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October 15, 2019

Autism & the Gut: Are they linked & what is the link? Part 3 The Gut-Brain Axis Series

by Nicola Schuler, CNTP, MNT and Dr. Miles Nichols

Three weeks ago, we wrote a blog on Autism & the Gut Part 1 and covered some facts about ASD as well as some of the contributing factors as they relate to genes and the environment. Recently, in Autism & the Gut Part 2, we discussed all of the contributing factors including gut health and its important impact on ASD. This week, in Autism & the Gut Part 3, we will outline specific action steps that you can take with diet, supplements and lifestyle habits, to address ASD.

Autism Spectrum Disorder: What Can You Do?

Gut health

In the case of ASD, it is important to improve gut health. This can be done by addressing the issues discussed last week in Part 2. These are dysbiosis, leaky gut, food sensitivities, yeast overgrowth, imbalanced SCFA’s and NT balance. Also look for other GI issues that may exist (such as parasites, SIBO or other infections / overgrowths of the gut).

We strongly recommend working with a qualified functional medicine clinic to properly assess gut issues through lab testing. A good functional medicine practitioner can guide you through the process of finding the most significant gut issues and working on those, in addition to identifying toxins and other root causes we’ve discussed in this article. If you would like to book a free 15-minute discovery call with our clinic, please click here. We work with people all over the world.

Tools that can be used to modify the gut microbiome are diet, supplements, probiotics, prebiotics, fecal microbiota transplant (FMT), microbiota transfer therapy (MTT) and antibiotics (Kang DW, 2019).

Diet

  • Diet influences the composition of the gut bacteria and overall health of one’s gut. We talked about a general gut healing diet and what to avoid for gut health in our recent article on anxiety. The approach discussed is always recommended for good gut health.
  • A gluten-free and/or casein- or dairy-free (GF/CF) diet has been found to improve ASD behaviors, physiological symptoms, and social behaviors (Li Q, 2017). Gluten and casein increase zonulin, which is a protein that increases gut permeability. Removing gluten and casein from the diet will improve leaky gut. Two trials have demonstrated the benefits that excluding gluten and casein have for symptoms of ASD (Whiteley P, 2010).
  • Avoid glyphosate. By only buying and eating organic food, glyphosate can be avoided. In addition to being used on the obvious GM crops, it is now also used as a desiccant to facilitate harvest in many other non-GM crops, like wheat, legumes and others. It is commonly found in alcohol, namely beer and wine, as it is sprayed on the crops used to make the alcohol. By going strictly organic-only, glyphosate exposure can be eliminated.
  • The GAPS Diet (The Gut and Psychology Diet) may be helpful in some cases of ASD. It removes foods that are damaging to gut bacteria and are difficult to digest, replacing them with nutrient-dense foods that heal the gut lining thereby addressing leaky gut. It is a fairly strict elimination diet that requires removing grains, pasteurized dairy, starchy vegetables and refined carbs. It is particularly helpful for neurological issues such as autism (Campbell-McBride, 2019).
  • There is some evidence that the ketogenic diet (a high-fat low-carbohydrate diet) leads to decreases in the total gut microbial counts, increased sociability, reduced repetitive behaviors, and improved social communication in an ASD animal model (Li Q, 2017). Animal research does fail in human trials about 92% of time, so it remains to be seen whether this will be effective for humans.
  • Prebiotics encourage the growth of beneficial bacteria. We encourage adding them to the diet of someone with ASD. We list prebiotic foods to add here.
  • It is helpful to work with an experienced FM practitioner to see which dietary approach will work best as research shows this can be case-dependent. To book a complimentary 15-minute phone consultation to see whether functional medicine is a good fit for your child, please click here.
  • It can be challenging to change the diet of children with ASD. Children with ASD typically tolerate only a narrow range of foods and have more feeding problems than children without ASD. They tend to refuse more foods and eat a limited food repertoire than typically developing children. Many parents complain that their children with ASD are very selective, ‘picky’ eaters. Children with ASD will reject foods for different reasons, including issues with the food presentation, texture, the use of certain utensils, and the mix of different types of food on the same plate. It can require patience to get a child with ASD to adapt their diet. Dr. Campbell-Mcbride explores this topic and recommends how to handle this situation in her book The GAPS Diet, Gut and Psychology Syndrome.

Supplements

  • In the case of ASD, children typically eat fewer fruits, vegetables, and proteins than non-affected children (Li Q, 2017).
  • They have a significantly lower daily intake of potassium, copper, folate, and calcium (Li Q, 2017). Research has looked at folate, vitamin D, omega 3, iron and zinc deficiencies with some links to ASD (Modabbernia A, 2017) and another study finds that zinc, copper, iron, and vitamin B9 are specific micronutrients related to ASD (Nuttall, 2017).
  • Vitamin D deficiency seems to be quite common in children with ASD (Modabbernia A, 2017).
  • We would recommend supplements in the case of ASD:
  • A good multi-vitamin & mineral supplement can help cover the bases with vitamin and mineral deficiencies. Specific testing for micronutrients can help to target treatment much better so consider working with a FM practitioner for this type of testing. Unfortunately, most multi-vitamins contain some nutrients that are problematic so we recommend using professional brands. We recommend Mitocore by Ortho Molecular in our clinic and you can buy it from our online store here.
  • Increased intake of omega 3 reduces hyperactivity, increases good bacteria in the gut and reduces risk of brain disorders (Amminger GP, 2007). You can use Olde World Icelandic Cod Liver Oil from our online store here.
  • In addition, test for vitamin D and iron status and supplement these if necessary. Too much of either is a problem so we recommend working with a practitioner to find the right dosage.
  • Lactobacillus probiotics help treat dysbiosis by controlling Clostridia overgrowth and aid the digestion of casein and gluten (Pelto L, 1998). Probiotics help to prevent intestinal inflammation, regulate intestinal tight junctions and barrier function, thereby improving leaky gut (Li Q, 2017). Probiotic treatments have a proven ability to normalize the microbiota and improve gut symptoms (Li Q, 2017). You can use Ortho Biotic probiotic from our online store here.
  • L-glutamine has been shown to improve barrier function and reduce intestinal permeability (Foitzik T, 1997). Protocol for Life Balance is a good brand that you can get from our online store here.
  • Digestive enzymes can aid the breakdown of food proteins and can improve digestive function. We often use Digestzymes by Designs for Health in our clinic, found here.
  • Vitamin B6 and magnesium supplements improve social and language skills (Mousain-Bosc M, 2006). P-5-P is the active form of B6 and we like the product by the company Designs for Health. Magnesium Chelate contains the preferred glycinate form of magnesium and we like the product by Designs for Health. Both of these can be found in our online store here.
  • Manganese (Mn) is an important nutrient, required for multiple functions in the body. A recent study revealed that glyphosate, the active ingredient in the herbicide Roundup, has been shown to severely deplete Mn levels (Samsel A, 2015). Low Mn affects the gut brain axis and is associated with gut dysbiosis as well as neuropathologies such as autism, Alzheimer’s disease, depression, anxiety syndrome and Parkinson’s disease (Samsel A, 2015).

Fecal Microbiota Transplantation (FMT)

FMT is the transplant of healthy human feces to a patient with severe gut dysbiosis, in order to regulate the intestinal microbiota of the patient. When the normal gut microbiota are destroyed, for example by excessive antibiotic treatment or other negative substances like GMO foods, it can be challenging to recover a normal healthy bacterial flora. FMT can be extremely helpful in these situations (Kim YK, 2018). Unfortunately this is not FDA approved for ASD in the US at this time.

Microbiota Transfer Therapy (MTT)

MTT is a modified FMT protocol. It involves 14 days of antibiotic treatment followed by bowel cleansing and a high initial dose of standardized human gut microbiota for 7–8 weeks. An open-label clinical trial showed that MTT improved both GI symptoms (i.e., constipation, diarrhea, indigestion and abdominal pain) and ASD-related symptoms and normalized the microbiota of ASD patients (Kang DW A. J., 2017)

Heavy metals

Heavy metals, combined with an inadequate nutritional status and an impaired detoxification function, can increase the severity of ASD symptoms (Blaurock-Busch E, 2012). Eliminating exposure to heavy metals will help prevent neurodevelopmental disorders in children. In children with ASD, it is best to test for heavy metals. If there is an issue with metals exposure, then seek treatment by supporting the detoxification process of the body and/ or chelating heavy metals from the body if necessary. Seek out a skilled functional medicine practitioner for both of these approaches.

Support detoxification

ASD children have a reduced ability to detoxify toxins from the body (Blaurock-Busch E, 2012). It is therefore advisable to find a skilled FM practitioner to help support the detoxification process. This will help the body to eliminate toxins, metals, and the other chemical types we have discussed, which contribute to the overall ASD picture.

Avoid toxins

In addition to enhancing the detox function, it is important to minimize toxin exposures wherever possible. Avoid pollution, endocrine disruptors, plastics, pesticides, GMO’s, glyphosate, mold or mycotoxins. You can do this by eating a clean, organic diet, and avoiding toxins or chemicals as much as possible. This would include cleaning up the family’s personal care and household cleaning products, avoiding pollution wherever possible, minimizing plastics use especially in food preparation and storage, not smoking cigarettes and keeping alcohol consumption to a minimum.

Avoid stress

Stress is not named as a cause of ASD but a stressful situation can trigger a person with ASD. For this reason, it is advisable to reduce stress where possible and manage stress. Stress can be managed with meditation and other mindfulness practices. Practice mediation, yoga or tai chi and spend time outdoors in nature.

 

If you or someone you know is suffering from ASD, get in touch with our clinic today. Book a free 15-min discovery call to see how we can help you with your symptoms. We can answer your questions and help you book an initial consult with one of the functional medicine doctors in our clinic.

 

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September 30, 2019

Autism & the Gut: Are they linked & what is the link? Part 2: Autism, in The Gut-Brain Axis Series

by Nicola Schuler, CNTP, MNT and Dr. Miles Nichols

Last week’s blog on Autism & the Gut Part 1 covered some facts about ASD as well as some of the contributing factors as they relate to genes and the environment. This week, in Autism & the Gut Part 2, we continue discussing the environmental factors that contribute to ASD, as well as cover gut health and its impact on ASD. Then in Autism & the Gut Part 3, we will outline specific action steps that you can take with diet, supplements and lifestyle habits, to address ASD.

In addition to what we covered last week, such as pre-natal factors, maternal nutrient deficiencies and environmental chemicals, these are Environmental Factors that can contribute to ASD:

  • Endocrine disruptors: These are chemicals that disrupt the endocrine (hormone) system of the body. Exposure to these chemicals pre-natally and in very early life can affect brain development.
    • It is thought that the effect of excessive testosterone on specific brain regions might be a key mechanism to push the brain to an extreme male pattern of more systematizing and less empathizing, which is in line with ASD characteristics (Modabbernia A, 2017). Therefore, factors that alter hormonal balance (and particularly fetal testosterone) might contribute to risk of ASD.  For example, flame retardants are both associated with an increased level of free testosterone and an increased risk of ASD (Modabbernia A, 2017).
    • Recent studies have shown that chemicals associated with lower testosterone levels are also associated with lower risk of autistic behaviors (Modabbernia A, 2017).
    • Another link between endocrine disruptors and ASD is alteration in thyroid function. Several studies have shown evidence of prenatal maternal thyroid dysfunction and ASD in the offspring (Modabbernia A, 2017). Many endocrine-disrupting chemicals that disrupt thyroid hormone function have also been hypothesized to increase the risk of ASD (Modabbernia A, 2017).
    • Studies of phthalate (an endocrine disruptor) exposure showed a significant association between phthalate exposure and risk of ASD (Modabbernia A, 2017).
  • Metals: Heavy metals, such as lead, cadmium, mercury, etc. are established neuro-toxins with documented impacts on cognitive and developmental outcomes (Lyall K, 2017).
    • Studies found an association between heavy metal concentration (mostly mercury and lead) and severity of ASD (Modabbernia A, 2017).
    • Twelve studies described improvement in symptoms of ASD following chelation therapy (a technique used to remove heavy metals from the body) (Modabbernia A, 2017).
    • In a genetically sensitive individual, toxic metals cause significant oxidative stress. This leads to impaired methylation/processing of folate and alters the capacity for synchronizing neural networks as a result of an impaired dopamine function (Modabbernia A, 2017). This affects epigenetic mechanisms, leading to abnormal gene expression. Both mechanisms, impaired synchronization of neural networks and epigenetic alterations related to methylation, are closely linked to ASD (Modabbernia A, 2017).
  • Glyphosate: Glyphosate is the active ingredient in Roundup Ready, the most widely used herbicide in the world (Samsel A, 2015). Glyphosate is liberally used on core food crops, because it is perceived to be non-toxic to humans. The adoption of genetically engineered “Roundup-Ready” corn, soy, canola, cotton, alfalfa, and sugar beets has made it relatively easy to control weeds without killing the crop plant, but this means that glyphosate is present as a residue in foods.
    • As weeds among GM Roundup-Ready crops are developing ever-increasing resistance to Roundup, use of the herbicide is increasing. In fact, its usage has increased steadily since 1987, in step with the rise in ASD rates (Samsel A, 2015).
    • In one study, the authors wrote: “Despite its relatively benign reputation, Roundup was among the most toxic herbicides and insecticides tested.” (Samsel A, 2015)
    • One paper states that this may explain the recent increase in incidence of multiple neurological diseases (Samsel A, 2015).
    • Glyphosate indirectly affects Lactobacillus, leading to increased anxiety via the gut–brain access (Samsel A, 2015). Both low Lactobacillus levels in the gut and anxiety syndrome are known features of ASD, and Lactobacillus probiotic treatments have been shown to alleviate anxiety and ASD (Samsel A, 2015).
    • Glyphosate indirectly results in mitochondrial damage, a hallmark of many neurological diseases and a factor in ASD (Samsel A, 2015).
    • This is a controversial topic, but glyphosate is frequently named as an environmental factor driving the rise in ASD that we see today.
  • Inflammation & immune system function: ASD is associated with an altered immune status, increased oxidative stress, and inflammation in the brain.
    • Concentrations of pro-inflammatory immune system molecules are increased in patients with ASD compared to those in healthy people (Modabbernia A, 2017).
    • A maternal autoimmune disease can increase the risk of ASD through the effect of maternal inflammatory mediators and autoantibodies on fetal neurodevelopment (Modabbernia A, 2017).
    • Substances such as lead, mercury, pollutants, or perinatal complications can cause inflammation and oxidative damage in the brain, which can impair neural growth and development (Modabbernia A, 2017).
  • Neurotransmitter changes and interference with signaling pathways in the brain: Neurotransmitters (NTs) are chemicals in the brain responsible for signaling. We wrote in some detail about NTs in our article on anxiety.
    • Abnormalities in the NTs glutamate, serotonin and GABA have been linked to ASD (Modabbernia A, 2017).
    • Some of the issues discussed already, like lead, environmental pollutants and flame retardants, disrupt the activities of NTs; NMDA, glutamate and GABA respectively (Modabbernia A, 2017).
    • Some environmental risk factors interact with intracellular signaling pathways and can impair neurodevelopment. For example, exposure to PCB and PBDE (chemicals used in plastics, construction, flame retardants, etc.) seems to alter a signaling pathway, leading to abnormalities in dendritic growth and neuronal connectivity, a key feature of ASD (Modabbernia A, 2017).

Gut health – As we have seen in our previous articles on the Gut Brain Axis (Anxiety, ADHD 1, ADHD 2, ASD 1), the gut microbiome is an important environmental factor that influences symptoms of various conditions, including ASD. Research has increasingly observed that children with ASD have distinctive gut microbiomes compared to neurotypical children (Kang DW, 2019). Thus through the microbiome-gut-brain axis, gut health influences ASD.

Gastrointestinal (GI) symptoms, such as abdominal pain, gas, diarrhea, constipation and flatulence, are common in people with ASD (Li Q H. Y., 2017). Constipation is found to be the most prevalent symptom (85%) in children with ASD (Li Q H. Y., 2017).

Other common symptoms are gut inflammation, intestinal permeability, low levels of digestive enzymes/ poor digestion, reflux esophagitis, impaired detoxification and dysbiosis (Horvath K, 1999). The prevalence of GI symptoms ranges from 23 to 70% in children with ASD (Li Q H. Y., 2017).

It has been found that improvements in GI and ASD symptoms are significantly correlated (Kang DW, 2019). In other words, attaining relief of GI symptoms may improve behavioral severity in children with ASD (Kang DW, 2019).

Dysbiosis, or an imbalance in gut flora with more bad bacteria than good in the gut, has been found in cases of ASD. Diversity, or the variety of gut bacteria found in people with ASD, is about 25% lower than in healthy people (Kang DW A. J., 2017). Their guts are missing hundreds of different species of bacteria, often ones that are important to fermentation and producing short chain fatty acids that influence health (Kang DW A. J., 2017).

For example, the guts of children with ASD exhibit lower levels of Bifidobacterium and Firmicutes and higher levels of Clostridium, Bacteroidetes, Desulfovibrio, Caloramator and Sarcina (Li Q H. Y., 2017). Children with autism who present GI symptoms have lower abundances of the species Prevotella, Coprococcus, and unclassified Veillonellaceae than that found in GI symptom-free neurotypical children (Li Q H. Y., 2017).

Clinical trials using fecal microbiota transplants (FMT) have shown promise with ASD. One trial using high-dose FMT for 1-2 days and then 7-8 weeks of highly purified oral solution dosing found significant GI and behavioral improvements (Kang DW A. J., 2019). A 2-year follow-up found that these positive changes continued to improve over time (Kang DW A. J., 2019). However, FMT is not FDA approved for ASD at this time, so it may be some time before this therapy is available in the US.

Re-establishing a healthy gut microbiome benefits the gut-brain axis that has become dysfunctional in ASD (Kang DW A. J., 2017). Also, simply removing the pain and distraction of a dysbiotic gut can help children concentrate better and benefit from speech, behavioral and other therapies they may be undergoing (Kang DW A. J., 2017).

In addition to dysbiosis, leaky gut is involved in ASD. A higher percentage of abnormal intestinal permeability, or commonly called leaky gut, was observed in 36.7% of patients with ASD compared with 4.8% of control children (Li Q H. Y., 2017).

In fact, the integrity of both the gut barrier and the BBB were impaired in ASD individuals (Li Q H. Y., 2017). Increased intestinal permeability results in the entry of the toxins and bacterial products into the bloodstream.

These circulating inflammatory molecules are then able to cross the blood-brain barrier, creating inflammation and immune responses in the brain (Li Q H. Y., 2017). For example, lipopolysaccharide (LPS), components of the cell wall of gram-negative bacteria, is increased in the serum of ASD compared with healthy individuals and is associated with impaired social behavior (Li Q H. Y., 2017).

Food sensitivities are often a problem, which ties back to a dysfunctional gut. Over 40% of children with ASD have food sensitivity issues, most commonly to wheat and milk products (Horvath K P. J., 2002).

The breakdown of gluten by pancreatic and intestinal enzymes produces ‘exorphins’ or undigested proteins.  When leaky gut is present, these undigested proteins can then enter into circulation and the central nervous system where they have a morphine-like effect (Reichelt K, 2003).

An increase in proteins, including opiates, has been linked to disruption in social awareness and behavior (Reichelt K, 2003). This sequence of events can occur with casein, from dairy products, as well (Reichelt K, 2003). Finally, gluten and casein increase zonulin, which is a protein that increases gut permeability i.e. leaky gut.

There is also a relationship between gut fungi or yeast and ASD. Yeast in the gut, particularly candida albicans, can result in less carbohydrates and minerals absorption and a higher release of toxins (Li Q H. Y., 2017).

A lower yeast rate of 19.6% was identified in non-autistic healthy volunteers (Li Q H. Y., 2017). It was found that in children with ASD, candida was two times more abundant than in normal individuals and that 81.4% of the yeast strains were candida, especially candida albicans (Li Q H. Y., 2017).

Candida can release ammonia and toxins that can induce autistic behaviors (Li Q H. Y., 2017). The changes in the bacterial microbiota in ASD individuals result in the growth of candida, which worsens the dysbiosis and can induce abnormal behaviors (Li Q H. Y., 2017).

SCFAs also play a critical role in patients with ASD. We talked about SCFAs here. SCFAs are products of the gut bacterial fermentation of carbohydrates and provide benefits to the human body.

Different SCFAs can be imbalanced in the gut of ASD patients. For example, proprionic acid, PPA, is a short-chain fatty acid that is mainly produced by Clostridia, Bacteroidetes, and Desulfovibrio bacteria, which are more frequently found with ASD, and can cross the BBB and induce ASD-like behaviors (Li Q H. Y., 2017). Higher PPA can lead to impaired social behavior, likely by altering some neurotransmitters, such as dopamine and serotonin (Li Q H. Y., 2017).

Finally, the impact of glyphosate on the gut is complex and multi-faceted. We cannot go into the tremendous amount of detail here but Stephanie Seneff has done so in this paper (Samsel A, 2015). There are multiple ways in which glyphosate can contribute to and worsen ASD. We advise avoidance and will explain how you can do that later in this article series on ASD.

Treatments used to date for ASD include behavioral therapy, speech and social therapy, diet / nutrition and medical treatments. However no medical treatment has been approved to treat core symptoms of ASD, such as social communication difficulties and repetitive behaviors (Kang DW, 2019). Considering the link between the gut and brain, the first approach should be to address gut health.

— To Be Continued —

Due to the complexity of ASD, we can’t cover everything that we want to say in one blog post. So please tune in again next week for ASD: Part 3, when we will outline specific action steps related to diet, supplements and lifestyle that you can take to address ASD.

If you want to address ASD sooner, then please get in touch with us today, by booking a free 15 minute discovery call here. We can answer your questions and help you book an initial consult with one of the functional medicine doctors in our clinic.

—————-

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September 24, 2019

Autism & the Gut: Are they linked & what is the link? Part 1: Autism, in The Gut-Brain Axis Series

by Nicola Schuler, CNTP, MNT and Dr. Miles Nichols

In this week’s article on the gut-brain axis, we address autism and the gut. The gut and the brain are linked, with the gut-brain axis regulating brain function and behavior (Chunlong Mu, 2016). For a full explanation of the gut brain axis, please see our first article on anxiety and the gut.

The gut-brain axis plays a critical role in many neurological disorders. It affects neuropsychiatric disorders like anxiety, depression, schizophrenia and dementia (Kim YK, 2018), as well as neurodevelopmental disorders in children including autism, ADHD, learning disabilities, intellectual developmental disorder, motor disorders, and specific learning disorders (EPA, 2015).

In this article, we will explore the link between autism and the gut brain axis. Autism, or autism spectrum disorder (ASD), is a brain developmental disorder (Li Q, 2017).

ASD is defined by significant social, communication and behavioral challenges, often with a pattern of stereotyped repetitive behaviors, speech and nonverbal communication behaviors and challenges with communication and social interaction (Li Q, 2017).

As autism is classified as a spectrum disorder, it affects sufferers differently (Autism Speaks, 2019). Cognitive abilities of people with ASD range from extremely gifted to severely challenged. Some with ASD need significant support in daily life, while others need less and some can live entirely independently.

ASD is often accompanied by sensory sensitivities, gastrointestinal (GI) disorders, immune deficits, anxiety, depression, sleep disturbances, seizures and attention issues (Lyall K, 2017).

A diagnosis of ASD now includes several conditions that used to be diagnosed separately: autistic disorder, pervasive developmental disorder not otherwise specified (PDD-NOS), and Asperger syndrome. These conditions are now all called autism spectrum disorder (Centers for Disease Control and Prevention, 2018).

Important facts about ASD:

  • The prevalence is increasing (Autism Speaks, 2019). According to the CDC (Centers for Disease Control and Prevention, 2019):
  • In 2004, 1 in 166 children had ASD.
    • In 2006, 1 in 150 children had ASD.
    • In 2016, 1 in 68 children had ASD.
    • In 2018, 1 in 59 children had ASD, according to Autism Speaks, who used data from the CDC (Autism Speaks, 2018).
    • However, according to Pediatrics journal, using data from the 2016 National Survey of Children’s Health (NSCH), in 2018, 1 in 40 children had ASD (Kogan MD, 2018).
  • Some of this increase is due to better and earlier diagnosis, but there is debate about whether this explains all of the increase in ASD rates. This will become clear when we discuss causes. Our genes have not and cannot change so quickly, but our environment has. Thus some environmental changes or triggers are thought to be partially driving the increases seen.
  • Boys are four times more likely to be diagnosed with autism than girls (Centers for Disease Control and Prevention, 2019). Of the 1 in 59 children diagnosed with ASD in 2018: 1 in 37 are boys and 1 in 151 are girls.
  • However, the gender gap in autism has decreased (Autism Speaks, 2018). While boys were 4 times more likely to be diagnosed than girls in 2014, the difference was narrower than in 2012, when boys were 4.5 times more frequently diagnosed than girls (Autism Speaks, 2018). This is likely due to improved identification of autism in girls, who often do not manifest the stereotypical symptoms of autism seen in boys.
  • 31% of children with ASD have an intellectual disability (with an IQ <70), 25% are in the borderline range (IQ 71–85), and 44% have IQ scores in the average to above average range (IQ >85) (Autism Speaks, 2019).
  • ASD is one of the most serious neurodevelopmental conditions in the U.S. It has significant caregiver, family, and financial burdens. The annual total costs associated with ASD in the U.S. have been estimated to be approx. $250 billion (Lyall K, 2017). Lifetime individual ASD-associated costs are in the $1.5 to $2.5 million range (estimates in 2012 U.S. dollars) (Lyall K, 2017).

Most children are still being diagnosed after age 4, though autism can be reliably diagnosed as early as age 2 (Autism Speaks, 2019). Diagnosing ASD can be difficult. There is no medical test, such as a blood test, to diagnose it (Centers for Disease Control and Prevention, 2018).

Doctors look at the child’s behavior and development to make a diagnosis. It can sometimes be detected at 18 months or younger. By age 2, a diagnosis by an experienced professional can be considered to be very reliable (Centers for Disease Control and Prevention, 2018).

What are the CAUSES or Contributing Factors?

The causes of ASD are not completely understood. Studies on twins suggest that both genes and environment play roles in the development of ASD (Modabbernia A, 2017). The developing brain is vulnerable to environmental factors, which explains the causative association between environmental factors and ASD (Modabbernia A, 2017).

Some studies show ASD is primarily driven by genetic influences, and others report a nearly equal contribution from heritable genetic and non-heritable environmental factors (Lyall K, 2017). One study found that up to 40-50% of autism spectrum disorder (ASD) liability might be determined by environmental factors (Modabbernia A, 2017). Because environmental and epigenetic influences are not as well studied as genetic ones, there may be a much greater impact of environment than has appeared in studies so far.

Metabolism, gut, immune and mitochondrial dysfunction are frequent in ASD (Lyall K, 2017). Among children with ASD, gastrointestinal symptoms have also been associated with more frequent challenging behaviors (Lyall K, 2017).

It is clear that there are three areas to look at to explain ASD:

  • Genes
  • Environment
  • Gut health

Genes – It is possible to have a genetic disposition to the condition. The fact that genes partly contribute to ASD is strongly supported by twin and family studies (Lyall K, 2017). Several genes have been identified in ASD; post-synaptic scaffolding genes, i.e. SHANK3, contactin genes, i.e. CNTN4, neurexin family genes, i.e. CNTNAP2, and chromatin remodeling genes, i.e. CHD2 (Lyall K, 2017). The specific genes involved are part of common genetic pathways involved in ASD (Lyall K, 2017). The cumulative effect of multiple common gene issues, i.e. the polygenic risk, is now becoming recognized as an important risk factor for ASD and other psychiatric disorders (Lyall K, 2017).

Epigenetics is the study of gene-environment interaction. Unfortunately there is little information on gene-environment interaction in ASD causality, as only a few studies have been published to date (Lyall K, 2017).

Some epigenetic changes have been found in the brains of people with ASD, including hypo- and hyper-methylation, i.e. related to the MTHFR gene, and spreading of histone 3 lysine 4 trimethylation marks (Lyall K, 2017). We talked in detail about MTHFR here.

Research has found an increased risk of ASD associated with common mutations affecting the folate/methylation cycle i.e. the MTHFR mutation (El-Baz F, 2017). A significant association between severity and occurrence of autism has been found with two common MTHFR gene mutations, called C677T and A1298C (El-Baz F, 2017). Further studies are needed to explore other gene mutations that may be associated with autism, to establish the genetic basis of autism. (El-Baz F, 2017)

Other genetic variants for ASD implicate chromatin remodeling, another aspect of epigenetic regulation (Lyall K, 2017). Other reports suggest interactions between gene risk and prenatal exposure to air pollutants, genes in the one carbon metabolism pathway and maternal use of prenatal vitamins, and genetic variations and maternal prenatal infection (Lyall K, 2017).

Environment – This can be an outright cause or a trigger of ASD. Systematic reviews of the available research suggest more than 20 individual, familial, pre-, peri- and neo-natal factors with some evidence for ASD risk (Lyall K, 2017).

The maternal environment is especially important for the risk of developing autism spectrum disorders. In particular infections present in a mother during pregnancy, micronutrient deficiencies, obesity, and toxic exposures are likely to interact with genetic risk factors to disrupt fetal brain development (Nuttall, 2017).

One study suggests that approximately 75-80% of the observed increase in ASD since 1988 is due to an actual increase in the disorder rather than to changing diagnostic criteria (Nevison, 2014). It attributes the increase to environmental factors driving this increase (Nevison, 2014).

For example, polybrominated diphenyl ethers (used in flame retardants, building materials, electronics, furnishings, motor vehicles, airplanes, plastics, polyurethane foams, and textiles), aluminum adjuvants (used in vaccines), and the herbicide glyphosate have increasing trends that correlate positively to the rise in autism (Nevison, 2014).

Environmental factors driving ASD risk include:

  • Parental age: Every 10-year increase in maternal and paternal age increases the risk of ASD in the offspring by 18 and 21% respectively (Modabbernia A, 2017).
  • Inter-pregnancy interval: Increases in risk of ASD with a short (<12 months) period between pregnancies have been consistently reported. Reasons for this are not clear but relate to maternal nutrient deprivation, inflammation, and stress (Lyall K, 2017). Adequate recovery time between pregnancies is recommended.
  •  Pregnancy-related complications: Abnormal or breech presentation, cord complications, fetal distress, multiple births, low birth weight <1500 g, small for gestational age, congenital malformations, birth injury or trauma, hyperbilirubinemia, earlier birth (first vs. third born) and feeding difficulties at birth can all play a role (Modabbernia A, 2017).
  • Immune factors: Maternal hospitalization with infection (bacterial or viral) during pregnancy has been associated with increased risk of ASD (Lyall K, 2017). Familial history of autoimmune disease has also been associated with increased risk of ASD (Lyall K, 2017).
  • Medication use during pregnancy: Antidepressants, anti-asthmatics, and anti-epileptics (especially maternal valproate use for epilepsy and bipolar disorder) are associated with ASD in the children (Modabbernia A, 2017). Some association with SSRI anti-depressants exist but are not fully established in the research (Modabbernia A, 2017). However, these drugs can cross the placenta and blood brain barrier (BBB), as well as be transferred to the child through breast milk (Lyall K, 2017).
  • Nutrient deficiencies: Research has looked at folate, vitamin D, omega 3, iron and zinc deficiencies with some links to ASD (Modabbernia A, 2017). One paper finds that zinc, copper, iron, and vitamin B9 are specific micronutrients related to ASD (Nuttall, 2017). Specific toxins can induce a maternal inflammatory response which leads to fetal micronutrient deficiencies in these nutrients (Nuttall, 2017). The fetal deficiencies disrupt development of the early brain (Nuttall, 2017). Maternal micronutrient supplementation is advised as it is associated with reduced risk of ASD (Nuttall, 2017). Higher maternal intake of certain nutrients and supplements has been associated with reduction in ASD risk, with the strongest evidence for taking folate supplements before conception (Lyall K, Schmidt RJ, 2014). In later life, vitamin D deficiency seems to be quite common in children with ASD (Modabbernia A, 2017).
  • Environmental chemicals: We are exposed to a vast, almost countless, number of environmental and industrial chemicals in today’s world. Certain environmental chemicals exposures during the pre-natal period interfere with and disrupt normal brain development in the fetus. These chemicals can cross the placenta and the blood brain barrier, accumulating in developing brains (Lyall K, 2017). Others disrupt hormone pathways or act on inflammatory pathways that may have negative effects on brain development (Lyall K, 2017). Prenatal exposure to air pollution has emerged as a risk factor for ASD. These are hazardous air pollutants, such as chlorinated solvents, methylene chloride and diesel particulate matter and others (Lyall K, 2017). Chemicals in flame retardants can result in mitochondrial toxicity and lead to issues with energy balance in the brain (Modabbernia A, 2017). In general, chemicals can contribute to the mitochondrial dysfunction that is well documented in people with ASD (Modabbernia A, 2017).

— To Be Continued —

Due to the complexity of ASD, we can’t cover all of the factors contributing to ASD in one blog post. So please tune in again next week for ASD: Part 2 where we will continue with the environmental factors that contribute to ASD. We will also discuss gut health and how it contributes to ASD. Finally, in ASD: Part 3, we will outline what diet, supplements and lifestyle action steps you can take to address ASD.

If you want to address ASD sooner, then please get in touch with us today, by booking a free 15 minute discovery call here. We can answer your questions and help you book an initial consult with one of the functional medicine doctors in our clinic.

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September 10, 2019

ADHD & the Gut: Are they linked & what is the link? Part 2: ADHD, in The Gut-Brain Axis Series

by Nicola Schuler, CNTP, MNT and Dr. Miles Nichols

In this next article on the gut-brain axis, we address ADHD Part 2. Last week, we looked at ADHD and its link to the gut in ADHD Part 1. This week, we explore a list of factors contributing to ADHD and specifically what you can do in the case of ADHD.  

In Functional Medicine, we like to dig deep and look for the root cause(s). As there is no single cause of ADHD, in FM the approach we take is to look at all the factors found in research to be influencing ADHD.

We cannot change genetics but we can affect how genes express. We cannot change any prenatal events as mentioned last week such as maternal stress, poor diet, smoking or alcohol use during pregnancy and/or a low birth weight.

We can, however, change and improve a number of health factors, which will improve the condition of ADHD.

Nutrient status & Diet: ADHD is associated with unhealthy diets and nutrients deficiencies (Chou WJ, 2018). Children with ADHD had significantly lower serum (blood) levels of vitamin B12, folate, vitamin B6, ferritin and monounsaturated fatty acids (Wang LJ, 2019).

They also had higher levels of serum saturated fatty acids and a higher omega 6 to omega 3 fatty acid ratio, which is inflammatory (Wang LJ, 2019).

Children with ADHD had a higher intake of nutrient-poor foods such as high sugar and high fat foods, and less vegetables, fruit and protein-rich foods (Wang LJ, 2019). Children with ADHD ate a higher intake of refined grains and a lower portion of dairy, calcium and vitamin B2 (Chou WJ, 2018).

It is clear from research that there is an association between unhealthy dietary patterns and ADHD. An unhealthy diet leads to the poor nutritional status of people with ADHD. In addition, food dyes and additives in the diet (Banerjee TD, 2007), common allergens such as eggs and micronutrient and mineral deficiencies (Wang LJ, 2019) have been implicated in ADHD. Improving diet and nutrition is expected to improve ADHD symptoms (Wang LJ, 2019).

Children with ADHD have been shown to have lower vitamin D levels when compared to children with healthy controls. Children with ADHD had an average blood level of 19.11 ng/ml whereas the control group average was 28.78 ng/ml (Sharif MR, 2015).

Of course, it is understandable that it can be difficult in some cases to help a child to eat a healthier diet with the peer and societal influences that push a standard American diet. However, with some diligent work and patience, a healthy diet can be achieved. Supplementation of some of the common nutrient deficiencies with a high quality professional grade B complex and cod liver oil may help.

Gut microbiome health: As we have discussed, the health of the microbiome is critical with ADHD. Dysbiosis and gut inflammation are factors that can lead to ADHD.

It is important to find a FM practitioner who will test for a variety of GI issues, such as dysbiosis, SIBO, overgrowths, infections, parasites, fungus, low SCFA’s or SCFA’s imbalance or any other type of infection or issues affecting gut health. After getting a clear picture of gut health, treating any issues found is critical.

Antibiotics use: Antibiotics disrupt the gut microbiome. They kill all bacteria in the gut, including the good ones. Antibiotics are commonly prescribed for infants and children. This negatively affects the gut microbiota and health and development outcomes.

One study found that children who had received antibiotics in the first 6 months of life had significantly lower overall cognitive and verbal comprehension abilities, increased risk of problems with cognition, impulsivity, hyperactivity, ADHD, anxiety and emotional problems (Slykerman RF, 2019). The study concluded that early exposure to antibiotics may be associated with detrimental neurodevelopmental outcomes (Slykerman RF, 2019). Limit antibiotics use wherever possible.

Acetaminophen: Tylenol contains an active ingredient called acetaminophen. Because it is available over the counter, many parents use Tylenol to treat pain and fever. It is typically used for mild to moderate pain relief and often used to relieve fever in children. However, research has identified that short-term maternal use of acetaminophen during pregnancy was negatively associated with ADHD in offspring and that long-term use during pregnancy was substantially associated with ADHD (Ystrom E, 2017).

Toxin exposure:  It is widely accepted that exposure to various toxins, such as the afore-mentioned food dyes, additives and artificial colors, lead contamination and exposure to other heavy metals, cigarette and alcohol exposure, and other potential toxins or chemicals, are environmental factors that contribute to ADHD (Banerjee TD, 2007).

It is important to minimize these exposures wherever possible, by eating a clean, organic diet, and avoiding toxins or chemicals as much as possible. This would include cleaning up the family’s personal care and household cleaning products, avoiding pollution wherever possible, not smoking cigarettes and keeping alcohol consumption to a minimum.

Another source of toxins that often goes undiscovered and can cause serious issues are mycotoxins, or toxins from mold. It is estimated that 1 in 2 American homes is water damaged (Spengler, 1994) and mold is not always visible. Our clinic specializes in helping people identify if they have been exposed to mold in the past or present and how to clear the toxins from the body.

Heavy metals: Exposures to heavy metals, particularly mercury, arsenic, lead, antimony and cadmium, can be contributors to ADHD. One study found that lead, cadmium and antimony were associated with susceptibility to ADHD and symptom severity in school-age children (Lee MJ, 2018).

Eliminating exposure to heavy metals will help prevent neurodevelopmental disorders in children. In children with ADHD, it is best to test for heavy metals.

If there is an issue with metals exposure, then seek treatment by supporting the detoxification process of the body and/ or chelating heavy metals from the body if necessary. Seek out a skilled functional medicine practitioner for both of these approaches.

MTHFR gene mutation: MTHFR is the name of both a gene and an enzyme in the human body called methylenetetrahydrofolate reductase. The gene tells the body how to make the enzyme. This enzyme is important to process folate properly. It turns folate into its bioavailable form, methylfolate, through the process methylation. The methylfolate then converts amino acids for many body functions, including the production of serotonin and dopamine.

If the MTHFR gene is mutated, it cannot produce the enzyme correctly, which disrupts various processes further downstream. One of these processes is the production of serotonin and dopamine, which are key players in ADHD, autism, and mood disorders (ADDitude, 2019). The malformation of the MTHFR gene causes the body to change folate into methylfolate at a reduced capacity (as low as 10% for homozygous and 50% for heterozygous) (ADDitude, 2019).

A person with the MTHFR mutation can have too much folate, and not enough methylfolate, which impairs various processes downstream. MTHFR is also critical in the process of detoxification. If it’s not working properly, heavy metal and mineral levels can become excessive or imbalanced, which can cause hyperactivity, mood disorders, and more (ADDitude, 2019). It is best to seek help from a functional medicine doctor if this is an issue or is suspected.

HPA axis: Stress can contribute to ADHD. It is not often named as a cause of ADHD but a stressful situation can trigger a person with ADHD. For this reason, it is advisable to reduce stress where possible and manage stress. Stress can be managed with meditation and other mindfulness practices. One study based on adults found that self-reported ADHD symptoms, emotional dysregulation and clinician ratings of ADHD symptoms improved for those who practiced mindfulness meditation relative to those who did not (Mitchell JT, 2017).

Yoga is another modality to increase mindfulness and help to manage ADHD symptoms. A small study done with children in 2013 found that a regular yoga practice, alongside treatment for ADHD, led to ‘a significant improvement in the ADHD symptoms’ (Hariprasad VR, 2013). In the months following the study, the children practiced yoga irregularly and symptoms worsened again (Hariprasad VR, 2013).

Tai Chi has also been found to reduce symptoms. One small study involving Tai Chi twice per week resulted in the study participants experiencing less anxiety, better behavior, less daydreaming, more appropriate emotional responses and less hyperactivity after 5 weeks of Tai Chi (Hernandez-Reif M, 2000).

Similarly, it has been found that spending time outdoors and playing in green open spaces reduces overall symptom severity in children with ADHD (Taylor AF, 2011). Children with ADHD who play regularly in green play settings have milder symptoms than children who do not (Taylor AF, 2011).

Generally, meditation and gentle movement practices that are mindful can be helpful for regulating the stress response. Creating a good habit from a young age of daily meditation is an invaluable life skill. Even 3-5 minutes per day can make a difference. And children can and do learn to meditate. Even if it is only for a short time, it is still helpful.

Exercise: We know that exercise improves mood and behavior in children and adults and lowers chronic disease risks. One study looking specifically at behavioral health disorders in children found that aerobic exercise improved symptoms (Bowling A, 2017). The children taking aerobic exercise experienced 32% to 51% lower incidence of poor self-regulation and disciplinary time out of class when participating in the exercise. These effects were noticeably more pronounced on days that children participated in the aerobic exercise, but carryover effects on non-exercise days were also observed. Aerobic exercise shows promise for improving self-regulation and classroom functioning among children with complex behavioral health disorders (Bowling A, 2017).

Screen time on phones, computers, video games and TV: Research has definitively linked excessive and addictive use of digital media with physical, psychological, social and neurological adverse effects. Overall screen time and violent and fast-paced content can activate dopamine and the reward pathways, leading to ADHD-related behavior and sleep problems (Lissak, 2018). A case study involving 9-year-old boy with ADHD found that screen time induced ADHD-related behavior (Lissak, 2018). Research agrees that reducing screen time is an effective tool to decrease ADHD-related behavior (Lissak, 2018). A secondary effect of reducing screen time is increased sleep time, which improves overall health.

Practical things that you can do to address ADHD:

Diet:

  • Adopt a clean, organic whole foods diet. Limit sugar, refined carbohydrates and processed foods. Eat vegetables, fruits, high quality organic proteins and healthy fats such as omega-3 fatty acids found in certain types of oily fish, flaxseed and other foods. Fermented foods help gut health as they contain live probiotics. Prebiotic foods will aid gut health and specifically, the balance of SCFAs. For more specific information on a diet that supports gut-brain axis health, please refer to our article on anxiety and the gut-brain axis.
  • Remove food dyes and additives. Certain food colorings, dyes, additives and preservatives may increase hyperactive behavior in some children (The Mayo Clinic, 2017). Avoid foods with these colorings and preservatives:
    • sodium benzoate – found in carbonated beverages, salad dressings, and fruit juice products
    • FD&C Yellow No. 6 – found in breadcrumbs, cereal, candy, icing, and soft drinks
    • FD&C Yellow No. 10 – found in juices, sorbets, and smoked haddock
    • FD&C Yellow No. 5 – found in pickles, cereal, granola bars, and yogurt
    • FD&C Red No. 40 – found in soft drinks, children’s medications, gelatin desserts, and ice cream
  • Remove commonly allergenic foods such as gluten/wheat, eggs, chocolate, dairy, tree nuts, peanuts and any other food you think you may be allergic to.

Supplements: can be helpful, as specific nutrient deficiencies have been identified with ADHD.

  • B12, Folate, B6: B vitamins have been found to be lower in people with ADHD (Wang LJ, 2019). Certain genetic mutations, such as MTHFR which we mentioned previously, can impair the body’s use of B vitamins. In this case, it would be helpful to work with a FM practitioner to determine your MTHFR status and address it accordingly with supplements and other measures.
  • Ferritin / iron: Children with ADHD are typically low in ferritin, which is the storage form of iron (Wang LJ, 2019). Test iron and ferritin levels first to determine if supplementation is necessary. (NOTE: Too much iron is a problem so please do not supplement iron without the guidance of a functional medicine or other qualified healthcare professional.)
  • Omega 3: It has been found that in ADHD, omega 3 fat levels are low (Wang LJ, 2019). This is an important nutrient for the brain, which can help to reduce neuroinflammation. Either eat fatty fish such as wild salmon, sardines, herring and anchovies or supplement with fish oil to get adequate levels of the omega 3 fats, EPA and DHA.
  • Vitamin D: Optimize vitamin D levels from sun exposure (avoid burning though) and/or supplemental vitamin D. First measure levels and determine if they are below 35 ng/ml. If so, supplementation and/or a healthy amount of sun exposure without sunscreen that does not produce sunburn will increase levels of vitamin D. When supplementing with Vitamin D, we recommend also supplementing with Vitamin K2. You can purchase products that have both in one capsule. Test vitamin D levels periodically to see if the dose is too high or too low. The sun may offer additional benefits beyond supplemental vitamin D so it is helpful to have a healthy level of sun exposure without burning.
  • Probiotics: There is some research suggesting that probiotics may be helpful with ADHD (Pelsser LM, 2009). Getting to the root cause of gut issues is, of course, preferable and that can be done by working with a skilled functional medicine doctor.
  • It is best to work with an experienced FM practitioner to determine what nutrient deficiencies you may have and how best to address them.

Mindfulness: Increase mindfulness with yoga, tai chi and meditation.

Exercise: Be sure to get plenty of exercise, including time to play outside in nature.

Address gut health: See a Functional Medicine practitioner to help you with gut health. Issues like dysbiosis and gut inflammation are important to address with ADHD. It is advisable to test for a variety of GI issues; dysbiosis, SIBO, overgrowths, infections, parasites, fungus, low SCFA’s or SCFA’s imbalance or any other type of infection or issues affecting gut health. After getting a clear picture of gut health, treating any issues found is critical.

 

If you or someone you know is suffering from ADHD, get in touch with our clinic today. Book a free 15-min discovery call to see how we can help you with your symptoms. We can answer your questions and help you book an initial consult with one of the functional medicine doctors in our clinic.

 

References:

Aarts E, E. T. (2017). Gut microbiome in ADHD and its relation to neural reward anticipation. PLOS One.

ADDitude. (2019, March 18). MTHFR: Another Piece of the ADHD-Genetics Puzzle. Retrieved August 14, 2019, from ADDitude: https://www.additudemag.com/mthfr-adhd-genetics-puzzle/

All About ADHD. (n.d.). Causes of ADHD. Retrieved July 30, 2019, from All About ADHD: https://www.adhd-information.com/adhd-causes.html

American Psychiatric Association. (2013). Diagnostic and Statistical Manual of Mental Disorders (DSM–5). American Psychiatric Association.

Banerjee TD, M. F. (2007). Environmental risk factors for attention‐deficit hyperactivity disorder. Acta Paediatrica.

Bowling A, S. J. (2017). Cybercycling Effects on Classroom Behavior in Children With Behavioral Health Disorders: An RCT. Pediatrics.

Cenit MC, N. I.-F. (2017). Gut microbiota and attention deficit hyperactivity disorder: new perspectives for a challenging condition. European Child & Adolescent Psychiatry, 1081–1092.

Centers for Disease Control and Prevention. (2018, September 21). Attention-Deficit / Hyperactivity Disorder (ADHD). Retrieved July 28, 2019, from www.cdc.gov: https://www.cdc.gov/ncbddd/adhd/data.html

Children and Adults with Attention-Deficit/Hyperactivity Disorder. (2019). General Prevalence of ADHD. Children and Adults with Attention-Deficit/Hyperactivity Disorde.

Chou WJ, L. M. (2018). Dietary and nutrient status of children with attention-deficit/ hyperactivity disorder: a case-control study. Asia Pacific Journal of Clinical Nutrition, 1325 – 1331.

Chunlong Mu, Y. Y. (2016). Gut Microbiota: The Brain Peacekeeper. Frontiers in Microbiology.

EPA, U. S. (2015, October). America’s Children and the Environment. Neurodevelopmental Disorders | Health.

Hariprasad VR, A. R. (2013). Feasibility and efficacy of yoga as an add-on intervention in attention deficit-hyperactivity disorder: An exploratory study. Indian Journal of Psychiatry.

Hernandez-Reif M, F. T. (2000). Attention Deficit Hyperactivity Disorder: Benefits from Tai Chi. Journal of Bodywork and Movement Therapies.

Kim YK, S. C. (2018). The Microbiota-Gut-Brain Axis in Neuropsychiatric Disorders: Patho-physiological Mechanisms and Novel Treatments. Current Neuropharmacology.

Lee MJ, C. M. (2018). Heavy Metals’ Effect on Susceptibility to Attention-Deficit/Hyperactivity Disorder: Implication of Lead, Cadmium, and Antimony. International Journal of Environmental Research and Public Health.

Lissak. (2018). Adverse physiological and psychological effects of screen time on children and adolescents: Literature review and case study. Environmental Research.

Ming X, C. N. (2018). A Gut Feeling: A Hypothesis of the Role of the Microbiome in Attention-Deficit/Hyperactivity Disorders. Sage Journals.

Mitchell JT, M. E. (2017). A Pilot Trial of Mindfulness Meditation Training for ADHD in Adulthood: Impact on Core Symptoms, Executive Functioning, and Emotion Dysregulation. Journal of Attention Disorders.

National Institute of Mental Health. (2019). www.nimh.nih.gov. Retrieved July 28, 2019, from NIH Nationa lInstitute of Mental Health: https://www.nimh.nih.gov/health/topics/attention-deficit-hyperactivity-disorder-adhd/index.shtml

NHS. (2018, May 30). Treatment ADHD. Retrieved August 14, 2019, from NHS: https://www.nhs.uk/conditions/attention-deficit-hyperactivity-disorder-adhd/treatment/#

Pelsser LM, B. J. (2009). ADHD as a (non) allergic hypersensitivity disorder: a hypothesis. Pediatric Allergy and Immunology.

Reneman D, B. C. (2019). White Matter by Diffusion MRI Following Methylphenidate Treatment: A Randomized Control Trial in Males with Attention-Deficit/Hyperactivity Disorder. Radiology.

Sharif MR, M. M. (2015). The Relationship between Serum Vitamin D Level and Attention Deficit Hyperactivity Disorder. Iranian Journal of Child Neurology.

Slykerman RF, C. C. (2019). Exposure to antibiotics in the first 24 months of life and neurocognitive outcomes at 11 years of age. Psychopharmacology.

Taylor AF, K. F. (2011). Could Exposure to Everyday Green Spaces Help Treat ADHD? Evidence from Children’s Play Settings. Applied Psychology.

Thapar A, C. M. (2013). What have we learnt about the causes of ADHD? Journal of Child Psychology and Psychiatry.

The Mayo Clinic. (2017, September 28). ADHD diet: Do food additives cause hyperactivity? Retrieved August 14, 2019, from The Mayo Clinic: https://www.mayoclinic.org/diseases-conditions/adhd/expert-answers/adhd/faq-20058203

Wang LJ, Y. Y. (2019). Dietary Profiles, Nutritional Biochemistry Status, and Attention-Deficit/Hyperactivity Disorder: Path Analysis for a Case-Control Study. Journal of Clinical Medicine.

Ystrom E, G. K. (2017). Prenatal Exposure to Acetaminophen and Risk of ADHD. Pediatrics.

 

 

 

 

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August 21, 2019

ADHD & the Gut: Are they linked & what is the link? Part 1: ADHD, in The Gut-Brain Axis Series

by Nicola Schuler, CNTP, MNT and Dr. Miles Nichols

In this next article on the gut-brain axis, we address ADHD and the gut this week. Recent research has established a strong link between the gut and the brain. The gut-brain axis regulates brain function and behavior (Chunlong Mu, 2016).

The gut-brain axis plays a critical role in many neurological disorders. It affects neuropsychiatric disorders like anxiety, depression, schizophrenia, dementia and autism (Kim YK, 2018). It also affects neurodevelopmental disorders in children including ADHD, autism, learning disabilities, intellectual developmental disorder, motor disorders, and specific learning disorders (EPA, 2015).

In this article, we will explore the link between ADHD and the gut brain axis.

ADHD (attention-deficit/hyperactivity disorder) is a brain disorder marked by a pattern of inattention and/or hyperactivity-impulsivity that interferes with normal functioning or development (National Institute of Mental Health, 2019).

You may have heard the name ADD, or attention deficit disorder. This is an out-of-date term. It was previously used to describe people who have problems paying attention but aren’t hyperactive. Instead of using the term ADD, such a person is now said to have the type of ADHD called predominantly inattentive.

The term ADHD became official in May 2013, when the American Psychiatric Association established the diagnostic criteria for different mental health conditions in the ‘Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition (American Psychiatric Association, 2013).

Some facts about ADHD:

  • ADHD is one of the most widespread neurodevelopmental conditions (Ming X, 2018).
  • The Center for Disease Control and Prevention (CDC) reports that 11% of all children (1 million) in the U.S. aged 4-17 have been diagnosed with ADHD in 2016. This represents a 43% increase since 2003. (Centers for Disease Control and Prevention, 2018).
  • In 2015, the CDC said the total number of Americans, adults and children, with ADHD continues to rise from 7.8% in 2003 to 9.5% in 2007 and to 11% in 2011 (Centers for Disease Control and Prevention, 2018).
  • ADHD rates are growing. Figures from 2003 to 2015/ 2016 show increases of 43% in children and 41% in all Americans with ADHD (Centers for Disease Control and Prevention, 2018).
  • The causes of the disorder remain unclear (Ming X, 2018). We do have some ideas on causes and they will be discussed later in this article so please do read on for information on causes of ADHD.
  • Boys have a higher incidence of ADHD than girls. In 2015-2016, Children and Adults with ADHD (CHADD) reported that 14% of children with ADHD were boys vs. 6.3% who were girls (Children and Adults with Attention-Deficit/Hyperactivity Disorder, 2019).
  • Co-occurring conditions are quite common in children (2-17 years of age). 63.8% of children with ADHD had at least one co-occurring condition: (Children and Adults with Attention-Deficit/Hyperactivity Disorder, 2019)
    • 51.5% had behavioral problems
    • 32.7% had anxiety problems
    • 16.8% had depression
    • 13.7% had autism spectrum disorder
    • 1.2% had Tourette syndrome
    • 1% (of adolescents) had a substance abuse disorder

Common symptoms of ADHD are:

  • difficulty focusing and concentrating on tasks
  • being easily distracted
  • forgetting to complete tasks
  • interrupting people while they’re talking
  • having difficulty sitting still

The National Institute of Mental Health further characterizes ADHD into three types; Inattention, Hyperactivity and Impulsivity: (National Institute of Mental Health, 2019)

  • Inattention: being easily sidetracked from the task at hand, lacking persistence, difficulty sustaining focus/concentration
  • Hyperactivity: appearing to move constantly, including when it is not appropriate, excessively fidgeting, tapping or talking, extreme restlessness or wearing others out with constant activity
  • Impulsivity: acting in a rash manner without first thinking about one’s actions, a desire for immediate reward or inability to delay gratification, being socially intrusive and excessively interrupting others

It is clear that the incidence of ADHD is growing. Part of this increase can be potentially attributed to better diagnoses. But in Functional Medicine (FM) we always want to dig deeper to get to the root causes and to understand why ADHD is on the rise. So what is going on?

In ADHD, there is an underlying metabolic and functional disorder in the brain. There are abnormalities in the neurotransmitter (NT) system in the brain, triggered by an imbalance of the neurotransmitters dopamine and noradrenaline (All About ADHD). These two NTs play an important role in the transmission of stimuli in nerve cells. When these neurotransmitters are out of balance, faulty information processing will result in the affected areas of the brain (All About ADHD).

With ADHD, the parts of the brain that are responsible for control and coordinating information processing are particularly affected (All About ADHD). This negatively impacts a person’s ability to concentrate, as well as their perception and impulse control (All About ADHD).

Causes of ADHD:

No single risk factor explains ADHD. Both inherited and non-inherited factors contribute and their effects are interdependent. (Thapar A, 2013)

In conventional medicine, it is widely accepted that ADHD is an inherited condition, although the precise cause or causes remain unclear. Studies have shown that children with a parent diagnosed with ADHD have a greater than 50% chance of having ADHD (Ming X, 2018).

However, only a small number of genes have been reported to have any effect in predicting ADHD and that effect is relatively small (Ming X, 2018).

The more likely explanation is that ADHD is due to a combination of genetic and environmental epigenetic factors. These environmental risk factors and potential gene-environment interactions increase the risk for the disorder (Banerjee TD, 2007). Environmental factors can be ‘inherited’. Growing up in and living in the same household means people – whether children or parents – are sharing their environment and are likely to be experiencing the same environmental factors.

Environmental factors influencing and potentially increasing the risk of developing ADHD are: (Banerjee TD, 2007) and (Ming X, 2018):

  • food dyes and additives in the diet
  • lead contamination and exposure to other heavy metals
  • micronutrient and mineral deficiencies
  • cigarette and alcohol exposure
  • maternal smoking during pregnancy
  • low birth weight
  • perinatal stress
  • neurotransmitter disruption

It is estimated that between 10% and 40% of the difference in heredity may be due to environmental factors (Ming X, 2018). Yet these known environmental factors do not account for all of the difference in heritability (Ming X, 2018).

More recent research into causes has highlighted the role of the gut, and specifically the microbiome-gut-brain axis, in ADHD (Ming X, 2018) and (Cenit MC, 2017). Please see our recent article on anxiety and the gut-brain axis for a full explanation of the microbiome-gut-brain axis.

In ADHD, it has been found that:

  • Dysbiosis, or an altered gut microbiome, and specifically increased Bifidobacterium species of gut bacteria, exist in patients and may contribute to the clinical expression of ADHD (Ming X, 2018).
  • Dysbiosis is associated with gastrointestinal symptoms, such as constipation, diarrhea, abdominal pain, and flatulence. A number of studies have noted an increase in these gastrointestinal symptoms in neurodevelopmental disorders and specifically in ADHD (Ming X, 2018).
  • Dysbiosis can lead to gut inflammation, due to a large amount of pro-inflammatory microbes. This can cause increased intestinal permeability and inflammation, allowing microbes into circulation through a leaky gut, which may lead to low-grade systemic inflammation and immune dysregulation (Ming X, 2018).
  • This low-grade systemic inflammation may gradually damage the blood–brain barrier and possibly cause the neuroinflammation seen in ADHD (Ming X, 2018).
  • Diet influences ADHD symptoms by affecting the gut microbiome through its impact on brain functioning and behavior. One proposed mechanism for these effects of gut microbiota is through their ability to synthesize neurotransmitters (NTs) and their precursors (Aarts E, 2017). Precursors of the NTs involved in ADHD (dopamine, noradrenaline and serotonin) are produced by the gut microbiota. Their precursors are amino acids (phenylalanine, tyrosine and tryptophan) which may pass through the gut lining, enter into circulation, and cross the blood-brain barrier (Aarts E, 2017). Once in the brain, they could potentially influence NT production. As a result, differences in gut bacteria may impair brain function and behavior relevant to ADHD (Aarts E, 2017). In fact, a higher amount of the gut bacteria Bifidobacterium in babies has been associated with increased risk of developing ADHD in childhood (Aarts E, 2017).

In conventional medicine, treatment used for ADHD is medication, behavioral treatment and/or a combination of medication and behavioral treatment. The most commonly prescribed medication for ADHD is Ritalin. Ritalin is not a cure for ADHD but it can improve concentration, reduce impulsivity and promote calmness (NHS, 2018). It does have side effects such as an increase in blood pressure and heart rate, difficulty sleeping, loss of appetite, headaches and stomach aches (NHS, 2018).

One recent study has just come out with findings that Ritalin changes the brain structure in children with ADHD (Reneman D, 2019). These effects were not found in adults with ADHD in the same study. The scans of the children’s brains showed changes in their brain structure in a short period of 4 months on Ritalin (Reneman D, 2019). These differences were in the left hemisphere of the brain and involved the process of coating nerve fibers, such as nerve fiber density, size and myelination (Reneman D, 2019). Patients can be on Ritalin and other medications for years, despite there being little knowledge about its long-term effect on the brain.

In Functional Medicine, we like to dig deeper and look for the root cause(s). As there is no single cause of ADHD, in FM the approach we take is to look at all the factors found in research to be influencing ADHD.

We cannot change genetics but we can affect how genes express. We cannot change any prenatal events as mentioned above such as maternal stress, poor diet, smoking or alcohol use during pregnancy and/or a low birth weight.

We can, however, change and improve a number of health factors, which will improve the condition of ADHD. Please stay tuned for a list of these factors and specifically what you can do in the case of ADHD in next week’s article ‘ADHD & the Gut: Are they linked & what is the link? Part 2’ of ‘The Gut-Brain Axis Series’.

 

References:

Aarts E, E. T. (2017). Gut microbiome in ADHD and its relation to neural reward anticipation. PLOS One.

ADDitude. (2019, March 18). MTHFR: Another Piece of the ADHD-Genetics Puzzle. Retrieved August 14, 2019, from ADDitude: https://www.additudemag.com/mthfr-adhd-genetics-puzzle/

All About ADHD. (n.d.). Causes of ADHD. Retrieved July 30, 2019, from All About ADHD: https://www.adhd-information.com/adhd-causes.html

American Psychiatric Association. (2013). Diagnostic and Statistical Manual of Mental Disorders (DSM–5). American Psychiatric Association.

Banerjee TD, M. F. (2007). Environmental risk factors for attention‐deficit hyperactivity disorder. Acta Paediatrica.

Bowling A, S. J. (2017). Cybercycling Effects on Classroom Behavior in Children With Behavioral Health Disorders: An RCT. Pediatrics.

Cenit MC, N. I.-F. (2017). Gut microbiota and attention deficit hyperactivity disorder: new perspectives for a challenging condition. European Child & Adolescent Psychiatry, 1081–1092.

Centers for Disease Control and Prevention. (2018, September 21). Attention-Deficit / Hyperactivity Disorder (ADHD). Retrieved July 28, 2019, from www.cdc.gov: https://www.cdc.gov/ncbddd/adhd/data.html

Children and Adults with Attention-Deficit/Hyperactivity Disorder. (2019). General Prevalence of ADHD. Children and Adults with Attention-Deficit/Hyperactivity Disorder.

Chou WJ, L. M. (2018). Dietary and nutrient status of children with attention-deficit/ hyperactivity disorder: a case-control study. Asia Pacific Journal of Clinical Nutrition, 1325 – 1331.

Chunlong Mu, Y. Y. (2016). Gut Microbiota: The Brain Peacekeeper. Frontiers in Microbiology.

EPA, U. S. (2015, October). America’s Children and the Environment. Neurodevelopmental Disorders | Health.

Hariprasad VR, A. R. (2013). Feasibility and efficacy of yoga as an add-on intervention in attention deficit-hyperactivity disorder: An exploratory study. Indian Journal of Psychiatry.

Hernandez-Reif M, F. T. (2000). Attention Deficit Hyperactivity Disorder: Benefits from Tai Chi. Journal of Bodywork and Movement Therapies.

Kim YK, S. C. (2018). The Microbiota-Gut-Brain Axis in Neuropsychiatric Disorders: Patho-physiological Mechanisms and Novel Treatments. Current Neuropharmacology.

Lee MJ, C. M. (2018). Heavy Metals’ Effect on Susceptibility to Attention-Deficit/Hyperactivity Disorder: Implication of Lead, Cadmium, and Antimony. International Journal of Environmental Research and Public Health.

Lissak. (2018). Adverse physiological and psychological effects of screen time on children and adolescents: Literature review and case study. Environmental Research.

Ming X, C. N. (2018). A Gut Feeling: A Hypothesis of the Role of the Microbiome in Attention-Deficit/Hyperactivity Disorders. Sage Journals.

Mitchell JT, M. E. (2017). A Pilot Trial of Mindfulness Meditation Training for ADHD in Adulthood: Impact on Core Symptoms, Executive Functioning, and Emotion Dysregulation. Journal of Attention Disorders.

National Institute of Mental Health. (2019). www.nimh.nih.gov. Retrieved July 28, 2019, from NIH National Institute of Mental Health: https://www.nimh.nih.gov/health/topics/attention-deficit-hyperactivity-disorder-adhd/index.shtml

NHS. (2018, May 30). Treatment ADHD. Retrieved August 14, 2019, from NHS: https://www.nhs.uk/conditions/attention-deficit-hyperactivity-disorder-adhd/treatment/#

Pelsser LM, B. J. (2009). ADHD as a (non) allergic hypersensitivity disorder: a hypothesis. Pediatric Allergy and Immunology.

Reneman D, B. C. (2019). White Matter by Diffusion MRI Following Methylphenidate Treatment: A Randomized Control Trial in Males with Attention-Deficit/Hyperactivity Disorder. Radiology.

Sharif MR, M. M. (2015). The Relationship between Serum Vitamin D Level and Attention Deficit Hyperactivity Disorder. Iranian Journal of Child Neurology.

Slykerman RF, C. C. (2019). Exposure to antibiotics in the first 24 months of life and neurocognitive outcomes at 11 years of age. Psychopharmacology.

Taylor AF, K. F. (2011). Could Exposure to Everyday Green Spaces Help Treat ADHD? Evidence from Children’s Play Settings. Applied Psychology.

Thapar A, C. M. (2013). What have we learnt about the causes of ADHD? Journal of Child Psychology and Psychiatry.

The Mayo Clinic. (2017, September 28). ADHD diet: Do food additives cause hyperactivity? Retrieved August 14, 2019, from The Mayo Clinic: https://www.mayoclinic.org/diseases-conditions/adhd/expert-answers/adhd/faq-20058203

Wang LJ, Y. Y. (2019). Dietary Profiles, Nutritional Biochemistry Status, and Attention-Deficit/Hyperactivity Disorder: Path Analysis for a Case-Control Study. Journal of Clinical Medicine.

Ystrom E, G. K. (2017). Prenatal Exposure to Acetaminophen and Risk of ADHD. Pediatrics.

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August 7, 2019

Anxiety & the Gut: Are they linked & what is the link?

by Dr. Miles Nichols and Nicola Schuler, CNTP, MNT

A tremendous amount of recent research has established a link between the gut and the brain. There is a gut-brain axis, which regulates brain function and behavior (Chunlong Mu, 2016).

The gut-brain axis plays a critical role in neuropsychiatric disorders like anxiety, depression, schizophrenia, dementia and autism (Kim YK, 2018).

Anxiety has been shown to be deeply affected by the gut–brain axis. In this article, we will explore this connection in more detail and suggest ways to address anxiety using the latest research on the gut-brain link.

  • Anxiety disorders are the most common mental illness in the U.S., affecting 40 million adults in the United States age 18 + (1% of the population) every year (Anxiety and Depression Association of America Facts & Statistics).
  • Approximately one in four adults in the US will suffer from an anxiety disorder at some point in their lives. (Murrough JW, 2015)
  • Worldwide, 4 out of every 100 people suffer from an anxiety disorder, but North America appears to have a higher than average rate (8 in 100), while East Asia had the lowest rate (3 in 100). (Mulpeter, 2017)
  • Patients with anxiety disorders experience substantial physical and emotional discomfort and have elevated rates of substance use and medical illnesses. (Murrough JW, 2015)
  • Anxiety disorders are more common among women, who were nearly twice as likely to be affected as men. Other at-risk groups include adults under age 35, and people with chronic diseases such as cardiovascular disease, COPD, diabetes, and cancer. (Mulpeter, 2017)

Anxiety can be mild to debilitating. The main feature of anxiety disorders is excessive fear and anxiety and behavioral disturbances that occur as a result. Common anxiety signs and symptoms include (Mayo Clinic, Anxiety disorders):

  • Feeling nervous, restless or tense
  • Having a sense of impending danger, panic or doom
  • Having an increased heart rate
  • Breathing rapidly (hyperventilation)
  • Sweating
  • Trembling
  • Feeling weak or tired
  • Trouble concentrating or thinking about anything other than the present worry
  • Having trouble sleeping
  • Experiencing gastrointestinal (GI) problems
  • Having difficulty controlling worry
  • Having the urge to avoid things that trigger anxiety

How does the gut brain axis work in relation to anxiety?

The gut brain axis refers to biochemical signaling between the gut and the brain. Broadly defined, the gut–brain axis includes the nervous system, the immune system and the endocrine (or hormone) system.

The ‘microbiome–gut–brain axis’ explicitly includes the role of gut flora in the biochemical signaling events that take place between the GI tract and the brain. This is important because gut microbiota, i.e. bacteria in the gut, regulate neurophysiological behaviors through neural, endocrine and immune pathways (Collins, 2012).

  • Vagus nerve: Neurons are nerve cells which transmit nerve impulses and communicate with each other. Neurons are in the brain and the gut and they communicate with each other via the vagus nerve. The vagus nerve is a large nerve connecting the brain and the gut, sending signals in both directions, and is involved in control of mood, immune response, digestion, and heart rate (Breit S, 2018).  Breathing, meditation and yoga stimulate the vagus nerve and decrease mood and anxiety symptoms (Breit S, 2018).
  • HPA axis: The gut brain axis includes the HPA axis. The HPA axis is part of the endocrine (hormone) system and regulates stress and the stress hormones. Stress, especially chronic stress, affects and changes the microbiome (Liu L, 2018). Stress activates the HPA axis and increases cortisol (a stress hormone) levels leading to increases in anxiety levels and intestinal microbiota changes (Liu L, 2018). Thus the change in the microbiome affects mood. Conversely, the intestinal microbiota can also inhibit the increase of cortisol through the HPA axis to relieve anxiety and depression (Liu L, 2018). Therefore, the HPA axis plays a bi-directional role in the gut-brain axis.
  • Neurotransmitters or NT’s: Neurotransmitters are chemical messengers produced in the brain. They transmit signals from one neuron to another neuron, muscle cell, or gland cell. They control feelings and emotions. The neurotransmitter serotonin contributes to feelings of happiness (Anguelova M, 2003). Gamma-aminobutyric acid, or GABA, is another NT which helps control feelings of fear and anxiety (Mazzoli R, 2016). Neurotransmitters are also produced by gut cells and the trillions of microbes living there. For example, a large proportion of serotonin is produced in the gut (Anguelova M, 2003).
  • Short-chain fatty acids or SCFAs: The trillions of microbes that live in the gut also make other chemicals that affect how the brain works (Clarke G, 2014). Gut microbes produce short-chain fatty acids such as butyrate, propionate and acetate. They are related to regulating the immune system and their absence or reduced status in the gut can contribute to inflammation in the gut (Hirschberg S, 2019). In a study on anxiety, low levels of SCFA-producing bacteria were found in patients with anxiety as compared to healthy controls without anxiety (Jiang HY, 2018).
  • Immune system: The gut plays an important role in immunity. 70-80% of immune cells are located in the gut. Gut bacteria provides crucial signals for immune system function. The gut controls what enters the body and what does not. If there is intestinal permeability, or leaky gut, inflammation occurs. The immune system will over-react and this can lead to disorders associated with inflammation like depression, Alzheimer’s and autoimmunity. Chronic low-grade inflammation causes cytokines, inflammatory molecules, to be released into the blood, further affecting the immune system. Intestinal microbiota contain molecules that can cause inflammation. The indirect effects of intestinal microorganisms on the immune system can cause changes in the circulating levels of pro-inflammatory and anti-inflammatory cytokines, which in turn have direct impacts on brain function (Kim YK, 2018).

Anxiety & the Gut

Anxiety is a multi-factorial disorder prompted by certain environmental factors in genetically susceptible individuals (Cenit MC, 2017). There is an element of complex gene-environment interactions and gut microbiota changes that precede the onset of neuropsychiatric diseases such as anxiety (Cenit MC, 2017).

Risk factors include genetics, brain chemistry, personality, and life events. (Anxiety and Depression Association of America Facts & Statistics). Anxiety can be triggered by a difficult or traumatic event (i.e. an accident, divorce, death of a loved one), trauma, chronic stress and in many other situations.

While genetics play a role in the possibility of developing anxiety, there are people with the same genetics who develop anxiety and others who never experience anxiety as an issue. In this article we will focus on modifiable risk factors that you can take some action towards changing.

There is a clear link between the gut brain axis and anxiety. About 60% of anxiety and depression patients have disturbed gastrointestinal function, such as in irritable bowel syndrome (IBS) (Liu L, 2018).

Treatment to date for anxiety is often therapy, typically in conjunction with anti-anxiety or anti-depression medications such as SSRIs (selective serotonin reuptake inhibitors). In the case of generalized anxiety, treatment response rates for SSRIs of between 60 and 75% are generally reported in studies, compared to response rates of between 40–60% for placebo (Lach G, 2018). While these rates are not insignificant, the issue with using SSRIs is that they do not address the root causes of the anxiety.

It is more effective to identify and address the root cause or causes of anxiety and avoid taking medication for the rest of your life. Furthermore, these drugs can have unintentional side effects. Antidepressants are well known to have antimicrobial effects and can damage the health of the gut microbiome (Lach G, 2018). This will reshape not only brain biochemistry, but also the gut microbiota, and not for the better (Lach G, 2018). The negative implications of antidepressants on gut health may result in intensifying anxiety over the long term, in a vicious cycle.

Furthermore, anxiety has various causes. If the root cause or causes are not addressed, treatment success rates over time are low (Kim YK, 2018). Emerging evidence of the interactions among the brain, gut, and microbiome can help those suffering from anxiety and the mechanisms underlying these complex interactions (Kim YK, 2018).

Gut health is critically important in cases of anxiety.  Before we address specific solutions to anxiety, let’s take a look at what can negatively impact the health of the gut microbiome (Mu C, 2016):

  • Diet
    • Sugar & excess refined carbohydrates
    • GMOs
    • Highly processed foods
    • Lack of fiber
    • Excess caffeine
    • Excess alcohol
  • Genetic make-up of the individual
  • Inflammation, particularly if in the gut
  • GI issues like dysbiosis (an unbalanced gut flora), leaky gut and many others
  • Antibiotics, SSRIs for depression or anxiety, NSAIDs and other medications
  • Circadian rhythm dysregulation
  • Stress – physical or emotional
  • Environmental toxins – mold, chemicals & others
  • Habits – news/ media, electronic use, lack of sleep, addictions, etc.
  • Abusive relationships, excessively stressful job, and history of trauma that has not been adequately processed/ resolved

Solutions:  What can you do?

Fix your gut: Like many other conditions we have written about in our blog, it is necessary to work on gut healing when addressing anxiety.

Inflammation in the gut is a key factor in neuropsychiatric conditions like anxiety. We’ve mentioned leaky gut but there can be other sources of gut inflammation.

Dysbiosis (an imbalance of good and bad bacteria in the gut), bacterial overgrowth like SIBO (small intestinal bacterial overgrowth), yeast overgrowth like Candida, a shortage of SCFAs, histamine intolerance, parasites, IBS, and other gut issues can all cause gut inflammation.

We recommend working with a functional medicine practitioner to identify any GI issues, infections or overgrowths when addressing anxiety.

Additionally, it can be helpful to work with an expert on issues like rebalancing neurotransmitter levels, increasing SCFAs in your gut, stimulating vagus nerve function, rebalancing an imbalanced HPA axis or stress response, and ensuring that your overall gut function is optimal.

Diet: Certain foods are particularly helpful for the gut-brain axis.

Some of the most important ones are:

  • Omega-3 fats: These are good fats found in wild salmon, sardines, anchovies, mackerel and herring as well as in high quantities in the brain. Studies in humans and animals show that Omega-3 fats can increase good bacteria in the gut and reduce risk of brain disorders (Robertson RC, 2017), (RJT Mocking, 2016).
  • Probiotic-rich fermented foods: Yogurt, kefir, sauerkraut, natto, kimchi and kvass all contain healthy microbes that are beneficial to gut health.  One study found that fermentation enhances the specific nutrient and phytochemical content of foods, which is associated with mental health (Selhub EM, 2014). In addition, the microbes (Lactobacillus and Bifidobacteria species) associated with fermented foods may also influence brain health via direct and indirect pathways (Selhub EM, 2014).
  • Prebiotic foods:  Prebiotics have been reported to improve inflammation and to alleviate psychological distress (Kim YK, 2018).  These foods contain non-digestible fibers that promote the growth of beneficial gut microbiota such as Lactobacillus and Bifidobacterium, benefiting the microbial-gut-brain axis (Kim YK, 2018). Prebiotic foods include lentils, apple cider vinegar, dandelion greens, raw garlic, raw or very lightly cooked onion, leeks, raw asparagus, green bananas, green plantains, potatoes that have been cooked then cooled 24 hours (served cold or at room temperature, as is common in potato salad), apples and others.
  • Polyphenol-rich foods: Clove, berries, raw cocoa, green tea, olive oil and coffee all contain polyphenols, which are plant chemicals that are digested by gut bacteria. Polyphenols increase healthy bacteria in the gut and can improve neuro-inflammation, inflammation in the brain, commonly found with depression and anxiety (Matarazzo I, 2018). These foods have been reported to promote cognitive function (Filosa S, 2018). One of our favorite polyphenol-rich foods we recommend to patients is pomegranate juice. While we normally don’t recommend fruit juices due to sugar content, research on pomegranate has shown such a high concentration of polyphenols that it tends to favorably impact blood sugar, likely due to its beneficial effects on the gut (here’s a link to an article we did on pomegranate).
  • Tryptophan-rich foods: Tryptophan is an amino acid that is converted into the neurotransmitter serotonin. Serotonin regulates mood, anxiety, stress, aggression, feeding, cognition and sexual behavior (Olivier B, 2015). Low serotonin is thought to be associated with anxiety (Olivier B, 2015). By increasing tryptophan through diet, the gut is better nourished to make serotonin. Foods that are high in tryptophan include turkey, eggs and cheese.

 Probiotics

Probiotics are live microorganisms that stimulate the growth of gut bacteria and enhance gut health.  Studies on probiotics have shown that low-grade inflammation is reduced, gut permeability is restored, and the composition of the gut microbiome changes (Kim YK, 2018). Probiotics modulate the processing of information that is strongly linked to anxiety and depression and influence the stress response. (K Schmidt, 2014).

Multiple studies have looked at specific strains of probiotics and found the following:

  • Lactobacillus casei Shirota – Improved mood in those who initially had poor mood, Better long-term memory (Kim YK, 2018)
  • L. helveticus, B. longum – Improvement of anxiety and depression symptoms (Kim YK, 2018)
  • L. acidophilus, L. casei, L. rhamnosus, L. bulgaricus, B. lactis, B. breve, B. longum, S. thermophiles – Improvement of anxiety and depression symptoms (Kim YK, 2018)
  • B. bifidum, B. lactis, L. acidophilus, L. brevis, L. casei,  L. salivarius, Lactococcus lactis – Improvement of self-reported mood and sadness (Kim YK, 2018)
  • L. casei Shirota – Decreased anxiety symptoms (Kim YK, 2018)
  • Lactobacillus rhamnosus – Reduced stress-induced anxiety- and depression-like behaviors in mice, Decreased levels of stress-induced hormones and changed levels of the NT GABA throughout the brain (Sharon G, 2016)
  • Lactobacillus rhamnosus and Lactobacillus helveticus – Reduced anxiety-like behaviors in mice in another study (Sharon G, 2016)
  • Bacteroides fragilis – Corrected anxiety-like and repetitive behaviors in mice, Partially restored an impaired microbiome, Restored intestinal barrier function (Sharon G, 2016)

Prebiotics

  • Prebiotics increase the level of Bifidobacterium, a healthy gut bacteria in the intestinal tract, benefitting the microbial-gut-brain axis (Kim YK, 2018)
  • The effect of prebiotics and increased Bifidobacterium can increase levels of Lactobacillus, Bacteroide and Bifidobacterium, other probiotic strains, in the gut (Kim YK, 2018)
  • Prebiotics increase the production of SCFAs as a result of the healthier gut flora profile (Kim YK, 2018)
  • In both animal and human studies, prebiotics have improved inflammation and reduced psychological distress (Kim YK, 2018)
  • One study showed prebiotics reduced stress and its effects, which positively impacts the microbiome (Kim YK, 2018)

Fecal Microbiota Transplantation (FMT)

FMT is the transplant of healthy human feces to a patient with severe gut dysbiosis, in order to regulate the intestinal microbiota of the patient. When the normal gut microbiota are destroyed, for example by excessive antibiotic treatment or other negative substances like GMO foods, it can be challenging to recover a normal healthy bacterial flora. FMT can be extremely helpful in these situations (Kim YK, 2018).

FMT can be an effective treatment for IBS. IBS showed a remission rate of 36-89% after FMT treatment (Kim YK, 2018). Recently, the first FMT trial in a neuropsychiatric area took place. In this eight-week clinical trial to evaluate the impact of FMT on GI and psychiatric symptoms, both GI and psychiatric symptoms were significantly reduced and Improvements were measured to have lasted eight weeks after treatment (Kim YK, 2018).

Many factors can affect anxiety and mood. Some may be a relatively simple and quick fix that you can do on your own like diet changes, while others may be more complex like FMT. Some other approaches to consider with anxiety include:

  • Balance blood sugar – Living on the blood sugar rollercoaster with excessive swings in blood sugar create and/or worsen mood issues like anxiety and depression.
  • Reduce caffeine consumption – Caffeine is a stimulant and can make you feel on edge or anxious. This is especially true for people who are slow metabolizers of caffeine.
  • Identify food sensitivities and allergies and eliminate those foods – Common allergenic foods like gluten, dairy, soy and corn can contribute to symptoms.
  • Address a potential magnesium deficiency – Research has shown that magnesium can help decrease anxiety in magnesium–deficient people (Boyle NB, 2017).
  • Reduce, where possible, and manage stress levels
  • Practice mindfulness and meditate daily
  • Work with an expert to process any past traumas
  • Deep diaphragmatic breathing – Breathing exercises can help to stimulate the vagus nerve and slow both heart rate and blood pressure.

If you or someone you know is suffering from anxiety, get in touch with our clinic today. Book a free 15-min discovery call to see how we can help you with your symptoms. We can answer your questions and help you book an initial consult with one of the functional medicine doctors in our clinic.

References:

Anguelova M, B. C. (2003). A systematic review of association studies investigating genes coding for serotonin receptors and the serotonin transporter: I. Affective disorders. Mol Psychiatry.

Anxiety and Depression Association of America Facts & Statistics. (n.d.). Retrieved July 9, 2019, from Facts & Statistics: https://adaa.org/about-adaa/press-room/facts-statistics

Boyle NB, L. C. (2017). The Effects of Magnesium Supplementation on Subjective Anxiety and Stress-A Systematic Review. Nutrients.

Breit S, K. A. (2018). Vagus Nerve as Modulator of the Brain-Gut Axis in Psychiatric and Inflammatory Disorders. Front Psychiatry.

Cenit MC, S. Y.-F. (2017). Influence of gut microbiota on neuropsychiatric disorders. World J Gastroenterol.

Chunlong Mu, Y. Y. (2016). Gut Microbiota: The Brain Peacekeeper. Frontiers in Microbiology.

Clarke G, S. R. (2014). Minireview: Gut Microbiota: The Neglected Endocrine Organ. Mol Endocrinol.

Collins, S. M. (2012). The interplay between the intestinal microbiota and the brain. Nat. Rev. Microbiol. 10.

Filosa S, D. M. (2018). Polyphenols-gut microbiota interplay and brain neuromodulation. Neural Regen Res.

Hirschberg S, G. B. (2019). Implications of Diet and The Gut Microbiome in Neuroinflammatory and Neurodegenerative Diseases. Int J Mol Sci.

Jiang HY, Z. X. (2018). Altered gut microbiota profile in patients with generalized anxiety disorder. J Psychiatr Res. .

K Schmidt, P. C. (2014). Prebiotic intake reduces the waking cortisol response and alters emotional bias in healthy volunteers. Psychopharmacology (Berl).

Kim YK, S. C. (2018). The Microbiota-Gut-Brain Axis in Neuropsychiatric Disorders: Patho-physiological Mechanisms and Novel Treatments. Current Neuropharmacology.

Lach G, S. H. (2018). Anxiety, Depression, and the Microbiome: A Role for Gut Peptides. Neurotherapeutics.

Liu L, Z. G. (2018). Gut–Brain Axis and Mood Disorder. Front Psychiatry.

Matarazzo I, T. E. (2018). Psychobiome Feeding Mind: Polyphenolics in Depression and Anxiety. Curr Top Med Chem.

Mayo Clinic, Anxiety disorders. (n.d.). Retrieved July 9, 2019, from Mayo Clinic: https://www.mayoclinic.org/diseases-conditions/anxiety/symptoms-causes/syc-20350961

Mazzoli R, P. E. (2016). The Neuro-endocrinological Role of Microbial Glutamate and GABA Signaling. Front Microbiol.

Mu C, Y. Y. (2016). Gut Microbiota: The Brain Peacekeeper. Front. Microbiol.

Mulpeter, K. (2017, January 31). These Groups Are Most at Risk for Anxiety Disorders. Retrieved July 9, 2019, from Health: https://www.health.com/anxiety/anxiety-disorders-women

Murrough JW, Y. S. (2015). Emerging Drugs for the Treatment of Anxiety. Expert Opin Emerg Drugs.

Olivier B, O. (2015). Serotonin: a never-ending story. Eur J Pharmacol.

RJT Mocking, I. H. (2016). Meta-analysis and meta-regression of omega-3 polyunsaturated fatty acid supplementation for major depressive disorder. Transl Psychiatry.

Robertson RC, S. O. (2017). Omega-3 polyunsaturated fatty acids critically regulate behaviour and gut microbiota development in adolescence and adulthood. Brain Behav Immun. .

Selhub EM, L. A. (2014). Fermented foods, microbiota, and mental health: ancient practice meets nutritional psychiatry. J Physiol Anthropol.

Sharon G, S. T. (2016). The Central Nervous System and the Gut Microbiome. Cell.

 

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July 29, 2019

Mast Cell Activation Syndrome: What is it and could it be affecting your health? Part 2

by Dr. Miles Nichols and Nicola Schuler, CNTP, MNT

Mast Cell Activation Syndrome: Part 2

Last week, we published Part 1 on Mast Cell Activation Syndrome, in which we discussed what it is, symptoms and diagnostic criteria, including a quiz on MCAS. In this week’s article, MCAS Part 2, we cover causes, triggers, treatment and most importantly, what you can do about MCAS.

As a review, Mast Cell Activation Syndrome or MCAS is a collection of symptoms resulting from mast cells or MCs which have been inappropriately activated (Afrin, 2013).  When MCs become overactive, they can cause serious problems in the body.

For a fuller explanation, please refer back to MCAS: Part 1. Also please take our quiz on MCAS if you suspect it may be affecting you.

Cause:

The cause of MCAS is not known. There is certainly a genetic component to the syndrome but this is currently not fully understood (Afrin, 2013). In our clinical observation, those with mold illness and Lyme disease tend to have a very high incidence of MCAS also. Gut imbalances, overgrowths, and infections are also part of the root in many cases.

Triggers:

It is helpful to look to triggers of MCAS while also addressing causes.

Potential Mast Cell Triggers:  (Symptoms And Triggers Of Mast Cell Activation, 2019)

  • Heat, cold or sudden temperature or weather changes
  • Stress: emotional or physical, including pain
  • Allergies, which can be both IgE-mediated or non–IgE-mediated triggers such as:
  • Environmental allergy to pollution, pollen, pet dander, etc.
  • Chemical allergy to chemical odors, perfumes, scents, industrial chemicals or dyes
  • Allergy to a particular food or beverage including alcohol
  • Exercise
  • Fatigue
  • Medications (opioids, NSAIDs, antibiotics and some local anesthetics)
  • Venoms (bee, wasp, mixed vespids, spiders, fire ants, jelly fish, snakes, biting insects, flies, mosquitos and fleas, etc.)
  • Infections
    • Viral
    • Bacterial
    • Fungal
  • Sunlight

In addition to these better known triggers listed above, lesser known triggers could be:

Heavy metals toxicity:

Heavy metals like aluminum and mercury have been shown to destabilize mast cells. In fact, these metals are used in vaccines in order to elicit a heightened inflammatory immune response. Lead, cadmium, and bismuth have also been found to activate mast cells and cause mast cell mediator release (S. Bent, 1992).

Gut health:

If you have been following us and our blog articles for any length of time, you will know that often we come back to gut health as a cause, trigger or contributing factor in most conditions. MCAS is no different.

Various gut infections, issues or dysbiosis in the gut can contribute to MCAS. Specifically, parasites, bacterial and/or viral infections, or bacterial and/or fungal overgrowths in the gut can activate mast cells (R. Saluja, 2012). Parasitic worms, also known as helminths, can over stimulate mast cells (Lee TD, 1986). The fungus Candida albicans can lead to an over stimulation or reaction in mast cells (José Pedro Lopes, 2015). Gut dysbiosis may cause mast cell disorders as the interactions between different strains of gut bacteria and MCs are quite complex (Afrin LB, 2015).

CIRS:

CIRS or Chronic Inflammatory Response Syndrome occurs as a result of exposure to mold. It results from a particular genetic susceptibility to mold which causes a reduced ability to clear mycotoxins (mold toxins) from the body. This syndrome can lead to a constant activation of mast cells or MCAS (Kritas SK, 2018).

Is there a Treatment for MCAS?:

Therapies for MCAS generally aim to control and improve the condition by inhibiting overactive mediator production and release, by blocking released mediators, and/or managing the consequences of excessive mediators (Afrin, 2013). Many therapies are available. Of course we recommend working with a skilled functional medicine office that has experience with MCAS, gut issues, Lyme, and mold.

There is currently no way to predict which set of therapies will best control an individual person’s condition. A systematic, trial-and-error approach usually succeeds in finding significant relief from symptoms. Comprehensive functional lab tests looking for root causes are very important.

Lifespan for most MCAS patients appears normal, but quality of life can be mildly to severely impaired if no correct diagnosis and effective treatment is given (Afrin, 2013).

What can you do about MCAS?: In order to fully get to the root cause(s) of MCAS, it is essential to look at these steps in great detail:

  • Identify and treat any infections – GI or others
  • Gut healing
  • Heavy metals detox
  • Identify toxins and allergens, then avoid or treat
  • Screen for CIRS (mold illness) and Lyme + co-infections – treat if present

Other helpful ways to address MCAS are:

Diet: To help manage MCAS and your symptoms, you can go on a Low Histamine Diet. We have recently written an article on histamine intolerance with the full details of a low histamine diet so please see here for details. Histamine is one of the many mediators released by mast cells. By lowering histamine, you will lower this mediator and the potential mast cell activation. You may need to experiment a little to see exactly which foods trigger your reactions. Low histamine is a great place to start then you can track foods and symptoms to tailor the diet more individually.

Supplements: It can also be useful to use supplements to increase DAO production and lower histamine. We included some details on these in our article on histamine intolerance. These include vitamin C and quercetin which help to reduce histamine load. You can also take a DAO supplement like DAO Hist-Digest, which we have formulated for our patients. DAO supplements are designed to increase diamine oxidase (DAO) enzyme, an enzyme that helps break down histamine in the gut. Pre-cursors to DAO can also help and include B6 (in P5P form), copper and B2. Co-factors for DAO production also include B12, iron and vitamin C.

Avoid certain medications: There are medications that decrease DAO activity; anti-arrythmics, some antibiotics, some painkillers, antidepressants, some psychiatric meds, antihistamines, antihypertensives, antimalarials, bronchodilators, diuretics, mucolytics, muscle relaxants and antiseptics. These are best avoided as DAO is required to break down histamine. It is best to also avoid medications that liberate, and therefore increase, histamine. These include some painkillers, antiflogistics, antibiotics, anti-hypotensives, antihypertensives, antitussives, cytostatics, diuretics, iodine-containing contrast mediums, local anaesthetics, muscle relaxants and narcotics. Certain medications inactivate B6, which is necessary to produce DAO. These include antihypertensives, antibiotics and hormonal contraception drugs containing estrogen.

Probiotics impact histamine levels: Some probiotics increase histamine levels (Lactobacillus Casei, Lactobacillus Delbrueckii, Lactobacillus Bulgaricus) so are best avoided with MCAS. Other probiotic strains decrease histamine. They can degrade histamine and are preferable to use in the case of histamine intolerance: Lactobacillus Plantarum, Lactobacillus Rhamnosus, Bifidobacter species and possibly soil based organisms like bacillus subtilis. Please see our article on histamine intolerance.

Mast cell stabilizers can help. There are a vast number of natural mast cell stabilizers:

  • Various flavonoids including quercetin (capers, apples), EGCG (green tea) and silymarin (milk thistle) (Walsh, 2013)
  • Coumarins including ellagic acid (strawberries, raspberries, blackberries, cherries) (Walsh, 2013)
  • Phenols including resveratrol (grapes) and curcumin (turmeric) (Walsh, 2013)
  • Terpenoids including menthol, the cannabinoids (cannabis), ginkgolide and bilobalide (Ginkgo biloba), and the curcuminoids (turmeric, mustard seed) (Walsh, 2013)
  • The amino acid theanine (green tea, mushrooms) (Walsh, 2013)

H1 and H2 blockers: H1 and H2 blockers are over the counter antihistamines.  They can be helpful for many people in minimizing symptoms. However, they do not get to the root causes and in some cases can exacerbate MCAS over the long-run. We may use them on a case-by-case basis in our clinic, if we think they will help a patient.

Reduce and manage stress: Stress causes the body to release a number of hormones. One in particular, CRH, Corticotropin-Releasing Hormone, can activate mast cells and cause them to release their mediators. This can make someone more vulnerable to allergic and autoimmune conditions (Elenkov IJ, 1999).

Sweat out toxins: Toxins such as the heavy metals arsenic, cadmium, lead, and mercury (Sears ME, 2012), phthalates (found in many cosmetic and personal care products) (Genuis SJ, 2012) and Bisphenol A (BPA) (found in plastic food and drink containers) (Genuis SJ B. S., 2012) can all destabilize mast cells and potentially trigger MCAS. Making sure that you sweat is one way for these toxins to leave the body. Going to the sauna to sweat and exercising regularly to induce sweating are ways in which you can mobilize toxins and increase toxic outflow from your body.

Sleep /Manage circadian rhythm: Mast cell activity and mediator-release follows the circadian rhythm of the body. It will increase if the sleep wake cycle is disturbed. For this reason, focus on getting regular high-quality sleep and practice good sleep hygiene in order to keep mast cell activity to a minimum (Pia Christ, 2018).

Others issues like excessive estrogen and low methylation can contribute to high histamine levels. These are best addressed with the help of an experienced functional medicine practitioner.

 

If you suffer from MCAS, allergies or simply have undiagnosed symptoms, then get in touch with us today. We can help to identify whether or not you have MCAS and more importantly, help you get to the root causes and work towards minimizing symptoms. Book a discovery call today with someone from our staff. We can answer your questions and help you book an initial consult with one of the functional medicine doctors in our clinic.

 

References:

Become Mold Illness Free. (2019). Retrieved 6 25, 2019, from Mold Illness Made Simple: https://www.moldillnessmadesimple.com/

Chris Kresser. (2019, 5 28). Retrieved 6 26, 2019, from https://chriskresser.com: https://chriskresser.com/could-your-histamine-intolerance-really-be-mast-cell-activation-disorder/

Mast Cell Activation Syndrme Variants. (2019). Retrieved 6 25, 2019, from The Mastocytosis Society Mast Cell Diseases: https://tmsforacure.org/overview/mast-cell-activation-syndrome-variants/

Overview & Diagnosis. (2019). Retrieved 6 25, 2019, from The Mastocytosis Society Mast Cell Diseases: https://tmsforacure.org/overview/

Symptoms And Triggers Of Mast Cell Activation. (2019). Retrieved 6 25, 2019, from The Mastocytosis Society Mast Cell Diseases: https://tmsforacure.org/symptoms/symptoms-and-triggers-of-mast-cell-activation/

Afrin LB, K. A. (2015). Mast Cell Activation Disease and Microbiotic Interactions. Clinical Therapeutics, 941-53.

Afrin, L. B. (2013). Presentation, diagnosis, and management of mast cell activation syndrome. In L. B. Afrin, Mast Cells: Phenotypic Features, Biological Functions and Role in Immunity (pp. 155-232). Nova Science Publishers, Inc.

Akin C, V. P. (2010). Mast cell activation syndrome: Proposed diagnostic criteria. The Journal of Allergy and Clinical Immunology, 1099-104.

Akin, C. (2017). Mast cell activation syndromes. The Journal of Allergy and Clinical Immunology.

Anand P, S. B. (2012). Mast cells: an expanding pathophysiological role from allergy to other disorders. Naunyn-Schmiedeberg’s Archives of Pharmacology, 657-70.

Elenkov IJ, W. E. (1999). Stress, corticotropin-releasing hormone, glucocorticoids, and the immune/inflammatory response: acute and chronic effects. The Annals of the New York Academy of Sciences.

EZ da Silva, M. J. (2014). Mast cell function: a new vision of an old cell. Journal of Histochemistry and Cytochemistry, 698–738.

Genuis SJ, B. S. (2012). Human elimination of phthalate compounds: blood, urine, and sweat (BUS) study. Scientific World Journal.

Genuis SJ, B. S. (2012). Human excretion of bisphenol A: blood, urine, and sweat (BUS) study. International Journal of Environmental Research and Public Health.

Gerhard J Molderings, S. B. (2011). Mast cell activation disease: a concise practical guide for diagnostic workup and therapeutic options. Journal of Hematology & Oncology, 10.

José Pedro Lopes, M. S. (2015). Opportunistic pathogen Candida albicans elicits a temporal response in primary human mast cells. Scientific Reports.

Kritas SK, G. C. (2018). Impact of mold on mast cell-cytokine immune response. Journal of Biological Regulators & Homeostatic Agents, 763-768.

Lee TD, S. M. (1986). Mast cell responses to helminth infection. Parasitology Today, 186-91.

Lichtenberger, D. F. (2015, April 11). DukeHeartCenter/3-mcas-frank-lichtenberger. Retrieved 6 25, 2019, from www.slideshare.net: https://www.slideshare.net/DukeHeartCenter/3-mcas-frank-lichtenberger

Pia Christ, A. S. (2018). The Circadian Clock Drives Mast Cell Functions in Allergic Reactions. Frontiers in Immunology.

  1. Saluja, M. M. (2012). Role and Relevance of Mast Cells in Fungal Infections. Frontiers in Immunology, 146.
  2. Bent, C. G. (1992). The effects of heavy metal ions (Cd2+, Hg2+, Pb2+, Bi3+) on histamine release from human adenoidal and cutaneous mast cells. Inflammation Research, C321–C324.

Sears ME, K. K. (2012). Arsenic, cadmium, lead, and mercury in sweat: a systematic review. International Journal of Environmental Research and Public Health.

Tae Chul Moon, A. D. (2014). Mast Cell Mediators: Their Differential Release and the Secretory Pathways Involved. Frontiers in Immunology, 569.

Valent, P. (2013). Mast cell activation syndromes: definition and classification. European Journal of Allergy and Clinical Immunology, 417-424.

Walsh, D. F. (2013). Twenty‐first century mast cell stabilizers. British Journal of Pharmacolgy.

 

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July 18, 2019

Mast Cell Activation Syndrome:  What is it and could it be affecting your health? Part 1

by Dr. Miles Nichols and Nicola Schuler, CNTP, MNT

Mast Cell Activation Syndrome: Part 1

This is Part 1 of our 2-part series on Mast Cell Activation Syndrome. In Part 1, we will discuss what is Mast Cell Activation Syndrome, symptoms and diagnostic criteria. Next week in Part 2, stay tuned for information on causes, triggers, treatment and most importantly, what you can do about MCAS.

Introduction:

Mast Cell Activation Syndrome or MCAS is a collection of symptoms resulting from mast cells or MCs which have been inappropriately activated (Afrin, 2013).  When MCs become overactive, they can cause serious problems in the body.

MCAS and its symptoms can present as chronic and persistent or recurring periodically (Afrin, 2013). It usually appears relatively early in life via unknown mechanisms. It is possible that an interaction of environmental factors with inherited risk factors is the cause (Afrin, 2013).

It initially appears often in childhood or adolescence but symptoms are non-specific. Often all of MCAS’s symptoms are non-specific, which can lead to decades of mysterious illness and incorrect diagnoses before a correct diagnosis of MCAs is determined (Afrin, 2013).

Mast cell activation syndrome is different from mastocytosis. In mastocytosis, there is an excessive growth or amount of mast cells. Mastocytosis can also occur when the mast cells produced have some sort of genetic defect (Gerhard J Molderings, 2011). Mastocytosis is very rare and not usually triggered by an irritant (Gerhard J Molderings, 2011).

In MCAS, due to some type of trigger (we will discuss possible triggers in Part 2 next week), mast cells become overactive in some people, leading to the development of mast cell activation syndrome (Valent, 2013). Mast cell activation causes chronic inflammation that causes mild to life-threatening symptoms (Valent, 2013).

Symptoms:  The chart below gives a detailed overview of all of the symptoms of MCAS (Lichtenberger, 2015).

MCAS‐related symptoms may be mild, moderate, severe, or even life‐threatening  (Valent, 2013). The severity of MCAS depends on a number of different factors, including genetic susceptibility, the number of mast cells involved, which chemicals are released in the reaction, the type of allergen, the presence of a specific IgE allergy and the possible presence of certain comorbidities (i.e.: one or more additional conditions co-occurring with the primary condition of MCAS) (Valent, 2013).

MCAS was first recognized in 1991 and not identified as a condition until 2007 (Afrin, 2013). Diagnostic criteria were not in place until 2010 (Akin C, 2010).

So what is it?

Definition: Mast cells are white blood cells in the immune system. Mast cells are involved in various important functions such as certain immune system processes like inflammation, defense against pathogens and allergic reactions (EZ da Silva, 2014). They are also involved in the formation of new blood cells, wound healing, the development of immune tolerance, and the maintenance of blood-brain barrier function (EZ da Silva, 2014).

As part of the immune system, mast cells produce inflammatory histamine, cytokines and other chemicals.  These chemicals that they release are referred to as ‘mediators’. There are over 200 different types of mediators that they release, including histamine, tryptase, prostaglandins, leukotrienes and others (Tae Chul Moon, 2014). Cytokines can be positive or problematic, but are generally thought to be pro-inflammatory overall and we see this evidenced by MCAS significantly involving inflammation.

MCAS occurs if something goes wrong with the mast cells. In MCAS, a normal amount of mast cells are present but they are over-activated out of proportion to the perceived threat, causing them to release excessive amounts of mediators (Gerhard J Molderings, 2011).

Mast cell activation commonly happens in the case of an allergy. The allergic reaction begins when the allergen interacts with IgE antibody complexes which are on the surface of sensitized mast cells (Walsh, 2013). This causes a series of downstream signaling events within the mast cell. This process leads to the release of chemical mediators such as histamine from mast cells as well as the production of cytokines and chemokines, which are inflammatory molecules of the immune system. The actions of these mediators as well as other immune cells are responsible for the effects of an IgE‐mediated allergic reaction (Walsh, 2013). Mast cells are central to both the development and maintenance of allergic diseases.

MCAS can occur as an indirect result of another disease or condition and be unrelated to an allergy. An IgE-type allergy can be a cause of secondary MCAS, but other diseases can cause secondary MCAS also (Mast Cell Activation Syndrme Variants, 2019).

It used to be thought that histamine was the primary mediator released by mast cells. But we now know that there are hundreds of mediators involved. Due to the vast number of possible mediators and the large diversity of both direct and indirect, local and remote effects caused by these mediators released by MCs, MCAS can present itself quite differently in different people (Akin, 2017).  Thus the symptoms of MCAS can vary by person, based on which mediators are released by the overactive mast cells:

Possible Effects of Some Mast Cell Mediators (Symptoms And Triggers Of Mast Cell Activation, 2019)

MEDIATOR POSSIBLE EFFECTS
Histamine Flushing, itching, diarrhea, hypotension
Leukotrienes Shortness of breath
Prostaglandins Flushing, bone pain, brain fog, cramping
Tryptase Osteoporosis, skin lesions
Interleukins Fatigue, weight loss, enlarged lymph nodes
Heparin Osteoporosis, problems with clotting/bleeding
Tumor Necrosis Factor-α Fatigue, headaches, body aches

This list is not exhaustive and is just to serve as an example. Mast cells secrete many different types of mediators responsible for numerous symptoms (Symptoms And Triggers Of Mast Cell Activation, 2019). Furthermore, mast cells are found in all human tissue in the body, so MCAS can potentially have an effect within every organ system of the body (Gerhard J Molderings, 2011). It has been found to be associated with conditions such as obesity, diabetes, skin conditions, irritable bowel syndrome (IBS), depression, autoimmune conditions and possibly others (Anand P, 2012).

In fact, some clinicians are beginning to think that histamine intolerance issues could be MCAS, which would make it a more common condition as histamine intolerance is seen more frequently than MCAS is (Chris Kresser, 2019).

Diagnosis:

There are three criteria to officially diagnose MCAS:

  1. the symptoms recur in separate episodes or are chronic
  2. tryptase, one of the possible mast cell mediators, is measured as elevated during and after an episode and
  3. symptoms decrease in a ‘complete and major’ response to medications that inhibit histamine and other mediators (Overview & Diagnosis, 2019).

Testing:

There is no definitive test for MCAS but there are a number of biomarkers that can aid in coming to a diagnosis. The markers below can be useful in confirming a diagnosis of MCAS and in tracking the progress of treatment (Become Mold Illness Free., 2019). Most of these biomarkers are mediators released by mast cells:

  • DAO
  • Histamine
  • Ratio between DAO and Histamine
  • Tryptase
  • Chromogranin A
  • Prostaglandin F2 alpha
  • Prostaglandin D2
  • Heparin
  • N-methylhistamine

In addition to these diagnostic criteria and tests, there is a questionnaire to recognize symptoms of mast cell activation disease in a standardized manner (Afrin LB M. G., 2014).

We will continue next week with Part 2 of Mast Cell Activation Syndrome, when we will discuss causes, triggers, treatment and most importantly, what you can do about MCAS. Please be sure to read MCAS Part 2.

 

References:

Become Mold Illness Free. (2019). Retrieved 6 25, 2019, from Mold Illness Made Simple: https://www.moldillnessmadesimple.com/

Chris Kresser. (2019, 5 28). Retrieved 6 26, 2019, from https://chriskresser.com: https://chriskresser.com/could-your-histamine-intolerance-really-be-mast-cell-activation-disorder/

Mast Cell Activation Syndrme Variants. (2019). Retrieved 6 25, 2019, from The Mastocytosis Society Mast Cell Diseases: https://tmsforacure.org/overview/mast-cell-activation-syndrome-variants/

Overview & Diagnosis. (2019). Retrieved 6 25, 2019, from The Mastocytosis Society Mast Cell Diseases: https://tmsforacure.org/overview/

Symptoms And Triggers Of Mast Cell Activation. (2019). Retrieved 6 25, 2019, from The Mastocytosis Society Mast Cell Diseases: https://tmsforacure.org/symptoms/symptoms-and-triggers-of-mast-cell-activation/

Afrin LB, K. A. (2015). Mast Cell Activation Disease and Microbiotic Interactions. Clinical Therapeutics, 941-53.

Afrin, L. B. (2013). Presentation, diagnosis, and management of mast cell activation syndrome. In L. B. Afrin, Mast Cells: Phenotypic Features, Biological Functions and Role in Immunity (pp. 155-232). Nova Science Publishers, Inc.

Akin C, V. P. (2010). Mast cell activation syndrome: Proposed diagnostic criteria. The Journal of Allergy and Clinical Immunology, 1099-104.

Akin, C. (2017). Mast cell activation syndromes. The Journal of Allergy and Clinical Immunology.

Anand P, S. B. (2012). Mast cells: an expanding pathophysiological role from allergy to other disorders. Naunyn-Schmiedeberg’s Archives of Pharmacology, 657-70.

Elenkov IJ, W. E. (1999). Stress, corticotropin-releasing hormone, glucocorticoids, and the immune/inflammatory response: acute and chronic effects. The Annals of the New York Academy of Sciences.

EZ da Silva, M. J. (2014). Mast cell function: a new vision of an old cell. Journal of Histochemistry and Cytochemistry, 698–738.

Genuis SJ, B. S. (2012). Human elimination of phthalate compounds: blood, urine, and sweat (BUS) study. Scientific World Journal.

Genuis SJ, B. S. (2012). Human excretion of bisphenol A: blood, urine, and sweat (BUS) study. International Journal of Environmental Research and Public Health.

Gerhard J Molderings, S. B. (2011). Mast cell activation disease: a concise practical guide for diagnostic workup and therapeutic options. Journal of Hematology & Oncology, 10.

José Pedro Lopes, M. S. (2015). Opportunistic pathogen Candida albicans elicits a temporal response in primary human mast cells. Scientific Reports.

Kritas SK, G. C. (2018). Impact of mold on mast cell-cytokine immune response. Journal of Biological Regulators & Homeostatic Agents, 763-768.

Lee TD, S. M. (1986). Mast cell responses to helminth infection. Parasitology Today, 186-91.

Lichtenberger, D. F. (2015, April 11). DukeHeartCenter/3-mcas-frank-lichtenberger. Retrieved 6 25, 2019, from www.slideshare.net: https://www.slideshare.net/DukeHeartCenter/3-mcas-frank-lichtenberger

Pia Christ, A. S. (2018). The Circadian Clock Drives Mast Cell Functions in Allergic Reactions. Frontiers in Immunology.

R. Saluja, M. M. (2012). Role and Relevance of Mast Cells in Fungal Infections. Frontiers in Immunology, 146.

S. Bent, C. G. (1992). The effects of heavy metal ions (Cd2+, Hg2+, Pb2+, Bi3+) on histamine release from human adenoidal and cutaneous mast cells. Inflammation Research, C321–C324.

Sears ME, K. K. (2012). Arsenic, cadmium, lead, and mercury in sweat: a systematic review. International Journal of Environmental Research and Public Health.

Tae Chul Moon, A. D. (2014). Mast Cell Mediators: Their Differential Release and the Secretory Pathways Involved. Frontiers in Immunology, 569.

Valent, P. (2013). Mast cell activation syndromes: definition and classification. European Journal of Allergy and Clinical Immunology, 417-424.

Walsh, D. F. (2013). Twenty‐first century mast cell stabilizers. British Journal of Pharmacolgy.

 

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July 4, 2019

HISTAMINE INTOLERANCE

by Dr. Miles Nichols and Nicola Schuler, CNTP, MNT

 

What is histamine?

Histamine is a chemical that is found in foods and is made in the body (1). Histamine is released from mast cells, within the immune system, when an allergen is detected by the body (1).

Histamine is also is produced in the body from the amino acid histidine, which is a type of protein (1). Histamine occurs in food as a by-product of the fermentation of histidine. It is a chemical which is produced by bacteria during fermentation, storage or decay.

Histamine plays an important role in the immune system. It causes an immediate inflammatory response. It serves as a warning to the immune system, telling the body about any potential attackers. Histamine causes blood vessels to swell, or dilate, so that white blood cells can quickly find and attack the infection or problem.

Histamine plays other roles in the body as well. As a neurotransmitter, it communicates important messages to and from the brain and spinal cord (1). These messages are related to arousal and attention. This partly explains why OTC anti-histamines that cross the blood-brain barrier, such as diphenhydramine or Benadryl, act as sedatives (1).

Histamine is also involved in stimulating the parietal cells, found in the stomach, to secrete stomach acid, which is critical for breaking down food in the stomach and for good digestion (2). Too much histamine can be one cause of excessive secretion of stomach acid. This can lead to acid reflux / heartburn (GERD).

Histamine Intolerance is an increased sensitivity to histamine and/or an excessive build-up of histamine in the body.

An excessive amount of histamine is suspected to result from various sources:

  • Allergic response(s)
  • Eating large quantities of histamine-containing foods or beverages
  • Consumption of foods or other substances that cause histamine to be released
  • Impaired ability for enzymes in the body to break it down (3)

The enzymes that can break down histamine are diamine oxidase (DAO) and histamine N-methyl transferase (HNMT) (3).

There are two primary categories of issues:

  1. An increased amount of histamine in the body
  2. Decreased activity of the enzymes that break down histamine and remove it from the body

In addition to these categories, approximately 1% of the population experience adverse reactions to what is considered a “normal” level of histamine in food (3). This typically presents more often in people who are middle-aged (3). High levels of histamine can make a person feel unwell but the majority of people tolerate the amounts found in a regular diet without any issues.

A histamine reaction is the body’s natural immune response, but if histamine is not broken down properly, it can lead to histamine intolerance (HI). This is why OTC medications like Claritin can help with an allergic histamine reaction. Claritin is an anti-histamine which blocks and decreases histamine’s action.

What are the symptoms of excess histamine?

The onset and severity of histamine intolerance symptoms can vary greatly between individuals, but common complaints are (3):

  • Flushing
  • Migraines and headaches
  • Respiratory problems including: asthma, nasal congestion, sneezing, difficulty breathing
  • Skin conditions like: itching, rashes, dermatitis, hives or eczema, swelling
  • Gastrointestinal problems such as: nausea, reflux, vomiting, abdominal pain/cramps, diarrhea
  • Dizziness, low blood pressure, and irregular heartbeat
  • Difficulty falling & staying asleep
  • Anxiety
  • Abnormal menstrual cycle
  • Fatigue
  • Joint pain

 How is it diagnosed?

Diagnosis of histamine intolerance has been based on low serum levels of DAO (the enzyme responsible for breaking down histamine), the presence of gastrointestinal disorders and the improvement of symptoms with a low histamine diet (4). Some additional blood markers like whole blood histamine and a few others can also point to histamine issues.

What are the causes of high histamine?

Intolerance to histamine is primarily thought to be caused by previous or current gastrointestinal problems (such as SIBO or small intestinal bacterial overgrowth, dysbiosis, leaky gut, inflammation of the gut), toxic burden, and/or genetics.

There is evidence that dysbiosis, or an alteration of the gut microbiome, is related to the incidence of all food intolerances, and especially to histamine intolerance (5). Dysbiosis is an imbalance in the types and amounts of bacteria in the gut. It means there are too many pathogenic or bad bacteria and too few good or health-promoting bacteria in the gut microbiome. It is very often associated with disease.

One study analyzed the microbiome of people with histamine intolerance (5). They found increased amounts of certain pathogenic bacteria like Proteobacteria, and a reduced level of good bacteria such as Bifidobacteriaceae / Bifidobacterium (5). This imbalance and lower bacterial diversity can both point to dysbiosis, or a problematic balance of bacteria in the gut. Additionally, this study found an impaired intestinal barrier, or leaky gut, in this patient group (5).

Histamine has a negative effect on gut permeability. Dysbiosis in histamine intolerant patients may contribute to mucosal inflammation of the gut (5). This in turn could favor the development of a leaky gut as well as the reduction of intestinal DAO leading to elevated histamine levels and symptoms in sensitive people (5).

Mast Cell Activation Syndrome (MCAS)

Toxic burden can also be a cause of mast cell activation syndrome (MCAS). Mast cells are cells that produce histamine. When mast cells are activated, they produce and release a high level of histamine, in addition to other chemicals. MCAS is a condition where there seems to be overly active mast cells and high histamine levels. This creates an inflammatory response and contributes to very similar symptoms as histamine intolerance.

As mentioned, gut dysbiosis and gut conditions like small intestinal bacterial overgrowth (SIBO) can be a cause of histamine issues (including MCAS). There are also common issues where toxins accumulate and that also seems to be correlated with higher levels of MCAS. Not all of the causes of MCAS are known.

About 1 in 4 people have a genetic predisposition in which there is a change in the HLA-DR gene. This gene is involved with the immune system’s ability to identify certain kinds of toxins and to eliminate them from the body effectively. In people with this genetic predisposition, there is an increased potential for these toxins to bioaccumulate and cause inflammation. In many cases mold toxins, or mycotoxins, are one of the toxins that are not appropriately identified.

This is a significant issue, given that about 1 in 2 American homes have been shown to have water damage and may have high levels of mold toxins. Because only 1 in 4 people have the gene, not everyone in the home will become ill. This makes mold toxin illness a common issue that is often underdiagnosed.

Although the reason why there is a link between MCAS and mold toxin illness remains unknown, many clinicians who treat mold issues see a high correlation between these two conditions.

Our blog post next week will focus on MCAS so be sure to look out for that article and read further on MCAS.

Enzymes involved in decreasing histamine

The main histamine enzyme in the gut is diamine oxidase (DAO), while other areas like the skin, spinal cord, lungs and other organs rely on an enzyme called histamine N-methyltransferase (HNMT) (5). Though both enzymes play an important role in histamine break down, DAO is the main enzyme responsible for breaking down ingested histamine. Any deficiency in DAO will likely result in symptoms of histamine intolerance (5).

The causes of high histamine (3, 5)

  • Allergies (IgE reactions)
  • Bacterial overgrowth (SIBO)
  • Leaky gut (intestinal permeability)
  • GI bleeding
  • Dysbiosis
  • Gut inflammation
  • Mold toxin illness
  • Fermented alcohol like wine, champagne, and beer and histamine-rich foods
  • Diamine oxidase (DAO) deficiency

Causes of low DAO (6)

  • GI disorders such as gluten intolerance, celiac disease, leaky gut, SIBO, inflammatory bowel disease
  • Inflammation from Crohn’s, ulcerative colitis, and inflammatory bowel disease
  • DAO-blocking foods: alcohol, energy drinks, and black, mate and green teas
  • Nutrient deficiencies for co-factors of DAO (vitamin B6, vitamin C, copper, vitamin B12, and iron)
  • Genetic mutations that lead to a reduced DAO enzyme activity (common in people of Asian-descent)
  • Medications that block DAO or prevent its production including: Non-steroidal anti-inflammatory drugs (ibuprofen, aspirin), Antidepressants (Cymbalta, Effexor, Prozac, Zoloft), Immune modulators (Humira, Enbrel, Plaquenil), Antiarrhythmics (propanolol, metaprolol, Cardizem, Norvasc), Antihistamines (Allegra, Zyrtec, Benadryl) and Histamine (H2) blockers (Tagamet, Pepcid, Zantac)

Although histamine blockers, a class of acid-reducing drugs, seem like they would help prevent histamine intolerance, these medications can actually deplete DAO levels in the body.

Treatment

Symptoms either improve or disappear with a low histamine diet (4). One study found a significant increase in serum DAO levels in patients with strict and even occasional compliance to a low histamine diet (4). The study authors concluded that a low histamine diet not only improves symptoms in HI, but also leads to an increase in serum DAO which correlates with the degree of diet compliance (4).

It is also critical to work on gut health to alleviate histamine intolerance. We know that dysbiosis and other GI issues are often present with histamine intolerance (3, 5, 6). Eradicating any gut infections, overgrowths or inflammation will be vital for rebalancing the gut and ensuring a healthy balance of gut flora.

The Basics of the Low Histamine Diet

Eat freshly cooked and prepared real food! Packaged and processed food can have high histamine levels. Eating fresh food is important because histamine levels increase the longer food is not refrigerated. Histamine levels can also increase in left-over or fermented food.

Unfortunately, the histamine content of different foods can vary quite substantially depending on the maturity of the food, storage time, and processing (7). So histamine levels can differ considerably within the same food product. For example, the histamine content in Emmental cheese varies from <0.1 to 2000 mg/kg and in smoked mackerel from <0.1 to 1788 mg/kg (7). These variations make it difficult to estimate the histamine content of individual meals. However, it is entirely possible to decrease histamine load by concentrating on low histamine foods and avoiding foods high in histamine (like cheese and fish) or foods that block DAO activity.

Low Histamine Foods to Eat:

  • Freshly cooked grass fed, wild, organic meat or poultry: red meat, steak, ham, chicken and turkey
  • Freshly caught wild fish
  • Cooked pastured eggs
  • Gluten-free grains: rice, quinoa, corn, millet, amaranth, teff
  • Pure peanut butter (although peanut butter can be contaminated with a mold toxin called aflatoxin)
  • Legumes (except soybeans & red beans)
  • Fresh fruits: mango, pear, watermelon, apple, kiwi, cantaloupe, grapes
  • All fresh vegetables (except tomatoes, spinach, avocado, and eggplant)
  • Dairy substitutes: coconut milk, rice milk, hemp milk
  • Cooking oils: olive oil, coconut oil
  • Leafy herbs
  • Herbal teas
  • Decaffeinated coffee
  • Honey & maple syrup

 

Some tips to keep in mind for food preparation:

  • Try to cook most of your own meals to avoid histamine
  • Avoid or limit eating canned foods and ready meals
  • Avoid heavily processed or junk foods: food dyes/artificial colors can be big triggers
  • Keep the kitchen clean
  • Refrigerate vigilantly as histamine forms on food as it spoils

 

Foods to Avoid:

To reduce histamine from food, avoid:

  • Foods high in histamine
  • Foods that release histamine
  • Foods that suppress DAO

Unfortunately, some research says certain foods are high in histamine and other research disagrees in some cases. Some foods are consistent across research studies. For this reason, we focus on the foods that are consistent across research studies. You may find that our list does not mention foods that other lists or research say is high in histamine. However, if one research study says a food is high in histamine and another says it is low, we have eliminated that food in order not to recommend avoiding things unnecessarily. It is important to have a varied healthy diet with few food restrictions, especially when we are not sure about whether those foods have high levels of histamine or not.

Histamine-Rich Foods (3):

  • Yeast or anything that contains it: alcohol, bread, pastries, and baked goods
  • Fermented foods: sauerkraut, vinegar, soy sauce, kefir, yogurt, kombucha, etc.
  • Vinegar-containing foods: pickles, mayonnaise, olives
  • Cured deli meats: bacon, salami, pepperoni, luncheon meats and hot dogs
  • Soured foods: sour cream, sour milk, buttermilk, soured bread, etc.
  • Dried fruit: apricots, prunes, dates, figs, raisins
  • Some citrus fruits: lemon and mandarin
  • Some other fruit: pineapple, banana, and avocado
  • Aged hard or semi-hard cheese including goat cheese (soft fresh cheese is okay)
  • Nuts: all nuts, especially walnuts, cashews
  • Smoked fish or canned anchovies
  • Bone broth
  • Certain spices: curry, mustard seed / mustard, and soy sauce

Histamine-Releasing Foods:

  • Alcohol
  • Banana
  • Nuts
  • Pineapple
  • Shellfish
  • Many artificial preservatives and dye

 

DAO-Blocking Foods (6):

  • Alcohol

In addition to alcohol releasing histamine and inhibiting DAO, there is also enzyme competition as some enzymes that can break down histamine are also involved in breaking down alcohol. The body may have to choose one of the two and this can further exacerbate histamine issues.

 

Probiotics and histamine: Probiotics impact histamine levels. Some increase histamine levels and others decrease histamine.

These probiotics can produce histamine – consider avoiding with histamine intolerance:

  • Lactobacillus Casei
  • Lactobacillus Delbrueckii
  • Lactobacillus Bulgaricus

These probiotics can degrade histamine and are preferable to use in the case of histamine intolerance:

  • Lactobacillus Plantarum
  • Lactobacillus Rhamnosus
  • Bifidobacter species
  • Possibly soil based organisms like bacillus subtilis
  • Some report benefit from Saccharomyces Boulardii

 

How to manage histamine intolerance:

  • In order to manage histamine intolerance, it is useful to follow a low histamine diet for 3 months. Avoid foods that either release histamine or block the action of DAO.
  • It can be helpful to take a DAO supplement.
  • Experiment with supplements that are pre-cursors to endogenous DAO production: vitamin B6 (in P-5-P form), copper and B2 (7). In addition, vitamin C can help to degrade excess histamine (7). Vitamin B12 may also help in some cases (we prefer methylcobalamin form of B12).
  • Some herbs like nettles and nutrients like quercetin can also help.
  • Healing the gut is an important step. This involves addressing SIBO and other potential gut infections or issues (parasites, celiac, inflammation, dysbiosis or others), as well as healing leaky gut.
  • Then re-introduce histamine foods, one food every 3 days, and observe reactions very carefully to see what can be tolerated without symptoms. Once symptoms are better under control and the overall histamine load is lower, it may be possible to tolerate some histamine foods, in a few months’ time.

 

There are many other factors involved with histamine intolerance and MCAS. For example, methylation is one issue that we did not discuss in this article, but low methylation can be associated with increased histamine. If you feel that you have several of the symptoms mentioned in this article, we recommend seeking guidance from a practitioner experienced with histamine intolerance and/or MCAS.

Please get in touch with us to help you manage and improve your histamine intolerance. We consult with clients world-wide. Use this link to get in touch: https://livinglovecommunity.com/book-15-min-discovery-call/

 

References:

  1. Purves D, Augustine GJ, Fitzpatrick D, et al. 2001. Neuroscience. 2nd edition. Sunderland (MA): Sinauer Associates; 2001. The Biogenic Amines. https://www.ncbi.nlm.nih.gov/books/NBK11035/
  2. University of Washington. Regulation of Acid Secretion. https://courses.washington.edu/conj/bess/acid/acidreg.html. Accessed June 17, 2019.
  3. Kohn 2014. Is There a Diet for Histamine Intolerance? J Acad Nutr Diet. 114: 1860.
  4. Lackner S, Malcher V, Enko D, Mangge H, et al. 2018. Histamine-reduced diet and increase of serum diamine oxidase correlating to diet complance in histamine intolerance. Eur J Clin Nutr. 73, 102–104.
  5. Schink M, Konturek PC, Tietz E, et al. 2018. Microbial Patterns Patients with Histamine Intolerance. J Physiol Pharmacol. 69, 4, 579-593. DOI: 10.26402/jpp.2018.4.09.
  6. MTHFR Support Australia. 2018. DAO Deficiency and Histamine: The Unlikely Connection. https://mthfrsupport.com.au/2016/09/dao-deficiency-and-histamine-the-unlikely-connection/. Accessed June 17, 2019.
  7. Reese I, Ballmer-Weber B, Beyer K et al. 2017. German Guideline for the Management of Adverse Reactions to Ingested Histamine. Allergo J Intl. 26: 72. doi.org/10.1007/s40629-017-0011-5.
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June 25, 2019

What is the Difference between Near and Far Infrared Light Therapies?

by Dr. Miles Nichols and Nicola Schuler, CNTP, MNT

Infrared radiation (IR), or infrared light, is a type of energy that’s invisible to the human eye but that can be felt as heat (1). IR is a type of electromagnetic radiation.

Electromagnetic radiation is a continuum of frequencies produced when atoms absorb and then release energy (1). From highest to lowest frequency, electromagnetic radiation includes gamma-rays, X-rays, ultraviolet radiation, visible light, infrared radiation, microwaves and radio waves (1). Together, these types of radiation make up the electromagnetic spectrum.

Within the electromagnetic spectrum, infrared waves occur at frequencies above those of microwaves and just below those of red visible light. Waves of infrared radiation are longer than those of visible light.

You might be thinking that radiation sounds bad for the body especially when you hear that microwaves are next on the spectrum.

However, there are two types of radiation:

  1. Ionizing – can damage DNA (genes)
  2. Non-ionizing – tends not to damage DNA

Infrared radiation is a non-ionizing form of radiation, which does not damage DNA (2). Ionizing radiation exposure can damage DNA. Ionizing forms are far ultraviolet radiation and x-rays.

Infrared radiation can be categorized into three groups according to wavelength, namely near infrared (NIR, 0.8–1.5 µm), middle infrared (MIR, 1.5–5.6 µm), and far infrared (FIR, 5.6–1000 µm) (3).

Infrared energy explains the concept of thermal imaging. Some infrared energy can be seen as heat. Some objects are so hot they emit visible light, such as fire (2). Other objects, such as humans, are not as hot and only emit infrared waves (2).

The human eye cannot see these infrared waves but instruments that can sense infrared energy, like night-vision goggles or infrared cameras, allow us to see the infrared waves emitting from humans and animals (2).

Everything in the universe emits some level of IR radiation (1). The two most obvious sources are the sun and fire. All living organisms benefit from the natural electromagnetic radiation of the sun.

Thermal radiation (or infrared) is a band of energy that has been used effectively for millennia to treat and ease certain maladies and discomforts (4). Heated saunas are one of the oldest methods of delivering radiation in a controlled environment and within a convenient treatment time (4).

What is Far InfraRed:

Far InfraRed Radiation or FIR relates to the longer wavelengths of radiation in the infrared spectrum, between 5.6 and 1000 micrometers (3). FIR wavelength cannot be perceived by the eyes, but its heat penetrates up to 1.5 inches (almost 4 cm) beneath the skin (4). FIR has been found to stimulate cells and tissue and is considered a promising treatment method for certain medical conditions (4).

There are new techniques for delivering FIR radiation to the human body. In fact, you may have heard of a far-infrared sauna. If not, you can Google the term and find lots of information and products.

Specialty lamps and saunas, delivering pure FIR radiation (eliminating completely the near and mid infrared bands), have become safe, effective, and widely used for the therapeutic benefits of FIR (4).

Clothing made with fibers containing FIR emitting ceramic nanoparticles, which is woven into the fabric, is being used to generate FIR radiation, and attain health benefits from its effects (4).

Benefits of FIR:

There are multiple medical applications of FIR that can improve health and reduce or even treat disease:

  • Reduces pain and inflammation (4)
  • Promotes cell repair post exposure to FIR (4)
  • Enhances circulation in the skin (4)
  • Protects against oxidative stress (4)
  • Enhances weight loss (4)
  • Stimulates cell proliferation, increases tissue regeneration (4)
  • FIR sauna therapy has been used to improve cardiac and vascular function and reduce oxidative stress in patients with chronic heart failure (5).
  • FIR saunas have a beneficial effect on quality of life in patients with type II diabetes. Physical health, general health, stress and fatigue all improved in the treatment group receiving FIR (6).
  • A study of patients with rheumatoid arthritis and ankylosing spondylitis showed a reduction in pain, stiffness, and fatigue during far infrared sauna therapy (8).
  • FIR has the effect of reducing the proliferation of some cancer cell lines (4). This suggests that FIR radiation may be used as an effective medical treatment for some cancer cells (4).
  • FIR therapy reduced symptoms of exercise-induced muscle damage in highly-trained athletes after a trail running race (8).
  • Modulates sleep: one study used a blanket containing FIR emitting ceramic discs and reported improved quality of sleep in the study subjects (9).
  • Gloves have been made out of FIR emitting fabrics and these gloves can be used to treat arthritis of the hands and Raynaud’s syndrome (10).
  • FIR therapy is effective in relieving pain in patients with chronic pain, chronic fatigue syndrome and fibromyalgia (3).
  • FIR benefitted patients who experienced persistent and progressively increasing phantom limb pain after amputation (3).
  • FIR stimulation alleviated depression in patients with insomnia by increasing serotonin (3).
  • FIR can reduce the pain of wounds after standard medical wound treatments. Wounds exposed to FIR had lower healing times (11).

Risks:

FIR is generally quite safe compared to other medical interventions. However, there are risks of infrared radiation exposure to the skin and the eyes. A potential concern is an increase in photo-aging (skin aging due to light) (12).

Infrared radiation can also harm tattooed skin and cause skin inflammation (13). The lens of the eye is very sensitive to infrared radiation and long-term exposure can contribute to cataract formation (14).

How to access FIR:

There are three main ways to benefit from FIR radiation:

  • FIR saunas
  • FIR ray devices
  • FIR emitting ceramics and fabrics (4)

FIR saunas are quite popular and there are many brands of FIR saunas that can be purchased for home use. In addition to saunas, there are also FIR lamps and clothing that can be purchased. For recommendations on a far-infrared sauna, call our office at 720-722-1143 or use our contact page.

What is Near Infrared:

Near Infrared Radiation or NIR relates to the shorter wavelengths of radiation in the infrared spectrum; NIR, 0.8–1.5 µm (3). NIR is used in the therapy called Photobiomodulation or PBM. We have just written an extensive article on Photobiomodulation, which you can find here.  It is a form of light therapy that uses near-infrared light over the brain, inside the nasal cavity, or over injuries or wounds (15).

The light is used to heal, improve tissue repair in wounds, bones and tendons, reduce pain and inflammation and restore and stimulate multiple physiological processes which repair damage caused by injury or disease (15). The healing occurs wherever the beam is applied. The light stimulates the cell’s natural healing and pain relief processes.

Benefits:

Photobiomodulation is used for a huge variety of health issues as it has a significant anti-inflammatory effect. (Again, please refer to our article on PBM for the full details)

  • The key applications of PBM for the future are in the areas of inflammation and autoimmunity (16).
  • Cognitive performance or brain injury (16)
  • Wound healing (16)
  • Arthritis (16)
  • Muscle healing (16)
  • Inflammatory Pain (16)
  • Lung inflammation and asthma (16)
  • Abdominal fat, obesity and type 2 diabetes (16)
  • Cancer (17)
  • Achilles tendinopathy (16)
  • Thyroiditis (16)
  • Psoriasis (16)
  • Hair loss (16)
  • Cognitive performance, memory and mood (18)
  • Cosmetic and aesthetic improvements (18)

Risks:

There are no known risks or side effects associated with PBM.

How to Find out More:

If you live in Colorado or are willing to travel to the Greater Denver Area, please book a discovery call with our clinic to find out more about PBM therapy. You can also call or text “PBM Therapy” or “FIR Sauna” to 720-722-1143. Click here to book a complimentary 15-minute discovery call now.

Which Type of Infrared Radiation – NIR or FIR – is Recommended to be Better for Health?

Based on multiple factors, we recommend NIR therapy over FIR therapy if you have to choose one. However in many cases we may suggest both!

This is because the sun emits 37% of its total energy in the near infrared range, and 3% in the far infrared range (19). Humans are biologically designed to use near infrared light, more so than far infrared light (19). It is now understood that the human body is partially photosynthetic and that we need sun light and near infrared for optimal health (19).

Near infrared is received at the cellular level in a way that far infrared is not. As we discussed in our article on PBM, the effect of near infrared on the cells of the body is an increase in cellular energy production that can then be used to repair and rejuvenate at the cellular level. Far infrared does not have the same cellular effect on the mitochondria of the cells (19). Thus, Near Infrared can provide greater rejuvenating effects over FIR.

Near Infrared as a wavelength has deeper tissue penetration. NASA has measured tissue penetration as deep as 23cm with near infrared (19), whilst FIR penetrates to only 4cm into the skin (4).

Thus, we recommend Photobiomodulation therapy (using Near Infrared Radiation) in most cases as an effective means to treating specific conditions and improving health versus using Far Infrared therapy. That being said, there can be enormous value to the detoxification from sweating that can be stimulated through FIR sauna therapy. This is very beneficial in many cases, but can also be achieved with standard saunas and does not require FIR technology in the sauna. For those purchasing a sauna, we do recommend the FIR technology to add some extra benefit.

 

References:

  1. Live Science. 2019. What is Infrared? https://www.livescience.com/50260-infrared-radiation.html. Accessed June 11, 2019.
  2. NASA Science. 2019. Tour of the Electromagnetic Spectrum. https://science.nasa.gov/ems/07_infraredwaves. Accessed June 11, 2019.
  1. Shui S, Wang X, Chiang JY, Zheng L. 2015. Far infrared therapy for cardiovascular, autoimmune and other chronic health problems: A systematic review. Exp Biol Med. v.240(10); 2015 Oct.
  1. Vatansever F, Hamblin 2012. Far infrared radiation (FIR): Its biological effects and medical applications. Photonics Lasers Med. doi: 10.1515/plm-2012-0034.
  2. Fujita S, Ikeda Y, Miyata M, Shinsato T, Kubozono T, Kuwahata S, Hamada N, Miyauchi T, Yamaguchi T, Torii H, Hamasaki S, Tei C. Effect of Waon therapy on oxidative stress in chronic heart failure. Circ J. 2011;75(2):348–56.
  3. Beever R. The effects of repeated thermal therapy on quality of life in patients with type II diabetes mellitus. J Altern Complement Med. 2010;16(6):677–81.
  4. Oosterveld FG, Rasker JJ, Floors M, Landkroon R, van Rennes B, Zwijnenberg J, van de Laar MA, Koel GJ. Infrared sauna in patients with rheumatoid arthritis and ankylosing spondylitis. A pilot study showing good tolerance, short-term improvement of pain and stiffness, and a trend towards long-term beneficial effects. Clin Rheumatol. 2009;28(1):29–34.
  5. Hausswirth C, Louis J, Bieuzen F, Pournot H, Fournier J, Filliard JR, Brisswalter J. Effects of whole-body cryotherapy vs. far-infrared vs. passive modalities on recovery from exercise-induced muscle damage in highly-trained runners. PLoS One. 2011;6(12):e27749.
  6. Inoué S, Kabaya M. Biological activities caused by far-infrared radiation. Int J Biometeorol. 1989;33(3):145–50.
  7. Ko GD, Berbrayer D. Effect of ceramic-impregnated “thermoflow” gloves on patients with Raynaud’s syndrome: randomized, placebo-controlled study. Altern Med Rev. 2002;7(4):328–35.
  8. Lin YH, Li TS. 2017. The Application of far Infrared in the Treatment of Wound Healing: A Short-Evidence Based Analysis. J Evid Based Complementary Altern Med.2017 Jan;22(1):186-188.
  9. Holzer AM, Athar M, Elmets CA. 2010. The other end of the rainbow: infrared and skin. J Invest Dermatol.2010 Jun;130(6):1496-9. doi: 10.1038/jid.2010.79.
  10. Chiang C, Romero L. 2009. Cutaneous lymphoid hyperplasia (pseudolymphoma) in a tattoo after far infrared light. Dermatol Surg.2009 Sep;35(9):1434-8. doi: 10.1111/j.1524-4725.2009.01254.x.
  11. Aly EM, Mohamed ES. 2011. Effect of infrared radiation on the lens. Indian J Ophthalmol.2011 Mar-Apr;59(2):97-101. doi: 10.4103/0301-4738.77010.
  12. Joovv. 2019. Photobiomodulation and Cancer: What is the Truth? www.//joovv.com/blogs/joovv-blog/photobiomodulation-cancer-truth. Accessed May 28 2019.
  13. Hamblin MR. 2017. Mechanisms and applications of the anti-inflammatory effects of photobiomodulation. AIMS Biophysics, 2017, 4(3):337-361. doi: 3934/biophy.2017.3.337.
  14. Hamblin MR, Nelson ST, Strahan JR. 2018. Photobiomodulation and Cancer: What is the Truth? Photomed Laser Surg.2018 May;36(5):241-245. doi: 10.1089/pho.2017.4401.
  15. Hamblin MR, de Sousa MVP, Agrawal T. 2017. Handbook of Low Level Laser Therapy. Singapore: Pan Stanford Publishing.
  16. Lifestyle Integration. Near Vs. Far Infrared Benefits. https://www.lifestyleintegration.com.au/learning-centre/articles/119-near-versus-far-infrared-benefits.html. Accessed June 11, 2019.
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