New book talks about preventing and treating childhood brain disorders

Does your child have ADHD, autism, Tourette’s, OCD, dyslexia, learning disabilities, or another brain-based disorder?

Or perhaps you’re having second thoughts about conceiving because the risks of giving birth to a child who develops autism, ADHD, or other brain development disorders is so much higher today.

Couples opting out of parenting due to autism risk

If so, Dr. Robert Melillo’s new book, Autism: The Scientific Truth About Preventing, Diagnosing, and Treating Autism Spectrum Disorders–and What Parents Can Do Now, was written for you. Dr. Melillo was compelled to write this book based partly on emerging research, but more so on disheartening conversations with young couples.

“I was coming across young, smart, professional couples who were choosing not to have children because the risk of autism, ADHD and other disorders is so much higher today,” says Dr. Melillo. “The rate of autism has increased 2,000 percent in the last 20 years and ADHD now affects at least one in 10 children. What these parents don’t know is that new research shows environmental and lifestyle factors influence childhood brain development, and that in the majority of cases we can prevent and even rehabilitate autism, ADHD, and related disorders.”

Environmental and lifestyle influences on genes before conception is key

Dr. Melillo is a friend and colleague of mine who is a pioneer in new understandings and approaches to childhood autism, ADHD, Tourette’s, OCD, dyslexia, learning disorders, and more. He has a gift for being able to illustrate how a parent’s diet, physical activity, stress hormone levels, immune health, and exposure to environmental chemicals can affect a child’s brain development, beginning in utero.

This is called epigenetics—when environmental factors influence gene expression. It doesn’t mean genes are mutated, but instead diet and lifestyle determine whether genes turn on or off. If we turn off the genes for healthy brain development in the mother or the father before conception, those genes can pass on to the children in the turned-off position. Researchers have been able to trace this in up to 11 generations.

Simply improving the maternal diet before pregnancy can alter gene expression in the offspring and their susceptibility to certain diseases for up to four or five generations. For couples hoping to have children, epigenetics means they can reduce the risk of giving birth to a child who will develop autism, ADHD, or another disorder by choosing dietary and lifestyle factors that favor healthy brain development.

Using functional neurology to help children with autism, ADHD, Tourette’s and OCD

We can also positively influence genes after the child is born by improving external influences, such as by removing inflammatory foods from the diet and supporting good nutrition and brain health. Because a child’s brain is so malleable, we can also activate specific areas of the brain to recover missed stages of development (such as learning to crawl) in a practice called functional neurology.

Listen to Dr. Melillo speak about preventing and treating autism

Early childhood milestones are vital to proper brain development and meeting them too late, too soon, or not at all is typical for many children with autism, ADHD, and other brain development disorders. Functional neurology is yielding unprecedented results, with Dr. Melillo’s Brain Balance Centers reporting 82 percent of children with ADHD becoming symptom-free by objective measurements in 12 weeks, and most making significant academic advancements.

Brain development disorders cause immune and digestive disorders too

It’s not uncommon for a child with autism, ADHD, Tourette’s, or OCD to also suffer from multiple food intolerances, stomach pain, chronic constipation, leaky gut, asthma, eczema, yeast infections, and other immune and digestive issues.

This is because brain disorders hinder the function of those systems. Until you deal with the brain development disorder, the myriad health protocols parents employ can sometimes amount to little more than putting out fires.

I use functional neurology and brain chemistry practices with all of my patients now with profound results, as the brain often plays a role in chronic autoimmune and health issues, the subject of my soon-to-be-released book, Why Isn’t My Brain Working? The best part is these approaches do not involve bandaging symptoms with prescription drugs, but rather repairing “broken” wiring in the brain and using clinical nutrition to improve brain health for lasting healthy function.

Dropped connections in the brains of children with autism, ADHD, Tourette’s, and OCD

The human brain is divided into two hemispheres that work together. It is the ability of the human brain to fire in both hemispheres simultaneously that distinguishes us from other species in terms of intelligence and complexity. However, the slightest disruption in the timing of this firing can have devastating affects on brain function. In autism, ADHD, Tourette’s, OCD, and other brain development disorders the brain is extremely good at firing short-range connections within one hemisphere of the brain, which may make a child gifted in particular areas, such as math.

However, we see poor simultaneous firing of long-range connections between the left and right hemispheres. This poor long-range firing is also evidenced by a smaller than normal corpus callosum in children with autism, the bridge between the left and right hemispheres across which communication travels. This poor long-range firing can begin in utero or during the first few years of life due to epigenetic influences.

As a result of this lopsided stimulation, one side of the brain may become over developed while the other side never catches up to normal, which makes communication between the two sides difficult. It’s like a brand new computer trying to communicate with an old, outdated computer.

In autism, ADHD, Tourette’s, and OCD, we see a left brain that is overdeveloped compared to a weaker right brain. This explains why these children have unusually strong skills in some areas and unusually weak skills in others. Dyslexia or learning and processing disorders are examples of right brain over development. Researchers have been able to identify these imbalances by looking at how different areas of the brain vary in size, electrical imbalances, and concentrations of blood flow.

Understanding the importance of proper brain development

To see whether your child (or you) may have a brain imbalance, I recommend reading Dr. Melillo’s first two books, Disconnected Kids and Reconnected Kids. Disconnected Kids offers checklists of signs and symptoms and suggested exercises to stimulate areas of weakness. It offers a breakthrough in understanding, which Reconnected Kids builds upon.

If you want to lower your risk of giving birth to a child with a brain development disorder or if your child has autism, ADHD, Tourette’s, OCD, or another brain development disorder, then Dr. Melillo’s Autism: The Scientific Truth About Preventing, Diagnosing, and Treating Autism Spectrum Disorders–and What Parents Can Do Now is a must have.

We changed publishers, which required the book to go out of print for a few months. I apologize for the inconvenience and the delay, and thank you for your patience.

I’m also working on a second edition of the thyroid book with more information on thyroid health, autoimmune hypothyroidism, thyroid hormones, and more, which I hope to have available early next year.

Why Do I Still Have Thyroid Symptoms When My Lab Tests Are Normal?

More functional medicine books on the way

Other books in the works cover brain chemistry, leaky gut, adrenal health, hormones, and more.

After I published Why Do I Still Have Thyroid Symptoms? I was shocked to see it become a best-selling book. I really did not think anyone would read it. After its release readers worldwide sent so many emails, faxes, phone calls and stories about how the book made a positive impact on their lives that it completely changed me forever.

I knew at that point I had to publish more books and share my information directly with the public instead of just at post-graduate seminars for health care professionals. I am now on a mission to share the insight and personal research I have developed with the general public.

The role of functional medicine in chronic disease

I am not anti-medicine. I have a high degree of respect and admiration for the practice of medicine and medical physicians. However, there a void exists in the current education and practice of medicine when it comes to chronic conditions such as Hashimoto’s hypothyroidism, despite the accepted models of care in the scientific community that include diet, nutrition, and lifestyle changes.

Using the research to develop effective strategies

Because I lecture nationally about the latest scientific research to health care professionals, patients with complex conditions are often referred to me. The combination of needing to perform at a high level as a post-graduate educator and as a clinician seeing complex patients created a demanding cycle that led to the information I will be sharing with you.

At this point in my career, I have seen patients from around the world with all sorts of various complex conditions. I am not always able to help them but I can usually find strategies to improve the quality of their life in some way. Sometimes it is profound and sometimes it is not. Nevertheless, I have been driven to develop the highest clinical competence I can achieve and share that with readers in my upcoming books.

Thank you for reading and sharing the information. I hope it continues to help provide answers and relief to those in need.

In the thyroid book I introduced the concepts of TH-1 and TH-2 and their role in autoimmune diseases, such as Hashimoto’s. It turns out another key player in the autoimmune scenario is TH-17, and that we can work with nitric oxide and glutathione (which I wrote about earlier) to tame autoimmune destruction caused by TH-17.

TH-17: The new kid on the block

There are many TH (again, TH means T helper cell) players actually, but TH-17 is one worth turning the spotlight on for a moment.

When the immune system triggers an autoimmune response, the autoimmune reaction expresses predominantly through either the TH-1 or TH-2 system, as explained in chapter three of Why Do I Still Have Thyroid Symptoms?.

When activated, the TH-1 and TH-2 systems release cytokines, or immune messenger cells, called IL-17. These cytokines in turn promote tissue destruction at the site of the autoimmune attacks, which for our purposes is the thyroid gland.

TH-17 cells are a fairly recent discovery, and believed to be connected with autoimmune destruction when found in abundance. TH-17 is the system that adds fuel to the autoimmune fire and determines the severity of tissue destruction.

It’s important to understand that TH-17 isn’t all bad—it also plays an anti-microbial role in the body’s mucous linings, preventing infection from microbes such as candida or staphylococcus. But when it comes to the immune system, too much of a good thing ends up creating an imbalance with bad results.[1]

Using nitric oxide to modulate autoimmune activity

IL-17 does its dirty work of destroying tissue by activating a compound called inducible nitric oxide.

Nitric oxide is a gas in the body that acts as a signaling compound, triggering things to happen. It plays a role in many normal physiological processes, but also in disease. There are three forms of nitric oxide, two of which are beneficial, and one of which is destructive.

Exercise enthusiasts take an amino acid supplement called arginine to boost nitric oxide, as the beneficial forms of nitric oxide promote blood flow and the dilation of blood vessels. Bodybuilders like this because increasing blood flow to their muscles enables them to lift heavier weights, work out longer, and recover faster, thus building more muscle. Good nitric oxide activity has also been shown to lower the risk of cardiovascular disease. [2]

The good and the bad of nitric oxide

Unfortunately, arginine may also increase a very pro-inflammatory and damaging form of nitric oxide called inducible nitric oxide.

Researchers have found that when an autoimmune reaction creates a surge in TH-17 activity, it stimulates an enzyme called inducible nitric oxide synthase (iNOS) to produce more inducible nitric oxide. When TH-17 goes up, iNOS goes up, and inducible nitric oxide sets about destroying body tissue, such as the thyroid gland, erroneously targeted by the dysregulated immune system.[3] [4] [5]

In other words, TH-17 gives the orders to attack, but inducible nitric oxide is the perpetrator that carries out the dirty work. Unfortunately, people who take arginine may be subjecting themselves to unnecessary increases in iNOS activity, and hence more inflammation.

Like TH-17, iNOS isn’t all bad. It’s pro-inflammatory role comes in handy to combat viruses, bacteria, and other pathogens.[6] But the health imbalances that lead to autoimmune disease are the same ones that over stimulate the production of iNOS that destroy body tissue.[7]

We can test TH-17 levels just as we can test for TH-1 and TH-2. This is helpful because if a lab panel shows TH-17 cytokines to be elevated, this tells us tissue is actively being destroyed and it’s vital to quench that process.

The good news and the bad news about nitric oxide

Body builders who take arginine think nitric oxide is good. A practitioner seeking to tame the destruction of an autoimmune process may look upon nitric oxide as bad. Which is it? It depends on the form of nitric oxide the body is producing.

So far I have talked about inducible nitric oxide, which a TH-1 or TH-2 triggered autoimmune attack activates via TH-17 to destroy tissue. For people experiencing autoimmune flare-ups, this system is in overdrive.

However, we can combat this destruction by activating the two beneficial forms (technically called isomers) of nitric oxide called endothelial nitric oxide and neuronal nitric oxide.

Endothelial nitric oxide

Endothelial nitric oxide is found in the lining of blood vessels. It aids in tissue recovery and regeneration, enhances blood flow, dissolves plaques, and dilates blood vessels. One thing that dramatically activates endothelial nitric oxide is exercise. When you exercise, the increase in blood flow turns on the endothelial nitric oxide system, which helps dissolve plaque in the arteries.

Unfortunately, autoimmune disease often compromises this system, thus hindering the delivery of blood to body tissue.[8] This not only makes body tissue, such as the thyroid gland, more vulnerable to inflammation and destruction, but it also makes it more difficult for these tissues to recover and heal.

A weak endothelial nitric oxide system helps explain cold hands and feet, the loss of hair, weak nails prone to fungal infections, and other symptoms frequently found in conjunction with autoimmune diseases.

Poor blood flow robs the brain of blood, and hence oxygen and nutrients, and brain function deteriorates.

Poor blood flow to the digestive tract is one cause of leaky gut and poor gut function. Coupled with inflammation and poor glutathione activity, the person with a chronically activated autoimmune disease can never seem to repair her gut. This is why a strict autoimmune diet to protect the gut is necessary in these cases.

Overall, the research shows endothelial nitric oxide plays a big role in preventing and taming autoimmune disease, due to its inhibition of over activity of both the TH-1 and TH-2 systems.

Neuronal nitric oxide

Neuronal nitric oxide acts on the brain and nervous system, enhancing the ability of the brain and nervous system to adapt to change, communicate between neurons, and recover. Because good brain health is vital to absolutely every organ and system in the body, we want neuronal nitric oxide levels to be sufficient and active.

How to boost the good nitric oxide and dampen the bad

So we know endothelial nitric oxide helps tame the autoimmune response and aids in tissue recovery. We know we have a “bad” nitric oxide, inducible nitric oxide, which is over active during TH-17-stimulated autoimmune attacks. We also know that taking arginine is not desirable, because although it might boost endothelial and neuronal nitric oxide, it may also boost the destructive inducible nitric oxide. These are the facts I considered as a practitioner when I began exploring these mechanisms and how to further help my autoimmune patients.

The clinical goal is to modulate the TH-1, TH-2, TH-3, and TH-17 systems (by modulate, I mean influence them to behave appropriately), increase endothelial nitric oxide, and dampen the inducible nitric oxide response.

Eventually, after my ongoing review of the research and clinical experience, it became apparent glutathione pathway integrity and nitric oxide modulation (boosting the good and dampening the harmful) offered profound responses.

Nutritional compounds for nitric oxide modulation

Through reading published studies, I found a variety of nutritional compounds that have been shown to boost endothelial nitric oxide without also boosting the pro-inflammatory inducible nitric oxide. I use these nutrients together as I find they have the best effects when working synergistically:

• Adenosine
• Huperzine A
• Vinpocetine
• Alpha Glycerylphosphorylcholine (Alpha GPC)
• Xanthinol niacinate
• L-Acetylcarnitine

In my practice the use of these compounds together in an emulsified liquid formula has had profound effects in managing some of my most severe autoimmune cases, and, together with glutathione recycling, has been an exciting discovery for me as a practitioner.

For the best results take these compounds before exercise, even if it’s a walk around the block. Exercise will get the blood flowing and enhance the effects of the endothelial and neuronal nitric oxide activation.

Glutathione recycling and nitric oxide modulation—a beautiful partnership

A nitric oxide modulating and glutathione recycling approach is available through a qualified health care practitioner trained in these approaches.

The nice thing about supporting glutathione recycling and nitric oxide is that it doesn’t matter whether you are TH-1 or TH-2 dominant.

I find these approaches have been successful with my very fragile patients who react to so many foods and supplements and can’t handle the TH-1 or TH-2 stimulating compounds.

After the patients followed a gluten-free diet for 11 months their TSH levels came down with the same T4 requirement as the non-celiac Hashimoto’s patients.

Gluten sensitivity linked with Hashimoto’s hypothyroidism

This is yet another study that demonstrates the clinical association between gluten sensitivity and Hashimoto’s hypothyroidism. It is very rare to find a person with Hashimoto’s who does not have some degree of gluten sensitivity or full-blown celiac disease.

Gluten overstimulates the immune system

Gluten sensitivity is basically defined as any immune response to gluten.

Celiac disease is defined generally as an autoimmune response to intestinal tissues upon gluten exposure, as well as overall activation of the immune system Various labs classify celiac disease using different criteria, including genetic testing and intestinal biopsy.

Either way, such an immune response is never good for a person with Hashimoto’s or other autoimmune disease.  The immune system is already imbalanced and overactive during an active autoimmune condition. A consistent immune reaction to a regular food in the diet only makes the immune system more volatile, further exacerbating the autoimmune condition.

This overall activation of the immune system creates inflammation and explains why symptoms of gluten sensitivity vary. For some the inflammation may target the joints, creating pain and swelling. For others skin rashes and skin disorders ensue. Many others suffer inflammation in the brain, resulting in brain fog, mood and anxiety disorders, or memory loss.

The list of inflammation-induced symptoms brought on by a gluten sensitivity goes on and depends upon the person’s genetic makeup. Needless to say such systemic inflammation also flares up an autoimmune condition.

Experience shows a gluten-free diet is a must

In my experience, most Hashimoto’s patients fall somewhere between gluten sensitivity and celiac disease.  Nevertheless, almost all patients with Hashimoto’s improve on a strict gluten-free diet, even if they do not fit the established criteria of celiac disease. By strict I mean you are 100 percent gluten-free. Because the immune reaction to gluten has been shown to last up to six months after exposure, cheat days or occasionally eating gluten will derail the therapeutic benefits of a gluten-free diet.

Practitioners wrong when they say gluten OK

I have seen many patients over the years with Hashimoto’s whose health care practitioners have told them they can eat gluten because they had a normal gluten antibody test (meaning there is no sensitivity) or they did not have the gene for gluten sensitivity. This a horrible mistake and a complete disconnect with the realities of what a serious immune trigger gluten is for most people with Hashimoto’s, unassociated with celiac disease.

Problem lies with incomplete gluten testing

I am now convinced that part of the problem with negative gluten antibody tests is improper testing. The general gluten antibody test conducted by most labs today is only testing a small portion of the gluten protein, alpha-gliadin.

In reality, an individual can have an immune response to various parts of the gluten protein, including omega-gliadin, gamma-gliadin, wheat germ agglutinin, and deamidated gliadin.

In my practice the only valid and complete gluten assessment is a panel called the Wheat/Gluten Proteome Sensitivity and Autoimmunity test by Cyrex Laboratory in Phoenix, Arizona. The panel also provides testing for transglutaminase antibodies, the marker for autoimmunity against intestinal tissue. This marker strongly suggests celiac disease or at least an autoimmune reaction in the small intestine in response to gluten.

Other factors in gluten testing

If you are a thyroid patient who tested negative for alpha-gliadin antibodies and have been told it is OK to eat gluten, that advice could be harmful to your condition as you may be reacting to one of these other components of gluten.

Also, newer research shows that people may have a gluten cross-reactivity, meaning they react to other foods as if they are gluten, another scenario for which Cyrex Labs screens. Lastly, if your immune system is depressed and exhausted, you may not be able to make enough antibodies to register positive on a lab panel, even though an immune reaction is taking place. In this instance, restoring immune health will often then produce a positive antibody response to gluten on a lab test.

Both the scientific and clinical evidence linking gluten with Hashimoto’s and autoimmune disease in general is too powerful and abundant to ignore. A strict gluten-free diet is the first and most important step to managing your Hashimoto’s hypothyroidism.

Marisol Aponte plays roller derby and is a fitness coach who has learned how to train effectively despite hypothyroidism.

But some athletes are surprised to learn their dwindling performance and failure to build muscle stems from improperly managed hypothyroidism.

The fact that athletes are typically fit and slender makes it easy for doctors to overlook their symptoms. And like 90 percent of Americans with hypothyroidism, most athletes have Hashimoto’s, an autoimmune condition that thyroid hormone medications alone do not properly address. As a result, performance declines until the athlete may be forced to stop competing and participating in a lifestyle she loves.

Studies show hypothyroidism affects athletic performance in a number of ways. It creates more muscle weakness and cramping, impairs cardiac function and blood flow, and hampers the ability of muscles to use fatty acids for energy, thus limiting endurance.

Athletes should avoid over training

Athletes set themselves apart by their ability to push themselves physically and mentally when most people would give up. However repeatedly pushing the body too far can produce negative health consequences.

What I commonly see in athletes, particularly endurance athletes, is adrenal fatigue, excess inflammation, and sometimes a form of anemia caused by the breakdown of red blood cells, another consequence of over training. These factors could lend a hand in triggering an autoimmune thyroid condition in someone genetically predisposed, and they can certainly exacerbate and existing thyroid condition.

I have seen many athletes boost flagging performance by adapting changes that include:

• Lightening up their training schedules
• Managing adrenal imbalances
• Eliminating foods to which they are intolerant
• Repairing inflamed and permeable guts
• Managing any autoimmune conditions

What’s required to modulate adrenal function and tame inflammation will be different, but most see improved performance and more enjoyment from their sport after tending to these issues.

Taking more thyroid hormones is not the answer

It may be tempting to take very high doses of thyroid hormones to boost metabolism and hence performance, but this is a trap. Too much thyroid hormone can cause resistance to the thyroid and hypothyroid symptoms. Also, studies show taking excess thyroid hormone can overstimulate the production of dopamine, which could predispose one to a dopamine deficiency. In fact Muhammad Ali took very high doses of thyroid hormone during his fighting career and later developed Parkinson’s disease, a disease of dopamine deficiency. Although we don’t know the thyroid hormone overuse caused his Parkinson’s, it may have played a role.

It’s more important to address the underlying cause of the thyroid imbalance and address that. For most that will mean managing an autoimmune attack on the thyroid gland. For some athletes, due the high amount of stress they subject themselves to, it could mean lowering stress and supporting the body’s stress-handling mechanisms. It is best to work with a qualified practitioner and read Why Do I Still Have Thyroid Symptoms? to learn the best way to manage your thyroid condition.

Following are some stories from athletes with hypothyroidism, and what they have learned about working with their condition.

Hypothyroid health coach says key is to avoid over training

Marisol Aponte plays roller derby, is a kettle bell instructor, and competes in triathlons. Because she was diagnosed with hypothyroidism as a child, she has had many years to finesse a training regimen that allows her to stay active without worsening symptoms. She finds she cannot train as hard as someone with a healthy thyroid because of the adrenal fatigue it causes. To keep her endurance strong without taxing her adrenals, she gets her cardio workouts from sprint interval training, long-duration low-intensity activities such as swimming, and weight-bearing exercises such as kettle bell training.

She has found supporting her digestion with an enzyme supplement helps her assimilate protein better to ensure muscle building, and she eats a healthy diet that is strictly gluten-free. Since adapting a healthier diet and modifying her training regimen she has been able to halve the dosage of her thyroid medication.

Hypothyroid cyclist can’t keep up

Lorraine, 46, didn’t think there was such a thing as exercising too hard. She lifted weights, cycled regularly, and rode in the Triple Bypass, a 120-mile bike ride up and over three of Colorado’s 11,000-foot mountain passes. She routinely did training rides of 80 miles, however when her health began to fail she struggled to make it 10 miles. She also noticed she was unable to lift much weight at the gym, and that she couldn’t build muscle. A doctor diagnosed her with hypothyroidism and after about six months on thyroid hormones she felt better, until her performance began to decline again. Then the doctor increased her dose and the cycle repeated itself. All along her TSH was normal, leading her doctor to dismiss her symptoms.

“Basically my doctor called me a liar,” says Lorraine. “I wanted to commit hari kari because I kept being told nothing was wrong with me. It’s criminal.”

Fortunately Lorraine began working with Shane Steadman, DC, DACNB and read Why Do I Still Have Thyroid Symptoms? She follows an autoimmune protocol, has eliminated gluten, dairy, nuts, and nightshades from her diet, and uses nutritional compounds to support her fatigued adrenal glands. Dr. Steadman explained to her how over training can exhaust the adrenal glands, and Lorraine has cut back on the intensity of her workout schedule, a formerly foreign concept.

“I always pushed myself through exercise because I felt I should be able to do it,” she says.

As a result she shed some unwanted pounds and her performance has improved significantly. She is back to building muscle at the gym and has seen her endurance return. But because she suffered for so long with adrenal fatigue, she knows it will take time to fully rebuild her strength, and that she must be vigilant to temper the intensity of her workouts.

Long distance swimmer questions hypothyroidism

Linda, a reader living in England, believes her recently diagnosed autoimmune thyroid condition started in 2006, the same year her performance as a long-distance swimmer began to suffer. She managed her second swim across the English Channel that year, although it was “touch and go,” and since has met with dwindling success in other long-distance swims. Nevertheless, she is training to swim the Catalina Channel in California this summer, although the effects of her improperly managed thyroid condition distress her. It has prevented her from swimming the English Channel a third time thanks to severe cramping and crippling pain that caused her to fall short of her target by five miles. She also struggles with other thyroid symptoms, chronic anemia, and repeat respiratory infections.

It wasn’t until she read Why Do I Still Have Thyroid Symptoms? that she began to question whether her thyroid condition was sabotaging her success, even though she takes thyroid hormone medications. When she brought up intestinal permeability, the role of gluten, and other concepts in the book with her endocrinologist, he dismissed them as irrelevant and said thyroid hormone medications were the only way to manage an autoimmune thyroid condition.

Linda will begin working on her thyroid condition long-distance with a U.S.-based practitioner, which will hopefully boost her swimming performance to previous levels.

Hypothyroid runner must be careful not to overdo

Troy is a runner in his twenties who has Type I diabetes in addition to Hashimoto’s. Although he enjoys staying active, he says it can be a struggle to balance his desire to train regularly without triggering hypothyroid symptoms.

“I can’t train consistently because of my Hashimoto’s,” says Troy. “I also can’t train too hard or I can’t recover and I get hypothyroid symptoms. I’m still trying to find the right balance. When I was able to get into a good routine that’s when I got my best time for a 5K. I don’t compete a lot but I feel like some of my times are pretty good for having two autoimmune diseases.”

Finding the right balance

Hypothyroid athletes must train a little differently than their peers. Although they may not train as hard or as long, some find they can still be just as fit and competitive through prudent training, a careful diet, and by listening to their body instead of blindly pushing themselves too hard.

Glutathione and stress

In the thyroid book I introduced glutathione, our body’s most powerful antioxidant, and how integral it is to modulating the immune system. Ideally the body makes sufficient glutathione to help keep everything running smoothly, however it becomes depleted in the face of extreme or chronic stress.

Modern life  bombards us with stressors, the most common being ongoing insulin surges from sugary, high-carb diets, immune aggravation from food intolerances, chronic gut infections (too much bad bacteria or parasites), hormonal imbalances, lack of sleep, and of course our hectic, information-overloaded lifestyles.

Many people suffer from all of the above on a daily basis and also may smoke, drink too much, or even overtrain athletically, compounding an already precarious situation. Of course autoimmune disease itself is a significant stressor, further depleting the body’s precious supply of glutathione.

In fact, I might go so far as to say it is difficult for the body to produce an autoimmune attack if the glutathione system is functioning properly.

Boosting glutathione levels though a liposomal cream or intravenously—as glutathione taken orally is ineffective—is a key strategy in combating the damage of stress. However these levels can be quickly depleted if the body cannot recycle glutathione to keep the supply on hand to meet the many stressors.

Glutathione’s job is to take the bullet

Before I can explain how glutathione recycling works, I first need to explain more about how specifically glutathione protects us. Glutathione is like the bodyguard or Secret Service agent whose loyalty is so deep that she will jump in front of a bullet to save the life of the one she protects. When there is enough of the proper form of glutathione in the body to “take the bullet”, no inflammatory response occurs. However when glutathione becomes depleted it triggers a destructive inflammatory process.

Glutathione recycling explained

Glutathione recycling is a separate function from just boosting glutathione levels through a liposomal cream, intravenously, a nebulizer, a suppository, or other means. These forms of glutathione delivery will help one’s antioxidant status but they do not raise levels of glutathione inside the cells. Glutathione is the main antioxidant for mitochondria, the little factories inside each cell that convert nutrients into energy. Some cells have more mitochondria than others depending on the cell’s function. This is important because an autoimmune disease destroys the mitochondria in the affected cells, thus causing tissue destruction, and glutathione protects these mitochondria.

Reduced glutathione versus oxidized glutathione

But not just any form of glutathione does this—it needs to be reduced glutathione. There are two main forms of glutathione in the body: reduced glutathione (GSH) and oxidized glutathione (GSSG).

Reduced glutathione, or GSH, is the bodyguard who “takes the hit” from free radicals that damage cells. Free radicals are molecules that are unstable because they have unpaired electrons and are looking for another electron to steal in order to become stable. They steal electrons from the mitochondria, thus destroying them and causing inflammation and degeneration.

However when there’s plenty of GSH in the cell, the GSH sacrifice themselves to the free radicals—throwing themselves in front of the bullet—in order to protect the mitochondria. Thus the GSH ends up with an unpaired electron and becomes unstable, at which point it becomes GSSG, or oxidized glutathione, which is technically a free radical itself.

Doesn’t this make GSSG dangerous to the cell then? When there is sufficient glutathione in the cell, the unstable GSSG naturally pairs with available glutathione in the cell with the help of an enzyme called glutathione reductase, returning back to its reduced glutathione state so it’s ready for action once again.

The key thing to remember is that two enzymes play important roles in these processes:

• Glutathione peroxidase triggers the reaction of GSH to GSSG, which is when glutathione “takes the hit” to spare the cell
• Glutathione reductase triggers the conversion of GSSG back to useable GSH.

These enzymes come into consideration when we look at how to support the glutathione system nutritionally.

The link between poor glutathione recycling and autoimmune disease

Studies show a direct correlation between a breakdown in the glutathione system and autoimmune disease. The ability to constantly take oxidized glutathione and recycle it back to reduced glutathione is critical for managing autoimmunity.

Fortunately studies also show various botanicals, nutritional compounds, and their cofactors have been shown to activate glutathione reductase and the synthesis of reduced glutathione. By boosting this enzyme and supplementing glutathione levels we can increase glutathione levels and glutathione recycling to quench inflammation once it starts, or, even better, to prevent inflammation in the first place.

Studies have also shown that efficient glutathione recycling helps boost the TH-3 system, the branch of the immune system that helps balance the TH-1 and TH-2 systems and prevent autoimmune reactivity. (I explain TH-1 and TH-2 systems of immunity in my book.) Proper glutathione activity not only helps protect cells, research shows it also modulates cell proliferation and immunity, and helps tissues recover from damage.

Glutathione recycling helps repair leaky gut

Good glutathione recycling helps tame autoimmune diseases in another way. One thing I have found universal in all my autoimmune patients is poor gut integrity. They all suffer from some degree of leaky gut and repairing the gut is vital to the recovery process. Studies show glutathione may play an important role in gut barrier function and the prevention of intestinal inflammation.

A compromised glutathione recycling system can worsen intestinal destruction—the person with multiple food sensitivities and a gut that never heals may be victim of this mechanism. Although repairing a leaky gut is vital to taming an autoimmune response, we can see now glutathione recycling is another vital piece to the puzzle of  restoring gut health.

Supporting glutathione recycling

So how do we support glutathione recycling? The first thing is to reduce the stressors depleting this vital system. The bulk of my thyroid book is devoted to this: balancing blood sugar, addressing food intolerances, restoring gut health, and managing adrenal function are foundational.

Other considerations are neurotransmitter imbalances and hormonal imbalances, which may require specialized guidance from a qualified health care practitioner.  And of course making any lifestyle changes you can, such as getting enough sleep, paring down an overactive schedule, making exercise a priority each day, creating time to do things you love, and so on.

Once you have addressed these factors (which for many people can actually take care of the problem) and autoimmune dysfunction persists, then boosting glutathione recycling may be necessary. Below I cover the basic botanicals and nutritional compounds researchers have found support glutathione recycling pathways.

• N-acetyl-cysteine (NAC): NAC is a key compound to glutathione activity. It is rapidly metabolized into intracellular glutathione.
• Alpha-lipoic acid (ALA): ALA directly recycles and extends the metabolic life spans of vitamin C, glutathione, and coenzyme Q10, and it indirectly renews vitamin E, all of which are necessary for glutathione recycling.
• L-glutamine: Research has shown that l-glutamine is important for the generation of glutathione. It is transported into the cell, converted to glutamate, and readily available to intracellular glutathione synthesis.
• Selenium: Selenium is a trace element nutrient that serves as the essential cofactor for the enzyme glutathione peroxidase, which converts GSH to GSSG so glutathione can “take the hit” by free radicals to spare cells.
• Cordyceps: Cordyceps has been shown to activate both glutathione and peroxidase synthesis in the body. It has also been shown to protect cells by engaging the glutathione enzyme cycle.
• Gotu kola (Centella Asiatica): Research has clearly demonstrated that oral intake of gotu kola rapidly and dramatically increases the activity and amount of glutathione peroxidase and the quantity of glutathione.
• Milk thistle (Silybum marianum): Milk thistle has been shown to significantly increase glutathione, increase superoxide dismutase (another powerful antioxidant) activity, and positively influence the ratios of reduced and oxidized glutathione.

Taken together these botanicals and compounds activate the glutathione peroxidase and reductase enzymes that promote a healthy glutathione recycling system.

For people with severe leaky gut issues I suggest they take these compounds as they work on repairing leaky gut. Also, it’s important to use these in conjunction with a liposomal glutathione cream discussed in the book. These compounds work more on recycling glutathione than boosting overall levels. This way the glutathione you do take, whether through a cream, an IV, a nasal spray, or other method is assured to stay in your body longer and get inside your cells where they can do their best work.

Glutathione recycling is imperative to taming autoimmune disease

Promoting glutathione recycling helps protect cell mitochondria, enhance tissue recovery, modulate an imbalance between TH-1 and TH-2, and boost immune regulation. The overall effect is to dampen both the autoimmune reaction and damage to body tissue. It also helps body tissue and the intestinal tract regenerate and recover. Keeping overall glutathione levels up by supporting glutathione recycling helps buffer the body’s cells from the many stressors hurled at us each day.

Other practitioners and I have witnessed patients rebuild their glutathione recycling system. As a result they are much less or no longer sensitive to chemicals around them, they have fewer autoimmune flare-ups, and they recover much faster from their flare-ups.

Potassium iodide in radiation emergencies

In 1982 the FDA approved potassium iodide to protect the thyroid gland from radioactive iodine in radiation emergencies. In an accidental event or attack on a nuclear power plant, volatile fission product radionuclides may be released.

Of these products, radioactive iodine is one of the most common and is particularly dangerous to the thyroid gland because it may lead to thyroid cancer. By saturating the body with a source of stable iodide prior to exposure, inhaled or ingested radioactive iodine tends to be excreted, which prevents radioiodine uptake by the thyroid.

Iodide only helps the thyroid gland

Potassium iodide cannot protect against any other causes of radiation poisoning and is limited to protecting the thyroid. All cells of the body are vulnerable to radiation and iodine cannot decrease other risks such as leukemia or other types of insult to cells of the body that may occur from radiation toxicity.

Glutathione recycling critical for radiation stress

Several research studies have found that that the glutathione recycling system is critical in dealing with the oxidative stress of radiation.Our bodies’ defense against these harmful compounds involves our antioxidant systems.

Glutathione is an antioxidant made in our bodies to help protect our cells from radiation and other free radicals.  Theoretically, the more glutathione we have, the more protection we have against free radical activity.

Compounds to boost glutathione recycling

Several natural compounds have been shown in research studies to increase glutathione levels.These include N-acetyl cysteine, Cordyceps, Guto Kola, Milk Thistle, L-glutamine, and alpha lipoic acid.

I personally use these compounds ands and have recommended them to patients as a single formulation called Glutathione Recycler from Apex Energetics.I also have been using a glutathione liposomal cream called Oxicell to be applied to the thyroid gland itself.

Adrenal adaptogens may protect against free radicals

Lastly, several research studies have shown that plant compounds called adaptogens such as Siberian Ginseng, Ashwagandha, Holy Basil, Rhodiola, and Boerhaavia Diffusa may have radiation free-radical protecting properties.

I use a formulation called Adaptocrine from Apex Energetics to provide these adaptogens.I have listed some of the research references at the end of this article on my blog regarding the role of glutathione and adaptogens, but these compounds and products have not been evaluated or approved by the FDA for radiation crises, nor are they considered mainstream management for radiation exposure.

Reports of Hashimoto’s flare-ups have gone up since the crisis

Lastly, the use of iodine in Hashimoto’s patients has become an issue of concern since many Hashimoto’s patients cannot tolerate iodine without activating their autoimmunity.  Many cases of Hashimoto’s flare-ups and thyroiditis have been reported to me by health care provider across the country since the recent media promotion of potassium iodine supplementation.

No good answer on emergency iodine use with Hashimoto’s

There is no good answer for this dilemma because both taking iodine and not taking iodine may not be good options for those suffering from Hashimoto’s.If iodine cannot be tolerated by the individual the use of the above protocol to enhance glutathione activity, the use of glutathione cream rubbed into the thyroid gland, and the use of adaptogens may be of help in protection without inducing iodine promoted adverse reactions.

References

1: Morales A, Miranda M, Sánchez-Reyes A, Biete A, Fernández-Checa JC. Oxidative damage of mitochondrial and nuclear DNA induced by ionizing radiation in human hepatoblastoma cells. Int J Radiat Oncol Biol Phys. 1998 Aug 1;42(1):191-203.

2: Morse ML, Dahl RH. Cellular glutathione is a key to the oxygen effect in radiation damage. Nature. 1978 Feb 16;271(5646):660-2.

3: Koval’ TV, Nazarova OO, Matyshevs’ka OP. [Change in glutathione content in rat thymocytes under apoptosis induced by H2O2 or irradiation]. Ukr Biokhim Zh. 2008  Mar-Apr;80(2):114-9. Ukrainian.

4: Manu KA, Leyon PV, Kuttan G. Studies on the protective effects of Boerhaavia diffusa L. against gamma radiation induced damage in mice. Integr Cancer Ther. 2007 Dec;6(4):381-8.

5: Verma P, Sharma P, Parmar J, Sharma P, Agrawal A, Goyal PK. Amelioration of Radiation-Induced Hematological and Biochemical Alterations in Swiss Albino Mice  by Panax ginseng Extract. Integr Cancer Ther. 2010 Aug 11.

6: Lee TK, O’Brien KF, Wang W, Johnke RM, Sheng C, Benhabib SM, Wang T, Allison RR. Radioprotective effect of American ginseng on human lymphocytes at 90 minutes postirradiation: a study of 40 cases. J Altern Complement Med. 2010 May;16(5):561-7.

7: Park E, Hwang I, Song JY, Jee Y. Acidic polysaccharide of Panax ginseng as a defense against small intestinal damage by whole-body gamma irradiation of mice.  Acta Histochem. 2011 Jan;113(1):19-23.

8: Goel HC, Bala M, Prasad J, Singh S, Agrawala PK, Swahney RC. Radioprotection by Rhodiola imbricata in mice against whole-body lethal irradiation. J Med Food. 2006 Summer;9(2):154-60.

9: Arora R, Chawla R, Sagar R, Prasad J, Singh S, Kumar R, Sharma A, Singh S, Sharma RK. Evaluation of radioprotective activities Rhodiola imbricata Edgew—a high altitude plant. Mol Cell Biochem. 2005 May;273(1-2):209-23.

10. Kuttan G. Use of Withania somnifera Dunal as an adjuvant during radiation therapy. Indian J Exp Biol. 1996 Sep;34(9):854-6.

It is worth checking TPO antibodies before conceiving

Since the book was published I have received countless emails from women whose thyroid problems began after pregnancy. This is fairly common for a number of reasons:

• Shifts in immune function during and after pregnancy
• Shifts in hormone function during and after pregnancy
• Already existing stressors to the body (blood sugar imbalances, food intolerances, gut infections, other autoimmune diseases, etc.)
• Genetic tendency

How pregnancy can trigger Hashimoto’s

Autoimmune diseases in general are more common in women and research suggests women’s more complex hormonal systems, which become exaggerated during and after pregnancy, play a role in that.[1] [2]

Also, during the third trimester a pregnant woman becomes TH-2 dominant, then TH-1 dominant postpartum. Combined with the other risk factors listed above, these periods of polarized immune dominance can tip an immune system that’s already on edge, thus triggering Hashimoto’s.

Pregnancy and pituitary function

Pregnancy can also cause hypothyroidism by depressing pituitary function. The pituitary gland is located at the base of the brain and operates as a control tower for the body’s hormones. Chronic stressors such as gut infections, food intolerances, blood sugar imbalances, and hormonal imbalances for instance (many women have a combination of all of these) can depress pituitary function.[3] [4] [5] [6] [7]

As a result the pituitary fails to signal the thyroid to release enough TSH to stimulate thyroid activity. In other words, the thyroid gland may be perfectly fine but nobody is telling it to go to work because the exhausted pituitary has fallen asleep on the job.

For many women this manifests not only as low thyroid function, but also postpartum depression. Because so many women enter pregnancy in some sort of adrenal stress, the increased demands of pregnancy overwhelm the pituitary gland.

Postpartum thyroiditis

Postpartum thyroiditis, a condition in which the thyroid gland swells, occurs in approximately five to seven percent of women within two to four months after delivery of a baby, and is the result of autoimmune disease. This is another common culprit for postpartum depression. Thyroiditis presents as a painless, small, firm goiter, or enlarged thyroid gland. Typically the woman notices either an enlarged thyroid, symptoms of hyperthyroidism (anxiety, restlessness, insomnia, weight loss, and difficulty concentrating), or both.

Hyperthyroid symptoms usually occur two to ten months after delivery—most commonly at three months—with recovery taking place during the next two to three months after the onset of hyperthyroidism. Symptoms can include nervousness, anxiety, insomnia, anorexia, and heart palpitations. It is important to distinguish postpartum thyroiditis from Graves’ disease with proper lab testing.

Hypothyroid symptoms (depression, fatigue, cold hands and feet, constipation, weight gain, etc.) occur two to twelve months after delivery—most commonly at six months. Eighty percent of women with postpartum thyroiditis return to normal thyroid function around the one-year mark, however, 30 to 50 percent develop permanent hypothyroidism within nine years.[8] [9]

TPO antibodies before pregnancy raise the risk

Women with no thyroid symptoms but who have elevated TPO antibodies have a 25 percent higher risk for developing postpartum thyroiditis.[10 ] I suggest women considering pregnancy screen for thyroid antibodies prior to conception or at least in the prenatal evaluation. Additionally, women who develop postpartum thyroiditis and have elevated thyroid antibodies have a 70 percent risk of it happening again in future pregnancies.[11]

Reducing the risk of autism, allergies, eczema, and more in the baby

Working to prevent hypothyroidism will help make those early exhausting days with a new infant more doable. More importantly, however, is that it may help ensure a healthier baby.

When a woman goes into pregnancy with a leaky gut, blood sugar imbalances, multiple food intolerances, and adrenal fatigue, I believe she is putting her baby at risk for developing one of the increasingly common modern health disorders, including an autism spectrum disorder, eczema, asthma, food allergies, and food intolerances.[12] [13] [14] [15] [16] [17]

Researchers are increasingly finding that autoimmune disorders are at the root of many cases of autism, with the immune system attacking brain or nerve tissue of the child. Children born with an immune system that is a ticking time bomb are vulnerable to anything that can launch a self-attack, whether it is a vaccine, food intolerance, blood sugar imbalance, or heavy metal toxicity.

Hashimoto’s in children

I have received a surprising number of emails from women over the last year whose children have Hashimoto’s. In some the disease is so advanced that the child’s brain development is affected. Having a genetic tendency for Hashimoto’s doesn’t mean it has to be triggered. Stabilizing an immune imbalance before pregnancy may help prevent Hashimoto’s in a child.

Of course nobody knowingly or purposely brings such things to a child, but given the state of the average American’s health, I feel addressing these factors can decrease the risk that a child will be born with one of the immune conditions so common today.

[2] Krysiak R, Okopien B, Szxkrobka W, Herman ZS. [Thyroid disorders in pregnancy and after delivery] [Article in Polish] Przegl Lek 2007;64(3):159-64.

[3] Rettori V, Jurcovicova J, McCann SM. Central action of interleukin-1 in altering the release of TSH, growth hormone, and prolactin in the male rat. J Neurosci Res 1987;18:179-183.

[4] Bartalena L, Grasso L, Brogioni S, et al. Interleukin-6 on pituitary-thyroid-axis in the rat. Eur J Endocrinol 1994;131:302-306.

[5] Lyson K, McCann SM. The effect of interleukin-6 on pituitary hormone release in vivo and vitro. Neuroendocrinology 1991;54:262-266.

[6] Ozawa M, Sato K, Han DC, et al. Effects of tumor necrosis factor-alpha/cachetin on thyroid hormone metabolism in mice. Endocrinology 1998;123:1461-1467.

[7] Rettori V, Milenkovic L, Beutler BA, et al. Hypothalamus action of catechin to alter pituitary hormone release. Brain Res Bull 1989;23:471-475.

[8] Stagnaro-Green A.  Clinical review 152: postpartum thyroiditis.  J Clin Endocrinol Metab.  2002;87:4024-7.

[9] Premawardhaha LD, et al.  Postpartum thyroiditis and long-term thyroid status: prognostic influence of thyroid peroxidase antibodies and ultrasound echogenicity.  J Clin Endocrinol Metab.  2000;85:71-5.

[10] Stagnaro-Green A.  Clinical review 152: postpartum thyroiditis.  J Clin Endocrinol Metab.  2002;87:4024-7.

[11] Muller AF, Drexhage HA, Berghout A. Postpartum thyroiditis and autoimmune thyroiditis in women of childbearing age: recent insights and consequences of antenatal and postnasal care.  Endocr Rev. 2001;22:605-30.

[12] Sex-specific programming of offspring emotionality after stress early in pregnancy. J Neurosci 2008 Sep3;28(36):9055-65.

[13] Activation of the maternal immune system alters cerebellar development in the offspring. Brain Behav Immun 2008 Aug 9.

[14] Preliminary evidence for a modulation of fetal depaminergic development by maternal immune activation during pregnancy. Neuroscience 2008 Jun 23;154(2):701-9. Epub 2008 Apr 25.

[15] Maternal infection leads to abnormal gene regulation and brain atrophy in mouse offspring: implications for genesis of neurodevelopmental disorders. Schizophr Res 2008 Feb;99(1-3):56-70. Epub 2008 Jan 9.

[16] Maternal autoimmune diseases, asthama and allergies, and childhood autism spectrum disorders: a case-control study. Arch Pediatr Adolesc Med. 205 Feb;159(2):151-7.

[17] Maternal health in pregnancy and intellectual disability in the offspring: a population-based study. Ann Epidemiol 2006 Jun;16(6):448-54. Epub 2005 Sep 22.

Dairy commonly triggers a gluten-like reaction. Surprisingly coffee can too. If symptoms don’t improve on a GF diet, these may be the culprits.

Gluten intolerance not as black-and-white as once thought

Testing for gluten-intolerance incomplete until now — New lab offers breakthrough

Gluten has been linked in the literature to 55 diseases so far, most of them autoimmune. The effect of gluten on brain and nervous tissue is significantly worse and more far-reaching than researchers realized. Yet thanks to poor lab testing and general misinformation many people continue to eat gluten, unaware it is harming them.

Fortunately a revolutionary breakthrough in gluten reactivity testing at Cyrex Labs, founded on years of leading immunological research, is now available to help determine whether this ubiquitous food is damaging your health.

Problems with standard tests for gluten intolerance

• Standard blood tests for gluten intolerance have a less than 30 percent accuracy rate. Would you tolerate that accuracy rate for a cancer, heart disease, or even pregnancy test? Gluten has to have significantly destroyed the gut wall for blood testing to be effective, and for many people that isn’t the case…especially if the brain, heart, or some other part of the body is the main target of attack.

• Current salivary tests produce false negatives due to the assessment of only one antibody of one wheat protein. Stool tests produce false negative and false positives due to specimen-interfering factors that alter the outcome of results.

• Current tests only screen for one component of wheat. Yet people can react to a single protein in wheat, or a combination of many proteins, peptides, and enzymes associated with wheat. Cyrex Labs tests for twelve of the most antigenic (meaning most likely to provoke a reaction) pathogens associated with wheat.

• Some people also have cross-reactivity to gluten. For instance, eating dairy can trigger a gluten-like immune response because the body sees them as one in the same.

Cyrex Labs hones in on the specifics of gluten intolerance

After many years of research and development Cyrex Labs in Arizona now offers thorough and comprehensive testing for gluten intolerance. Cyrex was founded by Aristo Vojdani, Ph.D., M.Sc., C.L.S., a leading researcher in the fields of autoimmune disease and neuroimmunology who has published more than 100 scientific papers.

Cyrex Labs offers four arrays, with a fifth to be introduced in spring of 2011:

Array 1:  Gluten Sensitivity Screen

A simple, affordable way to test for a general gluten sensitivity using saliva — great for preventative health if autoimmune issues run in the family

The saliva is the best way to detect a gluten sensitivity early, even before symptoms manifest. The gut has to be severely damaged in order for a blood test to be useful. Because it uses a saliva sample, this test is easy to use with children.

This is a great test for people who have a family history of autoimmune disease, even if they’re asymptomatic. Since so many autoimmune disease are triggered by gluten, this test shows the patient a gluten-free diet can prevent him or her from going down the same road as family members.

The Gluten Sensitivity Screen includes:

Total secretory IgA. Antibodies are used in testing to determine whether the immune system is reacting to something. Secretory IgA, a type of antibody, is manufactured in the mucosa of the gut lining. It’s job is to keep invading
pathogens, such as viruses, bacteria and food proteins from attaching to the gut lining. When the layer of mucosa that protects the lining of the digestive tract breaks down or becomes dysfunctional, total secretory IgA may be too low or too high. This means you could have too few or too many antibodies to test properly, even though you are gluten-intolerant. This marker screens for that.

Gliadin IgA + IgM antibodies. IgA antibodies are used to screen for gluten intolerance. However if IgA antibodies are low due to weak immunity, another type of antibody called IgM will be high. Screening for both gives a more accurate view of immune status and thus test results.

Transglutaminase IgA + IgM combined antibodies. Transglutaminase is an enzyme in the digestive tract targeted in an autoimmune attack triggered by gluten. If this marker comes back positive you know gluten is destroying gut tissue through an autoimmune attack.

Array 2:  Intestinal Antigenic Permeability Screen

A test that identifies how gluten is robbing you of gut health

Gluten causes inflammation in the gut, which eventually leads to intestinal permeability, or “leaky gut.” Leaky gut allows undigested food particles, bacteria, and other pathogens to escape into the bloodstream where they can trigger allergies, sensitivities, and inflammation in other parts of the body.

Several different mechanisms cause leaky gut:

• Breakdown of cells
• Loosening of the junctures of the gut lining
• Bacterial infection

This test pinpoints which of these is causing leaky gut so your practitioner knows what to specifically target for faster and more efficient gut repair.

Array 3: Wheat/Gluten Proteome Sensitivity and Autoimmunity

More than one wheat protein can cause gluten-intolerance — Cyrex Labs tests for twelve

Being gluten-intolerant isn’t as black-and-white as once thought. Actually gluten is a misnomer, “gliadin” is the portion of wheat that triggers an immune response in people (since “gluten” is commonly used I will stick with that term). It also has been discovered wheat is made up of more than 100 different components that can cause a reaction, not just one.

Until now testing for gluten intolerance has only been against one of those components, alpha gliadin. Through extensive research Cyrex pinpointed the twelve components of wheat that most often provoke an immune response.

This new test greatly expands the parameters of gluten intolerance testing, catching those who may have previously tested negative because they don’t react to the alpha gliadin.

Opioid testing

Array 3 also tests whether gluten has a drug-like opiate effect on an individual. Some people have enzymes in their digestive tract that break gluten down into opioids that act like heroin or morphine. Embarking on a gluten-free diet can cause terrible withdrawal symptoms in these people. One practitioner tells of a patient whose withdrawal symptoms were so severe she went to the emergency room.

Another problem with opioids is they disrupt brain function by attaching to receptor sites normally meant for neurotransmitters. Neurotransmitters are brain chemicals that help dictate our personality, moods, behavior, bodily function, and more.

This opioid effect on neurotransmitter receptors explains why gluten plays a role in so many cases of ADD/ADHD, autism, or behavioral problems in children; or brain fog, depression, anxiety, and migraines in adults. When one mother put her autistic son on a gluten-free diet, he began eating the binding out of books as he was so desperate for his gluten-opioid “fix.”

Array 3 screens for antibodies to the opioids, which signals their presence in the brain.

Array 4:  Gluten-Associated Sensitivity and Cross-Reactive Foods

Twenty-four foods that cross-react with gluten or are newly introduced to a gluten-free diet

One of the most frustrating scenarios for both the practitioner and the patient is when a gluten-free diet fails to have any effect on a person who seems so clearly gluten-intolerant. Newer research shows this may be due to cross-reactivity.

In cross-reactivity the body mistakes another food for gluten and reacts accordingly. Array 4 tests for 24 different foods that may be causing cross-reactivity.

Dairy

Cross-reactivity is common with dairy as its structure so closely resembles that of gluten. In fact 50 percent of people who are sensitive to gluten are also sensitive to dairy.

Coffee is surprisingly cross-reactive with gluten

However Cyrex researchers were surprised to find instant coffee has the highest rate of cross-reaction with gluten. In other words, some people’s immune system mistakes instant coffee for gluten, triggering a reaction. This test informs people whether one needs to give up instant coffee to prevent gluten cross-reactivity.

Amaranth and quinoa

Array 4 also tests for foods that many people eat for the first time on a gluten-free diet, such as amaranth or quinoa. Never having been exposed to these foods could trigger the immune to respond as if these grains were foreign intruders, especially in the case of a leaky and inflamed gut.

This panel has great clinical significance as it explains why people still react even after giving up gluten and even dairy.

Array 5

Which parts of the body are affected by a gluten-intolerance

People typically shrug off the possibility of a gluten intolerance by saying, “I don’t have any digestive problems.” Little do they know that gluten produces digestive symptoms in only a minority of people. For the majority gluten damages the brain, the heart, the skin, the respiratory tract, or the joints.

Although it won’t be out until spring of 2011, Array 5 will test for which part of the body is the site of inflammation and degeneration caused by gluten intolerance.

Comprehensive immune testing

In the coming months Cyrex will offer comprehensive and accurate immune testing, such as the TH-1 and TH-2 testing described in Why Do I Still Have Thyroid Symptoms When My Lab Tests Are Normal? Cyrex will also unveil my “thyroid dream panel” in spring of 2011.

For more information, visit Cyrex Labs. Tests must be ordered by a licensed health care practitioner.

After a bipolar diagnosis, this patient was prescribed eight different psychotropic medications and received a dozen electroconvulsive treatments.

After six months of support for Hashimoto’s, her symptoms resolved and she is now drug-free, with the exception of thyroid hormone medication. Was her bipolar disorder simply misdiagnosed Hashimoto’s?

I receive many amazing stories from people around the country whose lives were turned around by proper care for their Hashimoto’s. However this story of a young woman who spent most of her thirties on psychotropic drugs and underwent more than a dozen electroconvulsive treatments while under anesthesia really struck a chord. Her story, as told by her naturopath, follows.

Could Hashimoto’s flare-ups have started her down a path of psych meds and electroshock treatments?

“My patient Jeanette, 42, had been diagnosed seven years earlier by her family physician with bipolar disorder. She had manic episodes of staying up late at night, buzzing with energy and working on various projects, and shopping to excess, spending money she and her husband didn’t have. After these energy surges she then would crash and fall into fatigue and depression. A friend suggested she might have bipolar disorder and she brought this up with her family doctor, who prescribed her two psychiatric drugs and referred her to a psychiatrist. However her diagnosis was never re-evaluated and she eventually ended up on eight different medications, including lithium and drugs for depression, anxiety, panic attacks, and insomnia.

During her seven years of treatment she had also been hospitalized six times for complications due to her medications or for manic episodes. During the last hospitalization she had her gallbladder removed and was diagnosed with high blood sugar and Hashimoto’s, an autoimmune thyroid disease, and placed on thyroid hormone medication. Prior to seeing me she received twelve or thirteen electroconvulsive treatments under anesthesia during a six-month period, as prescribed by her psychiatrist.

Uncontrollable tremors and flat affect

When Jeanette came to my office her hands and legs shook uncontrollably, the result of a tremor that had developed recently. She also had a flat affect, meaning she showed no emotion and her overall mood was dull and low. She also said she struggled with extreme fatigue.

Given the precarious nature of her mental health and that fact that she had had so many hospitalizations, I thought it prudent to start very slowly with her case management.

Going gluten-free and dietary changes

Because of her Hashimoto’s diagnosis, the first thing I did was put her on an autoimmune diet and remove gluten from her diet. I also asked her to remove dairy and sugar and add in healthy fats, lots of vegetables, and to eat more frequently to keep her blood sugar stable. I supported her nutritionally with essential fatty acids (including emulsified fish oil), emulsified vitamin D, nutrients for insulin resistance (since her blood sugar was high her last time in the hospital), and gallbladder support to give her the digestive support she needed since her gallbladder had been removed.

Gut detox and adrenal support

Immediately she started to notice improvement in how she felt. After following the diet for several months, I put her on a gut detoxification program with a hypoallergenic detox protein powder. I started her on adrenal adaptogen herbs and nutrients as her salivary adrenal panel showed an increase in cortisol and night. This means she was more awake and night when she should be tired, which indicates a dysfunction in the brain’s sleep-wake cycle. Adrenal adaptogens address this.

Supporting serotonin

I also gave her nutritional compounds to support serotonin activity based on the results of a neurotransmitter assessment. [Note: Serotonin is a brain chemical responsible for feelings of joy and well being. Serotonin activity can become compromised in hypothyroidism.] She also continued to work on stabilizing her blood sugar with a lower-carb diet and by eating regularly to avoid drops in blood sugar.

Dramatic turn around and now med-free

After starting this protocol she felt so much better she decided to stop taking all of her medications, unbeknownst to me. But as it turns out her tremors disappeared completely and she now sleeps great. Whereas before she was emotionless and dull, she is now a bubbly, sweet, and energetic person. Since going off her meds, however, her TSH has slowly climbed and she will begin taking thyroid hormone medication. We will have her progress gingerly with the dosage so as to avoid over stimulating her metabolism.

She currently feels great. In fact, she says she feels “completely normal.” She and her husband rejoiced recently when she became angry and argued with him. For seven years she had been so emotionless she never even got angry, and the return of her anger was a sign of improving health.

We’re not out of the woods yet. Although I do wonder if her bipolar diagnosis wasn’t simply misdiagnosed Hashimoto’s, given how common that is, we remain vigilant of her symptoms and have a holistic psychiatrist on standby.

Nevertheless, I feel fortunate and grateful to have learned this information from Dr. Kharrazian, Otherwise there would be no help for people like Jeanette.”

Padeen Quinn, ND, Portland, Oregon

Why Hashimoto’s is mistaken for bipolar disorder

Could eight medications, six hospitalizations, and a dozen electroconvulsive treatments under anesthesia all have been the result of misdiagnosed Hashimoto’s? If so, how many other people are enduring the same kind of misguided treatment?

It’s possible her bipolar symptoms were symptoms of Hashimoto’s, and unfortunately such a mistake is common today given the medical misunderstanding of Hashimoto’s. When autoimmune Hashimoto’s flares up, the immune system attacks and destroys the thyroid gland. As the thyroid tissue is destroyed, it spills excess thyroid hormone into the bloodstream. This causes symptoms that can easily be confused with the manic episode of bipolar disorder, such as hyperactivity, irritability, and an inability to sleep.

When the immune attack dies down, more thyroid tissue is lost and the person returns to a hypothyroid state that frequently includes depression and fatigue, which can look like the depressive state of bipolar disorder. Also for someone who has gone a period of time without sleeping much and operating on overdrive, a crash it to be expected.

Studies on Hashimoto’s and bipolar

Studies back up the connection between bipolar disorder and thyroid disorders.[1] A 2009 study showed a high rate of Hashimoto’s disease in those with bipolar disorder compared to the control group.[2] Additional studies have shown that outcomes in treatment for bipolar disorder are poor unless a thyroid condition is treated.[3] Bipolar is not only the mental disorder mixed up with Hashimoto’s. Research shows a significant correlation between the presence of thyroid antibodies used to identify Hashimoto’s and mood and anxiety disorders, including depression.[4] Subjects with Hashimoto’s disease show higher frequencies of lifetime depressive episode, generalized anxiety disorders and social phobias.[5] Complicating the issue is the fact that lithium, the drug used to treat bipolar, suppresses thyroid function.

Why serotonin support often helps in hypothyroidism

For Jeanette nutritional compounds to support serotonin activity also appear to have helped her greatly. Serotonin is an important brain chemical, or neurotransmitter, responsible for feelings of well-being and joy. This explains why poor serotonin activity is one of the most common culprits in depression. As it turns out hypothyroidism can decrease serotonin synthesis and the sensitivity of serotonin receptors,[6] giving one of the symptoms of serotonin deficiency.[7] This can manifest as depression, seasonal affective disorder (becoming depressed with lack of light), inner rage, paranoia, and a general loss of pleasure in life. Whenever I get a patient with high TSH and low T4, markers for hypothyroidism, I always assess whether poor serotonin activity is an issue.

Addressing poor serotonin activity is beyond the scope of this article, however it is a topic that will be included in my next book on brain chemistry. In the meantime, please work with your practitioner if you feel you suffer from poor serotonin activity.

After six months of support for Hashimoto’s, her symptoms resolved and she is now drug-free, with the exception of thyroid hormone medication. Was her bipolar disorder simply misdiagnosed Hashimoto’s?

References

[1] Chang KD, Keck PEJR. Differences in thyroid function between bipolar manic and mixed states. Biol Psychiatry. 1998 May 15;43(10):730-3.

[2] Kupka RW, Nolen WA, et al. High rate of autoimmune thyroiditis in bipolar disorder: lack of association with lithium exposure. Biol Psychiatry. 2002 Feb 15;51(4):305-11.

[3] Cole DP, Thase ME, et al. Slower treatment response in bipolar depression predicted by lower pretreatment thyroid function. Am J Psychiatry. 2002 Jan;159(1):116-21.

Frye MA, Denicoff KD, et al. Association Between Lower Serum Free T4 and Greater Mood Instability and Depression in Lithium-Maintained Bipolar Patients. Am J Psychiatry.156:1909-1914, December 1999.

[4] Carta MG, Loviselli A, et al. The link between thyroid autoimmunity (antithyroid peroxidase autoantibodies) with anxiety and mood disorders in the community: a field of interest for public health in the future. BMC Psychiatry. 2004 Aug 18;4:25.

[5] Carta MG, Hardoy MC. A case control study on psychiatric disorders in Hashimoto’s disease and euthyroid goitre: not only depressive but also anxiety disorders are associated with thyroid autoimmunity. Clin Pract Epidemiol Ment Health. 2005 Nov 10;1:23.

[6] Kulikov AV, Zubkov EA. Chronic thyroxine treatment activates the 5-HT2A serotonin receptor in the mouse brain. Neurosci Lett. 2007:416(3):307-309.

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