In the past, oxalate research was relegated to kidney-related disorders. Now much more is known.

Whether your interest is autism, cancer, chronic pain, autoimmunity, or generalized inflammation, understanding the role dietary oxalates can play is critical for your clients.

Inflammasome activation is a new discovery related to the immune system and oxalate – which can have some significant implications, especially with age-related disorders and chronic conditions.

What is the inflammasome? It is an innate part of the immune system involved with creating inflammation. It is now known that oxalate can tigger it. The inflammasome has been implicated with several age-related disorders including gout, type 2 diabetes, obesity, cancer, and neurodegenerative and cardiovascular disorders, [1] as well as autoimmune conditions.

So as we begin to understand a broader picture of the various ways high oxalates can be detrimental to optimal health, we can see how/why a low oxalate diet can be helpful for our clients.

Here is some of the latest research. The first study is on the inflammasome. The second is on oxalate and breast cancer, and we just mentioned the inflammasome connection to cancer. The final two research papers are on autism including a study on autism and oxalate, and a paper on diet for autism including the recommendation of a low oxalate diet.

Oxalate Triggers the Inflammasome

A review of the current literature surrounding oxalates and inflammasome activation is compelling.

In this scientific paper, researchers explain how when the body is burdened with oxalates (either through diet or endogenous production) the kidneys can be damaged by the build up. When this happens, blood levels of oxalate rise even more which can activate the inflammasome.

Researchers pointed out how reducing dietary oxalate is important in reducing inflammation that stems from inflammasome activation. In fact, the authors conclude: “Accordingly, inhibiting oxalate-induced inflammasome activation, or lowering plasma oxalate, may prevent or mitigate progressive renal damage in CKD, and also reduce morbidity and mortality due to systemic inflammation.”

Given that the inflammasome is associated with gout, type 2 diabetes, obesity, cancer, autoimmune conditions, and neurodegenerative and cardiovascular disorders it is critical for practitioners to understand the effects oxalate can have on the body, the inflammatory process, and disease, and the important role a low oxalate diet plays. With this new research, oxalates become even more important to consider when working with patients or clients facing age-related conditions involving the inflammasome. 

Reference: Ermer, T., Eckardt, K. U., Aronson, P. S., & Knauf, F. (2016). Oxalate, inflammasome, and progression of kidney disease. Current opinion in nephrology and hypertension, 25(4), 363. 

Breast cancer and oxalates – is there a link?

Research has tied excess oxalate build-up to breast cancer.

Two types of mice were involved in this study, namely BALB/c or BALB/c nude female mice. BALB/c mice had a wild type immune system.

The researchers found that injecting oxalates in the mammary fat pad region of BALB/c nude mice favored the growth of breast tumors. More specifically, the scientists reported that oxalates promoted the growth of MCF-7 and MDA-MB231 breast cancer cell lines as well as the normal breast cell line, MCF10A.

Moreover, the higher the oxalate concentration, the faster the breast tumors developed.

Interestingly, injecting oxalates in the animals’ back did not induce cancer suggesting that oxalates may cause only breast cells to proliferate abnormally.

BALB/c mice were also injected with oxalates but did not develop tumors although some of the animals did experience some swelling in the mammary fat pad area. Since this swelling disappeared within 24 to 48 hours, this could indicate that the oxalate may have triggered tumor formation, but the immune system of BALB/c mice was strong enough to destroy the cancer cells.

Given this new research, the potential role of oxalate in cancer should be researched much more extensively. And the use of a low oxalate diet and nutritional approach should be studied as well.

Reference: Castellaro, A. M., Tonda, A., Cejas, H. H., Ferreyra, H., Caputto, B. L., Pucci, O. A., & Gil, G. A. (2015). Oxalate induces breast cancer. BMC cancer, 15(1), 761.

How ascorbic acid may cause oxalate nephropathy

In this case study, a 69-year-old patient with benign prostate hyperplasia and small bowel resection presented with reduced urinary output, fatigue, and trouble speaking. The patient had been taking 2g of ascorbic acid daily for the past 2 years.

Since his creatinine and blood urea nitrogen remained elevated, he had to undergo 4 sessions of hemodialysis on the fifth day of admission.

A renal biopsy was performed to identify the cause of this patient’s acute kidney failure. The sample revealed presence of edema, tissue thickening and scarring, and inflammation. Calcium oxalate crystals were also present.

The study authors explain that:

  • Ascorbic acid in doses above 2g/day can cause oxalate crystals to deposit in the kidney. This can cause oxalate nephropathy which refers to oxalate-induced damage to delicate structures within the kidney. Nephropathy can eventually result in kidney failure.
  • The benign prostate hyperplasia caused chronic urinary retention which probably increased crystal deposition in the kidney.
  • Small bowel resection can also increase oxalate absorption by impairing fat absorption in the gut. Reduced dietary fat absorption can cause calcium to bind to fatty acids that aren’t absorbed. This reduces excretion of calcium oxalate in the feces.

Reference: Lin, W. V., Turin, C. G., McCormick, D. W., Haas, C., & Constantine, G. (2019). Ascorbic acid-induced oxalate nephropathy: a case report and discussion of pathologic mechanisms. CEN case reports, 8(1), 67-70.

Oxalates and Autism

Researchers studied oxalates in autism, and they measured a 2.5-fold greater level of oxalates in the urine, and a three-fold greater level of oxalate in the plasma, in children with autism.

Their finding was specifically, hyperoxaluria; a condition of high oxalate.

It’s significant to note that the study on autism and oxalate excluded the following groups from their selection criteria: those on a special diet, those with a history of seizures or antibiotic use, those with gastrointestinal disease (in addition to those with kidney stones). This is important to note, because all of these can be conditions of or cause hyperoxaluria.

The study’s selection criteria (omissions) may affect an underrepresentation of the range of oxalate (plasma and urinary) that would occur in a full range of autistic patients. Even with the exclusions, significant oxalate issues were identified. This warrants further study, without excluded variables, to investigate how results may differ. If these groups had been included, rates and levels of oxalate would most likely be even higher.

The study concluded that: “hyperoxalemia or hyperoxaluria may be involved in the pathology of autism spectrum disorders in children.” 1 It then continues to explain that based on the high oxalate finding, certain treatment options, such as a low oxalate diet, probiotic therapy, possibly with Oxalobacter formigenes, and a variety of supplementation may be helpful in these children.

Oxalates are significant in autism because clinically we see a great deal of oxidative stress, considerable inflammation, mitochondrial damage or dysfunction, as well as faulty sulfation and seizures—areas where oxalates can wreak havoc. The discovery and clear indication that high oxalate may be involved in the pathology of autism is both significant and hopeful. This research and the biochemical connections we are highlighting provide further hope and direction for helping children with autism.

 

Reference: Konstantynowicz, J., Porowski, T., Zoch-Zwierz, W., Wasilewska, J., Kadziela-Olech, H., Kulak, W., Owens S.C., Piotrowska-Jastrzebska J., and Kaczmarski, M. (2012). A potential pathogenic role of oxalate in autism. European Journal of Paediatric Neurology, 16(5), 485-491.

Dietary and therapeutic strategies for inflammation in autism spectrum disorders.

Brain development and function can be influenced by the environment, gut health, and diet in utero and after the child is born.

This is particularly important in autism. In this article entitled, “Interplay Between Peripheral and Central Inflammation in Autism Spectrum Disorders: Possible Nutritional and Therapeutic Strategies” the authors reviewed diet, nutrition, and other interventions such as probiotics and fecal transplants for helping individuals with autism. I am excited to see two diets that I have found very helpful in my nutrition practice for children with autism on this list: the low oxalate diet and the Specific Carbohydrate Diet (SCD).

In the paper, they explain how lab studies indicate that offspring of mothers who were obese during pregnancy were more likely to develop social communication impairment and repetitive behavior. Scientists explain that the low-grade inflammation caused by obesity could impair the brain’s neuronal circuit which controls behavior in the offspring.

Moreover, anything that adversely influences the development of the gut microbiome (such as the mode of delivery, stress, antibiotics, and diet) will also affect the gut-brain axis. Since gut microbes produce neurochemicals that play a role in social cognition, emotion, and behavior, improving gut health during pregnancy could decrease risks of ASD in the offspring.

As such, they discuss the following promising adjuvant therapies for ASD including:

  • A gluten-free and casein free diet – this free step-by-step guide can help you get started
  • The Specific Carbohydrate Diet
  • A diet low in oxalates
  • Adequate intake of micronutrients such as carnitine, zinc, selenium, vitamins A, D, E, and B-complex and omega-3s and omega-6s from real foods and/or high-quality supplements
  • Prebiotics and probiotics from the Lactobacillus and Bifidobacterium genus
  • Fecal transplants which involve transferring fecal microbiota from healthy donors to an unhealthy individual

While grain-free diets like SCD have gained attention in recent years, the low oxalate diet has been slow to become mainstream nutrition knowledge. So I’m thrilled to see it gaining traction in the nutrition world. I hope researchers continue to study this important diet for gut health, neurodevelopmental disorders, and many other conditions.

Reference: Cristiano, C., Lama, A., Lembo, F., Mollica, M. P., Calignano, A., & Mattace Raso, G. (2018). Interplay between peripheral and central inflammation in autism spectrum disorders: possible nutritional and therapeutic strategies. Frontiers in physiology, 9, 184.

Conclusion

Tailoring the right nutritional guidance for your clients or patients is important. As we can see through these studies. elevated oxalate can have a big impact on inflammation, oxidative stress, kidney function, mitochondrial function, and even cancer. Having a clear understanding of how (and when) to safely guide clients and patients through transitioning to a low oxalate diet can make all the difference in their lives.

To learn more on personalized nutrition and therapeutic diets, like the low oxalate diet, and how to use them in your practice as part of a BioIndividual Nutrition® plan, explore my BioIndividual Nutrition Training.

The right bioindividual nutrition plan for your client can bring about profound improvement and benefit.

In this article, I want to focus on some diets that have received a lot of attention in the news and nutrition community: the ketogenic diet and intermittent fasting.

But is this diet right for your client or patient and how do you know?

This is something that I cover extensively in the BioIndividual Nutrition Training program. I teach practitioners in my professional program to consider symptoms, diet history, conditions, lab results, genetics, microbiome, and more.

Today I want to present 5 studies that are using these diets for three important neurological and metabolic conditions: autism, Alzheimer’s, and diabetes.

The ketogenic or “keto” diet has been long-studied in regards to the benefit for individuals with intractable seizures and other neurological conditions. You may also have heard a friend or relative talking about the weight loss effects from a ketogenic diet. It can be very helpful for those looking to switch from carb burning to fat burning. The ketogenic diet can also improve blood sugar regulation in type 2 diabetes. Intermittent fasting, while not a ketogenic diet, does encourage lower carbohydrate consumption, and has also been shown to improve blood sugar control and risk markers of disease.

But, is it safe for your clients?

The science says… it can be. And I’ll share some research showing the ketogenic diet can provide adequate nutrition.

Just like any other diet out there, there are pros and cons and a specific profile of people who may find the greatest benefit. And getting support from a qualified nutrition practitioner and health care provider are important, especially for diets that restrict macronutrients as these do.

And similarly, there are ways to do a healthy ketogenic diet and intermittent fasting as well, as ways that are less than healthy in my opinion. All fats are not created equal so slathering on cheese or loading up on poor quality, high fat meats is technically keto (as long as protein is not too high) but not very healthy by my standards. Whereas a diet high in fats like avocado, nuts, seeds, coconut oil/MCT (depending on individual allergies/intolerances) can provide those nutrients in a healthy way.

So what does the research say? Below, I break down 5 different research studies looking at the ketogenic diet (and intermittent fasting) and how they may benefit your clients and patients.

The Ketogenic Diet and MCT Oil for Children with Autism
GFCF vs. Keto Diet in Autism
The Ketogenic Diet Provides Adequate Nutrition (in Alzheimer’s Disease)
A Ketogenic Diet Improved Blood Sugar Regulation in Type 2 Diabetes
People with Type 2 Diabetes May Reverse or Reduce Their Insulin Use with Intermittent Fasting

The Ketogenic Diet and MCT Oil for Children with Autism

Low in carbohydrates, moderate in protein, and high in fat, the ketogenic diet has shown promise in the treatment of ASD.

In this study, 15 children aged 2 to 17 were prescribed a modified ketogenic diet with supplemental medium-chain triglycerides (MCT) oil for 3 months.

Individuals with ASA suffer from mitochondrial dysfunction –mitochondria act like the cell’s “engine” and helps produce energy. The scientists wanted to see if adding MCT to the modified ketogenic diet could improve ketone and fatty acid production which would optimize mitochondrial efficiency.

The children’s caregivers received 2 hours of training on the modified ketogenic, gluten free diet and MCT protocol. This diet consisted of:

  • 20 – 25g of carbohydrates per day
  • Protein, twice the RDA requirements, based on the child’s weight and height
  • Various types of fats including 20% of pure MCT oil or coconut oil

At the end of the study, 50% of the children showed moderate to considerable improvement in ADOS-2 scores for the social affect component. No significant difference was observed in restricted and repetitive behavior scores.

Furthermore, 50% showed improvement on CARS-2 scores in the areas of imitation, body use, and fear or nervousness.

Findings from this study suggest that this modified diet could improve inflammation levels, gut health, and cellular health in ASD patients.

 

Study Reference: Lee, R. W., Corley, M. J., Pang, A., Arakaki, G., Abbott, L., Nishimoto, M., … & Lum-Jones, A. (2018). A modified ketogenic gluten-free diet with MCT improves behavior in children with autism spectrum disorder. Physiology & behavior, 188, 205-211.Physiology & behavior, 188, 205-211.

 

GFCF vs. Keto Diet in Autism

In this 6-month study, Egyptian researchers compared the effects of two different dietary interventions versus a normal (control) diet on core symptoms of autism.

The study population consisted of 45 children – 33 boys and 12 girls – aged between 3 and 8. The children were randomly assigned to three groups:

  •     Group 1: received the modified ketogenic diet (keto)
  •     Group 2: received a gluten-free, casein-free diet (GFCF)
  •     Group 3: the control group, received balanced nutrition

The results were exciting. Both the GFCF and Keto group have significant improvements compared to the control group (that did not do a special diet). There were some differences, but overall the results show that a special diet is very helpful to improving autism symptoms.

Autism severity decreased among children in groups 1 and 2 indicating that the Keto and GFCF diet were effective in improving autism symptoms.

The ketogenic diet yielded better results than the GFCF diet. The ketogenic diet can be a great diet for autism… for the right person. The keto diet can address some underlying mitochondrial issues and neuroinflammation that can be wonderful!! By improving the underlying biochemistry, the symptoms of autism can be significantly reduced (as we saw in the study).

However, 1/3 of the children dropped out of the Keto group. The fact that the keto diet is more restrictive is one of its challenges. No one dropped out of the GFCF group and great benefits were seen by that group too.

This research is further proof that a special diet helps people with autism.

And it shows: both a GFCF diet and a keto diet were effective. See more on my write up of this paper, here, at my autism nutrition website: NourishingHope.com.

Study reference: El-Rashidy, O., El-Baz, F., El-Gendy, Y., Khalaf, R., Reda, D., & Saad, K. (2017). Ketogenic diet versus gluten free casein free diet in autistic children: a case-control study. Metabolic brain disease, 32(6), 1935-1941.

 

The Ketogenic Diet Provides Adequate Nutrition (in Alzheimer’s Disease)

Researchers wanted to study whether the ketogenic diet is nutritionally dense and can provide adequate nutrition. 15 older adults with very mild, mild, or moderate Alzheimer’s disease were involved in this study.

The study partners of each participant were counseled by a registered dietitian and participants were instructed to consume a 1:1 ketogenic diet consisting of about 70% fat, 20% protein, and at most 10% of carbohydrates.

The participants’ study partners completed self-reported 3-day food records (i) at baseline, (ii) after one month, and (iii) after two months. To assesses ketosis, evening urinary ketones was monitored daily by participants and serum beta-hydroxybutyrate was measured after a 12-hour fast within 48 hours of each 3-day food record.

Although only 10 of the 15 participants adhered to the diet, results indicated that it is possible to consume a nutrient-dense ketogenic diet with MCT oil and:

  • Plenty of non-starchy vegetables
  • Avocados
  • Nuts and seeds

Study reference: Taylor, M. K., Swerdlow, R. H., Burns, J. M., & Sullivan, D. K. (2019). An Experimental Ketogenic Diet for Alzheimer Disease Was Nutritionally Dense and Rich in Vegetables and Avocado. Current Developments in Nutrition, 3(4), nzz003.

A Ketogenic Diet Improved Blood Sugar Regulation in Type 2 Diabetes

This study looked at 28 overweight participants with type 2 diabetes for a 16-week diet trial. It is interesting that the research team noted that prior to the use of exogenous insulin for the treatment of diabetes in the 1920’s, the traditional therapy was dietary modification. Diet recommendations during that time were very different than the current recommendations of a low-fat, high-carbohydrate diet and consisted of “meats, poultry, game, fish, clear soups, gelatin, eggs, butter, olive oil, coffee, tea.”

This study focuses on a keto diet’s effects on blood sugar and diabetes medication use in patients who prepared (or bought) their own high fat, low carb meals.

The majority of the participants were males and the mean age was 56. The study provided Low Carb Ketogenic Diet (LCKD) counseling, with an initial goal of consuming less than 20 g carbohydrate/day, and diabetes medication dosages were reduced at the start of the diet. Measurements, counseling, and medication were adjusted as needed every other week. Food records were completed and evaluated several times throughout the study.

The results were impressive!

Results included a 6.6% decrease in body weight, 42% decrease in triglycerides, 16% reduction in hemoglobin A1c, 17% decrease in mean fasting glucose, and 10% in reduction in uric acid levels. “The LCKD improved glycemic control in patients with type 2 diabetes such that diabetes medications were discontinued or reduced in most [17 out of the 21] participants.”

Yancy WS, Foy M, Chalecki AM, Vernon MC, Westman EC. A low-carbohydrate, ketogenic diet to treat type 2 diabetes. Nutrition & metabolism. 2005 Dec;2(1):1-7.

People with Type 2 Diabetes May Reverse or Reduce Their Insulin Use with Intermittent Fasting

Note: this study is on intermittent fasting rather than the ketogenic diet.

In a new study, Suleiman Furmli, MD, and his team reported that, under medical supervision, therapeutic 24-hour fasting regimens can help reverse type 2 diabetes. The fasting interventions could also reduce the use of medications in patients with type 2 diabetes and minimize surgical interventions in this population.

This small study involved 3 male patients aged between 40 and 67. The 3 participants also had high blood pressure and high cholesterol levels in addition to type 2 diabetes and were taking at least 70 units of insulin daily at the beginning of the study.

Two of the patients fasted three times weekly for 7 months. After the intervention, one patient discontinued insulin and metformin use while the other stopped his fixed-dose insulin mix.

The other patient fasted on alternating days for 11 months and was able to eliminate metformin and pre-mixed insulin.

HbA1c levels improved for all 3 participants who also lost weight and inches off their waists.

“On eating days, patients are encouraged to eat a diet low in sugar and refined carbohydrates, which decreases blood glucose and insulin secretion.”

Study reference: Furmli, S., Elmasry, R., Ramos, M., & Fung, J. (2018). Therapeutic use of intermittent fasting for people with type 2 diabetes as an alternative to insulin. Case Reports, 2018, bcr-2017.

As you can see there is science to validate the ketogenic diet and intermittent fasting for some individuals.

What is clear through these studies is how impactful the right diet can be for improvement in health and wellness and even reduction in symptoms and improvement in metabolic markers. A healthy ketogenic diet, when guided by an experienced and knowledgeable practitioner for the right individual can make the world of difference to individuals seeking relief from neurological issues, obesity, diabetes, and increased metabolic health. The ketogenic diet is one of over a dozen diets we study at the BioIndividual Nutrition Institute. If you are a practitioner seeking advanced level training on specialized diets like the ketogenic diet, I encourage you to explore my BioIndividual Nutrition Training.

 

 

Nutrigenomics studies how the genes of individuals interact with their diet and how it impacts their physiology and health. This was made possible by the Human Genome Project. Research continues to uncover why some individuals respond differently to the same type of foods, supplements, and beverages. One of the most significant advantages of studying nutrigenomics is the practical application of improving people’s health through personalized nutrition.

Nutrigenomics testing continues to expand our view on how food molecules impact human cells. In other words, the nutrigenomics definition is simply food interacting with your genes, as diet plays a key role in determining your health. However, it’s still not clear to most health professionals what people should eat to optimize their health and performance. Currently, diet recommendations are based on a one-size-fits-all model, which was created decades ago.

How Genes Impact Nutrition

Each individual is born with numerous variations within their DNA, known as “single nucleotide polymorphisms” (SNPs). With SNPs, most of the enzymes do not function at peak capacity, making it possible to increase this activity by using the right phytochemical.

Nutrigenomics makes it possible for healthcare professionals to create personalized nutrition recommendations based on an individual’s genetic profile. These individuals can optimize their health by eating a proper diet that best matches their genetics and lifestyle.

Personalized Nutrition, or BioIndividual Nutrition®, is the link between our genes and lifestyle/environment.

Personalized nutrition can target these specific SNPs, as this is much more effective than following general dietary guidelines. And our genes can help us determine which foods we might not tolerate, such as gluten.

Evolution of Nutrigenomic Testing

Nutrigenomic testing continues to evolve, as now tests can focus on different well-being or health issues. But genetic testing is not the full picture. There are other factors, such as whether a gene is expressing or not, which is not determined by testing. There is also a complex interplay among genes, and the recommendations are only as good as the research and intelligence behind the algorithms.  Nutrigenomic testing is one way we can personalize nutrition, but additional factors need to be considered. At the BioIndividual Nutrition Institute we train practitioners to consider: symptoms, health conditions, food reactions and dietary consumption, the microbiome, mitochondrial and metabolic function, nutrient deficiencies, genetic testing, and more.

Additional research is needed to understand complex gene-diet interactions better, as nutrigenomics offers plenty of potential for individuals looking to improve their health by following a personalized nutrition plan.

Individual Nutrition Counseling

Following individual nutrition counseling can play an important role in improving your health, as no two individuals are the same. For example, one in three people has a poor response to sugar. Teaching these individuals how to avoid these spikes in blood glucose can dramatically reduce their chance of developing diabetes.

Today’s standard nutrition guidelines are developed from questionnaires about the type of food people ate in the last year. However, this approach is flawed because many respondents are poor at trying to recall their food choices, and the average of all this data doesn’t offer any personalized guidance.

Individual Responses to Food

Trying to determine how genes affect obesity remains a challenge, as various studies show that this number ranges from 35 to 85 percent. [1] Following the same diet can impact people in different ways, as a recent study  focused on how participants processed the same type of food, which included identical twins. The study, called the PREDICT1 study, showed how a person metabolizing one macronutrient isn’t a predictor of how that individual will respond to other macronutrients.[2] Additional studies are needed to better determine the ideal diet for an individual.

Why Genes Play a Limited Role in Processing Fats and Carbohydrates

The PREDICT  study  also focused on the variety of gut microbes while analyzing their responses to different diets. The study included 300 British volunteers, 100 individuals from the United States, and 700 identical twins. Data was gathered for anything impacting the metabolism, such as exercise, body fat composition, sleep duration, and microbiota. The initial results focused on the insulin, glucose, and triglyceride levels of the participants after eating a standard meal.

The team found that genes only play a limited role in the processing of fats and carbs. For example, only half of the post-meal glucose levels and less than 30 percent of the triglyceride and insulin response could be connected to genetic influence among identical twins. More important factors in how the body metabolizes food seem to be sleep, exercise, stress levels, and the diversity of the gut microbiome.

Closing Thoughts

Following a personalized nutrition plan can make a big difference in helping people to live healthier lives. Nutrigenomics makes it possible to study the correlation between your diet and how it interacts with your genes. Understanding underlying factors affecting your client or patient’s symptoms and condition such as food reactions, the microbiome, mitochondrial and metabolic function, and nutrient deficiencies can help you determine the best personalized diet and nutrition plan to improve the health of the individual.

 


What makes one nutrition professional more clinically successful than another?

Specifically, why do some practitioner’s clients get radically better (despite years of struggle) when others cannot figure out how to resolve their troublesome symptoms?

I have learned some of the reasons why, and in this article I share 5 common errors that inhibit results.

…then I give you insight to avoid them and help improve your overall success.

I’ve helped hundreds of clients with disorders resulting from complex neurological and physiological needs, and I discovered some interesting and important information that can help you…

I tend to see the “tough cases,” the “non-responders,” in my nutrition practice.

By the time they’ve come to me, clients have already seen 3 or more practitioners that have provided nutrition advice, yet they still have not gotten better.

I’ve always investigated why their prior practitioners were unsuccessful. And as I explored each of their case history files, I uncovered what they had overlooked.

Here are 5 Errors to Avoid…

#1 Being Too Dogmatic

There will always be a latest trend in diet. A diet becomes popular because it works well for a subset of people, or for a finite period of time. Some practitioners jump on board and start recommending that ONE popular diet for MOST their clients. They become blinded by their love and loyalty to that diet and cannot see that a different approach might be necessary.

Practitioners who are dogmatic about one dietary approach, are not able to see that it’s the wrong diet for their client because they don’t know how to cater to the biodindividual nutrition needs of the unique person.

Nutritional needs change over time and combining several different diet principles can allow consistently better clinical success. For example, while following a grain-free diet such as SCD or GAPS, a low FODMAPs or low oxalate diet may ALSO be necessary. Dogmatic thinking prevents that small dietary tweak from happening, even though it could make the difference between success and failure! Knowing how to be flexible, yet targeted, is key.

There is no dogmatic thinking in the BioIndividual Nutrition training, we teach you how to think not what to think.

#2 Being Too Rigid

When a practitioner insists that a certain diet must be done a certain way, and becomes inflexible – even if its not working. For example, a client on a special diet that emphasizes certain foods like bone broth or sauerkraut multiple times per day, but the individual has a food reaction to the amines or glutamates in those foods.

The client does not feel well, but the practitioner insists that it cannot be the “sacred foods” on the special diet, and instead assumes the client must be making a mistake or needs to be more strict. But then the client gets worse, not better.

Even within a special diet, food choices and rules may need to be modified, i.e. removing allowed foods (or adding non-compliant foods) in order to see success on that diet. In the BioIndividual Nutrition training, you’ll learn the specific strategies you need to make these kinds of complex customized recommendations.

#3 Being Too Simplistic

Some practitioners focus solely on “health food” diet. The challenge is that one man’s medicine is another man’s poison. Even certain “health foods” can be a problem for some people to the point of causing serious reactions including pain, inflammation, or digestive challenges.

A common example is practitioners who recommend almond flour as a grain-free alternative, without realizing that many people who need special diets have sensitivities to salicylates or oxalates, the compounds found in high levels in this health food. As a result, the individual’s health may be negatively impacted and the practitioner will see negligible improvements in their client’s symptoms.

Understanding the complexity of naturally occurring food chemicals and compounds can be the difference between being a world-renowned nutrition expert, or not.

#4 Being Too Overwhelming

You can make the best diet recommendations, but if your patient is confused on how to implement the diet, feels overwhelmed, doesn’t have the resources to make the diet work, isn’t certain of what to eat, or doesn’t know how to fit it into their lifestyle, then they will not make the necessary changes.

Without strategies, resources, lists, charts, and guides for helping your clients implement the complexities of a new diet, implementation will be unlikely, and their health does not improve…that’s why my BioIndividual Nutrition training provides practitioners with client handouts and resources to improve the process of transitioning/sustaining a new diet and addresses their leading questions.

#5 Being Too Limited/Restrictive

Some practitioners understand the value of all the different therapeutic diets, but they are not able to determine which diet to implement, prioritize, stagger, alter, or combine. Therefore the practitioner recommends implementing three or four diets simultaneously, causing the client to have too few foods to choose from. The variety in the diet suffers, and the client may develop nutrient deficiencies or food sensitivities to the few foods they are able to eat.

To prevent this problem, practitioners need to learn about common symptoms, underlying biochemical imbalances, and how to prioritize the right diets at the proper time. Doing so will ensure success with even the most complex and sensitive patients.

This is an advanced strategy of combining special diets and preventing over-restriction, something I cover in detail in my practitioner course.

There IS more you can do to help your clients truly feel better!

To start integrating these advanced strategies in your practice and become the MOST successful practitioner in your field, enroll in the BioIndividual Nutrition training.

Summer enrollment is open.

Explore the BioIndividual Nutrition Training program now.

Gastrointestinal Disorders Prevalence

If you’re a nutrition or health practitioner, you’ve certainly had your fair share of clients with a gastrointestinal disorder or symptoms. 

I’m certain of that. That’s because digestive disorders are incredibly common. They affect 60-70 million people in the United States alone. IBS has a prevalence 15.3 million people, that 11.6% in the population.

And the gut is a major factor in health or disease. The gastrointestinal tract is often the first system damaged in chronic disease. We need digestion to break down and assimilate our food and nutrients. Digestive disturbances are common in: neurological disorders, fibromyalgia, chronic fatigue syndrome, skin disorders, autoimmune conditions, and.

And food is a major factor in gut health… as food is in contact with the digestive tract every time we eat. And food can be irritating, inflammatory, and imbalance the microbiome. Or food can be nourishing, healing, and supportive to our beneficial bacteria.

As such, it’s important to know how food affects the gastrointestinal tract and which therapeutic diets can help (which is the purpose of my article today). 

But before we talk about special diets, I wanted to share more on the gut-brain connection, as neurological disorders are one of the most common manifestations of GI issues that you’ll likely run into in your practice, if you haven’t already.

The Gut-Brain Connection

The gut and the brain are connected so when the gut is not working well, we can have difficulty with cognitive function and mood.

Let’s take serotonin, for example. Serotonin is a key neurotransmitter in the brain-gut axis. Ninety percent of serotonin is produced in the gut. The microbiome influences the level of serotonin and the functioning of the gut brain axis. It is very important for digestive functioning including motility. And it’s crucial for good mood and happiness When the gut is not working well, neither is the brain.

In fact, 30% of people with IBS have depression (vs. 18% of the healthy population), and 16% have anxiety (vs. healthy population). 

Digestive disorders are also very common in autism, ADHD, and related developmental disorders.

The good news is: As we heal the gut, neurological disorders improve, often dramatically.

Gastrointestinal Problems and Developmental Delays

Gastrointestinal problems and developmental delays are often connected. According to one study, children with autism, as well as ADHD and other developmental delays, have higher rates of medical conditions than their peers. These medical diagnoses include: diarrhea or colitis, food allergies, asthma, eczema, headaches and earaches.1 It’s a substantive finding, involving a large sample size: 41,000 children aged 3 to 17 years. 5,469 children had one or more of the following diagnoses: autism, intellectual disability, ADHD, learning disability or other developmental delay. 

The study found children with developmental disabilities were 3.5 times more likely to have had frequent diarrhea or colitis during the past year. As well as 1.8 times more likely to have had a food allergy during the past year. They were also significantly more likely to have skin allergy, asthma, ear infections, and severe headaches.

When they compared the developmental disability groups to each other they discovered: “Children with autism were twice as likely as children with ADHD, learning disability or other developmental delay to have had frequent diarrhea or colitis during the past year. They were seven times more likely to have experienced these gastrointestinal problems than were children without any developmental disability.”

These findings are important because parents are routinely told one has nothing to do with the other. However, the gut and brain are closely connected, such that the gut is often called “the second brain.” 

When the gastrointestinal system is not functioning properly, children and adults struggle with mood, behavior, focus, and thinking.

Your client may not be able to:

  • Break down and absorb nutrients properly, leading to deficiency that can affect cognition, mood, and behavior.
  • Digest the protein in wheat, dairy, and soy, which form opioid (morphine-like) compounds that negatively affect attention, learning, and behavior.
  • Maintain a healthy gut microbiome – pathogenic microorganisms can negatively affect our neurotransmitter levels and cause hyperactivity, aggression and other mood related symptoms.

One of the most important ways to address digestive issues is to look at the foods that are going into the gastrointestinal tract: i.e. “the diet.”

Also there are supportive supplements and other nutritional tools that can help your client:

  • Digestive enzymes – digests food to relieve the burden on digestion and help reduce irritation.
  • Probiotics – helps supply needed beneficial bacteria.
  • Prebiotics – feeds the growth of beneficial bacteria.
  • Anti-inflammatory supplements – reduces inflammation throughout the body for symptom relief and healing of the gut.

But without looking at the food going in and whether it’s causing inflammation, harm, and havoc to the underlying biochemistry and system, we cannot make full progress and help your clients improve their health.

Some foods are generally inflammatory to most humans like gluten, for example.2 Whereas others – most grains, salicylates or oxalates – are only a problem for certain people based on their bioindividual circumstance.

Problematic Foods and Therapeutic Diets for Gut Healing

Some of these strategies are more advanced and others more introductory. I’ll start with the foundation stones for families at the beginning of their journey before covering other diets that can be helpful for more diet-experienced individuals.

Gluten-Free, Casein-Free and Soy-Free Diet

Gluten, found in wheat and other grains, casein, found in dairy, and soy are all inflammatory proteins. The proteins are hard to digest, and when not properly broken down can form opiate compounds. Opiates (just like morphine) can slow motility of the gut causing constipation and further digestive discomfort, and cause inflammation. Constipation is very common with dairy intolerance – one study of children with constipation revealed that 80% of the patients had a cow’s milk allergy. 3 A gluten-free, casein-free and soy-free diet is a great diet to start with when chronic digestive issues are present.

Grain-Free Diets

Grains are hard to digest, as they require large amounts of carbohydrate digesting enzymes. And we know that people with autism are often low in the correct enzymes.4 The starch in grains also feed pathogens and small intestine bacterial overgrowth (SIBO), resulting in irritation and damage to the gut, causing diarrhea, constipation, pain, and distress.

There are several grain-free diets that can be helpful with digestive problems:

  • Specific Carbohydrate Diet (SCD)
  • GAPS Diet
  • Paleo Diet

Low Salicylate Diet

Salicylates occur in plant foods, including berries, grapes, tomatoes, almonds, herbs, and spices. But salicylates are also present in honey. In addition to behavioral symptoms, salicylates can cause digestive symptoms such as diarrhea, and can increase digestive pain when consuming FODMAPs.5 6

Low salicylate diets include:

  • Feingold diet
  • FAILSAFE diet

Low Oxalate Diet

Oxalates are inflammatory molecules that are found in certain foods, including: Nuts, spinach, Swiss chard, chocolate, and beans. Oxalates can kill good bacteria and perpetuate yeast and gut microbiome imbalance. And create inflammation in the gut.

Low FODMAPS Diet

FODMAPS is an acronym for various fermentable carbohydrates including oligosaccharides found in the onion family and polyols found in prunes. Fermentable carbohydrates feed bacteria, but when there is an imbalance such as small intestine bacterial overgrowth (SIBO) it can cause gas, bloating, pain, diarrhea and constipation. Studies have shown a Low FODMAPS diet can be helpful for IBD.7

Body Ecology Diet

The Body Ecology diet avoids sugar and foods that feed and perpetuate candida overgrowth, and includes foods that are healthy – while supplying good bacteria through fermented foods. It’s often used to address candida overgrowth and other “inner ecology” imbalances.

Low Histamine Diet

There are a variety of low amine and histamine approaches. As the name implies, histamine is one type of amine. You find amines in: bone broth, sauerkraut, fermented foods, wine, beer, chocolate, and cheese. Histamine and other amines can cause intestinal and systemic inflammation, diarrhea, and abdominal cramps. 

Low Glutamate Diet

Glutamate is an excitatory neurotransmitter – think the opposite of calm! Glutamate is often present in food. Glutamate often occurs in similar foods to histamine ike: sauerkraut, fermented food, bone broth – and occurs in high amounts in soy sauce and parmesan cheese, and additives like monosodium glutamate (MSG) and autolyzed yeast extract. Glutamate can affect the nervous system and can cause reactions such as inflammation systemically. Glutamate can also cause diarrhea, constipation, and gut issues.

Ketogenic Diet

The Ketogenic diet is a very low carbohydrate diet that uses ketones/fat for energy instead of glucose/sugar. Though very restrictive, keto can help with balancing the microbiome and supply the proper energy for the gut to heal for the right individual. Remember, this diet is very strict and high fat diets can often lack the beneficial fiber for the microbiome – so more studies are needed to find out when this diet supports or imbalances the microbiome. 8

Underlying Considerations for Choosing a Special Diet

Now that you know a little about the diets, let’s tackle four considerations that arise with gut health, including their potential implications, and possible dietary choices for these gastrointestinal issues.

Inflammation 

Inflammation affects the gut by aggravating the gut wall, causing leaky gut, leading to food sensitivities, and often contributing to chronic disease or autoimmunity, affecting every system. Symptoms can include diarrhea, constipation, gas, bloating, and pain. 

Dietary considerations: Food allergies and sensitivities, oxalates, salicylates, amines, histamine, FODMAPs, and grains.

Mitochondrial dysfunction

Mitochondria are the powerhouses of the cell responsible for making energy, and if they aren’t functioning well, it can lead to constipation, but also fatigue, pain, and disease in any organ or system of the body. 

Dietary considerations: oxalates, a ketogenic diet, or adequate carbohydrates.

Poor sulfation

Sulfation is a set of biochemical processes that use sulfate, and it’s a necessary process for intestinal barrier integrity (to avoid leaky gut) and aid digestion. An imbalanced gut microbiome can contribute to poor sulfation. Poor sulfation can cause reactions to phenols, salicylates, and amines – many are present in foods traditionally considered “healthy” like berries, spices, almonds, fruits and vegetables.

Additionally, when sulfate the building block for sulfation is low, problems with oxalates can result,

Dietary considerations include salicylates, amines, and other phenols, plus oxalates.

Microbiome imbalance

Good bacteria is essential for good digestive health, while pathogens contribute to digestive issues and disease. Eating a diet that supports good bacteria while starving out the bad pathogens can be tricky to balance. For example, high fiber foods are good for beneficial bacteria but cause reactions for clients with SIBO. Additionally, if there is an imbalanced microbiome these reactions to foods that might otherwise be healthy can result in reactions to salicylates, amines or oxalates.

Dietary considerations include: FODMAPS, salicylates, oxalates, and amines.

The key is eating foods that support digestion and feed beneficial bacteria, while not causing another reaction. Determining which foods your client or patient needs while avoiding those that cause or contribute to underlying problems is essential to helping them improve.

Understanding the Relationship Between Symptoms and Foods

Complicating matters further, practitioners often recommend many healthy foods for “gut healing diets” – such as bone broth, sauerkraut, spinach, and almonds. Such foods contain natural food compounds that can cause or exacerbate the exact GI issue the practitioner is working to resolve!

So as a practitioner, it’s important to understand the big picture of diets and gut health for your client.

Understanding the relationship between symptoms and foods will allow you to help your clients find the right healing diet.

Of course, if you are looking to take your knowledge to the next level, check out our BioIndividual Nutrition Training program.

Share what diet strategies have helped you help your clients – I love to hear success stories!

Explore Enrollment into the BioIndividual Nutrition Training

…CLICK THROUGH….

High gluten intake during pregnancy linked to increased risks of diabetes in children

Although more research is needed, a recent study suggests that maternal gluten consumption during pregnancy could increase the child’s risk of type 1 diabetes. 

Findings from this study also suggest that:

  • The risk of type 1 diabetes in the children increases proportionally per 10g/day increased gluten intake.
  • Over an average follow-up period of 15.6 years, children of women who consumed at least 20g of gluten per day had twice the risks of developing type 1 diabetes compared to children of women whose daily gluten intake was less than 7g.

Since celiac disease and type 1 diabetes “share” some HLA genes, pregnant women or those intending to conceive may want to consider swapping gluten-containing foods (such as wheat, rye, spelt, and barley) for other gluten-free nutritious foods. 

Study reference: Antvorskov, Julie C., Thorhallur I. Halldorsson, Knud Josefsen, Jannet Svensson, Charlotta Granström, Bart O. Roep, Trine H. Olesen, Laufey Hrolfsdottir, Karsten Buschard, and Sjudur F. Olsen. “Association between maternal gluten intake and type 1 diabetes in offspring: national prospective cohort study in Denmark.” bmj 362 (2018): k3547.

Prenatal fish oil supplementation may improve children’s growth

A mother’s diet during pregnancy can have a profound effect on the fetus and the results can last through childhood.

A new study investigating the effects of prenatal fish oil supplements shows that children born of women who took the supplements were more likely to have healthier growth during the first six years of life.

The study involved 736 pregnant Danish women who either took daily fish oil supplements (the experimental group) or olive oil supplements (the control group). The women started the supplements from week 24 of their pregnancy until one week after delivery.

The researchers assessed the children’s height, weight, head and waist measurements 11 times from birth to age six. They found that the children’s whose mothers took the fish oil supplements had a higher body mass index throughout their first 6 years of life compared to those whose mothers received the olive oil supplements.

The higher BMI was due to a higher percentage of lean muscle and bone mass, and not extra body fat, indicating that fish oil supplements may exert a general growth-stimulating effect in utero.

Study reference: Rebecca Kofod Vinding, Jakob Stokholm, Astrid Sevelsted, Tobias Sejersen, Bo L Chawes, Klaus Bønnelykke, Jonathan Thorsen, Laura D Howe, Martin Krakauer, Hans Bisgaard. Effect of fish oil supplementation in pregnancy on bone, lean, and fat mass at six years: randomised clinical trial. BMJ, 2018; k3312.

Babies born at home may have a healthier gut microbiome

New research indicates that babies born at home have a more diverse gut and fecal microflora compared to those born in hospitals. 

The researchers followed 35 infants and their mothers until the babies were 1 month old. 14 of the babies were born at home (four of them in water) and 21 in the hospital. 

Stool samples indicated that the hospital-born babies had greater inflammatory gene expression in epithelial cells which cover organ linings, skin, and mouth. Moreover, hospital-born infants had lower levels of Bacteroides, Bifidobacterium, Streptococcus, and Lactobacillus, and higher Clostridium and Enterobacteriaceae compared to babies born at home.

Why these differences in gut microbiota between infants born at home versus hospitals? 

Well, the scientists speculate that common hospital interventions, such as infant bathing and antibiotic eye prophylaxis, and the aseptic hospital’s environment could be involved. 

Although more research is needed, this study’s findings favors the idea of home births and/or revamping the hospital environment to mimic home conditions for non-high-risk births. Since the gut flora affects the immunity and metabolism, a healthy microbiome could reduce the babies’ risks of obesity, diabetes, asthma, and gut disorders later in life.

Study reference: Combellick, Joan L., Hakdong Shin, Dongjae Shin, Yi Cai, Holly Hagan, Corey Lacher, Din L. Lin, Kathryn McCauley, Susan V. Lynch, and Maria Gloria Dominguez-Bello. “Differences in the fecal microbiota of neonates born at home or in the hospital.” Scientific reports 8, no. 1 (2018): 15660.

Mom’s microbiome during pregnancy linked to child’s autism risk

Cutting-edge research suggests that the mother’s gut health during pregnancy plays a critical role in determining the child’s risk of developing ASD.

The researchers hypothesized that, in mice, an immune reaction to interleukin-17a (IL-17a), a molecule produced by the immune system, could trigger ASD-like behaviors. 

To test their hypothesis, the team used Jax and Tac mice from two different laboratories. Unlike the Jax mice, the Tac mice had gut microbes that made them susceptible to an IL-17a inflammatory reaction. 

Both groups were exposed to a virus designed to create an immune response. Only the Tac mice (the ones susceptible to inflammation) had pups that developed ASD-like behaviors.

To prevent an inflammatory response, the researchers then artificially blocked the IL-17a molecule in the Tac mice. The pups born did not show ASD-like behavior. 

Finally, the researchers exposed the Jax mice to the gut flora of Tac mice (making them more susceptible to inflammation). Interestingly, they found that pups born after this intervention showed ASD-like behavior. 

Practical tip: Although these findings may not be applicable to humans, pregnant women and those planning to conceive could opt for a gut-friendly (and microbe-friendly) diet and lifestyle. Probiotics (or fecal transplants, when medically necessary) may also positively influence the mother’s microbiome.

Study reference: Lammert, Catherine R., Elizabeth L. Frost, Ashley C. Bolte, Matt J. Paysour, Mariah E. Shaw, Calli E. Bellinger, Thaddeus K. Weigel, Eli R. Zunder, and John R. Lukens. “Cutting edge: critical roles for microbiota-mediated regulation of the immune system in a prenatal immune activation model of autism.” The Journal of Immunology 201, no. 3 (2018): 845-850.

Panic attacks and hyperventilation attacks – could they be linked to nutrition?

Panic attacks (PA) and hyperventilation attacks (HVA) are generally considered as ‘mental’ health issues. But a growing body of evidence indicates that what we eat and how we live strongly influence our mental and emotional state. 

One such piece of evidence from Japan suggests an interesting link between iron and vitamin B6 levels and PA or HVA.

This study involved pre-menopausal women with PA or HVA (research group, n = 21) and 20 healthy volunteers. None of the study participants had liver disease, kidney disease, endocrine or inflammatory issues and none were regularly taking food supplements.

Serum levels of vitamins B2, B6, B12, and iron were measured either during visits to the emergency department (research group) or after overnight fasting (control group).

What the research showed:

  • Iron and vitamin B6 levels were significantly lower in the study group compared to the control group.
  • The study participants had similar hemoglobin, thus ruling out iron-deficiency anemia as a cause of PA and HVA.
  • The two groups showed no significant difference in vitamins B2 and B12 levels. This suggests that reduced intake due to illness did not cause PA and HVA.

The authors suggest that, since iron and vitamin B6 are involved in the formation of serotonin in the brain, deficiency of these nutrients could suppress serotonin production and cause PA and HVA.

Journal reference: Mikawa, Yasuhito. “Low serum concentrations of vitamin B6 and iron are related to panic attack and hyperventilation attack.” (2013).

Can supplements help with depression?

We’ve been told that depression is caused by a chemical imbalance that may require lifelong medication. But what if specific nutrients could improve treatment outcomes in depression?

In a brand-new study, researchers investigated the efficacy of the following nutrients as adjunctive treatments for depression:

  • Vitamin D – Low levels of this vitamin have been associated with depression. One proposed mechanism is that vitamin D modulates the HPA axis and regulates neurotransmitter synthesis.
  • Vitamin B9 and B12 – Deficiencies of these vitamins can reduce homocysteine recycling which can impair neurotransmitter synthesis, membrane phospholipids, and cause anemia.
  • Vitamin C – Since depression can be triggered by oxidative-stress, antioxidant vitamin C could help alleviate symptoms. 
  • Zinc – This mineral may help downregulate neurodegenerative inflammatory pathways of depression. 
  • Selenium – Low selenium intake has been linked to increased risks of de novo major depressive disorders.
  • Omega-3 fatty acids – Since these fatty acids are key components of gene expression regulation and cell lipid metabolism, deficiencies can trigger depression. 
  • N-acetylcysteine – In one study, 1,000mg of N-acetylcysteine helped reduce manic and depressive symptoms significantly by neutralizing reactive oxygen species thereby preventing cell damage. 
  • Nicotinamide riboside acts as a co-substrate for enzymes that are involved in DNA repair.

Keep in mind: You can’t out-supplement a nutrient-poor diet or an unhealthy lifestyle. One of the (many) reasons is that unlike real foods, supplements do not come with cofactors the body needs to absorb specific nutrients. Don’t know where to start? My free guide can help you.

Journal reference: Volker, Dianne, and Jade Ng. “Depression: Does nutrition have an adjunctive treatment role?.” Nutrition & Dietetics 63.4 (2006): 213-226.

Effects of probiotics prebiotics, and phytobiotics on anxiety, depression, and  mental health

The microbiome exerts a major influence on neurological health since our brains and gut are linked. Research shows that an inflamed gut promotes the release of inflammatory molecules (cytokines) in the bloodstream. These cytokines are able to cross the blood-brain barrier and induce inflammation in the brain, creating neurological symptoms like depression, anxiety, and stress.

Improving the gut health with specific strains of probiotics can positively influence mental health. For example, Lactobacillus helveticus R0052, Bifidobacterium longum R0175, and Lactobacillus rhamnosus R0011 can ameliorate depression, anxiety, and stress respectively.

A new study shows that supplementing with probiotics, prebiotics, and phytobiotics (i.e. phytonutrients such as polyphenols) for 30 days work together to increase beneficial bacteria. This can, in turn, improve:

  • Global mood
  • Vigor
  • Depression
  • Tension
  • Fatigue
  • Confusion
  • Anger

Journal reference: Talbott, S., Stephens, B., Talbott, J., & Oddou, M. (2018). Effect of Coordinated Probiotic/Prebiotic/Phytobiotic Supplementation on Microbiome Balance and Psychological Mood State in Healthy Stressed Adults. The FASEB Journal, 32(1_supplement), 533-85.

 

The effects of diet and probiotics on anxiety and depression

Around 90% of serotonin receptors are located in the gut. As such, it makes sense that digestive health, and the gut’s microflora, can have a tremendous impact on mood. 

In a review of studies, scientists explain that numerous lab studies indicate that probiotics can improve anxiety-like and depressive-like behaviors. For instance:

  • When taken together for 14 days, Lactobacillus helveticus and Bifidobacteria longum helped reduce anxiety.
  • Lactobacillus rhamnosus decreased both anxiety-like and depressive-like behaviors when administered for 28 days.
  • A 21-day intake of Lactobacillus helveticus helped to reduce anxiety triggered by a high-fat diet. It is worth noting that the high-fat (non-hydrogenated lard and sunflower oil) diet in this particular study was, in fact, a Western-style diet rich in refined sugar. 

It appears that probiotics can protect the gut’s lining from the adverse effects of stress by decreasing the activity of the autonomic nervous system and the HPA axis (which is involved in stress response). This, in turn, leads to reduced plasma levels of adrenaline, noradrenaline, and corticosterone in stressed mice. 

Interestingly, probiotics may not alleviate anxiety induced by a high-fat (Western-style) diet in the absence of anti-inflammatory cytokines produced by immune cells. What this means is that fixing food before trying gut-modifying therapies may yield better results. 

Journal reference: Luna, Ruth Ann, and Jane A. Foster. “Gut brain axis: diet microbiota interactions and implications for modulation of anxiety and depression.” Current opinion in biotechnology 32 (2015): 35-41.

Use of orange essential oil as an alternative treatment for anxiety in children with type 1 diabetes

Essential oils have been used for hundreds of years for their relaxation properties. And in 2017, research showed that orange essence could help alleviate anxiety in children with type 1 diabetes. 

60 Iranian children aged 6 to 12 were enrolled in the study and allocated to the intervention (n=30) or the control group. 

In the experimental group, two drops of orange essence were used on a strip of gauze inside an open box kept at a 5-cm distance from the child’s nose. The children were asked to breathe in deeply for about 2 minutes. This procedure was repeated thrice weekly on Saturday, Monday, and Wednesday before bedtime for two weeks.

Diabetes care remained unchanged in the control group. 

All the children completed an anxiety questionnaire before and after the intervention.

Results indicate that the essential oil helped to significantly reduce (i) physiological anxiety, (ii) social anxiety, and (iii) tendency to worry in the intervention group.

The researchers report that, besides orange essence, lavender and rose essential oils are also commonly used for their anti-stress and anxiety relief properties.

Journal reference: Motaghi, Minoo, Milad Borji, and Mohsen Moradi. “The effect of orange essence aromatherapy on anxiety in school-age children with diabetes.” Biomedical and Pharmacology Journal10.1 (2017): 159-164.

Gut health and inborn errors of metabolism

Inborn errors of metabolism (IEMs) are rare disorders involving a faulty gene that makes it difficult for the body to convert food into energy.

The treatment for IEMs typically involves dietary manipulations, which along with genetics, can influence the health of the microbiome. For instance, excessive food intake or food restriction, can lead to gut dysbiosis, an imbalance in the type and/or quantity of bacteria present in the gut.

This gut dysbiosis can further alter the metabolic state of a person with an IEM by worsening the functions of the liver and the brain, the two major organs already affected by IEMs.

As such, an unhealthy microbiome can cause:

  • Neurocognitive issues (mood and behavior disorders, coordination problems, and cognitive disorders)
  • Issues with the gut-brain interactions, increasing risks of cardiovascular risk, multiple sclerosis, anxiety, depression, autism, and Alzheimer’s disease.
  • Liver problems (cirrhosis and non-alcoholic fatty liver disease)

Journal reference: Colonetti, Karina, Roesch, Luiz Fernando, & Schwartz, Ida Vanessa Doederlein. (2018). The microbiome and inborn errors of metabolism: Why we should look carefully at their interplay?. Genetics and Molecular Biology, 41(3), 515-532.

Each month I review nutrition studies related to a specific topic and share the results with you. This month is on the microbiome. The following studies discuss the microbiome related to: mental health, autism, pregnancy and autism risk, homebirth, artificial sweeteners, cleaning chemicals, PANDAS, and metabolism.

Effects of probiotics prebiotics, and phytobiotics on anxiety, depression, and mental health

The microbiome exerts a major influence on neurological health since our brains and gut are linked. Research shows that an inflamed gut promotes the release of inflammatory molecules (cytokines) in the bloodstream. These cytokines are able to cross the blood-brain barrier and induce inflammation in the brain, creating neurological symptoms like depression, anxiety, and stress.

Improving the gut health with specific strains of probiotics can positively influence mental health. For example, Lactobacillus helveticus R0052, Bifidobacterium longum R0175, and Lactobacillus rhamnosus R0011 can ameliorate depression, anxiety, and stress respectively.

A new study shows that supplementing with probiotics, prebiotics, and phytobiotics (i.e. phytonutrients such as polyphenols) for 30 days work together to increase beneficial bacteria. This can, in turn, improve:

  • Global mood
  • Vigor
  • Depression
  • Tension
  • Fatigue
  • Confusion
  • Anger

Journal reference: Talbott, S., Stephens, B., Talbott, J., & Oddou, M. (2018). Effect of Coordinated Probiotic/Prebiotic/Phytobiotic Supplementation on Microbiome Balance and Psychological Mood State in Healthy Stressed Adults. The FASEB Journal, 32(1_supplement), 533-85.

Early disturbance of the microbiome and the rise in autism

A paper reviewing the implications of the disruption of the bacterial microbiome in autism was published in August this year.

Take-home “gems”:

  • Since gut microbes are involved in the production of many vitamins, they influence the overall antioxidant status. Glutathione, the body’s chief antioxidant agent is severely depleted in autism.
  • Gastrointestinal complications are common in ASD and could be caused by increased intestinal permeability, inflammation, and an unhealthy gut microbiome.
  • Individuals with ASD have more firmicutes than bacteroidetes – the ratio of these bacteria can influence the severity of autistic symptoms.
  • Antibiotics can decrease the body’s ability to absorb iron, produce proteins, and digest certain foods. This can further increase the risks of inflammation, autoimmune issues, and gastrointestinal distress.
  • An unbalanced gut flora can lead to many cognitive issues associated with ASD since about 90% of serotonin is produced in the gut.
  • Some antibiotics can prevent mitochondria, the cell’s energy-producing generator, from working properly and thus, impairs brain development.

To keep their microbiome healthy, individuals with ASD may want to (i) support their digestion and gut health, (ii) try an anti-inflammatory diet, and (iii) avoid using antibiotics except when imperative.

Journal reference: Eshraghi, Rebecca S., et al. “Early disruption of the microbiome leading to decreased antioxidant capacity and epigenetic changes: Implications for the rise in autism.” Frontiers in cellular neuroscience 12 (2018): 256.

Mom’s microbiome during pregnancy linked to child’s autism risk

Cutting-edge research suggests that the mother’s gut health during pregnancy plays a critical role in determining the child’s risk of developing ASD.

The researchers hypothesized that, in mice, an immune reaction to interleukin-17a (IL-17a), a molecule produced by the immune system, could trigger ASD-like behaviors.

To test their hypothesis, the team used Jax and Tac mice from two different laboratories. Unlike the Jax mice, the Tac mice had gut microbes that made them susceptible to an IL-17a inflammatory reaction.

Both groups were exposed to a virus designed to create an immune response. Only the Tac mice (the ones susceptible to inflammation) had pups that developed ASD-like behaviors.

To prevent an inflammatory response, the researchers then artificially blocked the IL-17a molecule in the Tac mice. The pups born did not show ASD-like behavior.

Finally, the researchers exposed the Jax mice to the gut flora of Tac mice (making them more susceptible to inflammation). Interestingly, they found that pups born after this intervention showed ASD-like behavior.

Practical tip: Although these findings may not be applicable to humans, pregnant women and those planning to conceive could opt for a gut-friendly (and microbe-friendly) diet and lifestyle. Probiotics (or fecal transplants, when medically necessary) may also positively influence the mother’s microbiome.

Journal reference: Lammert, Catherine R., et al. “Cutting edge: critical roles for microbiota-mediated regulation of the immune system in a prenatal immune activation model of autism.” The Journal of Immunology 201.3 (2018): 845-850.

Babies born at home may have a healthier gut microbiome

New research indicates that babies born at home have a more diverse gut and fecal microflora compared to those born in hospitals.

The researchers followed 35 infants and their mothers until the babies were 1 month old. 14 of the babies were born at home (four of them in water) and 21 in the hospital.

Stool samples indicated that the hospital-born babies had greater inflammatory gene expression in epithelial cells which cover organ linings, skin, and mouth. Moreover, hospital-born infants had lower levels of Bacteroides, Bifidobacterium, Streptococcus, and Lactobacillus, and higher Clostridium and Enterobacteriaceae compared to babies born at home.

Why these differences in gut microbiota between infants born at home versus hospitals?

Well, the scientists speculate that common hospital interventions, such as infant bathing and antibiotic eye prophylaxis, and the aseptic hospital’s environment could be involved.

Although more research is needed, this study’s findings favors the idea of home births and/or revamping the hospital environment to mimic home conditions for non-high-risk births. Since the gut flora affects the immunity and metabolism, a healthy microbiome could reduce the babies’ risks of obesity, diabetes, asthma, and gut disorders later in life.

Journal Reference: Combellick, Joan L., et al. “Differences in the fecal microbiota of neonates born at home or in the hospital.” Scientific reports 8.1 (2018): 15660.

FDA-approved artificial sweeteners are toxic to gut bacteria

What do as aspartame, sucralose, saccharine, neotame, advantame and acesulfame potassium-k have in common?

Yes, they’re FDA-approved artificial sweeteners. But they’re also toxic to the gut microbiome.

In a study published in September, scientists found that gut bacteria became toxic when exposed to concentrations of only one mg/ml of the artificial sweeteners. It appears that the artificial sweeteners damage the membranes of the bacterial cells.

What you can do about it: Read labels on the foods and drinks that you buy, especially if you consume energy drinks – you may be unconsciously consuming artificial sweeteners.

Avoiding these products may not only help preserve your microbiome’s integrity but will also help protect the environment. The sweeteners contaminate drinking and surface water, and groundwater aquifers.

Journal reference: Harpaz, Dorin, et al. “Measuring artificial sweeteners toxicity using a bioluminescent bacterial panel.” Molecules 23.10 (2018): 2454.

Home cleaning products may increase risk of children becoming overweight by altering their microbiome

Canadian scientists analyzed fecal samples from 757 3- to 4-month-old infants to assess their gut flora. They also recorded the children’s weight at ages 1 and 3 years. The infants’ mothers self-reported their use of disinfectants, detergents, and eco-friendly products at home.

What the research found:

  • Household cleaning products adversely affected the children’s gut microbiome irrespective of birth mode, intake of antibiotics, or breastfeeding.
  • Regular use of disinfectants increased Lachnospiraceae species by 1.3 times which, in turn, increased the risks of overweight at ages 1 and 3.
  • Haemophilus bacteria levels dropped with daily use of disinfectants and regular use of household wipe products.
  • The children whose mothers used eco-friendly products daily had lower levels of Enterobacteriaceae. However, the scientists speculated that the mothers who used these products probably led a healthier lifestyle during pregnancy and transmitted fewer Enterobacteriaceae to their babies during vaginal delivery.

Practical Tip: Since, common household cleaners can cause children to become overweight by disrupting the bacteria in the body, avoid these cleaners. Instead switch to eco-friendly products; even simply baking soda and vinegar can often do the trick. It’s easy to do and it will make a big difference for you and your family.

Journal reference: Tun, Mon H., et al. “Postnatal exposure to household disinfectants, infant gut microbiota and subsequent risk of overweight in children.” CMAJ 190.37 (2018): E1097-E1107.

PANDAS and the gut microbiome

“PANDAS” is the acronym for pediatric autoimmune neuropsychiatric disorders associated with streptococcal infections.

It refers to a form of obsessive-compulsive disorder with symptoms such as tics, frequent urination, and rigid or repetitive behaviors caused by a streptococcal infection. These behaviors may increase sleep disturbances and mood disorders in children.

A new study shows that streptococcal infections modify the composition of the gut microbiome by favoring the growth of certain bacterial species. This, in turn, promotes inflammation in PANDAS patients.

In the study, scientists analyzed the gut of 30 PANDAS patients and compared them with 70 healthy individuals. They found that, regardless of age, the PANDAS patients had a less diverse gut flora compared to healthy individuals.

Moreover, younger PANDAS patients showed a decrease in short-chain fatty acids, D-alanine, tyrosine and dopamine pathways involved in some neuronal functions. These patients also had a lack of anti-inflammatory elements like unsaturated fatty acids and dioxin degradation.

Conversely, the healthy individuals had increased D-alanine metabolism and higher concentrations of Roseburia bacteria which help preserve the gut function. These bacteria promote the production of butyrate, a type of fatty acid that helps the gut function effectively.

More research is needed to better understand the role of the gut’s microbes to assess the disease and how to adapt treatment to the patient’s needs.

Journal Reference: Quagliariello, Andrea, et al. “Gut Microbiota Profiling and Gut–Brain Crosstalk in Children Affected by Pediatric Acute-Onset Neuropsychiatric Syndrome and Pediatric Autoimmune Neuropsychiatric Disorders Associated With Streptococcal Infections.” Frontiers in microbiology 9 (2018): 675.

Gut health and inborn errors of metabolism

Inborn errors of metabolism (IEMs) are rare disorders involving a faulty gene that makes it difficult for the body to convert food into energy.

The treatment for IEMs typically involves dietary manipulations, which along with genetics, can influence the health of the microbiome. For instance, excessive food intake or food restriction, can lead to gut dysbiosis, an imbalance in the type and/or quantity of bacteria present in the gut.

This gut dysbiosis can further alter the metabolic state of a person with an IEM by worsening the functions of the liver and the brain, the two major organs already affected by IEMs.

As such, an unhealthy microbiome can cause:

  • Neurocognitive issues (mood and behavior disorders, coordination problems, and cognitive disorders)
  • Liver problems (cirrhosis and non-alcoholic fatty liver disease)
  • Issues with the gut-brain interactions, increasing risks of cardiovascular risk, multiple sclerosis, Alzheimer’s disease, depression, autism, and anxiety.

Journal reference: Colonetti, Karina, Roesch, Luiz Fernando, & Schwartz, Ida Vanessa Doederlein. (2018). The microbiome and inborn errors of metabolism: Why we should look carefully at their interplay?. Genetics and Molecular Biology, 41(3), 515-532.


Home cleaning products may increase risk of children becoming overweight by altering their microbiome

Canadian scientists analyzed fecal samples from 757 3- to 4-month-old infants to assess their gut flora. They also recorded the children’s weight at ages 1 and 3 years. The infants’ mothers self-reported their use of disinfectants, detergents, and eco-friendly products at home.

What the research found:

  • Household cleaning products adversely affected the children’s gut microbiome irrespective of birth mode, intake of antibiotics, or breastfeeding.
  • Regular use of disinfectants increased Lachnospiraceae species by 1.3 times which, in turn, increased the risks of overweight at ages 1 and 3.
  • Haemophilus bacteria levels dropped with daily use of disinfectants and regular use of household wipe products.
  • The children whose mothers used eco-friendly products daily had lower levels of Enterobacteriaceae. However, the scientists speculated that the mothers who used these products probably led a healthier lifestyle during pregnancy and transmitted fewer Enterobacteriaceae to their babies during vaginal delivery.

Practical Tip: Since, common household cleaners can cause children to become overweight by disrupting the bacteria in the body, avoid these cleaners. Instead switch to eco-friendly products; even simply baking soda and vinegar can often do the trick. It’s easy to do and it will make a big difference for you and your family.


Mom’s microbiome during pregnancy linked to child’s autism risk

Cutting-edge research suggests that the mother’s gut health during pregnancy plays a critical role in determining the child’s risk of developing ASD.

The researchers hypothesized that, in mice, an immune reaction to interleukin-17a (IL-17a), a molecule produced by the immune system, could trigger ASD-like behaviors.

To test their hypothesis, the team used Jax and Tac mice from two different laboratories. Unlike the Jax mice, the Tac mice had gut microbes that made them susceptible to an IL-17a inflammatory reaction.

Both groups were exposed to a virus designed to create an immune response. Only the Tac mice (the ones susceptible to inflammation) had pups that developed ASD-like behaviors.

To prevent an inflammatory response, the researchers then artificially blocked the IL-17a molecule in the Tac mice. The pups born did not show ASD-like behavior.

Finally, the researchers exposed the Jax mice to the gut flora of Tac mice (making them more susceptible to inflammation). Interestingly, they found that pups born after this intervention showed ASD-like behavior.
Practical tip: Although these findings may not be applicable to humans, pregnant women and those planning to conceive could opt for a gut-friendly (and microbe-friendly) diet and lifestyle. Probiotics (or fecal transplants, when medically necessary) may also positively influence the mother’s microbiome.


People with type 2 diabetes may reverse or reduce their insulin use with intermittent fasting

In a new study, Suleiman Furmli, MD, and his team reported that, under medical supervision, therapeutic 24-hour fasting regimens can help reverse type 2 diabetes. The fasting interventions could also reduce the use of medications in patients with type 2 diabetes and minimize surgical interventions in this population.

This small study involved 3 male patients aged between 40 and 67. The 3 participants also had high blood pressure and high cholesterol levels in addition to type 2 diabetes and were taking at least 70 units of insulin daily at the beginning of the study.

Two of the patients fasted three times weekly for 7 months. After the intervention, one patient discontinued insulin and metformin use while the other stopped his fixed-dose insulin mix.

The other patient fasted on alternating days for 11 months and was able to eliminate metformin and pre-mixed insulin.

HbA1c levels improved for all 3 participants who also lost weight and inches off their waists.


Children with developmental disorders are more likely to be overweight or obese

A new study reveals that children with developmental delays, including ASD, can be up to 50% more likely to be overweight or obese compared to the general population.

This study involved 2,500 children aged two to five years old and included:

  • 668 children with ASD
  • 914 children with developmental delays or disorders
  • 884 children from the general population (the control group)

Compared to the control group, children with ASD or other developmental delays were 1.57 times and 1.38 times, respectively, more likely to be overweight or obese.

Children with severe ASD were 1.7 times more likely to be classified as overweight or obese compared to those with mild symptoms.

The authors note that diet and other medical conditions (such as digestive issues, poor sleep quality, medication-associated side effects, genetic disorders, and hormonal imbalances) may contribute to weight gain in children with ASD.


Note: While this study did not look at diet, in my experience it’s a gluten-free, casein-free diet may be able to prevent excessive weight gain in children with autism. You see, children with ASD often react adversely to gluten-containing grains and dairy products since consumption of these foods promotes the production of gluteomorphins and casomorphins, respectively. These opioid-like molecules are addictive and can trigger overeating. Moreover, gluten and dairy are pro-inflammatory and can also perpetuate weight gain. Research would be needed to see if this was one of the contributing factors, and/or whether as GFCF diet could address excess weight in children.


Short questionnaire may help identify digestive issues in children with autism

Digestive disorders are four times more common in children with autism compared to the general population. Unfortunately, children with ASD often have issues communicating digestive distress, and pinpointing the location of their discomfort, to their parents or primary care providers.

As such, GI disorders can be tricky to identify in this population.

To remedy to this, a group of pediatric gastroenterologists and psychiatrists created a questionnaire that relies minimally on the child’s ability to report or localize pain.

In this study, 131 parents of children with autism were asked a series of question designed to assess symptoms of three common digestive issues, namely constipation, diarrhea, and reflux disease.

Symptoms included:

  • Gagging during meals
  • Applying pressure to the abdomen
  • Arching the back

The researchers then asked pediatric gastroenterologists, who were unaware of the parents’ answers, to assess the children.

The data collected helped the researchers identify 17 questions that were able to correctly identify 84% of kids with GI disorders.

Because many children with autism are nonverbal and parents and doctors are often unaware that they have digestive distress. This will help healthcare practitioners identify gastrointestinal issues, so the child can get needed support.



Autism and gluten intolerance – what do genes say?

Did you know that most cells in your body have proteins known as human leukocyte antigens (HLA) on the surface?

Put (very) simply, HLA act as flagpoles on the cell’s surface and ‘present’ small pieces of protein to the immune system.

If the immune system identifies these protein fragments as foreign, it will trigger a reaction to prevent the foreign protein from damaging the body.

HLA genes, autism, and gluten intolerance

HLA genes have hundreds of versions (or alleles), but research has identified 2 main classes of HLA which present antigens to the immune system: HLA Class I and HLA Class II.

In a recent study, French scientists investigated the differences in the distribution of the HLA Class II alleles between healthy subjects and ASD patients. They also studied differences in the genetic makeup and characteristics of the HLA Class II alleles in the two groups.

Compared to healthy individuals, ASD patients are more likely to carry the HLA gene with the HLA-DRB1 *11-DQB1*07 structure, which increases the risks of celiac disease.

This could explain why many individuals with ASD and those with celiac disease suffer from similar gastrointestinal issues, have increased intestinal permeability and an unbalanced gut flora.

Results from this study support the use of a gluten-free diet to help relieve some of the symptoms of ASD.


High gluten intake during pregnancy linked to increased risks of diabetes in children

Although more research is needed, a recent study suggests that maternal gluten consumption during pregnancy could increase the child’s risk of type 1 diabetes.

Findings from this study also suggest that:

  • The risk of type 1 diabetes in the children increases proportionally per 10g/day increased gluten intake.
  • Over an average follow-up period of 15.6 years, children of women who consumed at least 20g of gluten per day had twice the risks of developing type 1 diabetes compared to children of women whose daily gluten intake was less than 7g.
  • Older, overweight or obese women, and those who had given birth more than once were likely to be more sensitive to gluten due to increased inflammation or increased intestinal permeability.

Since celiac disease and type 1 diabetes “share” some HLA genes, pregnant women or those intending to conceive may want to consider swapping gluten-containing foods (such as wheat, rye, spelt, and barley) for other gluten-free nutritious foods.


Early disturbance of the microbiome and the rise in autism

A paper reviewing the implications of the disruption of the bacterial microbiome in autism was published in August this year.

Take-home “gems”:

  • Since gut microbes are involved in the production of many vitamins, they influence the overall antioxidant status. Glutathione, the body’s chief antioxidant agent is severely depleted in autism.
  • Gastrointestinal complications are common in ASD and could be caused by increased intestinal permeability, inflammation, and an unhealthy gut microbiome.
  • Individuals with ASD have more firmicutes than bacteroidetes – the ratio of these bacteria can influence the severity of autistic symptoms.
  • Antibiotics can decrease the body’s ability to absorb iron, produce proteins, and digest certain foods. This can further increase the risks of inflammation, autoimmune issues, and gastrointestinal distress.
  • An unbalanced gut flora can lead to many cognitive issues associated with ASD since about 90% of serotonin is produced in the gut.
  • Some antibiotics can prevent mitochondria, the cell’s energy-producing generator, from working properly and thus, impairs brain development.

To keep their microbiome healthy, individuals with ASD may want to (i) support their digestion and gut health, (ii) try an anti-inflammatory diet, and (iii) avoid using antibiotics except when imperative.


FDA-approved artificial sweeteners are toxic to gut bacteria

What do as aspartame, sucralose, saccharine, neotame, advantame and acesulfame potassium-k have in common?

Yes, they’re FDA-approved artificial sweeteners. But they’re also toxic to the gut microbiome.

In a study published in September, scientists found that gut bacteria became toxic when exposed to concentrations of only one mg/ml of the artificial sweeteners. It appears that the artificial sweeteners damage the membranes of the bacterial cells.

What you can do about it: Read labels on the foods and drinks that you buy, especially if you consume energy drinks – you may be unconsciously consuming artificial sweeteners.

Avoiding these products may not only help preserve your microbiome’s integrity but will also help protect the environment. The sweeteners contaminate drinking and surface water, and groundwater aquifers.


PANDAS and the gut microbiome

“PANDAS” is the acronym for pediatric autoimmune neuropsychiatric disorders associated with streptococcal infections.

It refers to a form of obsessive-compulsive disorder with symptoms such as tics, frequent urination, and rigid or repetitive behaviors caused by a streptococcal infection. These behaviors may increase sleep disturbances and mood disorders in children.

A new study shows that streptococcal infections modify the composition of the gut microbiome by favoring the growth of certain bacterial species. This, in turn, promotes inflammation in PANDAS patients.

In the study, scientists analyzed the gut of 30 PANDAS patients and compared them with 70 healthy individuals. They found that, regardless of age, the PANDAS patients had a less diverse gut flora compared to healthy individuals.

Moreover, younger PANDAS patients showed a decrease in short-chain fatty acids, D-alanine, tyrosine and dopamine pathways involved in some neuronal functions. These patients also had a lack of anti-inflammatory elements like unsaturated fatty acids and dioxin degradation.

Conversely, the healthy individuals had increased D-alanine metabolism and higher concentrations of Roseburia bacteria which help preserve the gut function. These bacteria promote the production of butyrate, a type of fatty acid that helps the gut function effectively.

More research is needed to better understand the role of the gut’s microbes to assess the disease and how to adapt treatment to the patient’s needs.


 

Could targeting the immune system improve ASD symptoms?

Numerous studies indicate that the immune system, which usually protects the body against foreign invaders, can malfunction in people with autism, causing ASD symptoms.  

For instance, changes in the central immune system (located in the thymus and bone marrow where immature white blood cells develop) and the peripheral immune system (tissues with mature white blood cells) can lead to:

  • An overstimulation of immune cells
  • The production of autoantibodies (antibodies that attack the body itself)
  • An imbalance in inflammatory molecules
  • An increased permeability of the blood-brain barrier – this can exacerbate neurological symptoms

This research involved a review of several studies that looked at the use of various drugs and nutritional supplements in the treatment of ASD, via the immune system. The substances were studied because of their anti-inflammatory and immunomodulatory actions.

Drugs reviewed

The various drugs used showed varying results in terms of improvements in behavior, social interaction, memory, and decreased symptoms of autism based on different autism rating scales.

Supplements reviewed:

  • The antioxidants sulforaphane (found in broccoli) and luteolin (found in carrots, pepper, oregano, and olive oil) were found to improve bowel characteristics, eye contact, social interaction, memory, and speaking abilities. See more on sulforaphane and DIY broccoli sprouts.
  • Immunoglobulins, administered either orally or intravenously, showed improvements in digestive symptoms, attention, and hyperactivity. No changes were seen in the core symptoms of autism.
  • Vitamin D and omega-3 may decrease inflammation.
  • Gingko biloba is safe and well-tolerated but may not be effective in improving autistic symptoms.
  • L-Carnosine appeared to improve sleep quality.
  • N-acetylcysteine could help reduce irritability and aggressive behaviors.

Most of the studies were small and results may not be applicable to the whole autism population.

Journal reference: Marchezan J, Winkler dos Santos E, G, A, Deckmann I, Riesgo R, S: Immunological Dysfunction in Autism Spectrum Disorder: A Potential Target for Therapy. Neuroimmunomodulation 2018. doi: 10.1159/000492225

 

Gut health and inborn errors of metabolism

Inborn errors of metabolism (IEMs) are rare disorders involving a faulty gene that makes it difficult for the body to convert food into energy.

The treatment for IEMs typically involves dietary manipulations, which along with genetics, can influence the health of the microbiome. For instance, excessive food intake or food restriction, can lead to gut dysbiosis, an imbalance in the type and/or quantity of bacteria present in the gut.

This gut dysbiosis can further alter the metabolic state of a person with an IEM by worsening the functions of the liver and the brain, the two major organs already affected by IEMs.

As such, an unhealthy microbiome can cause:

  • Neurocognitive issues (mood and behavior disorders, coordination problems, and cognitive disorders)
  • Liver problems (cirrhosis and non-alcoholic fatty liver disease)
  • Issues with the gut-brain interactions, increasing risks of cardiovascular risk, multiple sclerosis, Alzheimer’s disease, depression, autism, and anxiety.

Journal reference: Colonetti, Karina, Roesch, Luiz Fernando, & Schwartz, Ida Vanessa Doederlein. (2018). The microbiome and inborn errors of metabolism: Why we should look carefully at their interplay?. Genetics and Molecular Biology, 41(3), 515-532.

 

Effects of probiotics prebiotics, and phytobiotics on mental health

The microbiome exerts a major influence on neurological health since our brains and gut are linked. Research shows that an inflamed gut promotes the release of inflammatory molecules (cytokines) in the bloodstream. These cytokines are able to cross the blood-brain barrier and induce inflammation in the brain, creating neurological symptoms like depression, anxiety, and stress.

Improving the gut health with specific strains of probiotics can positively influence mental health. For example, Lactobacillus helveticus R0052Bifidobacterium longum R0175, and Lactobacillus rhamnosus R0011 can ameliorate depression, anxiety, and stress respectively.

A new study shows that supplementing with probiotics, prebiotics, and phytobiotics (i.e. phytonutrients such as polyphenols) for 30 days work together to increase beneficial bacteria. This can, in turn, improve:

  • Global mood
  • Vigor
  • Depression
  • Tension
  • Fatigue
  • Confusion
  • Anger

Journal reference: Talbott, S., Stephens, B., Talbott, J., & Oddou, M. (2018). Effect of Coordinated Probiotic/Prebiotic/Phytobiotic Supplementation on Microbiome Balance and Psychological Mood State in Healthy Stressed Adults. The FASEB Journal, 32(1_supplement), 533-85.

 

The gluten-free diet, ASD and Down Syndrome

An often-asked question – do individuals with Autism Spectrum Disorder carry genetic markers of gluten intolerance?

After all, some studies indicate that gluten intolerance may cause, not only gastrointestinal symptoms, but extraintestinal issues including psycho-neurological disorders such as ASD. Moreover, the removal of gluten-containing foods from the diet has been shown to improve symptoms of ASD.  

The same is true for Down syndrome: individuals have an increased intolerance to gluten and improve upon removal.

However, while there is significant science and experience from physicians on the harm associated with gluten for individual with ASD and Down syndrome, this information is slow to reach in the mainstream nutrition or medical fields to the extent is should. Therefore, additional research is always welcome.

New research looking at both Autism and Down syndrome indicates that:

  • Antibodies to gliadin IgG (Antigliadin IgG) were likely present in children with ASD who consumed a regular diet as well as children with Down Syndrome.
  • As expected, children with ASD who consumed a gluten-free diet are less likely to carry antigliadin IgG antibodies.
  • Children with ASD and Down Syndrome were likely to have a genetic predisposition to celiac disease, indicating a sensitivity to gluten.
  • Children with ASD and Down Syndrome are unlikely to carry antibodies to deamidated peptides of gliadin IgA (AntiDGP IgA).

Download our complimentary Gluten-Free Casein-Free guide

Journal reference: Bavykina, I. A., Zvyagin, A. A., Petrova, I. V., & Nastausheva, T. L. (2018). Markers of gluten intolerance in children with autism spectrum disorders and Down’syndrome. Zhurnal nevrologii i psikhiatrii imeni SS Korsakova, 118(5. Vyp. 2), 64-68.

 

Prenatal fish oil supplementation may improve children’s growth 

A mother’s diet during pregnancy can have a profound effect on the fetus and the results can last through childhood.

A new study investigating the effects of prenatal fish oil supplements shows that children born of women who took the supplements were more likely to have healthier growth during the first six years of life.

The study involved 736 pregnant Danish women who either took daily fish oil supplements (the experimental group) or olive oil supplements (the control group). The women started the supplements from week 24 of their pregnancy until one week after delivery.

The researchers assessed the children’s height, weight, head and waist measurements 11 times from birth to age six. They found that the children’s whose mothers took the fish oil supplements had a higher body mass index throughout their first 6 years of life compared to those whose mothers received the olive oil supplements.

The higher BMI was due to a higher percentage of lean muscle and bone mass, and not extra body fat, indicating that fish oil supplements may exert a general growth-stimulating effect in utero.

Journal reference: Rebecca Kofod Vinding, Jakob Stokholm, Astrid Sevelsted, Tobias Sejersen, Bo L Chawes, Klaus Bønnelykke, Jonathan Thorsen, Laura D Howe, Martin Krakauer, Hans Bisgaard. Effect of fish oil supplementation in pregnancy on bone, lean, and fat mass at six years: randomised clinical trial. BMJ, 2018; k3312.

Histamine and Mast Cell Activation Syndrome – Everything You Need to Know

Do you experience random headaches? Or perhaps your tongue gets all swollen when you eat tomatoes?

As you’ll discover in this article, these symptoms aren’t ‘all in your head’ but could be related to how your body handles histamine. I’ll also talk about what nutritional strategies are available along with dietary tips you can implement easily.

But first, let’s begin with the basics.

What is histamine?

Histamine [2-(4-imidazolyl)-ethylamine] is an amine produced by various cells including mast cells, basophils, histaminergic neurons, platelets, and gastric enterochromaffin cells.

Histamine is also found in various amounts in foods containing the amino acid histidine. Fermentation, curing, and slow cooking, convert histidine to histamine thereby increasing the food’s histamine content.

Physiological functions of histamine

Let’s say you’ve been bitten by an insect. Your immune system will ‘see’ the insect’s venom and respond by triggering mast cells, a type of white blood cells which act as the guards of our innate immune system.

These mast cells will then trigger the release of histamine from storage sacs known as secretory granules [1].

Since histamine is a signaling molecule widely distributed throughout the body, it relays information between cells in the body via four types of receptors namely H1, H2, H3, and H4 receptors. And in doing so, histamine triggers the release of other immune cells while also dilating capillaries, causing swelling.

This swelling increases the capillaries’ permeability to immune cells, enabling them to rapidly find the invader (the insect’s venom in this case) and attack it so that it doesn’t have time to cause serious adverse effects.

Histamine’s other functions in the body

Since histamine acts via four different receptors, its role goes much beyond the production of an immune response.

For instance, histamine also acts as a neurotransmitter in the brain and research suggests that it can control whole brain activity [2]. Issues with the H1 receptor could cause defective locomotor and exploratory behaviors.

Moreover, histamine is also involved in:

  • The regulation of physiological functions in the gut
  • The sleep-wake cycle – issues with the H1 receptor can cause drowsiness [3, 4]
  • The production of gastric acid – medications which interfere with the H2 receptor can reduce gastric acid levels [5]

The body is usually well-equipped to prevent the build-up of histamine

Usually, once histamine has done its job (or after consuming a histamine-rich food), this amine will be enzymatically degraded via [5]:

  • Oxidative deamination by diamine oxidase (DAO) into imidazole acetaldehyde
  • Methylation by histamine N-methyltransferase (HNMT) into N4-methylhistamine

However, in some cases, the body may be unable to deal with the histamine produced or consumed.

When histamine goes haywire

There are three main types of histamine problems:

1. Mastocytosis

This is a rare genetic condition caused by an excess of altered mast cells. And the more mast cells a person has, the more histamine the body will produce [6].

2. Food-induced histaminosis

More commonly referred to as histamine intolerance, food-induced histaminosis is not a true food intolerance since it stems from the body’s inability to clear out the ingested histamine [7].

Although some foods are naturally richer in histidine/histamine, symptoms of histamine intolerance are caused by defects in the processing and elimination of histamine along with gut issues.

3. Mast Cell Activation Syndrome (MCAS)

MCAS is different from an intolerance caused by histamine consumption: it refers to an immunologic condition where the mast cells set off a hyper response to a threat.

This exaggerated reaction then leads to the release of an excess of histamine (as well as other chemical mediators like cytokines, prostaglandins, and interleukins), causing various symptoms as shown below. Put simply, MCAS is a reaction to the histamine released by the mast cells.

Common symptoms of MCAS

Since mast cells and their receptors are found throughout the body, MCAS can affect any organ system. For instance, MCAS can cause distress in the:

  • Central and peripheral nervous systems
  • Reproductive system
  • Respiratory system
  • Digestive system
  • Immune system

As you can imagine, histamine intolerance and MCAS causes a constellation of symptoms depending on which body systems are affected.

  • Headaches and migraines
  • Anxiety and/ or depression
  • Sleep disturbances
  • “Brain fog”
  • GI distress, heartburn, diarrhea
  • Redness, flushing or hives
  • Wheezing or shortness of breath
  • Nasal congestion or drip
  • Vertigo
  • Arrhythmia
  • Anaphylaxis
  • Hypotonia and hypertension
  • Circadian rhythm imbalance
  • Dysmenorrhea
  • Heart palpitations
  • Food and chemical sensitivities

What can trigger MCAS?

Mast cells can become overactive due to:

  • Pollen
  • Trauma
  • Insect bites
  • Environmental toxins
  • Inflammation or cytokines
  • IgE and IgG antibodies – Any type of food allergens and food sensitivities can trigger MCAS.
  • Gut dysbiosis or infections caused by bacteria, viruses, fungi, Lyme, and mold [8]. The toxins released by those organisms can cause severe symptoms by (i) triggering MCAS and (ii) inducing inflammation and oxidative stress.
  • Toxicity of heavy metals such as aluminum and mercury [9]
  • Salicylates (one type of phenol) – It is estimated that 0.6 to 2.5% of the population is sensitive to salicylates which can over-activate mast cells. The mast cells then release inflammatory molecules known as cysteinyl leukotrienes which then lead to various symptoms [10].
  • Oxalates – Oxalates appear to also trigger MCAS; although, this is mostly clinical evidence at this point.

Conditions associated with MCAS

In addition to the symptoms listed earlier, the following conditions are associated with MCAS, including autism and autoimmune disorders:

  • Autism
  • Allergies and Asthma
  • Food Allergy and Intolerance
  • Eosinophilic Esophagitis
  • Chronic Fatigue Syndrome
  • Multiple Chemical Sensitivity
  • CIRS (Chronic Inflammatory Response Syndrome)
  • POTS (Postural Orthostatic Tachycardia Syndrome)
  • Autoimmune disorders (Hashimoto’s thyroiditis, lupus, etc.)
  • Fibromyalgia
  • Celiac Disease
  • Irritable Bowel Syndrome
  • GERD
  • Interstitial Cystitis
  • Migraines
  • Anxiety
  • Depression
  • Sleeping Disturbances

Now that you know what MCAS is and how it can be triggered, let’s look at why some individuals have issues with histamine.

Why would a person have issues with degrading histamine?

Well, this may stem from various factors [7]:

  • A deficiency of DAO secondary to a genetic issue with DAO production (more common among people of Asian origin), gluten intolerance, and inflammation. Since DAO degrades histamine, a deficiency would cause histamine to build up in the body.

Moreover, drugs like NSAIDs, antihistamines, H2-blockers, antidepressants, immune modulators, and antiarrhythmics can also adversely affect the body’s DAO levels.

  • Genetic mutations in the DAO gene – These would reduce DAO’s efficiency in clearing out histamine.
  • A deficiency, or reduced activity, of HNMT – This can be caused by micronutrient deficiencies (such as deficiencies of vitamins B1, B2, B12, B6, and minerals like folate, zinc, and copper). These nutritional deficiencies impact the methylation pathway via which HNMT degrades histamine.
  • Consumption of histamine-rich foods or foods that naturally block DAO – This can trigger, or worsen, symptoms in individuals suffering from histamine intolerance especially if they have issues with DAO or HNMT.
  • Nutrient deficiencies – Sufficient vitamin B6 and copper are required for DAO production. Nutrient deficiencies can be caused by suboptimal digestive function, higher nutrient demands (such as in cases of stress, anxiety, or poor sleep quality), and a nutrient-poor diet.

The gut’s role in MCAS

As you’re probably aware, an unhealthy gut will increase risks of MCAS. For instance, increased intestinal permeability can cause a DAO deficiency which could then lead to histamine buildup in the body.

Moreover, histamine can be produced by pathogens and beneficial bacteria. Pathogens can also produce phenols – usually, the body is able to metabolize excess phenols. However, if someone has gut issues or inadequate levels of sulfate and liver enzymes, excess phenols can trigger histamine release.

MCAS and autism – is there a link?

Definitely!

You see, the brain also has mast cells – these are close to the neurons and microglia and are mostly found in the hypothalamus which is involved in behavior and language regulation [11].

It is well known that children with ASD are more sensitive to stress. And research by Dr. Theoharides shows that, in ASD, brain mast cells can be excessively activated by stress [12] leading to increased serum levels of neurotensin along with excess hypothalamic release of  corticotropin-releasing factor (CRF) [13]. (Allergens, toxins, and environmental, immune and neurohormonal triggers can also cause the brain mast cells to be overly activated in ASD.)

Now, both neurotensin and CRF stimulate mast cells to produce inflammatory and neurotoxic components that adversely affect the blood-brain barrier and cause inflammation in the brain [11].

Neurotensin also causes the mast cells to secrete mitochondrial DNA which can act as an innate pathogen that activates immune cells, including mast cells, thus causing autoinflammation [12]. Dr. Theoharides suggests that the inflammation induced by brain mast cells could drive headaches, ‘brain fog’, and other neurological symptoms associated with ASD [11].

What about salicylates?

Salicylate sensitivities are even more prevalent among individuals with autism and ADHD. Research suggests that individuals with autism and known food/chemical intolerances are deficient in phenol-sulfotransferase-P enzyme and/or have limited capacity to oxidize sulfur compounds [14].

Since phenol-sulfotransferase-P enzyme metabolizes phenols, amines, and some drugs, inadequate levels of this enzyme could lead to:

  • A build-up of phenols after exposure to foods and chemicals that contain phenols. This could then trigger MCAS.
  • Unpleasant reactions to medications such as antibiotics or sedatives and worsening of autism symptoms in some cases.
  • An accumulation of serotonin, dopamine, and serotonin. If these neurotransmitters are then further metabolized, it could result in the production of toxins which could impact sensory functions in ASD.

So, how can you identify MCAS? Well, there are various ways to test for this.

Testing for MCAS

1. Dietary Trial

A histamine trial involves the elimination of:

  • Foods rich in histamine
  • Foods that release histamine
  • DAO enzyme inhibitors such as alcohol, tea (black, green, mate), and various energy drinks

Foods rich in histamine

  • Fermented foods: sauerkraut, kombucha, fermented dairy including yogurt, kefir, sour cream, soy sauce, fish sauce
  • Vinegar and Vinegar-containing foods: pickles, olives, mustard
  • Cured meats: bacon, salami, hot dogs, sausage
  • Aged, dried, jerky, smoked and less fresh meat and fish, as well as anchovies and mackerel
  • Aged cheese
  • Nuts: Peanuts, walnuts, and cashews
  • Vegetables: avocados, mushrooms, eggplant, spinach, and dried tomatoes and tomato sauce
  • Dried fruit and citrus fruits
  • Long/slow simmered and roasted foods: such as bone broths and pot roast
  • Fermented alcohol: wine, beer, brandy, port, sherry, rum, champagne
  • Probiotic supplements

Foods that release histamine

  • Bananas
  • Chocolate
  • Alcohol
  • Milk
  • Nuts and peanuts
  • Fruit: Papaya, Pineapple, Strawberries
  • Tomatoes
  • Shellfish
  • Artificial preservatives and dyes

Note: Any diet can be high in histamine depending on which foods are included. So just because a diet is a therapeutic one, it does not mean that it is suitable for everyone.

For instance, the GAPS diet, especially the beginning phases, can be particularly high in histamine since these phases include lots of bone broth, fermented foods, and slow simmered meats. This is not limited to a GAPS diet. And any individual diet that includes large amounts of these foods would be a high histamine diet. This being said, with some awareness and attention, most diets can be adapted to be low in histamine.

2. Lab tests [12]

  • Serum tryptase – This is usually the test that some functional medicine doctors used to diagnose MCAS
  • Plasma heparin
  • Plasma histamine
  • N-methylhistamine
  • Plasma prostaglandin D2 (plasma PGD2) – NSAIDs are to be avoided for at least 5 days before testing since they can reduce plasma PGD2 levels
  • Urine prostaglandine D2 (urine PGD2) –
  • PGF2a
  • Serum chromogranin A – Proton pump inhibitors must be avoided at least 5 days before testing since they will interfere with test results.

You could also look at genetic SNPs for DAO and HNMT – mutations in HNMT have been shown to result in high levels of histamine in the brain [15]. This could lead to intellectual disability.

A high histamine to DAO ratio could mean that:

  • Dietary histamine intake is excessive (if currently on a regular diet)
  • Gut dysbiosis is causing over-production of histamine (if currently on a low histamine diet)
  • The body is unable to maintain optimal DAO levels

If histamine levels are normal but DAO levels are inadequate, this could indicate a genetic DAO deficiency.

3. Supplement challenge

If you are unable to test your histamine and DAO levels, you could try a supplement challenge. This involves consuming a low histamine diet while taking a DAO supplement at each meal. If your symptoms improve, this could indicate that your DAO levels are low.

What can you do about MCAS?

1.  Try a low histamine diet

The following foods are low in histamine.

  • Fresh meats
  • Fresh fish
  • Vegetables (except spinach, pickles, olives, eggplant, mushrooms)
  • Fruits (except bananas, papaya, pineapple, strawberries, citrus, dried fruit, tomato sauce)
  • Beans
  • Gluten-free grains
  • Butter and ghee

2.     Look into supplementation support with your practitioner

Some supplements that can help:

  • DAO enzymes
  • Mast cell stabilizers and anti-histamines
    • Quercetin
    • Luteolin (product:Neuroprotek)
    • Prickly pear
    • Vitamin C
    • B6
    • Omega-3 fatty acids (prostaglandins)
    • Alpha Lipoic Acid
  • Methylating Nutrients
    • Methyl B12, Methyl Folate, zinc, magnesium, riboflavin, B6/P5P, choline, SAM
    • And foods rich in them
  • Probiotics that can decrease histamine
    • bifidobacter species

Remember Dr. Theoharides’ research? Well, he created Neuroprotek, a nutritional supplement that contains natural flavonoids, like luteolin and quercetin. These antioxidants can reduce inflammation by inhibiting the release of inflammatory mediators from mast cells. The supplement also contains rutin and quercetin – these act “as ‘decoys’ to keep the intestinal and liver enzymes occupied to allow luteolin to escape metabolism and reach the brain” [17].

3.    Avoid high histamine supplements

These include:

  • Probiotics like Lactobacillus Casei and Lactobacillus Bulgaricus since these increase histamine levels.
  • Fish oil supplements are a bit tricky in that they can help reduce salicylate intolerance and prostaglandins (which cause inflammation) but they are high in amines. So, you may want to start with diet first and then add in the low-histamine supplements mentioned earlier. Then, with the guidance of your healthcare professional, you could include fish oil. If symptoms improve, then you could keep the fish oil supplements. However, you may need to remove these supplements if you notice that symptoms worsen.
  • NAC since it can block intestinal DAO although it does have some benefits. Again, you may want to assess tolerance.

Troubleshooting

You’ve tried avoiding foods rich in histamine and those that release histamine, but symptoms persist?

Then, you might want to look into:

  • Cooking methods – To reduce histamine content of broths, you’ll want to select bones with the meat and simmer the broth for a short period. You may also want to avoid slow cooked foods as well as those that are marinated, fermented, or cured. Also, if possible, consume fresh meat instead of frozen ones and avoid leftovers.
  • The Failsafe Diet – this trial diet, which I’ve previously discussed here, eliminates amines, phenols, and glutamates.
  • The low-oxalate diet – You can find out more about this diet in my video or article. Check out these recipes for easy ideas.

Now I’d like to hear from you: have you dealt with MCAS? What helped you?

A growing body of research is implicating mitochondrial dysfunction as a root cause of a wide spectrum of metabolic, lifestyle and degenerative diseases including: Chronic Fatigue Syndrome, Autism, Cancer, Diabetes, Alzheimer’s, Fibromyalgia and potentially many more. Essential to human survival at the most basic level we review the evidence that these specialized organelles are suffering in our modern environment.

Mitochondria and Energy Production

These minute powerhouses in every cell are responsible for regulating and storing cellular energy. They convert ingested energy, for example glucose, into a format the body can actively use, called ATP (Adenosine Tri Phosphate).

ATP carries energy within its atomic bonds which can be released for use in biochemical processes. Hydrolysis of ATP to ADP (Adenosine Di Phosphate) liberates energy: breaking the phosphate bond is exothermic (it gives off energy) due to the inherent instability of ATP which would ‘prefer’ to be in its ADP state.  After conversion of ATP to ADP, and release of the energy holding the phosphate in place, the ATP molecule (now ADP) is ‘spent’ and needs to be recycled.

Electrochemical reactions (collectively known as oxidative phosphorylation) take place inside the mitochondria along the electron transport chain to reattach a phosphate group to create ATP again. This endless recycling of ADP to ATP is needed to maintain energy production.

Even though each cell contains approximately one billion ATP molecules it is only sufficient to meet the cell’s energy requirements for a few minutes and constant activity is required to keep energy flowing  – amazingly humans manufacture and consume their own weight in ATP every day[1]. Cells needs energy to function optimally so even a minor impairment of mitochondrial function can have dramatic systemic ramifications.

The Scientific Study of Mitochondria

Mitochondria are actually bacterial in nature and they evolved with us endosymbiotically: mitochondrial DNA is inherited through the maternal line. [2] Unable to maintain themselves outside of eukaryotic cells, mitochondria have been co-opted into our energy production systems. However, they have their own genetic system distinct from the nuclear genome – they even use a different protein coding system for translation of mitochondrial DNA.[3]

Mitochondrial DNA is exquisitely sensitive to environmental challenges, specifically oxidative damage and stress, due to the high ratio of coding regions (versus non-coding regions) in the DNA; and a lack of protective histones supporting their DNA structure and environment.[4] Alarmingly, oxidative damage occurs at a rate five to ten times greater in mitochondrial DNA versus nuclear DNA and “damaged mitochondria promptly accelerate intra-cellular oxidation”.[5]

De Novo mutations have been specifically linked to both autism and schizophrenia indicating that the DNA damage leading to the disease is developed and not inherited.[6] Specific alterations in the mitochondrial DNA coding for complexes in the electron transport chain and pyruvate dehydrogenase have been identified in the frontal cortex of patients with autism which cause inadequate (anaerobic) utilization of glucose and an excess of unwanted metabolic byproducts.[7]

Mitochondria uniquely sit in two very different areas of biological research: structural (proteins, tissues, genome etc.) and bioenergetics (energy metabolism). These interfacing areas of research have until relatively recently been uncoupled and in vivo research has been difficult due to a lack of biomarkers and assays to detect mitochondrial damage. This lack of ability to diagnose problems with energy flow in and out of the mitochondria means the root cause of many diseases relating to mitochondrial function has been overlooked or ignored.[8]

Mitochondrial Function and Biogenesis

free-radicalsIn addition to their role in energy regulation, mitochondria are also involved in the maintenance of intracellular calcium levels and calcium buffering (required for cellular signaling)[9]. They also regulate cell numbers and defend against unwanted or dangerous cells by triggering programmed cell death (apoptosis).[10] Signaling between the human (nuclear) and mitochondrial genome is also controlled by the mitochondria themselves via the production of Reactive Oxygen Species (ROS).

Excessive ROS (also known as free radicals) is a metabolic byproduct and one of the triggers for apoptosis. For example, asbestos induced lung disease has been linked to elevated alveolar epithelial apoptosis  due to increased ROS caused by the asbestos damage.[11] Elevated levels of mitochondrial calcium can also trigger apoptosis and recent research indicates that apoptosis of nerve cells contributes to Alzheimer’s.[12]

While mitochondria have their own unique DNA, the majority of the proteins required to synthesize the organelle are recruited from nuclear coded proteins. This means they need to communicate effectively with nucleic DNA to produce the protein pieces required to join with existing subcomponents. Since the co-ordination required for mitochondrial biogenesis requires the expression of two different genomes, any epigenetic problems with DNA signaling due to a lack of nutrients or toxicity are amplified.[13]

Pharmacology and Mitochondrial Disease

Azidothyramidine was commercialized for the treatment of HIV/AIDs in the late 1980’s and transformed the disease from a death sentence to a chronic manageable condition. Unfortunately, prolonged treatment with the drug, and others nucleoside analogs, has severe or fatal side effects. Over 30% of patients treated experienced heart muscle damage and loss of vision with mitochondrial toxicity (via multiple routes) being the agreed cause.[14]

The association with pharmacologically active compounds and mitochondrial function is now so well recognized that pharmaceutical companies have developed high throughput screening to specifically look for mitochondrial damage during the drug development process. Other classes of compounds including antibiotic, antiepileptic, antidiabetic, antipsychotic, antidepressant, beta-blocker, and nonsteroidal anti-inflammatory drugs have also demonstrated the ability to damage mitochondria; many others may reveal the same problems with further research.[15]

Fueling the Mitochondria

Mitochondria can use different sources of fuel (glucose, protein and fat) both with and without oxygen depending on the cellular conditions. A delicate balance of regulatory mechanisms and hormones determines which of these fuel sources should be preferentially utilized. The byproducts of the different pathways also control a wide variety of downstream biological processes meaning that fuel availability (or capacity to utilize it) has wider implications.

Mitochondrial fuel selection, and metabolite production, is interlinked with responses in vital systems such as immune function[16]. For example an excessive production of ROS stimulates the inflammatory response[17] and can trigger chronic diseases.[18]

Energy Preferences

Organs have different metabolic requirements: the brain relies on glucose and a derivative of fatty acids called ketone bodies while muscle uses glucose for short bursts of energy but uses fatty acids for 85% of its needs. The heart relies exclusively on anaerobic metabolism of fatty acids and has a high density of mitochondria to meets its energy requirements. [19]

Aerobic glycolysis of glucose (in the presence of oxygen) is 5 times more efficient than anaerobic glycolysis as it fully breaks down the glucose. The buildup of lactic acid, as a result of anaerobic glycolysis, can be used to indicate a drop in mitochondrial performance as it no longer metabolizes the pyruvate to release the remaining energy – elevated lactate to pyruvate ratios are often seen in patients with autism.[20] When mitochondria are utilizing fuel less efficiently they produce more ROS (like a sooty fire) and this causes further damage to the delicate organelle.

Dietary modifications to reduce glucose have been found to improve some behavioral traits commonly associated with autism in mice models. Changes in plasma metabolites reduce the neuroinflammation and impaired neurogenesis seen in both animal and human models. [21]

The excess ROS production (due to inefficient fuel usage), combined with low levels of intrinsic antioxidants and lack of precursors needed for fatty acid metabolism (specifically carnitine) often associated with autism explains why some patients experience improved symptoms with a ketogenic (fat based) diet especially when combined with carnitine supplementation. [22]

Mitochondrial Diseases and Dysfunctions

There are an increasing number of diseases which have been attributed to mitochondrial function and many share general symptoms of fatigue and muscle pain due to impaired energy provision to organs with high energy demands.

At the other end of the disease spectrum, the fatal condition MELAS (mitochondrial encephalomyopathy, lactic acidosis, and stroke like episodes) causes extreme seizures, migraines and brain damage. Mutations in mitochondrial DNA mean the body is not able to meet its own energy needs, specifically during physical exertion.

While some mitochondrial diseases have a strong genetic element many are suspected to be as a result of environmental conditions which do not support efficient energy utilization. Mitochondrial dysfunction as a result of increased ROS production, lack of antioxidants and environmental pollutants has been coming under closer scrutiny as a trigger or even for conditions as diverse as autism and Gulf War Syndrome.[23] Another metabolic waste product, oxalates cause oxidative stress too and further damage the mitochondria leading to chronic disease.

The high energy demands of the brain make it more susceptible to a buildup of ROS if mitochondria are not functioning optimally. Additionally, the ROS directly damage the polyunsaturated fats which make up the majority of the brain tissue and mitochondrial damage has been implicated in a variety of neurodegenerative diseases including Alzheimer’s.[24]

Chronic stress has also been shown to inhibit mitochondrial function and induces reversible mitochondrial damage causing symptoms resembling Irritable Bowel Syndrome (IBS).[25] Sleep apnea is another condition which reduces mitochondrial function by causing frequent periods of hypoxia.[26] Glutamate has also been found to contribute to mitochondrial disease because it interferes with calcium homeostasis.[27]

Autistic Spectrum Disorder

The spectrum of symptoms, and wide variety in the severity of autism spectrum disorder, supports the notion that varying energy demands and fuel utilization throughout the body determine the degree of the impact from poorly functioning mitochondria. The huge degree of divergence points to multiple genetic susceptibilities which have been found to cluster around genes responsible for calcium and metabolic (MAPK) signaling. These foundational errors also indicate widespread “vulnerability to other chronic and systemic problems potentially including cancer, metabolic conditions and heart diseases” for both autistic patients and the public at large.[28]

Neurological symptoms are virtually always present and this is the organ with the highest energy usage and very stringent requirements about fuel sources (other high energy systems such as the bowels and muscles are also typically symptomatic).

Some patients also experience idiopathic symptoms including cardiovascular symptoms, growth retardation and fatigue which align with the known outcomes of poor mitochondrial function. [29] According to one study, defects in oxidative phosphorylation (the process by which ADP is remade into ATP) are identified in nearly 50% of patients with autism highlighting the need for metabolic evaluation to support individualized therapy.[30] Glutamate levels are also often elevated in ASD patients, further exacerbating mitochondrial toxicity.[31]

Cardiovascular Health

The heart is another organ which has high energy demands and 35% of the volume of cardiac muscles cells is taken up by mitochondria. Diabetic patients often experience cardiac problems higher than predicted levels (adjusting for hypertension and coronary artery disease) due to deficiencies in cardiac energy metabolism.[32] Various mechanisms have been identified which contribute to the multifactorial cardiac challenges, including: increased ROS production; impaired calcium regulation and incomplete biogenesis of new mitochondria.

The root cause of cardiovascular diseases, including atherosclerosis, is increasingly being linked to the mitochondria responsible for energy production and regulation. The vicious feedback loop of oxidative stress causing inflammatory responses and apoptosis further exacerbates a system under pressure leading to a variety of disease states.[33]

Cancer and Oncogenesis

Since the beginning of the 20th century, scientists knew that cancer cells had differences in their metabolism: preferentially utilizing glucose anaerobically and producing a lot of lactic acid (known as the Warburg effect) even when sufficient oxygen is available for aerobic metabolism. It is postulated that anaerobic glycolysis actually produces more of the biosynthetic intermediates needed for cellular growth and proliferation.[34]

Abnormal mitochondrial function has been found in multiple human cancer variants. In vitro replication of mitochondrial mutations, knocking out specific parts of the electron transport chain, has demonstrated cells with increased ROS (as a result of anaerobic glycolysis) have higher invasive behaviors and greater migration rates comparable to cancer cells.[35]

Additionally, some metabolic enzymes typically involved in the Krebs cycle usually actually act as oncosuppressors – this means that imbalances in fuel selection due to mitochondrial dysfunction also impacts genes promoting cell proliferation. [36]

The regulatory role of mitochondria in apoptosis is also under scrutiny for its role in cancer progression as compromised apoptotic function removes the usual protection the body has for removing dangerous cells.  Cancerous cells actually manage to deregulate the pathway which would typically save the rest of the body from tumor development.

Elevated ROS, from poorly functioning mitochondria, also increases cancer risk by damaging the DNA and stimulating pro-growth responses (tumor genesis). In an attempt to slow down the tumorigenic signaling, the body will typically respond by up-regulating the production of intrinsic anti-oxidants to reduce ROS levels.

The relationship between ROS, antioxidants and tumor genesis explains why research has repeatedly substantiated claims that fresh fruits and vegetables, packed with anti-oxidants, can prevent and even cure cancers and nutritional therapies reduce ROS while providing the nutrients needed for the body to heal itself.[37]

Evidence for other Mitochondrial Conditions

Metabolic Syndrome: Many of the risk factors for metabolic syndrome (obesity, elevated cholesterol, hypertension and diabetes) are linked with abnormal mitochondrial function. [38] Over nutrition is specifically linked with oxidative stress especially when combined with a lack of exercise.[39]

Asthma: Animal models have demonstrated the role of oxidative stress in the inflammatory response triggered during asthma. [40] Additionally, there is an increased likelihood of severe asthma attacks in obese individuals, pointing to mitochondria as the root cause of the disease.[41] The use of targeted antioxidant therapy in animal asthma models has already demonstrated a reduction in the fibrotic airway remodeling which is linked to disease progression.[42]

Chronic Fatigue Syndrome: The severity of symptoms presented by sufferers of CFS has been directly linked to the degree of mitochondrial disease. [43]

Fibromyalgia: The chronic pain of this condition has been linked to suboptimal mitochondrial function in the nervous system and patients are often low in enzymes required for complete energy metabolism, namely CoQ10.[44]

Irritable bowel syndrome: Mitochondrial DNA mutations have been found to be higher in patients with IBS and oxidative stress triggers damaging chronic inflammatory responses.[45]

Diabetes: Excessive production of ROS contribute to the pathophysiology of diabetes, specifically damaging nerves and the eyes.[46]

There is increasing evidence that mitochondrial dysfunction is responsible for, or strongly contributes to, many more chronic degenerative disorders, including: Alzheimer’s, Parkinson’s disease, Huntington Disease, Amyotrophic Lateral Sclerosis (ALS) oobesity and autoimmune diseases (lupus, Sjogren’s syndrome and rheumatoid arthritis).[47]

The New Paradigm

Science tends to put things in little, separate, boxes. Taking a step back and looking at the wider picture we can see that the various epidemics of modern disease present very different symptoms but the root cause could be remarkably simple.

Putting together the pieces of the puzzle, we can see that our ancient mitochondria can simply not cope with the insult of environmental toxins, from the food we eat; medicines we take; air we breathe; and chemicals we apply on our body. Most likely the lack of quality nutrients in the modern processed diet is also responsible for the reduced function and increasing mitochondrial damage.

Unless some drastic action is taken to improve the working conditions of these vital organelles, the progression and severity of lifestyle diseases is set to continue at an alarming rate. Figures for diabetes, cancers, cardiovascular disease and more are soaring and the abuse of our mitochondria seems to be the elephant in the room that has finally been noticed.

References

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[2] Michael W Gray, Gertraud Burger, and B Franz Lang, “The Origin and Early Evolution of Mitochondria”, Genome Biology 2001 June 5; 2(6): reviews 1018.1-reviews1018.5 http://www.ncbi.nlm.nih.gov/pmc/articles/PMC138944/

[3] Cooper GM, The Cell: A Molecular Approach, 2nd Edition. Sunderland (MA): Sinauer Associates; 2000. Mitochondria Available from: http://www.ncbi.nlm.nih.gov/books/NBK9896/

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[33] Ballinger SW, “Mitochondrial Dysfunction in Cardiovascular Disease”, Fee Radical Biol Med. 2005 May 15;38(10):1278-95, http://www.ncbi.nlm.nih.gov/pubmed/15855047

[34] Fogg VC, Lanning NJ, and Mackeigan JP, “Mitochondria in Cancer: At The Crossroads of Life and Death”, Chinese Journal of Cancer, 2011 Aug;30(8):526-539, http://www.ncbi.nlm.nih.gov/pubmed/21801601

[35] Jia Ma, Qing Zhang, Sulian Chen, Binbin Fang, Qingling Yang, Changje Chen, Lucio Miele, Fazlul H Sarkar, Jun Xia, and Zhiwei Wang, “Mitochondrial Dysfunction Promotes Breast Cancer Cell Migration and Invasion through HIF1a Accumulation via Increased Production of Reactive Oxygen Species”, Plos ONE, July 29, 2013, http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0069485

[36] Scatena R, “Mitochondria and Cancer: A Growing Role In Apoptosis, Cancer Cell, Metabolism, and Dedifferentiation”, Advances in Experimental Medicine and Biology, 2011 December 22, Ch. Advances in Mitochondrial Medicine, Volume 942; 287-308, http://www.ncbi.nlm.nih.gov/pubmed/22399428

[37] Gerson Institute, http://gerson.org/gerpress/

[38] Ulaganathan Mabalirajan and Balaram Ghosh, “Mitochondrial Dysfunction in Metabolic Syndrome and Asthma”, Journal of Allergy, 2013 June 5, 340476, http://europepmc.org/articles/PMC3687506/

[39] James AM, Collins Y Logan A, and Murphy MP, “Mitochondrial Oxidative Stress and the Metabolic Syndrome”, Trends in Endocrinology & Metabolism, September 2012 Volume 23(9);429-434, http://www.ncbi.nlm.nih.gov/pubmed/22831852

[40] P Hemachandra Reddy, “Mitochondrial Dysfunction and Oxidative Stress in Asthma: Implications for Mitochondria Targeted Antioxidant Therapeutics”, Pharmaceuticals (Basel) 2011Mar. 4(3):429-456, http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3066010/

[41] Ulaganathan Mabalirajan and Balaram Ghosh, “Mitochondrial Dysfunction in Metabolic Syndrome and Asthma”, Journal of Allergy, 2013 June 5, 340476, http://europepmc.org/articles/PMC3687506/

[42] Jaffer OA1, Carter AB, Sanders PN, Dibbern ME, Winters CJ, Murthy S, Ryan AJ, Rokita AG, Prasad AM, Zabner J, Kline JN, Grumbach IM, and Anderson ME, “Mitochondrial-Targeted Antioxidant Therapy Decreases Transforming Growth Factor-β-Mediated Collagen Production In a Murine Asthma Model”, American Journal Of Respiratory Cell and Molecular Biology, 2015 January;52(1):106-15, http://www.ncbi.nlm.nih.gov/pubmed/24988374

[43] Sarah Myhill, Norman E. Booth, and John McLaren-Howard, “Chronic Fatigue Syndrome and Mitochondrial Dysfunction” International Journal of Clinical Experimental Medicine, 2009, 2(1):1-16, http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2680051/

[44]  Cordero MD, de Miguel M, Carmona-Lopez, Campa F, and Moreno-Fernandez AM, “Oxidative Stress and Mitochondrial Dysfunction in Fibromyalgia” Neuro Endocrinlogy Lett. 2010; 31(2):169-73, http://www.ncbi.nlm.nih.gov/pubmed/20424583

[45] Wei-Feng Wang, Xin Li, Ming-Zhou Guo, Jian-De Chen, Yun-Sheng Yang, Li-Hua Peng, Yong-Hua Wang, Chun-Yan Zhang, and Hui-Hui Li, “Mitochondrial ATP 6 and * Polymorphisms in Irritable Bowel Syndrome with Diarrhea”, World Journal of Gastroenterology, 2013 June 28; 19(24): 3847-3853 http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3699044/

Asima Bhattacharyya, Ranajoy Chattopadhyay, and Sheila E Crowe, “Oxidative Stress: An Essential Factor in the Pathogenesis of Gastrointestinal Mucosal Diseases”, Physiological Reviews 2014 April: 94(2):329-354, http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4044300/

[46] William I Sivitz, and Mark A Yorek, “Mitochondrial Dysfunction in Diabetes: From Molecular Mechanisms to Functional Significance and Therapeutic Opportunities”,  Antioxidants & Redox Signaling, 2010 February 15; 12(4):537-577, http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2824521/

[47] United Mitochondrial Disease Fundation, Understanding Mitochondrial Disease,  http://www.umdf.org/site/pp.aspx?c=8qKOJ0MvF7LUG&b=7934637

Methylation-diet (1)I’m thrilled to announce the launch of Kara Fitzgerald and Romilly Hodges’ new book the “Methylation Diet and Lifestyle.” Methylation is a topic we cover extensively in our Advanced Practitioner training program at the BioIndividual Nutrition Institute. I’ve admired Kara Fitzgerald’s work for over 8 years. She’s brilliant at understanding the biochemistry of the body and the importance of nutrients and food. When I learned that she came out with a new book recently on the Methylation Diet, I knew this topic was PERFECT for our BioIndividual Nutrition members. Here’s the article Kara and Romilly wrote for us, as well as more on their book and an online webinar session we will be doing in August…

The Methylation Diet: MTHFR and Methylation Support—an Expanded Approach 
by Kara Fitzgerald and Romilly Hodges

This is a must-read for anyone who knows they have an MTHFR, or other methylation-related, gene polymorphism or is at risk for hypomethylation-related conditions including autism.

The Importance of Methylation

Defects in the body’s methylation process have been of interest to many health communities since MTHFR genetic testing, as well as functional testing for markers such as homocysteine, have become more widely-available and since the connection to different disease states—ADD, autism, cancer, diabetes, heart disease, Alzheimer’s disease, Parkinson’s disease, immune hypersensitivity, inflammation and more—is increasingly recognized. Even before that, the connection between maternal folate deficiency (one of the key methylation nutrients) and neural tube defects in children was observed and validated, leading to broad-based folic acid food fortification initiatives.

Methylation is such a fundamental process that each of our cells is continually using for many, many activities, ranging from cell division, immune cell formation, creating neurotransmitters, detoxification, and hormone metabolism, to regulating even how our genes get expressed.

There has just been this remarkable boom in methylation research, and as Functional Medicine practitioners we obviously want to fold that in to how we work with patients. This is what has led to the use of supplemental nutrient cofactors, such as folate, B12, B6, and so on, to support methylation pathways (Figure 1). The intention has been to overcome methylation deficits by pushing those reactions on to a greater level of activity, or bypassing blockages in the folate cycle completely, such as with methylated folates (5-methyltetrahydrofolate, the product of the MTHFR reaction). This is, no doubt, an important goal.

Figure 1: Core Methylation Pathways and Nutrient Cofactors

methylation pathwayThe problem with using this approach alone is that we just don’t know what the end outcome on overall methylation status, especially epigenetic methylation, is. Methylation in the body exists in a state of fluctuation but also, importantly, balance. There is research to show that too much methylation can be problematic too—excessive methylation on the epigenome is associated with cancer, autoimmunity, and allergies in particular. Epigenetic methylation is typically associated with gene repression, which can be beneficial in some circumstances, but not if we are repressing an important anti-cancer gene, or a gene that is important for immune balance.

So, of course we want to support proper methylation activity in the body, and yes we can use targeted supplemental methyl donors and cofactors where needed. However, there is so much more we can be doing to support healthy methylation beyond supplements. In our practice we have expanded our approach to incorporate evidence-based diet and lifestyle factors that not only are effective, but are extremely safe. This allows us to be more judicious and conservative in our use of supplementation, provides useful tools for those who actually don’t tolerate methylation supplementation (yes, this happens), and gives us a long-term support framework that can help patients over a lifetime.

We have so many more tools to support healthy methylation beyond supplementation.

Tools to Support Methylation

Food Choices

What does this look like? To start with, we look at sources of nutrients. Of course nutrients have a key role to play, but we can also get nutrients from food based sources, not just supplements (Figure 1). We specifically designed our Food Plans, Menu Plans and recipes to be rich in methylation nutrients, and compatible with other commonly-used dietary programs such as gluten-free and dairy-free.

Figure 1: Examples of Foods Rich in Methylation Nutrients

Methylation ‘Superfood’ Rich in these nutrients
Beets
Daikon radish
Dark leafy greens
Egg
Legumes
Liver
Betaine
Magnesium, potassium, B2, B6, folate
Potassium, folate, betaine
Methionine, cysteine, taurine, B2, B12, choline, sulfur compounds
Magnesium, potassium, folate, sulfur compounds
Cysteine, B2, B3, B6, folate, B12, betaine, choline

Support the Microbiome

We can also support nutrient status through the microbiome. Those little guys in our gut actually have a really important role to play in synthesizing nutrients for us, including B vitamins such as folate (Figure 2). In fact, many of them even synthesize the methylated forms of folate, and data has shown that supplementing specific bacterial species can even raise folate status, and lower homocysteine independently of any other changes. Prebiotic foods can support this activity even more.

Figure 2: Example Microbial Producers of Folate

Lactobacillus plantarum
Bifidobacterium bifidum
Bifidobacterium infantis
Bifidobacterium breve
Bifidobacterium longum
Bifidobacterium adolescentis
Bifidobacterium pseudocatenulatum

Avoid Nutrient and Methyl Depletors

Another way to support nutrient and methylation status is to minimize factors that actually deplete nutrients and methyl donors. This is a really important concept, termed ‘methyl donor drain’. One example of this at work relates to stress—when we are in a chronic state of fight-or-flight, we are using methyl donors both to produce, and also to break down, adrenaline. Those methyl donors are ‘spent’, so that they are no longer available for use in other methylation activity. And there are many other potential methyl donor drainers.

Methylation Balance

Beyond nutrients, it is really important to identify and implement those techniques that help promote methylation balance in the body. Again we can look to food here, among other factors, since there are specific food-based components—such as found in berries, rosemary, and more—that demonstrate adaptogenic effects on epigenetic methylation, providing those ‘checks-and-balances’ that will prevent inappropriate excessive methylation on our genome.

Inflammation and Additional Factors

These are some, but by no means all, of the concepts that we’ve incorporated into our program; we also work on inflammation, oxidative stress, mitochondrial fitness, sleep, exercise, environmental toxins (Figure 3), medication effects, dietary patterns and macronutrient ratios, meal timing and more. These factors address both the availability of methyl donors in the body, as well as that homeodynamic methylation balance.

Figure 3: Environmental Toxins That are Known to Alter DNA Methylation

Pesticides
Fertilizers
Automobile fumes
Bisphenol A (BPA)
Phthalates
Persistent Organic Pollutants (POPs)
Jet fuel
Benzene
Mold toxins (e.g. aflatoxin)
Arsenic
Mercury
Lead
Cadmium
Nickel

To find out exactly how these factors influence methylation and how to apply them for a holistic approach to methylation support, we have published our program in an eBook, which is available at www.drkarafitzgerald.com/practitioners/eBook. We encourage you to read it, apply it, and tell others about it. Methylation may be just one piece of the puzzle for autism and other conditions, but it is such a fundamental one. This approach is a much-needed evolution of how we need to be thinking about supporting healthy methylation.

Use the following code for a 10% discount on Methylation Diet and Lifestyle: BNI10

Sign up for our free webinar on August 16 at:  http://bioindividualnutrition.com/the-methylation-diet-webinar/

About the Authors:

Kara FitzgeraldDr. Kara Fitzgerald received her doctorate of naturopathic medicine from National College of Natural Medicine in Portland, Oregon. She completed the first CNME-accredited post-doctorate position in nutritional biochemistry and laboratory science at Metametrix (now Genova) Clinical Laboratory under the direction of Richard Lord, Ph.D. Her residency was completed at Progressive Medical Center, a large, integrative medical practice in Atlanta, Georgia. Dr. Fitzgerald is lead author and editor of Case Studies in Integrative and Functional Medicine, a contributing author to Laboratory Evaluations for Integrative and Functional Medicine and the Institute for Functional Medicine’s updated Textbook for Functional Medicine. She has been published in numerous peer-reviewed journals. Dr. Fitzgerald is on faculty at the Institute for Functional Medicine, and is an Institute for Functional Medicine Certified Practitioner. She is a clinician researcher for The Institute for Therapeutic Discovery. Dr. Fitzgerald regularly lectures internationally for several organizations and is in private practice in Sandy Hook, Connecticut.

Romily HodgesRomilly Hodges completed her Master’s degree in Human Nutrition at the University of Bridgeport, CT. She is a Certified Nutrition Specialist through the Board for the Certification of Nutrition Specialists, and completed her practice hours under the supervision of Dr. Deanna Minich, PhD and Dr. Kara Fitzgerald, ND. She has published in the Journal of Nutrition and Metabolism on food-based modulators of detoxification enzymes, and has been a contributing author to Sinatra & Houston, Nutritional and Integrative Strategies for Cardiovascular Medicine. She has been teaching assistant to Dr. Minich for the Certified Food and Spirit Practitioner Program and the Food and Spirit Advanced Detoxification Module. She is the staff nutritionist at the office of Dr. Kara Fitzgerald where she advises and supports patients in the implementation of complex, multi-layered dietary and nutritional protocols that are uniquely personalized to each individual’s needs.

Resolute_photoTell us about your specialty and clinical focus, and how you use nutrition to help?

While I currently see all nutrition clients, my passion lies in three main areas. The first is ADD/ADHD, Autism Spectrum Disorder (ASD), and Sensory Processing Disorder. Closely related is AutoImmune issues, due to the correlation that has been seen with ASD. This shows up especially when I counsel the whole family unit. Lastly, I’m rather passionate about the nutritional links to neurological issues including, but not limited to, anxiety and depression. This blends well with the ASD families, who are under tremendous strain and these neurological issues often come along with all else.

How do you incorporate BioIndividual Nutrition into your practice?

BioIndividual Nutrition is what I do! I work with the foundations of a nutrient dense whole food diet, digestion, adrenals/blood sugar regulation, hydration, essential fatty acids and minerals. Bringing the client’s body into balance is different every time, even when there are common themes. My plans are individually tailored both to what the client’s body needs and to their ability and motivation to make the necessary changes.

Do you have a favorite diet you use in your practice, or a set of favorite diets when working with clients. Tell us how and when you use them.

NH_FoodPyramidWebPageMany clients are already gluten free when they come to see me, or have attempted it in the past. Through education, I motivate them as to how the GF/CF diet can often bring great gains in their health. It’s the specifics of each client that are fascinating, and each person needs a nutrient dense, whole food diet tailored to their needs.

I stress the Nourishing Hope food pyramid. The pyramid, with proper modifications as to the actual selection of foods within each category, provides the visual many clients need in order to understand what is meant by nutrient dense, whole food. The conversation this generates is always helpful.

My most magical results working with a specific diet come with those who start the low salicylate or low histamine diets. The results often are immediate and astounding!

Are there any nourishing foods you consider important for most people with this condition?

Many of the superfoods are off limits for those following the salicylate/amine diet. That includes bone broth and fermented foods. My approach is to determine what foods they generally enjoy, and focus on what foods they can have, as opposed to only concentrating on what they need to eliminate. This again is where the pyramid is helpful to think through what their shopping list will contain and how their dinner plate will look. I’m not past drawing proportions and suggestions on a paper plate with a sharpie and sending it home with them!

What other factors do you consider essential in supporting clients? Are there other supplement or lifestyle choices people should consider?

My paradigm for supplementation is two-fold. There are times when a client’s body is not able to complete a function, such as the person who has had their gall bladder removed, or someone whose detox processes are inefficient. While food helps, there are supplements that can provide the support in these areas, and such supplements may be used long term.

Alternatively, while learning again to feed the body, some supplements provide the client with a nutrient framework for the body to do its amazing healing work. Through dietary adjustments, most of these supplements are short term support to ease the client through those first rough weeks or months.

I always remember that the brain is part of the body, and that how we engage with ‘outside’ our body, starts ‘inside’ – and the only building blocks we have to maintain and repair all of our body are the ones we put in our mouth. Therefore, food and nutrition are an entry to additional conversations regarding sleep, movement and exercise, meditation, environment (including toxins and toxic relationships), and attention to daily and seasonal rhythms. Food is a metaphor fResolute_diagramor so many things and food affects all other aspects of our lives. Often, when food begins to be dialed in, these other areas begin to take their proper place in even the busiest of schedules.

Anything else you’d like to share with practitioners interested in this subject?

Study this Venn diagram. If your interest lies at the junction of all four circles, you’ll know you’re headed in the right direction. Never settle. Trust your gut!!

How has the BioIndividual Nutrition Institute training helped you?

If the only tool you have is a hammer, everything starts to look like a nail. The more tools you have, and the more proficient you are using them, the easier and more professional the job.

Screen Shot 2016-04-15 at 12.58.51 PMThe BioIndivdual Nutrition Institute training provides a plethora of tools to guide me in my work and proficiency came quickly due to the way the material is presented. I’m able to help not only the ASD families, but also my distressed clients who have never made the link between specific foods and environmental factors, and their dis-ease.

Since I now have a better understanding of how the body interfaces with its environment – internal and external – I can provide reason and meaning for all the necessary changes I recommend to my clients. This in turn motivates them to try. Then, they learn that it’s only hard until it becomes routine.

Check out Resolute Michael’s Profile in our Online Directory

BIO: Resolute came to nutrition later in life, after a 30 year career as a casualty claims adjuster. When reading medical histories, she took note of the progression of chronic disease and the doctors’ heroic efforts to bring it all under control, often without success. During this time, she started having chronic health issues. She researched nutrition solutions, becoming quite passionate about eating whole foods in their natural form, and understanding the sad state of our food chain today. She was delighted when a whole food, nutrient dense diet worked to resolve her metabolic syndrome, anxiety, sinus congestion and digestive issues. Now, as a Nutritional Therapy Practitioner and a Certified BioIndividual Nutrition Practitioner, she compassionately counsels families and individuals as they take their own journeys toward the best health they can achieve. Resolute is also a Group Leader for the BioIndividual Nutrition Institute’s NTA Study Group.

Website: www.PrimalPerspectives.com

New science and clinical experience reveal concerns about oxalates that far exceed traditional kidney stone pathology. In order to best support their patients and clients, integrative practitioners, and especially diet and nutrition specialists would benefit from greater understanding of their influence.

Oxalates are highly reactive molecules; they present in our body as sharp crystals or crystalline structures with jagged edges that cause pain, irritation, and distress. They can bind with certain minerals; particularly calcium and magnesium, as well as iron and copper. Having high oxalate in the body can be problematic; and not giving proper consideration to one’s oxalate intake can impede the effectiveness of even the best healing diet protocol.

High oxalate in the body (hyperoxaluria) can be a factor in many chronic conditions; including digestive issues, autoimmune disorders, and neurological conditions. Oxalates affect mitochondrial function and can create inflammation; thus influencing every system in the body.

OxalatesDefinedThis article explores the repercussions of the oxalate cascade in a variety of chronic diseases; and my follow-up article will specifically investigate oxalates and autism – and how you, the knowledgeable practitioner, can help.

Understanding Oxalates

OxalateCrystalsAlthough most commonly identified with the formation of calcium oxalate kidney stones (oxalate bound to calcium), when unbound, free oxalate can interfere with cellular functions; affecting health on a broader, systemic level. Clinical studies and anecdotal experience indicate that oxidative stress, mitochondrial disruption and damage, and nutrient depletions, trigger widely varied symptoms including fatigue and inflammatory cascades, joint pain or pain anywhere in the body. Chronic low energy is very common because of a reduction in ATP in the mitochondria. Oxalates could be a hidden source of headaches, urinary pain, genital irritation, joint, muscle, intestinal or eye pain.

Other common oxalate-caused symptoms may include mood conditions, anxiety, sleep problems, weakness, or burning feet. Indicators can be digestive, respiratory, or even bedwetting for children.

It’s important to note that oxalates can inhibit the absorption of calcium, magnesium, and other minerals; which actually makes oxalates an “anti-nutrient.” Minerals in food become bound by oxalate – for instance calcium (thereby forming insoluble calcium oxalate) – and cannot then be absorbed properly by the intestinal tract. This can lead to mineral deficiencies, such as calcium and/or magnesium deficiency.

In the gut of a healthy person, oxalates typically bind together with these minerals (are not absorbed through the gut), then eliminated in the stool. While this inhibits absorption of nutrients, beneficially this ensures they are excreted rather than crossing the gut into the blood stream and causing cellular distress and damage.

High Oxalate

Once oxalate gets into cells where it can disrupt mitochondrial function; it can cause all sorts of systemic disturbances. Here are some of the varied effects of high oxalate in the cells and tissues – that we’ll explore through the course of this article:

  • Disrupt mineral absorption and usage
  • Impair cellular energy
  • Deplete nutrients like glutathione and interfering with biotin
  • Create oxidative stress[1]
  • Activate the immune system to trigger inflammatory cascades
  • Interfere with and damage mitochondrial function[2]
  • Damage cells and tissues
  • Cause seizures during toxic exposure to oxalate[3],[4],[5]
  • Cause faulty sulfation
  • Cause histamine release

Types & Sources of Oxalates

Exogenous and Endogenous

Oxalates stem from two main sources: exogenous (outside the body; from dietary intake) and endogenous (produced within the body, cell or tissue).

Exogenous oxalate can accumulate from a diet that is high in spinach, nuts, beans, or other high oxalate foods. This is why individualizing therapeutic diets is essential; because “by the book” some well-known special diets strongly rely on higher-oxalate foods (especially almonds/almond flour). Diets often heavy on these nut flours include: SCD, GAPS, and Paleo. And vegetarian diets are often high in oxalate; since they usually include many beans, grains, nuts and seeds, as well as high oxalate greens or starchy vegetables, like spinach or sweet potatoes.

High Oxalate Foods

  • Spinach
  • Swiss chard
  • Almonds and almond flour
  • All nuts
  • Chia seeds
  • Sesame seeds
  • Buckwheat
  • Quinoa
  • Most legumes
  • Potatoes
  • Sweet potatoes
  • Chocolate
  • Beets

Practitioners should be aware that diets high in oxalate could create a wide variety of problems for some people. Making informed choices or modifying a diet for oxalate can make a dramatic difference in lowering the oxalate load (note: it is important to reduce oxalates in the diet very slowly).

However, most of our body’s total oxalate content is created during normal body metabolism. “It is increasingly accepted that 80-90% of urinary oxalate is produced endogenously,” [6]  within the cell, and this can directly wreak havoc in the body.

The Origin of Oxalate Issues

Deficiencies and Endogenous Production

Each person’s ability to process oxalate varies, based on certain deficiencies, pathways or genetic differences. Some deficiencies, including vitamin B6 and B1 deficiency can cause the body to produce oxalate (endogenously) in problematic amounts. Other deficiencies such as vitamin A deficiency can cause the body to absorb excess oxalate through the gut.

Further, because one’s body chemistry can convert a substance into oxalate; such as supplements like ascorbic acid or the amino acid glycine (a key component in bone broth) – complications can arise. Fructose, xylitol, and other sugar alcohols can also convert to oxalate. Certain supplements, as well as a diet too high in meat, can be a problem for some people.

When the Gut is Unhealthy

The health of the gut and one’s microbiome influence whether or not a person has an issue with oxalate.

Oxalates can be a problem when: the gut is inflamed and hyper-permeable (i.e. leaky gut), fat is not digested and there is fat malabsorption, or when there is not enough good bacteria (especially particular forms) to break the oxalate down. Developing problems with oxalates is more likely if there aren’t enough minerals in the gut to bind the oxalate.

Oxalobacter Formigenes

Leaky gut and low beneficial bacteria can contribute to oxalate problems. Oxalobacter formigenes is a strain of beneficial bacteria that degrade oxalate. Unfortunately, even one, or a few courses of antibiotics can wipe out oxalobacter formigenes for months, if not indefinitely. Certain probiotics break down oxalate, not just the oxalobacter. If there’s a history of antibiotic use, dysbiosis or other conditions that negatively affect the microbiome, one should work on correcting the flora balance, as well as be suspicious of any concerns with oxalates.

Fat malabsorption

Excess undigested fat compound matters. The extra fat floating around in the gut can bind to calcium, which makes the calcium unavailable for oxalate binding, causing free oxalate to absorb into the body.

With optimal health, good digestion, and mineral intake, calcium would be available for binding to that oxalate; however, when there is excess fat the calcium binds to the fat, allowing the oxalate to be free to get into the bloodstream and into the cells. For people with oxalate issues, it is important to know whether fat malabsorption is at play.  A stool analysis can help you determine if fat malabsorption is at play. Some clients/patients may also present with symptoms of fat digestion issues such as floating or greasy stools. For those who have had a GI scope, gastroenterologists can often see signs of fat malabsorption. Once it is determined that fat is not digesting and absorbing, an individual may need to restrict fat intake in their diet to avoid further complication of oxalate issues, particularly in the short run, as they work on digestion whether with digestive enzyme, supporting bile production, or other means.

Sulfate, Poor Sulfation, and Mitochondrial Dysfunction

In addition to gut issues, sulfate and sulfation can be underlying factors in oxalate issues. When sulfate is low, and sulfation biochemistry is poor, oxalate problems can arise.

Sulfate is very important in the body; it’s needed for processing phenolic foods, and dozens of processes in the body including digestion, gut integrity, and neurodevelopment.

There is a two-way relationship between oxalate and sulfate/sulfation. Said another way: oxalates can cause low sulfate and low sulfate can cause oxalate problems. As noted, excess oxalates can lead to poor sulfation by oxalate interfering with the body’s ability to allow sulfate into the cell, inhibiting sulfation. On the other hand, with poor sulfation from low sulfate levels, oxalate more readily gets into a cell on the (unoccupied) sulfate transporter.

Another way that low sulfate can cause problems with oxalates, involves the role of the kidneys. Susan Owens, who heads the Autism Oxalate Project, said that insufficient sulfate inside the kidney tubule cells would interfere with the ability of the kidneys to remove oxalate from the blood and to deliver the oxalate to the urine. Therefore, inadequate sulfate could cause higher levels of oxalate in the system.

It’s a double-edged sword if you’ve got low sulfate. If there isn’t enough sulfate, you might not be regulating your oxalate very well. Depleted sulfate can allow for higher oxalate absorption, and the more oxalate you absorb, the less sulfate your body is likely to have.

Because there are so many conditions that have poor sulfation underlying them, it’s sensible to consider a low oxalate diet and other support for a variety of chronic health matters. We need to step well outside the mainstream thinking of just kidney stones.

Faulty sulfation is of influence to these chronic health conditions:

  • Autism[7],[8]
  • Food sensitivity[9]
  • Parkinson’s disease
  • Alzheimer’s disease
  • Migraine
  • Chronic fatigue syndrome[10]
  • Rheumatoid arthritis[10]
  • Lupus[10]
  • Inflammatory bowel disease[10]
  • Asthma[10]
  • Depression[10]
  • Hyperactivity[10]

Furthermore, when sulfate is low, it can cause phenol reactions to various foods. Therefore, those who have low sulfate may also have an issue with phenols and with oxalates in food. It’s not across the board, but these are some of the key relationships. People with depleted sulfate frequently do well on a low phenol and low oxalate diet. Of course, that cannot be true for everyone – which is why BioIndividual Nutrition is essential. Routinely though, when I’m supporting clients to lower oxalate, I will consider the potential benefit of a low phenol regime as well.

Effects of High Oxalate in the Body

Mitochondrial Dysfunction

Oxalates, inside the cell, can damage the mitochondria.[11]

Once oxalate impedes mitochondria function, it can affect every cell, organ, and system of the body. This is a primary reason that oxalates can become so problematic. But it’s also why the full scope of oxalate’s effect on chronic disease can be wide reaching and difficult to study through association.

But how does oxalate get into the cell and damage the mitochondria?

I earlier noted that when sulfate is low, oxalate can be “transported” into the cell on the sulfate transporter, and disrupt or damage the mitochondria. Additionally, oxalate can get into the cell by endogenous production, which happens in the cell and, therefore, doesn’t require being transported in. While high oxalate may or may not be the initial impetus of mitochondrial conditions, because of their tendency to get into the mitochondria and cause damage, it’s reasonable to assume that oxalate is an important factor to consider for those with mitochondrial issues.

Here are some of the conditions involving mitochondrial dysfunction:

  • Autism
  • Alzheimer’s
  • Neurodevelopmental disorders
  • Seizures
  • Parkinson’s
  • Hypertension
  • Retinopathy
  • Multiple sclerosis
  • Obesity
  • Cancer

Oxidative Stress, Inflammation, and Glutathione

Medical illustration about pain located in the head area. Digital illustration.

There are even more pieces to this puzzle. High oxalate can lead to oxidative stress, and subsequently inflammation and injury,[12],[13]  which can cause oxalate stone formation in the kidney, and damage to any soft tissue or area of the body where they interfere with cellular function.

High oxalates can elevate superoxide and deplete glutathione and antioxidant status.[14]  Conversely, antioxidants and free radical scavengers can decrease oxalate stone formation in the kidney, as well as reducing the inflammation caused by oxalate.

Oxidative stress, inflammation, and low glutathione status are common manifestations in many chronic diseases. Understanding this relationship and the potential sources of chronic inflammation and stress can help practitioners appropriately address the triggers that can be causing the problems, and in this case, oxalate is an important factor to consider.

Conditions linked to oxidative stress and inflammation:

  • Autism [15], [16], [17]
  • Asthma
  • Allergies
  • ADHD [18]
  • Autoimmune conditions
  • Depression [19], [20]
  • Anxiety [21], [22]
  • Inflammatory bowel disorders
  • Eczema
  • Schizophrenia [23], [24]
  • Obesity, heart disease, and diabetes

For people or practitioners addressing issues with oxidative stress, inflammation, and the aforementioned conditions, it’s important to consider oxalate’s potential systemic implications when devising therapeutic intervention.

Conclusion – Through The Lens of Autism

Oxalate can affect many systems of the body. Extensive research indicates a multitude of chronic health conditions where systems are impaired and oxalate is implicated.

Chronic Conditions Associated with High Oxalate:

  • Asthma
  • Autism[25]
  • Autoimmune thyroid or other autoimmunity
  • Chronic fatigue syndrome
  • Cystic Fibrosis[26]
  • Fibromyalgia
  • Hypothyroid[27]
  • IBD (inflammatory bowel disease)[28]
  • Interstitial Cystitis
  • Kidney Stones in family
  • Low muscle tone
  • Migraine and Headaches
  • Mitochondrial damage and dysfunction
  • Rett Syndrome[29]
  • Seizures
  • Vulvodynia

Julie_Speaking_Autism_Summit_2015For fifteen years I’ve researched and educated parents and clinicians about therapeutic diet and nutrition for autism. It’s a very complex chronic disorder, and studying its intricacies provides great insight into addressing a wide variety of health conditions.

From the list of conditions in this article alone, you can see the similarities of implicating factors are great. Autism and many other disorders share underlying mechanisms of inflammation, mitochondrial dysfunction, and faulty methylation and sulfation, as well as digestive disorders, leaky gut, and dysbiosis as we’ve discussed today.

As we continue to survey the underlying factors and consider how oxalate may play a role, it’s easy to appreciate, and not particularly surprising, that there are so many chronic disorders that may be affected by oxalate. The degree of overlap in those conditions is significant and worth exploring more deeply.

In my next article, I’ll dive into this topic even further – looking specifically at oxalate and autism. Through that overarching “lens” I’ll share what I’ve researched, learned, and experienced over the years and share what you can do – as a clinician or parent, to help your patient/client or child – when you suspect that oxalates may be an issue.

Julie Matthews
Certified Nutrition Consultant


Scientific References

[1] Lee, Hyo-Jung, et al. (2012). “Gallotannin suppresses calcium oxalate crystal binding and oxalate-induced oxidative stress in renal epithelial cells.” Biological & Pharmaceutical Bulletin 35(4): 539–544.

[2] Veena, C. K., Josephine, A., Preetha, S. P., Rajesh, N. G., & Varalakshmi, P. (2008). Mitochondrial dysfunction in an animal model of hyperoxaluria: a prophylactic approach with fucoidan. European Journal of Pharmacology 579(1), 330-336.

[3] Díaz, Cándido, et al. (2004). “Long daily hemodialysis sessions correct systemic complications of oxalosis prior to combined liver–kidney transplantation: case report.” Therapeutic Apheresis and Dialysis 8.1, 52-55

[4] Pfeiffer, H., et al. (2004). “Fatal cerebro-renal oxalosis after appendectomy.” International Journal of Legal Medicine 118.2, 98-100.

[5] Chen, Chien-Liang, et al. (2002). “Neurotoxic effects of carambola in rats: the role of oxalate.” Journal of the Formosan Medical Association 101.5, 337-341.

[6] Conyers, R. A., R. Bais, and A. M. Rofe. (1990). “The relation of clinical catastrophes, endogenous oxalate production, and urolithiasis.” Clinical chemistry 36, no. 10, 1717-1730.

[7] Waring, R. H., and L. V. Klovrza. (2000). “Sulphur metabolism in autism.” Journal of Nutritional and Environmental Medicine 10, no. 1, 25-32.

[8] Alberti, Antonino, Patrizia Pirrone, Maurizio Elia, Rosemary H. Waring, and Corrado Romano. (1999). “Sulphation deficit in “low-functioning” autistic children: a pilot study.” Biological Psychiatry 46, no. 3, 420-424.

[9] Scadding, G. K., R. Ayesh, J. Brostoff, S. C. Mitchell, R. H. Waring, and R. L. Smith. (1988). “Poor sulphoxidation ability in patients with food sensitivity.” BMJ: British Medical Journal 297, no. 6641, 105.

[10] Moss, Margaret, and Rosemary H. Waring. (2003). “The plasma cysteine/sulphate ratio: A possible clinical biomarker.” Journal of Nutritional and Environmental Medicine 13, no. 4. 215-229.

[11] Veena, C. K., Josephine, A., Preetha, S. P., Rajesh, N. G., & Varalakshmi, P. (2008). Mitochondrial dysfunction in an animal model of hyperoxaluria: a prophylactic approach with fucoidan. European Journal of Pharmacology 579(1), 330-336.

[12] Biswas, Subrata K., et al. (2007). “Which comes first: renal inflammation or oxidative stress in spontaneously hypertensive rats?” Free Radical Research 41.2, 216-224.

[13] Khan, Saeed R. (2005). “Hyperoxaluria-induced oxidative stress and antioxidants for renal protection.” Urological Research 33.5, 349-357.

[14] Khand, F. D., et al. (2002). “Mitochondrial superoxide production during oxalate-mediated oxidative stress in renal epithelial cells.” Free Radical Biology and Medicine 32.12, 1339-1350.

[15] Vargas, Diana L., et al. “Neuroglial activation and neuroinflammation in the brain of patients with autism.” Annals of neurology 57.1 (2005): 67-81.

[16] Li, Xiaohong, et al. “Elevated immune response in the brain of autistic patients.” Journal of neuroimmunology 207.1 (2009): 111-116.

[17] Rossignol, D. A., and R. E. Frye. “A review of research trends in physiological abnormalities in autism spectrum disorders: immune dysregulation, inflammation, oxidative stress, mitochondrial dysfunction and environmental toxicant exposures.” Molecular psychiatry 17.4 (2011): 389-401. 4 Donev, Rossen, and Johannes Thome. “Inflammation: good or bad for ADHD?.” ADHD Attention Deficit and Hyperactivity Disorders 2.4 (2010): 257-266.

[18] Donev, Rossen, and Johannes Thome. “Inflammation: good or bad for ADHD?.” ADHD Attention Deficit and Hyperactivity Disorders 2.4 (2010): 257-266.

[19] Miller, Gregory E., and Ekin Blackwell. “Turning Up the Heat Inflammation as a Mechanism Linking Chronic Stress, Depression, and Heart Disease.” Current Directions in Psychological Science 15.6 (2006): 269-272.

[20] Raison, Charles L., Lucile Capuron, and Andrew H. Miller. “Cytokines sing the blues: inflammation and the pathogenesis of depression.” Trends in immunology 27.1 (2006): 24-31.

[21] O’Donovan, Aoife, et al. “Clinical anxiety, cortisol and interleukin-6: Evidence for specificity in emotion–biology relationships.” Brain, behavior, and immunity 24.7 (2010): 1074-1077.

[22] Pitsavos, Christos, et al. “Anxiety in re- lation to inflammation and coagulation markers, among healthy adults: the AT- TICA study.” Atherosclerosis 185.2 (2006): 320-326.

[23] Saetre, Peter, et al. “Inflammation-relat- ed genes up-regulated in schizophrenia brains.” Bmc Psychiatry 7.1 (2007): 46.

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[25] Konstantynowicz, J., Porowski, T., Zoch-Zwierz, W., Wasilewska, J., Kadziela-Olech, H., Kulak, W., Owens S.C., Piotrowska-Jastrzebska J.,  and Kaczmarski, M. (2012). A potential pathogenic role of oxalate in autism. European Journal of Paediatric Neurology 16(5), 485-491.

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KrisBarrett_NETell us about your specialty and clinical focus, and how you use nutrition to help?

I work specifically with families who have children on the autism spectrum. I help families implement dietary intervention to help improve their children’s behaviour, sleep and health.

How do you incorporate BioIndividual Nutrition into your practice?

Because there is no “one diet suits all,” I work very closely with my clients to formulate the right combination of foods that will be best for them. I also take into account the extent of the child’s sensory and textural issues with foods and their symptoms to find the right starting place.  I think Bioindividual Nutrition is the perfect description of how I approach my clients as I don’t try and make any one particular diet fit, it’s all about what works for the individual.

Do you have a favorite diet you use in your practice, or a set of favorite diets when working with clients. Tell us how and when you use them.

My favourite beginner diet for kids with autism is the GFCF diet. Usually kids on the spectrum have very limited diets – mainly consisting of gluten and dairy foods! When these are removed, you can see positive changes very quickly. This is a great motivator for parents to continue the dietary changes and go even further into healing and understand the power of good nutrition.

After this great first step in diet!  Do you have any other important food/diet principles you find many children on the autism spectrum benefit from after you’ve removed gluten and dairy? 

Definitely looking at numbers/additives/preservatives to make sure the diet is clean – unfortunately is is very easy to do a “bad” GFCF diet, with loads of products being gluten and dairy free but  containing nasty additives. This is something I think everyone can benefit from. With many kids too we will need to look at salicylates.  Removing high salicylate foods temporarily while focusing on healing the gut can have a profound effect on many of the kids who are still experiencing behavioural and sleeping issues after gluten and dairy are removed.

Are there any nourishing foods you consider important for most people with this condition?

Definitely stocks and fermented foods. It’s all about the Gut so I love to teach people how to increase the nutritional value of everything they’re making by adding in these wonderfully healing foods.

What other factors do you consider essential in supporting clients? Are there other supplement or lifestyle choices people should consider?

I love fish oil, digestive enzymes and probiotics as a base for people starting out. I always recommend they see a biomedical doctor for individual testing so they can be prescribed other supplements that are going to be beneficial. And I always educate my clients about incorporating Healthy Home strategies alongside diet. For me this is a crucial part of the puzzle and you can’t do dietary intervention without also addressing the toxins that may be in personal care products, in your water or in your environment. And I’m big on making sure everyone gets plenty of sunshine (for Vitamin D), exercise and sleep!

You are also a mother who has helped your child recover from autism (a journey you outline in your book).  Those people in the “Nourishing Hope for Kids” BioIndividual Nutrition course can also see more on your son’s story there in the Case Study Module. Will you share with us now how important diet was for your son, some of the things you saw the most benefit from and how it helped? 

Diet was the foundation of his recovery, no doubt. He was such a sick little boy. As soon as I removed gluten and dairy, his eczema, asthma and constant ear infections just disappeared, never to return. He started to sleep better. I resisted removing corn for a long time, but when I did, his diarrhea stopped.
I did this a long time when there were no BNI practitioners, so I was cobbling things together for myself and it also took me a long time to understand about salicylates. He was a huge salicylate responder (bright red burning hot cheeks and ears when he ate them, crazy behaviour like I’d wound him up and big black circles under his eyes). When we took those out we got much calmer behaviour and better sleep. It was a few years into our journey before I went to full GAPS and then we got even better response with his gut and finally some formed stools. We only stayed on full GAPS for around 6 months because he is a mito kid and he was becoming super lethargic and weak, so we finally settled on a diet that suits him best, which is pretty much paleo but with the addition of some of the Body Ecology grains and the occasional rice and potato.
We did a lot of therapy with Tim (ABA, biomedical, speech, OT, cranial osteopathy, chiropractic, naturopathy, homeopathy, vision therapy & more!) but changing his diet had the biggest impact. Not only did it enable him to become well again, it calmed him down to actually be able to participate in all of the other therapies and achieve more from them. It helped his health, concentration, behaviour, sleep, bowels and honestly changed his life, and the life of our family. I shudder to think what would have happened to him had I not stumbled across the dietary path. I can’t state strongly enough how important it was and that it was the foundation upon which all of our other gains were built.

Anything else you’d like to share with practitioners interested in this subject?

Dietary intervention can change the lives of kids with autism. It’s incredibly powerful.  I would encourage any other practitioners to do some training (like the BNI Kids course) and attend seminars so they are confident with the approaches used for autism. Unfortunately there are a lot of families who need our help, so the more experienced practitioners we can have the better. My only other advice is to meet the families where they are at. They are under a lot of stress and often can’t implement changes as quickly as we’d advise. Lots of empathy and practical solutions will ensure they can make these changes for the long term.

KrisBarrett_DirectorySNIPPETHow has the BioIndividual Nutrition Institute training helped you?

The BNI training was incredibly detailed and gave me the confidence to quickly assess a client and advise initial starting points. For more complex situations I had the information on hand to then advise further interventions. I loved that the training was backed by scientific references which you can share with your clients so they have more understanding and confidence around what they are doing. I feel that BNI training gave me all the knowledge I will need to work with my clients with great success.

Check out Kris Barrett’s Profile in our Online Directory

BIO: Kris is a Certified Nutrition & Health Coach, Certified GAPS Practitioner, Certified BioIndividual Nutrition Practitioner and MINDD Practitioner who loves working with families of children with autism guiding them to health and happiness. Kris had absolutely no interest in food until her son Tim was diagnosed with autism in 2004 and she stumbled upon information from the US where families were seeing remarkable improvements in their ASD children after taking gluten and dairy out of their diets. She was desperate to help her son, so despite being challenged by even making a packet cake and the fact that Tim ate only 5 foods, she began a gluten and casein free diet that quite literally changed her son’s life.  In June 2014 Kris released her first book, No Cows Today : a mother’s story, a son’s autism recovery. She is thrilled to share her story in the hope it inspires others to consider dietary and biomedical intervention as part of their therapy programs.

WEBSITE : www.krisbarrett.com.au