they eat differently but they have things in common that are central to what it’s all about that makes a huge difference for people. I had this firsthand, up close, day-after-day. It was amazing.
Next time you take a trip and you do some research on diet, especially in the Mediterranean, make sure to give me a call. To get us started with this, please tell us what is a Mediterranean diet from your perspective?
It’s this incredible variety of foods that are served in Mediterranean countries all the way from Spain, France, Italy, Greece, Turkey and North Africa. Here are the things they have in common. Greek food looks different than Italian food but what they have in common is they use lots of vegetables and fruit. It’s fresh and it’s local oftentimes. The predominant oil is olive oil. They have nuts. They serve beans if not every day, 4 or 5 times a week. They drink lots of water and then they also have a little bit of red wine for protein. They tend to eat seafood 3 to 5 times a week, much more than we do here. With some clean poultry, they don’t have a lot of red meat. They don’t eat a lot of sugar and they don’t have preservatives and chemicals in their food. It’s mostly a plant-based diet with some clean animal protein. It’s real food that you make and it’s simple. It’s not complicated recipes. They’re easy things to make.
Simple, beautifully prepared, delicious whole foods, which is a good way to start to describe the Mediterranean diet. You said a whole bunch there, which is enough that people would copy down and take that to the supermarket and then put it on their plate and live a healthier life. I want to dial down to some of these topics because they’re a little controversial. The first one you said, which has been the hot topic of 2019, at least in the nutrition circles I move in, is beans. On a traditional Mediterranean diet and on the evidence-based research that you’ve looked at, how many times a week can someone or should someone consume beans? What does a portion of beans look like?
It’s half-cup served with vegetables as a side dish or part of the main course in soup. They’re eating them almost every day. Hummus or pureed beans in a paté that goes with something or beans in soup or being sprinkled on a salad. Lentils, red beans, white beans, there’s an endless variety of them. Some of the controversies have to do with electives. Before we talk about lectins, we should mention that all the foods that have any oxidant capacity, the ability to block oxidation, beans are number one. There’s not even a close second. It’s only which bean you could fight over which might be the best foods for blocking oxidation on the planet, which is a really important part of aging. They’re loaded with protein, B vitamins, calcium and fiber. They’re a nutritional powerhouse.
People mentioned that lectins block some of the nutrient content. Spinach does too, but we don’t say don’t eat spinach. Similarly, we shouldn’t say, “You can’t have beans.” I’ll admit that some people are lectin intolerant. I would guess for my clinical practice, it’s about 10% of people, they get more than a little bit of gas. They get real discomfort. Like any food whether it’s gluten or dairy or soy, if you’re intolerant, you should avoid it. I would say to 5% to 10% of people who have real discomfort when they eat beans, don’t eat them. The other 90% to 95% who get all those health benefits should eat them more often. That’s my take and from all the research I’ve read about lectins and beans.
We’re on the same page. If a practitioner is seeing ten patients per day, you’re maybe looking at 1 to 3 max people for where beans should be eliminated from their diet. The interesting thing that I find about beans is when you do a fruit frequency questionnaire and you dial down into beans and how much people are eating it. Sometimes their portions are huge. With that, there can be lots of different digestive complaints, there can be glycemic implications. There are lots of different things with beans.
Let me comment on glycemic, that’s important. Generally speaking, if you add beans to any meal that has any other carbs sources, whether its bread or potatoes or other vegetables, they lower and give you better blood sugar control. For diabetics and elevated blood sugar, beans are one of the best foods to give you a slight stable rise in blood sugar for many hours. When you look at the glycemic response to beans, it’s excellent and it improves the whole overall meal for blood sugar control.
Number two on my list here is seafood. If you look at most diets and most dietary recommendations, seafoods are on there twice a week. I have done a lot of research into the study around chronic pain and diets specifically. There’s some good research building that you need 4 to 5 servings of seafood per week. Some people are a little bit fearful of that because of contamination and mercury and things like that. Tell us why increasing seafood may be an important strategy for some people to optimize their health.
If it’s cold water seafood, then it provides long-chain Omega 3s, which are inflammatory. To me, three servings a week, about a 4 or 5-ounce serving is about what you get from having a gram a day of EPA and DHA, something that clearly has been shown in studies to block inflammation. The downsides to seafood are mercury and mercury contamination. I’m prone to mercury elevation and many of my patients have been over time. I’ve measured mercury in almost all my patients when they come in for an eval. We’ve done studies on which type of fish predict your mercury level and your EPA/DHA levels. It’s the big mouth fish that’s the big culprit. That’s swordfish, shark, kingfish, tuna, tuna bean, especially Ahi tuna is a major issue. Grouper, sea bass or others, all of those big mouth predatory fish, which are popular in restaurants, impact your mercury level.
I usually say avoid that. In the Mediterranean, they eat a lot of shellfish. The Mediterranean seas have been fished out. There’s not any big mouth fish hardly left, not on a regular basis. Most people are eating middle fish like sardines, what we would call bait and a lot of shellfish. They do have some other Dorado and they have a little sea bass that’s popular. They’re delicious. Some of the chemicals come from farm-raised fish. I’m never a huge farm raised fish fan because those have higher PCP levels in them than some of the other wild-caught ones. Those are my real tips for choosing the right seafood.
On this podcast, we’re focused on chronic pain. As we think about diet and the aging population and we’re talking about seafood, for those that are suffering from cognitive decline, is increasing seafood in the diet could potentially help them with that?
I’ve published studies from my clinic showing that eating more seafood clearly improves brain processing, speed memory, overall brain performance associated with less memory loss assuming you don’t have elevated mercury levels. You have to control and measure that for people who eat lots of seafood. If you eat the right types of seafood, it’s not a problem.
Going through your book, reading it, starting to look at the recipes in it and all the science, you’re someone who looks at the evidence base. I know you have a little bit of a twist to your Mediterranean diet. Tell us what that twist is.
There are two parts to this. One is think about historically who had all the benefits from a Mediterranean diet and who was following it. They were farmers, fishermen, herders, people who were active 6, 7, 8 up to 10 hours a day. I would love to have that much activity but I don’t have the time. I’m trying to get 7, 8, to 10 hours a week. I don’t get that every day. One, we have to modify it for the glycemic load because we don’t have as much activity as we saw back in the 1950s, 1960s when this study was first studied. The other aspect is in the Epic trial, there was this big trial in Greece looking at the Mediterranean diet. They looked at which components had the biggest benefit and which had the least. It turns out the grains had the least benefit of following any part of the Mediterranean diet. To me, it’s the glycemic load.
They broke it down into this other analysis they looked at, if you follow my Mediterranean diet and you had a low-glycemic version, you’ve got far more health benefit and better blood sugar or cholesterol response, better weight loss. That’s the twist for me is a low-glycemic, low sugar load version of a Mediterranean diet. There are still lots of vegetables and fruits but the grain portions are smaller or you can cut them out. I encourage people to avoid flour because it has such a high glycemic response. Sugar would be a rare treat because sugar feeds inflammation, abnormal blood sugar control. We’re supposed to eat fresh fruit for dessert, not some sugary confection.
You give people the option to either eliminate grains or the serving size. We’re talking about whole grains, correct?
Yes, only whole grains. Anybody who’s gluten-sensitive should have nothing to do with gluten.
The serving portion is smaller.
We’re talking a half cup of whole grain. Pasta is an appetizer in Italy. It’s not the main course. You don’t have a platter of it. You get 3, 4 tops, 5 little twirls on a fork and that’s it. Then you go on and eat your vegetables and protein for the main course.
I have a friend here in New York City. He’s of Italian descent. He’s born and raised in Italy and he has an Italian restaurant here in New York City. The restaurant’s called Etcetera Etcetera. He serves incredible gluten-free pasta that he makes in his kitchen there. His serving of pasta comes on a pretty much smaller than the palm of your hand. It’s delicious and it’s satisfying. I’m of Italian descent and I’ve eaten with my family in Italy. It warms my heart that there are people like us out there who understand how food can be beautiful and healthy and how it should be served because it’s part of your family and your culture, it’s a wonderful experience. I’m sitting down, I’m building my plate out. I have the option according to Dr. Steven Masley, to either eliminate grains or my grains can be less than half a cup, ideally whole grains, gluten-free if you have gluten intolerance or if you have celiacs. You’re also saying that beans can be there too because they help buffer the glycemic load. Lots of fruits and vegetables. Do you limit the fruit servings at all based on glycemic load?
After a meal, a cup of berries or most of the fruit do have a low-glycemic load. If you’re talking a one-cup portion, 0 to 10 is considered low and a cup of watermelon is 4 or 5. Almost all the melons are 4 or 5. An apple, pear, apricot, peach is low. Berries are usually the best. They have the lowest glycemic load and the most fiber and nutrients. Potato is the only vegetable I would limit. If people do eat potatoes, it should be the little ones with the skin on and you boil them because that gives them a lower glycemic load. Even if you refrigerate them before you eat them, it’s even lower. Mostly I tend to avoid the potatoes and greens and reds. The color is the critical part. Your plate should be beautiful and colorful and I would say at least have a two-cup portion of vegetables with lunch and dinner every day. That’s an essential part of a Mediterranean diet. They eat so many vegetables that we don’t have that quantity by any stretch.
That’s the bizarre key portion of the plate and their culture in general. They crave vegetables where we’ve taught people to crave sugar.
Animal protein portions are smaller. We’re talking 3, 4, not more than 5-ounce portions of fish or poultry. It’s not like a 12 to 16-ounce steak that you might see here. They would think that was for an entire family. It would never occur to them that was for one person.
We should talk about red meat specifically. We talked about seafood. If you’re increasing your seafood then other types of meat are going to decrease. What about red meats specifically? There’s lots of controversy around that.
Traditionally, they only eat it if a couple of times a month. It’s not part of their culture. It’s not that they’d never have it, they do, but it’s not like a daily or even a weekly event. When they do, it’s raised on a smaller farm. It’s local. It didn’t come from a feedlot where it was given hormones, pesticide, enriched grains and herbicide enriched plants. It’s not organically certified but it was organically raised on a small puddle land and it ran around and free-range and then it shows up in the market someday. It’s clean and they would have it on occasion to celebrate with. When they use red meat, it’s more of a flavoring. They might put a little bit of bacon with their green beans or something. They don’t have a huge slab. It’s quite a different use of animal protein than we do.
Almost look at it like a condiment.
Red meat is more of a condiment. You’ll see poultry and seafood often.
Nuts and seeds can be healthy snacks for people.
It’s very common to see people eating nuts and seeds. Olives and nuts are the most common snacks you would see people eating.
Talk to us about olive oil. It’s interesting when you look at FDA regulations and recommendations that we can make regarding olive oil here in the United States versus what they can do in Europe are quite different. How many servings of olive oil should someone include in their diet on a modified or a Mediterranean diet? What are some of the benefits of that?
In the pre-med study that was this heart cognitive weight loss, different versions of looking at the study, they gave them up to a liter per week. Generally, we’re talking anywhere from 2 to 4 up to 6 tablespoons of olive oil per person per day. I tend to think of about a tablespoon per person per meal is a portion that I would use in my recipes. They don’t cook with it at high heat. You’re using medium-low heat because if high heat, that oil gets damaged and you lose some of the beneficial properties. It turns bitter as well, so it doesn’t taste as good. Important to use low heat cooking with olive oil. If you’re going to do high heat cooking, you should use a different oil like avocado oil, almond oil or something else.
Two tablespoons of olive oil at a sitting, at your meal.
On your salad, there’s going to be a tablespoon of olive oil per person and maybe a teaspoon of vinegar. A table of olive oil drizzled over your vegetables and better being served with the same meal.
How do you respond to people with regards to lots of oils but olive oil specifically is the one that we’re talking about when they say, “That’s still processed food. If you have heart disease, you shouldn’t have any type of processed oil. If you’d like to eat a whole olive, that’s okay, but not olive oil.”
It doesn’t match the facts. When you look at what’s been published and randomized clinical trials, olive oil improves your cholesterol profile, blood sugar, blood pressure, decreases your cancer risk, lowers inflammation and has been shown to reduce your risk for heart attacks and strokes. In people following an American Heart Association Diet or a Mediterranean diet where they added extra olive oil, it lowered their rate of heart attacks and strokes. It improves their cognitive performance and it helped them lose weight. That’s what’s proven. I can’t help what people say and share. It’s hard to discredit olive oil. To me, if you squeeze it once and the oil comes out of the olive, that’s extra virgin. If you have to use heat and chemicals to get it out, that would be regular olive oil. That is processed. I do ask people to avoid what I call processed olive oil, which was something beyond mechanical pressing it. If you’re putting chemicals in it to pull out more oil, you’ve gone over the top.
Steven, you and I are out to dinner. We’re sitting down, we’re having this wonderful, beautiful Mediterranean meal. I’ve got two cups of vegetables. I’ve got some berries sprinkled on there. I’ve got some gluten-free grains. There are some beans on the salad as well. I’m having a nice piece of cold-water fish. I love fish and seafood. I eat it up to five times a week. Do I get to order wine if we’re eating together?
Yes. It should be red wine. Red wine has more medicinal benefits than white wine. Beer and hard liquor don’t have any medicinal benefits. I would say they’re more harmful than beneficial. The only alcohol I can recommend to people is red wine. The first thing we do when we sit down at that table is they’re going to give us a bottle of water. The only question is sparkling or flat. We’re going to have a bottle of water and then we’re going to get a glass or two of red wine. It’s not like we each get a bottle of red wine and we get to drink it. That’s overdoing it. The wine part does have to be in moderation than the benefit.
How big is a glass in those times?
Four and a half ounces per serving or five servings per 750 mil bottles. That’s 150 mils.
Some of our wineglasses nowadays, you can pour a whole bottle in the glass. I’ve seen people do that.
Instead of a glass, I should say a serving and specify what a serving is.
Talk to us about dairy. There are lots of intolerances out there and people are aware of these intolerances. They may or may not show up with trying out a Mediterranean diet.
Europeans and Mediterranean use dairy on a regular basis. It’s mostly a garnish. They sprinkled a little crumbled on there. They’re not large portions and they’re using minimally processed heavily probiotic-rich dairy products like Kefir or plain yogurt. When you buy yogurt in Europe, it’s mostly plain. In the US, the yogurt section is 30 feet long and it’s twenty brands with different sugar and fruit added to them, flavorings and processed stuff. I always ask my patients which has more sugar in it, yogurt with fruit or ice cream? They look at me like, “This is a trick question.” They knew it because I’m asking them. Its yogurt. It should be plain, no sugar added or skip it.
The type of dairy they eat is they don’t drink milk. They don’t put much milk in their coffee. When they use dairy, it’s either Kefir which is very probiotic-rich, plain yogurt or a little cheese grated on a dish. It’s Camembert or blue or it’s probiotic-rich. If you’re dairy intolerant then avoid it. Don’t eat dairy if it bothers you. Some people will give them all sorts of symptoms and joint aches and mucus. I would say, most people are not probiotic, dairy intolerant. They can eat plain yogurt. They can eat a little bit of garnish cheese on a dish like blue cheese or something. It’s not going to bother them and it’s nutrient-rich. That’s how it’s used in Europe. Very different than when we put these huge slabs or serve lasagna with pounds of cheese in it. They don’t do that. There’s quite a contrast in how they use dairy and how we use dairy.
They don’t have fluorescent yellow cheese either. Somehow, we have fluorescent yellow cheese in America. Whenever I counsel people on nutrition and we’re talking about the dairy aspect, the first thing they say is, “What am I going to use in my coffee? I use milk in my coffee.” If you think of the Mediterranean diet, I love visiting Spain because in Spain they have something called a Cortado, which is a single shot of espresso with a little bit of steam milk on top. It’s delicious. It gives you the caffeine fix but you’re not eating or drinking eighteen ounces of processed dairy, which can be harmful to some people. Steven, how many books have you written now on nutrition?
This is my seventh book now.
This is the first one where they put in pictures. The pictures came out nice. I was like, “These are awesome pictures.” They’re my favorite Mediterranean recipes and some photos to go with it.
Tell us what you hope will happen with this seventh book on the Mediterranean diet versus the six before it.
We could have a large-scale conversion here. Right now, we have a very small percent of the population following the Mediterranean diet. We know that regardless of your genetics or ethnicity health situation, we know if you add a Mediterranean diet, you’re going to decrease your risk for heart disease, for memory loss. It helps you lose weight. You feel better, it’s delicious food and it’s easy to follow. This is a chance to transform the health of America now. The closer we follow a Mediterranean diet, the better our health is going to be. We’re at a tipping point where so much of our food supply is processed and chemicals. Not the things that you would promote. I know I follow bunched and followed it for years. This is a realistic eating plan people could follow. I hope to spread the word and make it easy for people to eat healthy food, love it, delicious and stick with it long-term.
Talking or thinking about dietary recommendations as we head into 2020, there should be new USDA Dietary recommendations coming out. The current ones at times mimic a Mediterranean diet, but have never arrived there. Do you think we’ll see them move closer toward it? What should someone be cognizant of with our current USDA?
Remember, USDA food pyramid is designed to market US food products. It’s not designed to promote health. That’s the disconnect. People think this is what we’re supposed to recommend. No, they’re out-marketing US farmer products. They’re marketing things like sugar, sodas and grains that we produce as an economy. They’re boosting GNP and destroying the health of Americans at the same time. I have my own food pyramid in here and the grains are not at the bottom of it. It’s fruit and vegetables. The bottom of the pyramid for me is the lifestyle that goes with it. It’s the activity, the cooking, being active, being outdoors with nature and communicating being with other people. Especially over food, not eating in front of a computer, television or smartphone. It’s connecting with people over food. That’s the essential lifestyle part. To me, that’s the base of what the new food pyramid should be. I don’t expect the US food pyramid to get it. I’m not waiting for a change from them.
A little change will happen but we can keep our toes, fingers and ear lobes crossed for that. It’s interesting as you mentioned as the GDP is going up, people’s health is going down. Why they don’t see that inverse relationship and look across the pond and see all these countries that are eating this diet and quite frankly have a longer life expectancy. We’re looking at populations of people now in America that will have shorter life expectancies than potentially we have.
They don’t live 5, 6, 7 years longer. Their health span where they’re independent and active is more than a decade longer. The biggest difference isn’t how long they live, but how long they live well vibrantly. They’ve got more than a decade on us.
I have parents that are getting older and we have the Baby Boomers are the fastest-growing segment of our population. Talk to us about that. Let’s say what those last two months should look like in life versus potentially with some of the last 10 to 20 years look like for people.
In our ’90s, we should still be active in working part-time because we need something to do. We’re not disabled, we’re not in pain. We feel good each day. Do we have some health issues at 95? Probably, but not that it keeps us from going to the market, shopping, coming home, cooking food and having a joyous evening with family and working still. There’s nothing to stop any of that except for ourselves.
Holidays have passed and people may be looking back and saying, “My diet is not good. I over-indulge, I ate too much.” What can someone start to do to shift toward your Mediterranean diet?
I would look at some of the recipes in here. I’ve made it simple. I’ve got a special offer for your list. If they pre-ordered the book or buy it in the first month that’s out, I have cooking classes to give them to make it easier to follow some of these recipes. What are the tips that you can get? I’ll send you a link that you could put up and they can get my cooking classes to go with the book. That would be so helpful to what are the key points when you’re preparing food that you follow these steps. It makes it easier to cook, more delicious, more nutritious, and your family and friends will love it. That’s what I would like to offer. Some little tips and tricks that make it simpler to prepare meals. That’s something I got from traveling the Mediterranean. Don’t make it over complicated. Don’t add too many ingredients. Simple can be better when it comes to good quality food.
Five simple, delicious, healthy ingredients can make a wonderful meal.
It doesn’t have to be hard.
What I love about your approach is you’re a physician. You’re bringing a medical approach to this with you being a nutritionist. You’re also a chef. It’s a wonderful combination of all three that always winds up in your books. Can you tell us a healthy dessert that we might find in that book of yours back there? People want to feed their sweet tooth at times, which is understandable, but something that can be healthy and not damage that glycemic response.
There are a few choices. The simplest thing we would get often would be fruit. It’s either berries or melon or something and they might put it in a glass and then they pour a little sweet wine on it, a couple of tablespoons and a little bit of mint. It takes you two minutes to prepare that. It’s so easy. Dark chocolate is very popular in the Mediterranean and they’ll frequently have dark chocolate at least 75%, preferably 80% cocoa, not milk chocolate. They’ll have that for dessert. I even have a blueberry ricotta cheesecake in here. It’s an Italian version with plain ricotta, orange rind and blueberries. That’s a huge variety of things you can make that are for dessert that is still flavorful and healthy.
I recommend everyone to check out Dr. Masley’s book, The Mediterranean Method. Steven, tell everyone how they can learn more about you, about the book and all the great things you have to offer.
They can go to my website, DrMasley.com. I’ve got a blog and pre-recipes. I have a variety of information there that I’m happy to share with people that are free to help them transform their health.
Make sure to check out www.DrMasley.com. Make sure to download his free cooking tips. Check out his book, The Mediterranean Diet. A modified Mediterranean diet is the diet that I recommend for people. Most of the time, we have chronic pain, so make sure to check it out and check out his book. I want to thank Dr. Masley for being on the Healing Pain Podcast. Once again, we appreciate his time and work. We’ll see you all next week.
- The Mediterranean Method
About Steven Masley
Steven Masley, MD is a physician, nutritionist, trained-chef, best-selling author, and the creator of the #1 all-time health program for public television.
His work has been viewed by millions on PBS, the Discovery Channel, and over 700 media interviews. His latest book is titled: The Mediterranean Method.
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Bacteria are the oldest and most abundant organisms on Earth. They are also the ones that most easily adapt to environmental conditions and have an unsurpassed ability to coexist with other living beings, including us.
More than 1000 species of microorganisms (mostly bacteria, but also viruses, protozoa, archaea and fungi), exceeding by ~10 times the number of cells in the adult body, live within our gastrointestinal (GI) tract. This microbial collection, known as the gut microbiome, co-evolved with humans -and all animals- over thousands of years resulting in a mutually beneficial relationship.
Bacterial colonization of the gut happens at birth, and is shaped in the first few years of life under the influence of several factors including delivery (vaginal or Caesarean section), whether breastfed or formula fed, weaning, diet, antibiotic use, infections, and stress (1). The composition of gut bacteria remains quite constant in each of us, and tends to be similar within families, among close friends, and in people that live together (2). However, diet, exercise, stress, mood changes, disease, and environmental exposure to pathogens and contaminants can all modulate the balance of gut microbes and tilt the scale between disease and health (3).
Gut Bacteria: New Best Friends Against Pain?
It has long been known that specific groups of intestinal bacteria are over- or under-represented in people with painful GI conditions such as irritable bowel syndrome (IBS) and inflammatory bowel disease (IBD). However, only in the last few years the role of gut bacteria in pain regulation did become a hot topic of research. For instance, early this year, two separate studies (reviewed here and here) revealed that the gut microbiome profiles from people with widespread chronic pain (fibromyalgia) differed from those of healthy controls (including siblings and close relatives) (4, 5), prompting speculation about whether specific gut bacteria can ‘remotely’ trigger pain.
This 2-part blog series will explore what is known so far about the mechanisms by which gut microbiota alterations may trigger pain in the GI tract and elsewhere, and influence pain processing by the brain.
Gut Microbiota and Visceral Pain
It is now well established that alterations in the gut microbiota – gut dysbiosis- contribute critically to the development of GI disorders such as IBS, IBD, celiac disease, and food allergies (6, 7). Interestingly, a 2017 study in mice suggests that these conditions do not emerge suddenly, but result from modest, repeated insults that end up disabling the host’s defenses against inflammation. Their research showed that minor, recurrent infections caused by food poisoning reduce the levels of intestinal alkaline phosphatase – the enzyme that detoxifies LPS (endotoxin) the most abundant pro-inflammatory bacterial toxin. This effectively unmasks the pathogenic potential of commensal Gram negative bacteria and promotes chronic inflammation, colitis, and eventually IBD. Notably, the study showed that the heightened pro-inflammatory state of intestinal tissue persisted long after the initial infection was resolved by the host’s immune response (8).
In turn, animal studies and clinical trials in humans confirmed that gut microbes are important modulators of visceral pain that results from the above conditions (9). Many insights into gut microbiota properties and functions come from research on mice born and bred under strict sterile conditions that prevent bacterial growth in any part of the body. A study showed that these “germ-free” mice develop visceral hypersensitivity (hyperalgesia), and this can be reversed by colonization with normal microbiota from control mice. Moreover, germ-free mice showed volumetric changes in brain areas related to pain processing (e.g. anterior cingulate cortex and periaqueductal grey) that were also reversed by replenishment of gut bacteria from conventionally-bred mice (10). It is becoming clear, however, that the nature of pain also determines the influence that gut bacteria have on pain perception; illustrating this point, studies showed that germ-free mice experienced less pain, compared to normal mice, when exposed to LPS, carrageenan (a red seaweed extract), or pro-inflammatory cytokines (11).
Other studies, both in mice and humans, suggested that depletion of gut bacteria by antibiotics early in life may predispose to more intense and long-lasting visceral pain and disorders like IBD later in life, and stressed the benefits of probiotics and prebiotics for symptom reduction (9, 12, 13). Conversely, research showed that transplantation of fecal microbiota from IBS patients reproduced disease symptoms in rats (14).
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Antibiotics, a Double-Edge Sword
Broad-spectrum antibiotics eliminate not only pathogenic bacteria, but deplete also microbes that ferment butyrate and other essential, fiber-derived small-chain fatty acids (SCFAs) needed to maintain microbial homeostasis. In the absence of butyrate, gut metabolism is halted, mitochondrial beta-oxidation in colonocytes becomes disabled, and increased oxygen levels reach the GI lumen. The colon is essentially an oxygen-free (anaerobic) environment, populated by benign obligate anaerobes (mainly Firmicutes and Bacteroidetes). In the presence of oxygen, pathogenic facultative anaerobes such as E. coli outcompete the colon’s normal bacteria, leading to immune activation, inflammation, and manifestations of GI disease (3).
Stay Tuned… In the second part of this blog series we will talk about the gut microbiota-brain-axis, and how signals released by gut microbes affect pain processing in the brain.
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1- Thursby, E., & Juge, N. (2017). Introduction to the human gut microbiota. The Biochemical journal, 474(11), 1823–1836. doi:10.1042/BCJ20160510
2- Brito, I.L., Gurry, T., Zhao, S. et al. Transmission of human-associated microbiota along family and social networks. Nat Microbiol 4, 964–971 (2019) doi:10.1038/s41564-019-0409-6
3- Hills, R. D., Pontefract, B. A., Mishcon, H. R., Black, C. A., Sutton, S. C., & Theberge, C. R. (2019). Gut microbiome: profound implications for diet and disease. Nutrients, 11(7), 1613.
4- Minerbi, A., Gonzalez, E., Brereton, N.J.B., Anjarkouchian, A., Dewar, K., Fitzcharles, M-A., Chevalier, S., Shir, Y. (2019) Altered microbiome composition in individuals with fibromyalgia. Pain, Jun 18.doi: 10.1097/j.pain.0000000000001640 / PMID: 31219947
5- Clos-Garcia, M., Andrés-Marin, N., Fernández-Eulate, G., Abecia, L., Lavín, J. L., van Liempd, S., … Falcón-Pérez, J. M. (2019). Gut microbiome and serum metabolome analyses identify molecular biomarkers and altered glutamate metabolism in fibromyalgia. EBioMedicine, 46, 499–511. doi:10.1016/j.ebiom.2019.07.031
6- Zuo, T., & Ng, S. C. (2018). The Gut Microbiota in the Pathogenesis and Therapeutics of Inflammatory Bowel Disease. Frontiers in microbiology, 9, 2247. doi:10.3389/fmicb.2018.02247
7- Iacob, S., & Iacob, D. G. (2019). Infectious Threats, the Intestinal Barrier, and Its Trojan Horse: Dysbiosis. Frontiers in microbiology, 10, 1676. doi:10.3389/fmicb.2019.01676
8- Yang, W. H., Heithoff, D. M., Aziz, P. V., Sperandio, M., Nizet, V., Mahan, M. J., & Marth, J. D. (2017). Recurrent infection progressively disables host protection against intestinal inflammation. Science, 358(6370), eaao5610.
9- Pusceddu, M. M., Murray, K., & Gareau, M. G. (2018). Targeting the microbiota, from irritable bowel syndrome to mood disorders: focus on probiotics and prebiotics. Current pathobiology reports, 6(1), 1-13.
10- Luczynski, P., Tramullas, M., Viola, M., Shanahan, F., Clarke, G., O’Mahony, S., … & Cryan, J. F. (2017). Microbiota regulates visceral pain in the mouse. Elife, 6, e25887.
11- Amaral, F. A., Sachs, D., Costa, V. V., Fagundes, C. T., Cisalpino, D., Cunha, T. M., … & Vieira, L. Q. (2008). Commensal microbiota is fundamental for the development of inflammatory pain. Proceedings of the National Academy of Sciences, 105(6), 2193-2197.
12- Verdú, E. F., Bercik, P., Verma-Gandhu, M., Huang, X. X., Blennerhassett, P., Jackson, W., … Collins, S. M. (2006). Specific probiotic therapy attenuates antibiotic induced visceral hypersensitivity in mice. Gut, 55(2), 182–190. doi:10.1136/gut.2005.066100
13- Kronman, M. P., Zaoutis, T. E., Haynes, K., Feng, R., & Coffin, S. E. (2012). Antibiotic exposure and IBD development among children: a population-based cohort study. Pediatrics, 130(4), e794–e803. doi:10.1542/peds.2011-3886
14- Crouzet, L., Gaultier, E., Del’Homme, C., Cartier, C., Delmas, E., Dapoigny, M., … & Bernalier‐Donadille, A. (2013). The hypersensitivity to colonic distension of IBS patients can be transferred to rats through their fecal microbiota. Neurogastroenterology & Motility, 25(4), e272-e282.
When we think about bacteria, unpleasant things like cavities, infections and disease usually come to mind. In reality, our relationship with microbes is far more complex and interesting. Microorganisms thrive in our bodies, both inside and out, and co-evolved with humans over thousands of years as essential partners in health and disease.
Gut Microbiota: The World Within
About 100 trillion microbes live within the human gastrointestinal tract, the largest interface between the body (200-400 m2) and the external environment. This assembly, known as the gut microbiota, contains mostly bacteria (between 500 and 1,000 species), but also viruses, fungi, and protozoa. Scientists have identified a large set of unique bacterial genes (the microbiome) that exceeds by more than 100 times the number of genes (23,000) that comprise the human genome (1) This is why the gut microbiome is considered our “second genome”.
The composition of gut bacteria is inherited at birth, but afterwards is heavily influenced by lifestyle factors (diet, exercise, stress, environmental exposures) (2). Every individual has a unique mix of species, most of them innocuous, and some potentially harmful, that define a symbiotic relationship that is vital to normal health.
Gut Microbiota in Health
Main benefits of a normal gut flora include regulating energy production and use, protecting against pathogens, modulating the host’s immune response, and preserving the integrity of intestinal cells (3).
Gut bacteria produce enzymes that assist in the breakdown and absorption of foods. Bacterial enzymes help degrade proteins into absorbable amino acids, and facilitate production and transport of vitamins and minerals into the blood to be distributed to cells. Importantly, colonic bacteria are responsible for fermenting indigestible dietary polysaccharides (fiber) and, to a lesser degree, also proteins, into short-chain fatty acids (SCFAs) like acetate, butyrate, and propionate. Bacterial SCFAs induce insulin secretion, thus helping maintain glycemia over time, and promote satiety by activating hormonal secretions in specialized enteroendocrine (L) cells. SCFAs are also used as fuel by colonic bacteria; during dietary fiber deficiency, they feed instead on protective mucins secreted by intestinal cells, leading to erosion of the mucus barrier (4).
A diverse and balanced gut flora prevents colonization by pathogenic bacteria and viruses that damage the gut epithelium and induce inflammation. It also protects against environmental toxins (dust, pollen, chemicals) by triggering immune responses to neutralize their effects (5).
Gut Microbiota in Disease
Dysbiosis (or dysbacteriosis) refers to the alteration in the composition of microbial populations within the body, and is a characteristic feature of many metabolic diseases (6). A common cause of dysbiosis is the prevalence of a high fat/high sugar “Western diet” and a sedentary lifestyle (see below).
Antibiotics can also alter the balance of bacterial populations in the gut. Most conventional antibiotics indiscriminately kill or prevent the growth of both pathogenic and beneficial microbes, favoring expansion of opportunistic pathogens (7).
It has been known for some time that changes in the gut microbiota can affect the metabolism and effectiveness of therapeutic drugs (8). Recent evidence now shows that non-antibiotic drugs can also impede the growth of some bacterial strains, and facilitate antibiotic resistance (9).
Dysbiosis of the gut microbiota has been linked to intestinal disorders such as inflammatory bowel disease, irritable bowel syndrome (IBS), coeliac disease, and extra-intestinal disorders including autoimmune conditions (autoimmune hepatitis, type 1 diabetes, spondyloarthritis, multiple sclerosis and rheumatoid arthritis), allergy, asthma, metabolic syndrome, cardiovascular disease, obesity, and cancer. Colonic cancer, for instance, has been linked to protein fermentation by pathogenic bacteria following excessive consumption of red meats (10, 11).
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Gut Microbiota, Systemic Inflammation, and Obesity
Perhaps the most direct example of the influence of gut dysbiosis on human disease is found in obesity. A high fat/high carb diet unfavorably alters the gut microbial composition, leading to increased intestinal permeability. This facilitates the transfer to the blood of bacterial lipopolysaccharides (LPS, also called endotoxin), the major glycolipid component of the outer membrane of gram-negative bacteria, which make up ~70% of the total bacteria in the gut. This causes metabolic endotoxemia, a condition characterized by a pro-inflammatory and pro-oxidant environment, often observed in obesity, that results from endotoxin-mediated activation of Toll-like receptor 4 (TLR4) on the surface of immune cells and other cell types (e.g. skeletal muscle, adipocytes, and liver cells) (12, 13).
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How Diet Shapes The Human Gut Microbiota
In healthy individuals, the gut microbiota is dominated by two bacterial lineages (phyla), i.e. Bacteroidetes and Firmicutes, that compete for shared nutritional resources (14).
- Research in mice showed that a high fat diet increased the proportion of Firmicutes relative to the more beneficial Bacteroidetes, and this finding was confirmed in patients with obesity or diabetes. The reason behind this population switch is that different microbes thrive on different carbon sources. Bacteroidetes ( Bacteroides, Alistipes, Parabacteroides, and Prevotella), for instance, mostly use glycans (complex polysaccharides, i.e fiber) as fuel. Thus, people following plant-based (carbohydrate) diets have higher representation of Prevotella bacteria in the gut.
- In contrast, Firmicutes (Bacillus, Listeria, Staphylococcus, Streptococcus, Enterococcus, and Clostridium) can more easily exploit a larger variety of nutrients (amino acids, sugars, fatty acids) and their growth is positively correlated with caloric intake (15).
- High fat/high carb diets, on the other hand, were shown to stimulate the growth of Proteobacteria, another prominent phylum of bacteria found in the gut. This group includes a wide variety of pathogens such as Escherichia, Salmonella, Vibrio, Helicobacter, and Yersinia. These are actively fought by the immune system, but under permissive conditions such as a high fat/high carb diet, they can overrun the body’s defenses and contribute, through endotoxemia and inflammation, to a range of human diseases (14, 16).
Prebiotics and probiotics are commonly used to modulate the composition of bacterial communities in the gut. Prebiotic fibers are present in a several foods such as whole grains, fruits, root vegetables, and legumes, and are used to promote the growth of beneficial bacteria. Probiotics consist of live bacteria and yeast and are found in fermented foods such as yoghurt, kefir, sauerkraut, and tempeh. They are used to treat diarrhea, constipation, and some intestinal disorders, and to replenish gut flora after antibiotic use (17).
Nourish Your Gut
As you’ve seen, a balanced gut flora helps ensure adequate digestion, assimilation, defense and repair of a strong immune system. However, its benefits go well beyond. In future blogs we’ll discuss how nutrition, physical activity and exercise can help create an optimal gut microbiota environment, and how this changes over the course of chronic disease.
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1- Pasolli, E., Asnicar, F., Manara, S., Zolfo, M., Karcher, N., Armanini, F., … & Collado, M. C. (2019). Extensive unexplored human microbiome diversity revealed by over 150,000 genomes from metagenomes spanning age, geography, and lifestyle. Cell, 176(3), 649-662.
2- Rothschild, D., Weissbrod, O., Barkan, E., Kurilshikov, A., Korem, T., Zeevi, D., … & Shilo, S. (2018). Environment dominates over host genetics in shaping human gut microbiota. Nature, 555(7695), 210.
3- Thursby, E., & Juge, N. (2017). Introduction to the human gut microbiota. The Biochemical journal, 474(11), 1823–1836. doi:10.1042/BCJ20160510
4- Koh, A., De Vadder, F., Kovatcheva-Datchary, P., & Bäckhed, F. (2016). From dietary fiber to host physiology: short-chain fatty acids as key bacterial metabolites. Cell, 165(6), 1332-1345.
5- Bäumler, A. J., & Sperandio, V. (2016). Interactions between the microbiota and pathogenic bacteria in the gut. Nature, 535(7610), 85–93. doi:10.1038/nature18849
6- Gagliardi, A., Totino, V., Cacciotti, F., Iebba, V., Neroni, B., Bonfiglio, G., … & Schippa, S. (2018). Rebuilding the gut microbiota ecosystem. International journal of environmental research and public health, 15(8), 1679.
7- Francino M. P. (2016). Antibiotics and the Human Gut Microbiome: Dysbioses and Accumulation of Resistances. Frontiers in microbiology, 6, 1543. doi:10.3389/fmicb.2015.01543
8- Enright, E. F., Gahan, C. G., Joyce, S. A., & Griffin, B. T. (2016). The Impact of the Gut Microbiota on Drug Metabolism and Clinical Outcome. The Yale journal of biology and medicine, 89(3), 375–382.
9- Maier, L., Pruteanu, M., Kuhn, M., Zeller, G., Telzerow, A., Anderson, E. E., … Typas, A. (2018). Extensive impact of non-antibiotic drugs on human gut bacteria. Nature, 555(7698), 623–628. doi:10.1038/nature25979
10- Singh, B., Qin, N., & Reid, G. (2015). Microbiome regulation of autoimmune, gut and liver associated diseases. Inflammation & Allergy-Drug Targets (Formerly Current Drug Targets-Inflammation & Allergy), 14(2), 84-93.
11- Carding, S., Verbeke, K., Vipond, D. T., Corfe, B. M., & Owen, L. J. (2015). Dysbiosis of the gut microbiota in disease. Microbial ecology in health and disease, 26, 26191. doi:10.3402/mehd.v26.26191
12- Cani, P. D., Amar, J., Iglesias, M. A., Poggi, M., Knauf, C., Bastelica, D., … & Waget, A. (2007). Metabolic endotoxemia initiates obesity and insulin resistance. Diabetes, 56(7), 1761-1772.
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Nutrition impacts our health in multiple ways, and the current epidemic of obesity and diabetes provide direct, overwhelming proof of how poor nutrition can precipitate disease.
Not surprisingly, research is showing that dietary habits and lifestyle also influence the course of neurological conditions such as multiple sclerosis (MS), where other environmental and genetic factors seem to bear more weight (1, 2).
MS is a potentially disabling condition in which nerve fibers progressively lose the protective myelin sheath that surrounds them. This results in weakness, decreased motor coordination, impaired mobility and ambulation, and fatigue. While the exact causes are unknown, epidemiologic evidence points to a combination of autoimmune mechanisms, genetic factors, and lifetime environmental exposures associated with infections and inflammatory reactions. Nutrition has been signaled as a possible co-factor in MS by influencing the inflammatory cascade and changes in the gut microbiota (3, 4).
While basic research continues to unveil the molecular events that underlie MS, the potential benefits of dietary interventions are also being explored with the goal of improving the quality of life of people with MS.
How Can Nutrition Improve Function in Multiple Sclerosis?
A recent 2019 study appearing in The International Journal of MS Care and conducted by physical therapists at The State University of New York at Buffalo evaluated the associations between nutrition and ambulation, daily activity, quality of life (QOL), and fatigue in MS patients with mild-to-moderate disability (5).
The study included 20 individuals (14 women and 6 men; mean age: 57.9 years) with a mean time since MS diagnosis of 18.4 (range, 3–39) years. They presented a mean Expanded Disability Status Scale (EDSS) score of 4.1 (range 1.5-6.0), denoting mild-to-moderate disability. Eligible patients had no diabetes, inflammatory bowel disease, or dysphagia, and had not experienced active disease relapse within the past 30 days. All the outcome measures were collected on 2 different days separated by a minimum of 1 week.
Functional tests included:
- 6-Minute Walk Test (6MWT). It measures the distance that patients can cover within 6 minutes by walking as fast as they safely could.
- Timed 25-Foot Walk Test (T25FW). It measures the time it takes participants to “walk as quickly as possible but safely” to cover a distance of 25 ft.
- TUG Test. It measures the time it takes participants to rise from a chair at the word “go,” walk as quickly as possible but safely to a mark 10 ft away, turn around, walk back, and sit down again.
- Physical activity (mobility and energy expenditure) was measured using an accelerometer worn over the dominant hip for 7 days.
- Body Fat Percentage was calculated from bioelectrical impedance measurements on a segmental body composition monitor.
- 36-item Short Form Health Survey (SF-36): The self-administered SF-36 survey measures Quality of Life using eight subscales: physical functioning, role limitations due to physical problems, bodily pain, general health perceptions, vitality, social functioning, role limitations due to emotional problems, and mental health.
- 12-Item Multiple Sclerosis Walking Scale (MSWS-12). This self-report scale assesses patients perceptions of their walking ability during the previous 2 weeks.
- Modified Fatigue Impact Scale. This self-report survey measures the impact of fatigue on a patient’s daily life in terms of physical, cognitive, and psychosocial functioning.
Items 5 to 8 (biometric data and self-reports) were assessed on day 1 of the study, and items 1 to 4 (physical tests) on day 2. Potential associations between nutrient intake and physical/functioning outcomes were assessed by cross-analyzing responses to the tests above with two dietary assessments delivered on day 1 and returned by patients on study day 2:
- Three-Day Food Diary (3-DFD). Respondents were asked to record the type and amount of consumed products, dishes, and beverages at the time of consumption on 3 consecutive days (including 1 weekend day). To standardize reporting, participants were given specific instructions on how to appropriately record food and portion size.
- Food Frequency Questionnaire (FFQ). The FFQ collects information about food consumption over a specified period of time. Participants were asked to quantify the frequency (daily, monthly, yearly) of their intake over the past 12 months using standardized serving sizes of 116 food items
The overall analysis showed that consuming more fats than carbs was associated with improved physical performance and QOL in people with mild-to-moderate MS; in contrast, consuming high carb diets had a negative impact. Also, in line with previous research, the 3-DFD revealed that ingestion of cholesterol and some micronutrients (iron, magnesium, and folate) correlated with better ambulation, daily function, and QOL in both the SF-36 and during functional tests (6).
The finding that diets with higher fat contents may help MS patients perform better physically somewhat conflicts with previous reports. Swank and Goodwin, for instance, reported in 2003 on 150 MS patients who followed a low-fat diet for over 30 years, concluding that diets low in fats were associated with reduced disease progression and mortality (7). Newer studies, however, also stress the benefits of reduced carbohydrate intake for MS.
Weighing down this controversy is the shift in dietary patterns that started about 20 years ago in the US. Namely, the substitution of fats (blamed for increased rates of inflammatory conditions, cardiovascular disease, and obesity) by carbs. As a consequence, the current US food pyramid consists of 50% carbs, a change that resulted in increased rates of inflammatory conditions, cardiovascular disease, and obesity.
So would MS patients be better off by largely avoiding fats, or carbs? The answer of course is no. As Harvard’s Nutrition Source points out “Cutting back on saturated fat will likely have no benefit, however, if people replace saturated fat with refined carbohydrates.”
High Fat, Low Fat, High Carb, Low Carb or Somewhere in the Middle?
To understand this issue, let’s briefly examine the mechanisms underlying the health effects of fats and carbs. There are clear distinctions within food types.
Saturated lipids (like meat fats, and trans fats from hydrogenated oils used to make margarines, frozen foods, chocolates, etc.) are solid at room temperature, are harder for our bodies to break down, and were shown to reduce the ability of cells to sense insulin and contribute to obesity, atherosclerosis, and coronary disease (although there is some controversy); in contrast, unsaturated (mono- and poly-unsaturated) lipids contained in olive oil, avocado, and nuts, are a mainstay of the Mediterranean diet and were shown to help control blood glucose levels and regulate blood pressure, among other health benefits (8, 9).
And something similar happens with carbohydrates. Simple carbs are sugar molecules (mono- or disaccharides), like glucose, fructose, and sucrose that are obtained by refinement of more complex foods (wheat, sugar cane, corn). They provide fast but short-lasted energy, and promptly stimulate insulin release to normalize their surging blood levels. Fast insulin peaks, however, quickly reduce blood glucose and triggers the release of hunger hormones, which may lead to overeating. Over multiple, continuous cycles, insulin secretion in the pancreas may become impaired and cells may also begin to fail to respond to it (insulin resistance). In both cases the excess glucose keeps stressing cells and tissues, leading eventually to chronic inflammation, metabolic dysfunction, and disease. Interestingly, studies show that decreased insulin sensitivity with postprandial hyperinsulinemia prevail in newly diagnosed, untreated MS patients with a low EDSS score, contributing to disability (10, 11).
In contrast, complex carbs (present in fruits, vegetables, whole rice, and grains) are made of long chains of sugar molecules (polysaccharides) chained together. These are broken down more slowly by our bodies, leading to a gradual rise in blood sugar, and a gentler and more sustained rise in insulin levels. Glycemic control is thus more easily achieved, reducing the risk of cellular stress. Diets rich in complex carbs and low in refined carbs, like the Mediterranean diet, were associated with both reduced odds of developing MS, and lower risk of cardiovascular disease in people with MS (12, 13).
When diets high in both saturated fats and refined sugars (simple carbs) combine, the usual consequence is obesity, which raises the risk for insulin resistance, metabolic syndrome (characterized by hyperglycemia, hyperlipidemia, high blood pressure, and elevated cholesterol), diabetes, and cardiovascular disease (14). Both childhood obesity, especially in girls, and type 2 diabetes have been associated with increased risk of developing MS (15, 16).
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Nutrition and MS: What Does the Evidence Show?
The energy that our cells derive from simple carbs is depleted fast, and this results in fatigue, decreased functional performance, and reduced physical activity. Conversely, free fatty acids provide longer-lasting energy output and reduce insulin responses. This may partly explain why increased fat, and not carbohydrate, consumption was associated with better ambulation and QOL in people with MS (5).
Based on these perceived benefits, the ketogenic diet has gained popularity among people with MS; this diet includes high-fat (~75%), low-carbohydrate (~5%), moderate protein (~20%), reduces the reliance on glucose for energy needs and has shown to be beneficial in other neurological conditions such as epilepsy, Alzheimer’s and Parkinson’s disease. More research is needed, however, to confirm its benefits in patients with MS (17).
Other dietary approaches that variously aim at controlling fat, carb, and micronutrient intake have shown to provide some benefits to people with MS (18, 19). These include the original low-fat Swanks diet and the newer Wahls diet. The latter, also known as the Autoimmune Protocol (AIP), is a modified version of the Paleo diet that allows healthy meats, including organ meats, seafood, most vegetables, fruits, fats, and fermented foods, and excludes grains and gluten, eggs, nuts, seeds, and nightshade vegetables (tomatoes, potatoes, eggplant, peppers). A recent study suggested that the AIP is a promising complementary strategy in the management of MS (20).
With different approaches available, defining the best dietary intervention for MS would require attention to each patient’s condition and specific nutritional deficits and needs. An upcoming clinical trial comparing the low saturated fat (Swank) and the modified Paleolithic (Wahls™) diets in their ability to improve symptoms and QOL in people with MS should provide renewed insight into best nutrition practices to manage MS (21).
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