Parasites and Diabetes

Gut Bacteria May Predict PTSD Risk

Gut Bacteria May Predict PTSD Risk

Summary: People with PTSD had lower levels of three different gut bacteria than individuals who experienced trauma but didn’t develop the disorder, a new study reports.

Source: Stellenbosch University.

The bacteria in your gut could hold clues to whether or not you will develop posttraumatic stress disorder (PTSD) after experiencing a traumatic event.

PTSD is a serious psychiatric disorder that can develop after a person experiences a life-threatening trauma. However, not everyone exposed to a traumatic event will develop PTSD, and several factors influence an individual’s susceptibility, including living conditions, childhood experiences and genetic makeup. Stellenbosch University researchers are now also adding gut bacteria to this list.

In recent years, scientists have become aware of the important role of microbes existing inside the human gastrointestinal tract, called the gut microbiome. These microbes perform important functions, such as metabolising food and medicine, and fighting infections. It is now believed that the gut microbiome also influences the brain and brain function by producing neurotransmitters/hormones, immune-regulating molecules and bacterial toxins.

In turn, stress and emotions can change the composition of the gut microbiome. Stress hormones can affect bacterial growth and compromise the integrity of the intestinal lining, which can result in bacteria and toxins entering the bloodstream. This can cause inflammation, which has been shown to play a role in several psychiatric disorders.

“Our study compared the gut microbiomes of individuals with PTSD to that of people who also experienced significant trauma, but did not develop PTSD (trauma-exposed controls). We identified a combination of three bacteria (Actinobacteria, Lentisphaerae and Verrucomicrobia) that were different in people with PTSD,” explains the lead researcher, Dr Stefanie Malan-Muller. She is a postdoctoral fellow in the Department of Psychiatry at the Faculty of Medicine and Health Sciences.

Individuals with PTSD had significantly lower levels of this trio of bacteria compared to trauma-exposed control groups. Individuals who experienced trauma during their childhood also had lower levels of two of these bacteria (Actinobacteria and Verrucomicrobia). “What makes this finding interesting, is that individuals who experience childhood trauma are at higher risk of developing PTSD later in life, and these changes in the gut microbiome possibly occurred early in life in response to childhood trauma,” says Malan-Muller. She collaborated with researchers from the University of Colorado Boulder on the study.

One of the known functions of these bacteria is immune system regulation, and researchers have noted increased levels of inflammation and altered immune regulation in individuals with PTSD. “Changes in immune regulation and increased inflammation also impact the brain, brain functioning and behaviour. Levels of inflammatory markers measured in individuals shortly after a traumatic event, was shown to predict later development of PTSD.

Image shows gut bacteria.

“We therefore hypothesise that the low levels of those three bacteria may have resulted in immune dysregulation and heightened levels of inflammation in individuals with PTSD, which may have contributed to their disease symptoms,” explains Malan-Muller.

However, researchers are unable to determine whether this bacterial deficit contributed to PTSD susceptibility, or whether it occurred as a consequence of PTSD.

“It does, however, bring us one step closer to understanding the factors that might play a role in PTSD. Factors influencing susceptibility and resilience to developing PTSD are not yet fully understood, and identifying and understanding all these contributing factors could in future contribute to better treatments, especially since the microbiome can easily be altered with the use of prebiotics (non-digestible food substances), probiotics (live, beneficial microorganisms), and synbiotics (a combination of probiotics and prebiotics), or dietary interventions.”

ABOUT THIS NEUROSCIENCE RESEARCH ARTICLE

The research group is launching a large-scale, population based initiative to unravel the intricate connections between the gut microbiome and the brain, in collaboration with the South African Microbiome Initiative in Neuroscience. The study will focus on people that have been diagnosed with any kind of psychiatric disorder in comparison to healthy control groups. This study will identify more links between the gut microbiome and disorders that affect the brain.

Source: Wilma Stassen – Stellenbosch University
Publisher: Organized by NeuroscienceNews.com.
Image Source: NeuroscienceNews.com image is for illustrative purposes only.
Original Research:Abstract for “The Microbiome in Posttraumatic Stress Disorder and Trauma-Exposed Controls: An Exploratory Study” by Hemmings, Sian M.J.; Malan-Müller, Stefanie; van den Heuvel, Leigh L.; Demmitt, Brittany A.; Stanislawski, Maggie A.; Smith, David G.; Bohr, Adam D.; Stamper, Christopher E.; Hyde, Embriette R.; Morton, James T.; Marotz, Clarisse A.; Siebler, Philip H.; Braspenning, Maarten; Van Criekinge, Wim; Hoisington, Andrew J.; Brenner, Lisa A.; Postolache, Teodor T.; McQueen, Matthew B.; Krauter, Kenneth S.; Knight, Rob; Seedat, Soraya; Lowry, Christopher A in Psychosomatic Medicine. Published online October 2017 doi:10.1097/PSY.0000000000000512

CITE THIS NEUROSCIENCENEWS.COM ARTICLE
Stellenbosch University “Gut Bacteria May Predict PTSD Risk.” NeuroscienceNews. NeuroscienceNews, 25 October 2017.
<http://neurosciencenews.com/ptsd-gut-bacteria-7807/&gt;.

Abstract

The Microbiome in Posttraumatic Stress Disorder and Trauma-Exposed Controls: An Exploratory Study

Objective: Inadequate immunoregulation and elevated inflammation may be risk factors for posttraumatic stress disorder (PTSD), and microbial inputs are important determinants of immunoregulation; however, the association between the gut microbiota and PTSD is unknown. This study investigated the gut microbiome in a South African sample of PTSD-affected individuals and trauma-exposed (TE) controls to identify potential differences in microbial diversity or microbial community structure.

Methods: The Clinician-Administered PTSD Scale for DSM-5 was used to diagnose PTSD according to Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition criteria. Microbial DNA was extracted from stool samples obtained from 18 individuals with PTSD and 12 TE control participants. Bacterial 16S ribosomal RNA gene V3/V4 amplicons were generated and sequenced. Microbial community structure, α-diversity, and β-diversity were analyzed; random forest analysis was used to identify associations between bacterial taxa and PTSD.

Results: There were no differences between PTSD and TE control groups in α- or β-diversity measures (e.g., α-diversity: Shannon index, t = 0.386, p = .70; β-diversity, on the basis of analysis of similarities: Bray-Curtis test statistic = –0.033, p = .70); however, random forest analysis highlighted three phyla as important to distinguish PTSD status: Actinobacteria, Lentisphaerae, and Verrucomicrobia. Decreased total abundance of these taxa was associated with higher Clinician-Administered PTSD Scale scores (r = –0.387, p = .035).

Conclusions:
 In this exploratory study, measures of overall microbial diversity were similar among individuals with PTSD and TE controls; however, decreased total abundance of Actinobacteria, Lentisphaerae, and Verrucomicrobia was associated with PTSD status.

“The Microbiome in Posttraumatic Stress Disorder and Trauma-Exposed Controls: An Exploratory Study” by Hemmings, Sian M.J.; Malan-Müller, Stefanie; van den Heuvel, Leigh L.; Demmitt, Brittany A.; Stanislawski, Maggie A.; Smith, David G.; Bohr, Adam D.; Stamper, Christopher E.; Hyde, Embriette R.; Morton, James T.; Marotz, Clarisse A.; Siebler, Philip H.; Braspenning, Maarten; Van Criekinge, Wim; Hoisington, Andrew J.; Brenner, Lisa A.; Postolache, Teodor T.; McQueen, Matthew B.; Krauter, Kenneth S.; Knight, Rob; Seedat, Soraya; Lowry, Christopher A in Psychosomatic Medicine. Published online October 2017 doi:10.1097/PSY.0000000000000512

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Gut Microbes May Talk to the Brain Through Cortisol

Gut Microbes May Talk to the Brain Through Cortisol

Summary: Researchers identify a predictive relationship between serotonin, cortisol and fecal microbiota. The study provides additional support for previous findings that implicate gut bacteria in ASD.

Source: University of Illinois.

Gut microbes have been in the news a lot lately. Recent studies show they can influence human health, behavior, and certain neurological disorders, such as autism. But just how do they communicate with the brain? Results from a new University of Illinois study suggest a pathway of communication between certain gut bacteria and brain metabolites, by way of a compound in the blood known as cortisol. And unexpectedly, the finding provides a potential mechanism to explain the characteristics of autism.

“Changes in neurometabolites during infancy can have profound effects on brain development, and it is possible that the microbiome — or collection of bacteria, fungi, and viruses inhabiting our gut — plays a role in this process,” says Austin Mudd, a doctoral student in the Neuroscience Program at U of I. “However, it is unclear which specific gut bacteria are most influential during brain development and what factors, if any, might influence the relationship between the gut and the brain.”

The researchers studied 1-month-old piglets, which are remarkably similar to human infants in terms of their gut and brain development. They first identified the relative abundances of bacteria in the feces and ascending colon contents of the piglets, then quantified concentrations of certain compounds in the blood and in the brain.

“Using the piglet as a translatable animal model for human infants provides a unique opportunity for studying aspects of development which are sometimes more difficult or ethically challenging to collect data on in human infants,” Mudd says. “For example, in this study we wanted to see if we could find bacteria in the feces of pigletsthat might predict concentrations of compounds in the blood and brain, both of which are more difficult to characterize in infants.”

The researchers took a stepwise approach, first identifying predictive relationships between fecal bacteria and brain metabolites. They found that the bacterial genera Bacteroides and Clostridium predicted higher concentrations of myo-inositol, Butyricimonas positively predicted n-acetylaspartate (NAA), and Bacteroides also predicted higher levels of total creatine in the brain. However, when bacteria in the genus Ruminococcus were more abundant in the feces of the piglets, NAA concentrations in the brain were lower.

“These brain metabolites have been found in altered states in individuals diagnosed with autism spectrum disorder (ASD), yet no previous studies have identified specific links between bacterial genera and these particular metabolites,” Mudd notes.

The next step was to determine if these four bacterial genera could predict compounds in the blood. “Blood biomarkers are something we can actually collect from an infant, so it’s a clinically relevant sample. It would be nice to study an infant’s brain directly, but imaging infants is logistically and ethically difficult. We can, however, obtain feces and blood from infants,” says Ryan Dilger, associate professor in the Department of Animal Sciences, Division of Nutritional Sciences, and Neuroscience Program at U of I.

The researchers found predictive relationships between the fecal microbiota and serotonin and cortisol, two compounds in the blood known to be influenced by gut microbiota. Specifically, Bacteroides was associated with higher serotonin levels, while Ruminococcus predicted lower concentrations of both serotonin and cortisol. Clostridium and Butyricimonas were not associated strongly with either compound.

Again, Mudd says, the results supported previous findings related to ASD. “Alterations in serum serotonin and cortisol, as well as fecal Bacteroides and Ruminococcus levels, have been described in ASD individuals.”

Based on their initial analyses, the researchers wanted to know if there was a three-way relationship between Ruminococcus, cortisol, and NAA. To investigate this further, they used a statistical approach known as “mediation analysis,” and found that serum cortisol mediated the relationship between fecal Ruminococcus abundance and brain NAA concentration. In other words, it appears that Ruminococcus communicates with and makes changes to the brain indirectly through cortisol. “This mediation finding is interesting, in that it gives us insight into one way that the gut microbiota may be communicating with the brain. It can be used as a framework for developing future intervention studies which further support this proposed mechanism,” Dilger adds.

Image shows a gut.

“Initially, we set out to characterize relationships between the gut microbiota, blood biomarkers, and brain metabolites. But once we looked at the relationships identified in our study, they kept leading us to independently reported findings in the autism literature. We remain cautious and do not want to overstate our findings without support from clinical intervention trials, but we hypothesize that this could be a contributing factor to autism’s heterogenous symptoms,” Mudd says. Interestingly, in the time since the researchers wrote the paper, other publications have also reported relationships between Ruminococcus and measures of brain development, supporting that this might be a promising area for future research.

Dilger adds, “We admit this approach is limited by only using predictive models. Therefore, the next step is to generate empirical evidence in a clinical setting. So it’s important to state that we’ve only generated a hypothesis here, but it’s exciting to consider the progress that may be made in the future based on our evidence in the pre-clinical pig model.”

ABOUT THIS NEUROSCIENCE RESEARCH ARTICLE

Mudd and Dilger’s co-authors include Kirsten Berding, Mei Wang, and Sharon Donovan from the Division of Nutritional Sciences and the Department of Food Science and Human Nutrition at U of I.

Funding: The study was supported by Mead Johnson Nutrition.

Source: Lauren Quinn – University of Illinois
Image Source: NeuroscienceNews.com image is in hte public domain.
Original Research: Full open access research for “Serum cortisol mediates the relationship between fecal Ruminococcus and brain N-acetylaspartate in the young pig” by Austin T. Mudd, Kirsten Berding, Mei Wang, Sharon M. Donovan & Ryan N. Dilger in Gut Microbes. Published online July 13 2017 doi:10.1080/19490976.2017.1353849

CITE THIS NEUROSCIENCENEWS.COM ARTICLE
University of Illinois “Gut Microbes May Talk to the Brain Through Cortisol.” NeuroscienceNews. NeuroscienceNews, 21 August 2017.
<http://neurosciencenews.com/gut-microbes-cortisol-7338/&gt;.

Abstract

Serum cortisol mediates the relationship between fecal Ruminococcus and brain N-acetylaspartate in the young pig

A dynamic relationship between the gut microbiota and brain is pivotal in neonatal development. Dysbiosis of the microbiome may result in altered neurodevelopment; however, it is unclear which specific members of microbiota are most influential and what factors might mediate the relationship between the gut and the brain. Twenty-four vaginally-derived male piglets were subjected to magnetic resonance spectroscopy at 30 d of age. Ascending colon contents, feces, and blood were collected and analyzed for volatile fatty acids, microbiota relative abundance by 16s rRNA, and serum metabolites, respectively. A mediation analysis was performed to assess the mediatory effect of serum biomarkers on the relationship between microbiota and neurometabolites. Results indicated fecal Ruminococcus and Butyricimonas predicted brain N-acetylaspartate (NAA). Analysis of serum biomarkers indicated Ruminococcus independently predicted serum serotonin and cortisol. A 3-step mediation indicated: i) Ruminococcus negatively predicted NAA, ii) Ruminococcus negatively predicted cortisol, and iii) a significant indirect effect (i.e., the effect of fecal Ruminococcus through cortisol on NAA) was observed and the direct effect became insignificant. Thus, serum cortisol fully mediated the relationship between fecal Ruminococcus and brain NAA. Using magnetic resonance spectroscopy, this study used a statistical mediation analysis and provides a novel perspective into the potential underlying mechanisms through which the microbiota may shape brain development. This is the first study to link Ruminococcus, cortisol, and NAA in vivo, and these findings are substantiated by previous literature indicating these factors may be influential in the etiology of neurodevelopmental disorders.

“Serum cortisol mediates the relationship between fecal Ruminococcus and brain N-acetylaspartate in the young pig” by Austin T. Mudd, Kirsten Berding, Mei Wang, Sharon M. Donovan & Ryan N. Dilger in Gut Microbes. Published online July 13 2017 doi:10.1080/19490976.2017.1353849

Lectin, gluten, stomach, fasting, toxins, wheat, and foods

By Dr Mercola

From an evolutionary standpoint, any creature, including plants, has a built-in imperative to grow, thrive and propagate. Plants, being rooted into the ground, cannot outrun a predatory insect. Instead, plants use chemistry for self-defense. One of the plant kingdom’s self-defense systems is lectins — not to be confused with lecithin or leptin.

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Lectins are plant proteins, sometimes called sticky proteins or glyca-binding proteins, because they seek out and bind to certain sugar molecules on the surface of cells. There are many types of lectins, and the main difference between them is the type of sugar each prefers and binds to.

Some — including wheat germ agglutinin (WGA), found in wheat and other grass-family seeds — bind to specific receptor sites on your intestinal mucosal cells and interfere with the absorption of nutrients across your intestinal wall. As such, they act as “antinutrients,” and can have a detrimental effect on your gut microbiome by shifting the balance of your bacterial flora — a common precursor to leaky gut.

“I like to think of it as they hack into our communication system, or any predator’s communication system,” Gundry says. “For instance, in insects, they attack a sugar called sialic acid which, among other things, sits between the endings of nerves. One nerve talks to the other nerve by acetylcholine jumping through that space.

Sialic acid allows that to happen. Lectins bind to sialic acid and so interrupt nerve transmission. If you think about it, paralyzing an insect is a great defense system because if the insect can’t move, bingo, you’ve solved the problem. One of the things I’ve learned through the years through my patients is we’re just a giant insect to a plant.

What may happen to an insect fairly instantaneously by eating some plant lectins may take years in us, who are giant insects, to manifest. It may manifest as neuropathy, it may manifest as brain fog, arthritis or heart disease. But the longer I do this, the more I’m convinced that almost every disease process … can be traced back to … plant lectins.

That’s a long-winded explanation for how plants don’t like us. They absolutely don’t want to be eaten. They’ve had 400 million years to work out defense systems — a really long time.”

The Role of Your Microbiome

One of the things that struck me about Gundry’s approach is that it targets the mitochondria and the microbiome, both of which are vital for optimal health. Few physicians, even those in the integrative medicine field, fully understand the importance of mitochondrial function, but Gundry certainly does. And, while the human genome has received a majority of the scientific attention, the bacterial microbiome genome is actually far more important. As noted by Gundry:

“Our microbiome is, I think, our early warning system, because about 99 percent of all the genes that make up [the human body] are actually nonhuman, they’re bacterial, viral and fungal … [from which] we’ve uploaded most of the information about interacting with our environment … because the microbiome is capable of almost instantaneous changing and information processing that we actually don’t have the ability to do.

We’re beginning to realize … that the microbiome is not only how we interact with plant materials … like lectins, but probably more importantly, our microbiome teaches our immune system whether a particular plant compound is a friend or foe [based on] how long we’ve known that plant compound.

There are lectins in everything. But the longer we’ve interacted with lectins and the longer our microbiome has interacted with them, the more our microbiome kind of tells our immune system, ‘Hey, guys, it’s cool. We’ve known these guys for 40 million years. Chill out. They’re a pain, but we can handle them.’

From an evolutionary perspective, if you look at modern foods — say the grains and the beans, which we started interacting with 10,000 years ago, which is a blink of time — our microbiome [regards them as] foreign substances … [T]here’s no lectin speed dating in evolution.”

The Importance of Mitochondrial Function

With regard to mitochondria, “mitochondrial flexibility is one of the unique things that make us human,” Gundry says, comparing the human race to a “fat-storing ape.” Whether you ascribe to the evolutionary theory or not, humans and apes have many genetic similarities, but the ability to store fat is a unique human feature. No other great apes can do that.

Chimps, gorillas and orangutans carry 3 percent body fat. Few humans could ever achieve that low of a body fat percentage unless we were near death from starvation.

“The reason we’re designed to [store fat is to] be able to access fat for fuel,” Gundry says. “The reason why [humans] have been able to take over all parts of the world … [is] because we can cycle back and forth, having our mitochondria use fat for fuel or glucose for fuel. We’re designed to shift very quickly … even within 24 hours.

[Most people] no longer have that metabolic flexibility [because] we’ve been constantly bombarding our mitochondria with an overload of glucose as a fuel, and that really underlies, I think, most disease processes.”

How Intermittent Fasting Boosts Mitochondrial Flexibility

One of the strategies Gundry recommends and uses to improve his own metabolic flexibility is intermittent fasting. For nearly a decade now, he’s been fasting for 22 hours a day, five days a week, from January through June 1, which means he eats all his calories for the day during a two-hour window. On the weekends, he eats lunch and dinner.

“I don’t eat breakfast. I don’t eat lunch. I eat my calories between 6 and 8 o’clock at night. I do that because my wife and I are at home at that time. If I was really smart, I would [eat] earlier in the day, but, you know, you’ve got to be practical in one way or another …

In summer, I’ll have a smoothie with some MCT oil in it, half an avocado, some romaine lettuce, spinach, half a lemon and a little bit of vanilla or stevia. Then I won’t eat lunch. At dinner, same sort of thing, I try to pack all of my calories in between 6 and 8 o’clock at night … 

[June 1], I finished my winter fast, if you will. Now, why do I do that? [Historically], food was a rare thing to find [during the winter]. Again, our metabolic advantage is we’re really good at starvation. It’s what allowed us to survive.

We know that during food scarcity, not only do our mitochondria rev up, but more importantly, our entire immune system and genetic monitoring basically says, ‘Look, times are tough. We don’t know when the next good food supply is going to come. We’ve got to make it through to that next period. We’re going to look at every cell in our body. We’re going to look at whether they’re pulling their own weight.

Are they odd? Are they not very fuel-efficient? We’re going to jettison that. We’re going to create apoptosis until these cells commit suicide.’ It’s kind of like if we were in a hot air balloon and we’re heading for the mountain and we’re going to crash, we’ve got to start throwing things overboard to get more lift.

I think that’s a fundamental principle that you’ve known for a number of years and that I’ve certainly preached for a number of years. The more we understand that that’s how successful aging occurs and study successful agers, one of the things that’s fascinating, particularly in an animal model, is that this intermittent fasting, this challenging [your mitochondria], is the way to do it.”

Although I used to do 14- to 16-hour intermittent fasts, because I felt that it was wise to increase glycogen stores prior to strength training, I have come to realize that’s not true. In fact, it’s counterproductive, as carbs after strength training can increase insulin and diminish IGF-1 response and blunt the anabolic stimulus. So now I am fasting for 18 to 20 hours a day and do all my strength training in a fasted state.

That may sound challenging, but I can confidently assure you, from personal experience, that once you are fat adapted there are no cravings. Additionally, I recently interviewed Dr. Dale Bredesen, who wrote the book “The End of Alzheimer’s: The First Program to Prevent and Reverse Cogntive Decline,” in which he discusses how ApoE4 is a genetic risk factor for Alzheimer’s but ONLY if you don’t intermittent fast. If you do, it will likely actually decrease your risk for the disease as its biological function is to allow us to go for longer periods of time without food.

The Importance of Ketogenic Cycling

Gundry also understands the importance of cycling in and out of nutritional ketosis. While your body is still burning sugar as its primary fuel, you’ll want to be quite strict about not going over your net carb allotment. But once your body has regained the metabolic flexibility to burn fat, it’s really important to cycle in and out or on and off.

I suggest doubling, tripling or even quadrupling your net carbs two days a week, because the metabolic “magic” actually happens during the refeeding phase. As noted by Gundry:

“You have to look at it evolutionarily. It really was feast or famine. When we hit large amounts of food, whether it was a fruit tree or whether it was honey or a wildebeest or a mastodon, there was no food storage system. People tend to forget that nobody walked out of their cave and said, ‘What’s for breakfast?’ There was no refrigerator to have organic berries in every day.

When we chanced upon fuel, then our beautiful design [allowed us to] eat large quantities of [food] and store it as fat. Because, very shortly, whether it was a period of drought, whether it was a period of winter, we were going to regress. I’d like people to think of circadian rhythms. Obviously, we have a 24-hour clock. We have a moon clock. We have seasonal clocks.

What I like people to think of is that we have a period of every year where [we’re in] a growth cycle … That’s the time of growth and it’s a time to reproduce. Then there’s a time of involution, whether it’s a tree dropping its leaves, whether it’s an animal hibernating.

That’s the time where we kind of take stock of everything. That yin and yang, that flow that would happen every year on seasonal basis has completely been lost. We have to have periods where we consume excess calories, then we have to have periods where the exact opposite happens.

Years ago, after my first book came out, I was invited to Phoenix, Arizona, by a blogger named John Kiefer. Kiefer said you should burn fat for fuel most of the time. But every week, you should have what’s called “carb nite loading.” He chanced upon this by accident, but he made a career out of it. I picked his brain and he picked my brain. I think he’s absolutely right.”

Lectins Are Strongly Associated With Autoimmune Diseases of All Kinds

Since we just talked about carb-loading at least once or twice a week (once you’ve regained the ability to burn fat for fuel), it’s worth stressing that these ought to be healthy carbohydrates, and ideally lectin-free. While intermittent fasting and eating a ketogenic (high-fat, low-carb, moderate protein) diet will dramatically reduce your risk of chronic disease, lectins may still cause trouble. One of the primary issues is autoimmune diseases.

“One of the things I talk about in the book that really made me hyper-focused on lectins was a friend of mine who was a very early adopter of my first program. I call him Tony in the book. Tony had really bad vitiligo. That’s … where the [skin] pigmentation is lost. Vitiligo is an autoimmune disease.

What happens is we attack the pigment-forming cells in our skin called melanocytes. Melanocytes are actually modified neural cells. They migrate from the neural crest to our skin in embryonic development. When Tony started my program, a few months later, he came up to visit me. He said, ‘You’re not going to believe this. My vitiligo is gone.’ I’m looking at him and I’m going, ‘Wow. That’s impressive.’

He said, ‘How did that happen?’ I could have said, ‘Well, this is a very anti-inflammatory diet. It’s high in antioxidants.’ But because I’m a researcher, I said, ‘No. That’s too simple.’ I said, ‘Melanocytes. Neural Cells. What’s the target of lectins in insects? Neural cells! Could it be that lectins are why [his body is] attacking his neural cells? What I’ve done is I’ve removed lectins from his diet.’

I lost track of him for a number of years. I was on a health panel in New York City two years ago. I saw him and he’s covered with vitiligo again. I said, ‘What happened?’ He says, ‘You know. I fell off [the diet]. I really need to get back on.’ I said, ‘This is a great experiment. Come on. Here’s the list. Go for it.’

We were just on a panel at Harvard two months ago. He’s chairing the panel. He says, ‘I’ve got to show you — everybody — the vitiligo’s gone because I took lectins back out of my diet. It sounds silly but here’s the proof.'”

Molecular Mimicry

One way by which lectins cause harm is through molecular mimicry. They resemble proteins in the thyroid gland, in your joint spaces and in nerves. They mimic myelin sheath proteins.

The reason why lectins will in one person cause vitiligo or psoriasis, and in another attack the thyroid or cause rheumatoid arthritis, is still unknown. What is known is that one of the underlying factors in all of these disease processes is the penetration of the gut wall by lectins and their co-travelers, lipopolysaccharides (LPSs), also known as endotoxins, which tend to elicit very strong immune responses.

“One of the things I found in all my autoimmune patients is they had profoundly low levels of vitamin D … Interestingly, when you finally seal the gut … all of a sudden, their vitamin D levels went sky high and I could back down on the dosage.

Vitamin D is essential to tell the stem cells at the bottom of the crypts in the villi to grow and divide. Without vitamin D stimulating them, they just sit there and don’t repair the gut. I think plants are so intelligent, it’s shocking. I think one of the plant strategies is that if you have low vitamin D, because you can’t absorb it, then you can’t repair your gut. You’re a horrible predator. You won’t reproduce. You won’t walk.

Vitamin D is really one of the keys to autoimmune disease. Lectins are the other key. I’ve been blessed by knowing thousands of autoimmune patients who I call “canaries,” because they react almost instantaneously to lectins. It’s interesting. Everybody has their own certain lectin or lectins that they really react to.

This morning I had a woman who has rheumatoid arthritis. Her rheumatoid markers or anti-CCP3 markers have gone up. Her IL-17 had gone up. I said, ‘All right. What are you doing? What’s going on?’ She said, ‘No, no. I’m perfect. I know your list backwards and forwards.’ I said, ‘No. There’s something.'”

A Sample Case History of Crohn’s Disease

As it turns out, she’s been eating raw (unpeeled) almonds, and almond peels contain lectins. Another patient’s markers went up after going on a cashew binge, forgetting that cashews are an American bean and hence high in lectins. The answer for autoimmune patients, Gundry says, is to remove lectins from the diet and add vitamin D, which together will help “heal and seal” the gut, thereby preventing the autoimmune response.

“I mention a young woman who has Crohn’s disease in the book. Her well-meaning doctor at the Mayo Clinic told her that food had nothing to do with Crohn’s disease. She had been cured of Crohn’s disease with my program. He told her it was the placebo effect. We still laugh at that one. She ate a couple of Christmas cookies after she got off the phone with him.

Of course, it was like throwing a bomb in her stomach. She had horrible cramps and diarrhea. We skyped and she said, ‘Why don’t doctors see this?’ Like I talk about in the book, we can’t see unless our eyes are open …

I was lucky enough that when I met the guy who changed my life, Big Ed, who cleaned out his arteries with diet and supplements, [I had] my eyes open. I said, ‘This is not chance. How did [he] do this?’ Luckily, because of my evolutionary background, I was able to piece it together.”

Which Foods Have the Most Problematic Lectins?

Lectins are found in many of our most cherished foods, such as: 2,3

Potatoes Eggplants Tomatoes Peppers Goji berries Lima beans
Cashews Peanuts Sunflower seeds Chia seeds Pumpkin seeds Kidney beans
Squash Corn Quinoa Soybeans Wheat Lentils

Another common lectin is the A1 casein protein, found in most of today’s dairy cows. I’ve talked a lot about the benefits of raw milk on my site. The devil’s in the details however, and aside from being high in sugar, even raw dairy may cause problems if it has A1 casein.

“Casein A2 is the normal protein in milk, besides whey. It’s present in sheep, goats and water buffalos. But, most of the cows in the world are now casein A1 producers. They make a lectin-like protein called casein A1, which is metabolized in our gut to make beta-casomorphin, which is a very interesting thing. They can attach to the beta cell of the pancreas and incite an autoimmune attack on the pancreas.

I and others are pretty convinced that [many cases] of Type 1 juvenile diabetics is because of the casein A1 in milk. I’ve been convinced through the years that not only is it the problem, but people who think they’re lactose intolerant or that milk gives them mucus, it’s the casein A1 … Raw milk is great, as long as it came from the right cow … [Some] Jerseys are A1 and [some are] A2. Holsteins are A1.”

More and more people are now starting to recognize this, and there are even grassroots movements pushing for A2 milk in California and Ohio. Jeni’s Ice Cream gets all her milk from Snowville Creamery, which is an A2 farm. “I’ve actually talked to those people. They get it,” Gundry says. There have even been attempts to introduce A2 milk on a larger scale, but each attempt has been crushed by the American Dairy Council, for obvious reasons.

Wheat — Going Beyond Gluten

Wheat germ agglutinin (WGA) is another problematic lectin, found in wheat. Compared to WGA, gluten is a minor problem. According to Gundry, WGA is one of the most efficient ways to induce heart disease in experimental animals. WGA binds to insulin receptor sites. Normally, a normal hormone will dock on a receptor site, give its information and then release. Pseudo hormones like WGA, on the other hand, dock on the receptor permanently. Gundry explains:

“If they hit the insulin receptor on a fat cell, they turn on lipoprotein lipase and pump sugar into the fat cell, turning it into fat constantly. In muscle cells, the exact opposite happens.

They’ll attach to the insulin receptor in the muscle cell [and] block insulin from delivering sugar into the cell. I see so many long-distance runners who are carboholics, who look like concentration camp survivors because they’re really cachectic and sarcopenic because they block the insulin receptors in their muscles …

The lectins, like WGA and galactans in beans are miraculous ways of making us store fat … [T]he only way we’ve ever been able to fatten an animal for slaughter is to give them grains, beans and some antibiotics. If that’s how we fatten animals, that’s how we fatten us. It works really well.”

Not All Bread Is the Same

If you’ve ever traveled to Europe, you may have indulged in some bread and noticed you didn’t experience the same type of problems you have when eating bread in the U.S. The reason for this is because the lectins are removed when you use traditional methods of raising bread, which is still popular in Europe.

“Europe [has] always used traditional methods raising bread. They use yeast or sourdough. Yeast and bacteria are actually pretty good at breaking down the gluten molecule and other lectins,” Gundry explains.

Europe also does not permit the use of glyphosate to desiccate wheat, which has become common practice in the U.S. Glyphosate is also used on many conventional grains, including beans and flax, so it’s in the animal meats we eat, it’s in our baked goods, and even in wine produced in the U.S. According to Gundry, glyphosate potentiates gluten to people who are not even gluten-sensitive, and interferes with your liver’s ability to manufacture the active form of vitamin D.

Glyphosate also chelates important minerals, disrupts the shikimate pathway, decimates your microbiome and increases leaky gut, which allows more of the LPSs into your bloodstream. Since it works synergistically with the lectins, it really delivers a double-whammy.

“[Glyphosate] hits cytochrome P450. It’s one of the reasons the Europeans are so far [ahead] on health,” Gundry says. “It’s one of the reasons why so many of my patients can go to Europe, eat their traditional diet and think they’re cured and now they can start eating bread. They come back and eat a piece of bread and, bam — the whole thing starts all over again.”

On Vegetarianism and Other Diets

As mentioned, Gundry was a professor at Loma Linda University, a Seventh Day Adventist facility. Seventh Day Adventists are typically vegetarians, and while not an Adventist, Gundry did eat a vegetarian diet for about 15 years during his time there.

“I’ve never been sicker in my life. I used to weigh 228 pounds despite running 30 miles a week and running half marathons on the weekend and going to the gym one hour every day, wondering why I had high blood pressure, prediabetes and heart disease … Quite frankly, we have a fabulous orthopedic department at Loma Linda, because grains are pretty doggone mischievous for that.

Through the years, I’ve been good friends with the head of the Adventist Health Studies, a cardiologist. One of the things I’ve learned from following the Adventists and following Gary Fraser is that … certain animal proteins do contribute to aging. In the Adventist health study, the vegan Adventists have the longest life span. Behind them are the lacto-ovo vegetarians, then behind them are the pescetarians. Then finally, there are the real cheaters who eat chicken …

It is interesting that the longest living of the Adventists, who are very long-living, are the vegans. I take care of a lot of vegans because of my association with Loma Linda. As a general rule, the vegans are some of the unhealthiest people I have met. The reason is they’re grain- and bean-itarians. They are not vegetable eaters.

I have nothing against a high vegetable diet … The other thing we see in the vegans is they somehow think they will convert short-chain omega-3 fats into EPA, the long-chain omega-3 fats. They absolutely and positively do not.

Our brain is about 70 percent fat; 50 percent of that fat is DHA. There are beautiful longitudinal studies showing people with the highest omega-3 index have the largest brains as they age, and the largest areas of memory in the hippocampus. People with the lowest levels of omega-3 index have the most shrunken brains and the smallest areas of memory. Vegans have no excuse anymore. There’s algae-based DHA.”

Fruit and Berries — Seasonal Treats

Gundry’s first rule is that what you stop eating is more important than what you start eating. “It’s absolutely true,” he says. “If you take away certain foods, you’ll be amazed [to find] that it’s certain foods that are the troublemakers.” His second rule is, take care of your gut microbiome. Rule No. 3 is “fruit might be as good as candy.” While he doesn’t expound on the importance of burning fat for fuel in his book, that’s really part of the equation. Once you’re able to burn fat, fruit can be a healthy carbohydrate to add once or twice a week.

“Exactly. I think part of the problem is the vast majority of Americans are insulin-resistant. One of the things that people should realize is that the modern fruit has been bred for sugar content … One of the things I ask people to do initially is give fruit the boot.

Fructose is a major toxin. We take fructose directly to our liver and detoxify it into triglycerides and uric acid. It always amazes me the number of people with gout who consume more concentrated fruit, like wine or beer. Beer is one of the underlying reasons that they have gout.

The other thing people should realize is that fructose is a direct renal toxin. The more fructose I can get out of people, the better. Having said that, once you get to a point where you have metabolic flexibility, I think things like berries are probably one of the best ways to carbohydrate load on the day you decided to do that … Sweet potatoes are great as well, [and] I’m a big fan of taro root.

Years ago [in June] … my wife and I were at a Santa Barbara farmers market. I was taking these gorgeous organic peaches and putting them into my bag. She says, ‘Hey, wait a minute. Aren’t you the guy who says give fruit the boot?’ I said, ‘Yeah, yeah. But it’s June and it’s time to eat fruit.’ She says, ‘OK, smart guy. Let’s do this. This summer, we’re going to give up fruit to see what happens’ …

So, we gave up fruit for one summer. We didn’t change anything else in our diet. My wife lost 6 pounds and I lost 8 pounds. It brought home to me that, again, our ancestors and the reason we have two-thirds of our tongue devoted to sweet taste is we are great fruit predators. Fruit was only available once a year. We utilized that fruit to gain weight for the winter … [Now] we can have it 365 days a year, but that’s not normal. So, always keep that in mind.”


Connie: Eat gluten free, avoiding refined and processed foods.

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The Human Gut Microbiome as a Screening Tool for Colorectal Cancer

scfa.JPGOur results suggest that relative abundance data from the human gut microbiome differentiates individuals with healthy colons from those with adenomas and carcinomas. Most importantly, there was a significant difference in the gut microbiome of people with colonic adenomas compared with those with healthy colons. This has considerable importance in secondary prevention because screening for early-stage colorectal cancer hinges on the ability to detect early pathologic changes. In this regard, we found that failure to detect at least 1 of the 5 OTUs served as a signal of the presence of adenoma. The probability of having an adenoma rose more than 50-fold with this added information about microbiome. Taken with the existing literature about the importance of the gut microbiome in health and disease, our study further suggests that the microbiome may play a crucial role in the etiology of colorectal cancer.

A strength of our study design was that we collected samples from 3 clinical groups that represented the multistage progression in colorectal cancer (healthy, adenoma, and carcinoma). This allowed us to identify a panel of bacterial populations that could indicate both the progression from healthy tissue to adenoma and the progression from adenoma to carcinoma. Interestingly, when we looked at each patient, we rarely observed significant enrichment of every bacterial population among the OTUs incorporated in the logit models. For example, 11 of the 30 carcinoma patients had no detectable levels of Fusobacterium. However using the relative abundance data for the remaining panel of microbial biomarkers, such as Porphyromonas, Bacteroides, and Enterobacteriaceae, we were able to accurately classify these subjects. This strongly suggests that there may be multiple underlying mechanisms by which the microbiome is involved in colorectal cancer and that colorectal cancer is likely a polymicrobial disease.

Our findings are supported by previous evidence. Three research groups reported that Fusobacterium spp. were enriched on the surface of tumors compared with adjacent healthy tissue (22, 37, 38). Building upon these clinical studies, animal and tissue culture-based studies have provided evidence that Fusobacterium may contribute to tumor multiplicity through the recruitment of immune cells to tumors (22, 37). These mechanistic studies agree with our findings that Fusobacterium may be a marker for the presence of tumors. In addition, enterotoxigenic Bacteroides fragilis (ETBF), a pathogenic variant of a common commensal, has been shown to directly influence the development of colorectal cancer in murine genetic models through the production of a metalloprotease toxin (39). In our samples, subjects with carcinomas showed an increase in the relative abundance of one Bacteroides population (OTU 1882) compared with subjects with adenomas. However, PCR-based screens for the toxin producing genes did not reveal the presence of ETBF. In addition, we observed a significant decrease in the relative abundance of Bacteroides populations (OTUs 1889 and 1913) associated with the advancement of tumorigenesis. Finally, a polyketide synthetase operon from Escherichia coli was shown to influence the progression of tumors using a murine model of inflammation-derived tumorigenesis (21, 23). Although we did see an enrichment for non–E. coli Enterobacteriaceae in the carcinoma subjects relative to the healthy subjects, we were unable to detect significant differences in the relative abundance of E. coli across the 3 clinical groups.

It is tempting to speculate on the enrichment of Fusobacterium and Porphyromonas spp. in subjects with colorectal cancer. Both of these bacterial taxa are common commensals of the mouth and a wealth of literature has linked them to chronic inflammation and periodontal disease (40, 41). It is possible that the mouth is a reservoir for these pathogens, allowing for colonization of the gastrointestinal tract under abnormal environmental conditions. During colorectal carcinogenesis, dramatic physiologic changes occur in the microenvironment of colonic lesions (42). Tumor-associated fluxes in nutrients and shifts in inflammatory mediators may favor colonization by opportunistic pathogens such as Fusobacterium and Porphyromonas. As demonstrated by Kostic and colleagues, colonization by such pathogens can support the development and progression of colorectal cancer (22, 37). We were unable to detect a significant association between either population and carcinoma severity or location. Additional studies are needed to examine how and at what stage these bacterial populations are affecting the development of colorectal cancer and how they may be linked to the oral microbiome and related to oral disease.

As highlighted above, there is a clear association with the enrichment of pathogenic bacterial populations and colon tumorigenesis; however, in this study we emphasize that the depletion of potentially protective bacteria likely plays a similar role colorectal cancer pathology. We identified several bacterial populations that were significantly depleted in colorectal cancer. Individuals with both adenomas and carcinomas showed a dramatic loss in OTUs associated with the genera Clostridium and Bacteroides, and the family Lachnospiraceae (43–45). Each of these bacterial taxa are well known producers of short chain fatty acids (SCFA) in the colon. SCFAs are important microbial metabolites that supply nutrients to colonocytes and help maintain epithelial health and homeostasis. Specifically, the SCFA, butyrate, has been shown to have substantial antitumorigenenic properties, including the ability to inhibit tumor cell proliferation, initiate apoptosis in tumor cells (46), and mediate T-regulatory cell homeostasis (44). Loss of these important bacterial populations in concert with an enrichment of pathogenic populations likely plays a synergistic role in potentiating tumorigenesis.

Joseph P. Zackular, Mary A.M. Rogers, Mack T. Ruffin IV and Patrick D. Schloss

Gut bacteria regulate happiness

APC scientists have shown that brain levels of serotonin, the ‘happy hormone’ are regulated by the amount of bacteria in the gut during early life. Their research is being published today in the leading international psychiatry journal, Molecular Psychiatry.

This research shows that normal adult brain function depends on the presence of gut microbes during development. Scientists at the APC used a germ-free mouse model to show that the absence of bacteria during early life significantly affected serotonin concentrations in the brain in adulthood. Serotonin, the major chemical involved in the regulation of mood and emotion, is altered in times of stress, anxiety and depression and most clinically effective antidepressant drugs work by targeting this neurochemical.

The research also highlighted that the influence is sex dependent, with more marked effects in male compared with female animals. Finally, when the scientists colonised the animals with bacteria prior to adulthood, they found that many of the central nervous system changes, especially those related to serotonin, could not be reversed indicating a permanent imprinting of the effects of absence of gut flora on brain function.

Some of the general pathways for dopamine and serotonin in the human brain are illustrated.

General pathways for dopamine and serotonin along with a few brain areas are illustrated. VTA in this illustration stands for the ventral tegmental area. Image in the public domain.

This builds on earlier work, from the Cork group and others, showing that a microbiome-gut-brain axis exists that is essential for maintaining normal health which can affect brain and behaviour. The research was carried out by Dr Gerard Clarke, Professor Fergus Shanahan, Professor Ted Dinan and Professor John F Cryan and colleagues at the Alimentary Pharmabiotic Centre in UCC.

“As a neuroscientist these findings are fascinating as they highlight the important role that gut bacteria play in the bidirectional communication between the gut and the brain, and opens up the intriguing opportunity of developing unique microbial-based strategies for treatment for brain disorders”, said Professor John F Cryan, senior author on the publication and Head of the Department of Anatomy & Neuroscience at UCC.

This research has multiple health implications as it shows that manipulations of the microbiota (e.g. by antibiotics, diet, or infection) can have profound knock-on effects on brain function. “We’re really excited by these findings” said lead author Dr Gerard Clarke. “Although we always believed that the microbiota was essential for our general health, our results also highlight how important our tiny friends are for our mental wellbeing.”

Notes about this behavioral neuroscience research and article

Contact: APC of University College Cork
Source: Alimentary Pharmabiotic Centre at Biosciences Institute in University College Cork news release
Image Source: NeuroscienceNews.com image adapted from public domain image at Wikimedia Commons from DrugAbuse.gov.
Original Research: Abstract for “The microbiome-gut-brain axis during early life regulates the hippocampal serotonergic system in a sex-dependent manner” by G Clarke, S Grenham, P Scully, P Fitzgerald, R D Moloney, F Shanahan, T G Dinan and J F Cryan in Molecular Psychiatry June 12, 2012; doi:10.1038/mp.2012.77

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