Functional Medicine Webinar Recording

Thanks to all who joined us in LIVE the Functional Medicine Webinar!

It was a sincere pleasure to share the benefits of functional medicine with you. I hope you found it a useful tool for living a happier and healthier life.

If you missed it, catch the replay below.
https://vimeo.com/279374383

PS: Have you registered for my next webinar? It is called “Don’t Let Adrenal Fatigue Impact Your Life” and it is happening on Friday, July 27th at 10:00 am PDT. Click here to register: http://onnalomd.synduit.com/AFW0001

Why Functional Medicine by Dr. Onna Lo Zoom Webinar from Onna Lo MD on Vimeo.

Why Functional Medicine by Dr. Onna Lo Zoom Webinar from Onna Lo MD on Vimeo.

Guide To Boosting Your Cognitive Health Part 2:  Lifestyle Tips

Last week we shared an article about how to boost your cognitive health using nutrition. Click here to read that post: Guide To Boosting Your Cognitive Health Part 1: Nutrition

Whether you yourself are suffering, your loved one is struggling, or you are an advocate of healthy living- you will want to take note of the tips offered in this guide.

This guide is based on Dr. Bredesen’s #1 Bestseller, The End of Alzheimer’s: The First Program to Prevent and Reverse Cognitive Decline,  His substantial work in the field of reversing cognitive decline is instrumental for anyone suffering from this themselves or supporting a loved one going through this process.  

Here are some great tips that would truly benefit all of us, especially those of you who are trying to find the right protocol to support your brain health.  1) Exercise 

5-6 times per week for 30-60 minutes, raising heart rate and including both cardiovascular and strength training exercises. Exercise increases brain-derived neurotrophic factor (BDNF), which has important anti-Alzheimer’s effects. It also helps to improve oxygenation, improve sleep, reduce overall stress, reduce fat and associated adipokines, improve insulin sensitivity, and improve overall brain and body physiology in numerous ways. Exercise is one of the best ways to prevent cognitive decline, and is an important part of the protocol to reverse cognitive decline.2) Sleep

Sleep has multiple mechanisms to reduce cognitive decline. For example, it induces melatonin, which reduces the amyloid-beta associated with Alzheimer’s disease. Also, it is critical to memory consolidation and it alters cellular anatomy to foster the removal of abnormal and toxic species from the brain. Thus, sleep has multiple mechanisms to support the reversal of cognitive decline.

Most people have a sleep debt, due to chronic lack of optimal sleep, both in quantity and quality. It is crucial to ensure that you do not have sleep apnea. If you do have sleep apnea, it is very important to treat it whether by CPAP, oral device, altering sleeping position, or other methods. Melatonin:

It can be helpful to use melatonin at bedtime. A physiological dose is 0.5mg, which can be taken by mouth or sublingually, depending on formulation. Some take higher doses, up to 20mg, and it is a relatively benign supplement, so you can adjust your dose.

If the dose is too high, you may notice that you awaken after about three hours of heavy sleep, and you may feel sluggish the next morning. If the dose is right, you should notice increased dreaming and awaken feeling refreshed. Melatonin has many effects, among them reducing amyloid-beta, reducing reactive oxygen species, and tumor suppression.

If you find that you are awakening in the middle of the night and ruminating, unable to return to sleep, you may find that Tryptophan (500mg) or 5-hydroxytryptophan (100 mg) helps to prevent this. Please discuss this with your practitioner, especially if you are on an SSRI (selective serotonin reuptake inhibitor) for depression, or a related SNRI (serotonin and norepinephrine reuptake inhibitor).Helpful Sleep Tips:

In order to optimize cognition, try to get as close to 8 hours of sleep each night as possible. It is best to go to bed before midnight, although some people find that their circadian rhythms do not allow this. It is also best to make sure that the room is as dark as possible. Many people like to use an eye mask for this purpose or blackout curtains. In addition, have your bedroom be as quiet as possible and free of EMFs. Lastly, wind down in the evening instead of exercising or working right up until bedtime. 3) Reduce Stress

Stress is one of the most important contributors to cognitive decline, and stress-related molecules such as cortisol and corticotropin releasing factor receptor 1 are mediators of neural cell death and cognitive decline. Therefore, an important part of the overall program is to reduce stress-related effects, and there are many ways to do this, so please choose the ones that you enjoy. Relaxation Ideas:

Some people choose meditation, and indeed meditation has a positive effect on cognition. Others love music, walks in the park, yoga, visiting museums, lovemaking, or many other things (or all of those things). The Neural Agility recording, designed for brain neurophysiology, is “meditation on steroids,” and many enjoy that. This should be done 5 times per week, in the evenings, for 30 minutes, relaxed and lying down with the lights down. Finding joy and relaxation in life is very important to reduce the brain-damaging stress that many of us feel in our busy lives.4) Mental Exercise

There are many ways to do mental exercises. Try Posit, Dakim, Lumosity, learn a new language, do Sudoku, or crossword puzzles, etc. The key is to do these in the presence of improved biochemistry. Do not do these exercises to the point of exhaustion. A typical session is 40-60 minutes for 4 or 5 times each week. If you are new to this habit, it is ok to start with shorter sessions and increase the duration with time. Remember, some mental exercise is better than none at all. Make it a priority to stay mentally active. In essence, you “use it or lose it.”5) Auditory Physiology

This is like “meditation on steroids.” Use with headphones and listen from your phone, iPod or computer in the evening. It is ideal to practice this 5 times per week, for 30 minutes each time. Rest as you lay down on your back in a dark room and relax. These specialized tones can affect the release of powerful brain chemicals that can regulate mood, improve sleep, and reduce aggression as well as depression. Listen here: http://www.fariastechnique.com/music-for-interhemispheric-synchronization  and Dr. Bredesen recommended this program : http://www.activemindsglobal.com/products/revita-mind/

6) Hygiene

Dr. Kenneth Seaton from Australia spent his career studying the relationship between hygiene, inflammation, and cognition. One of the measures he used to gauge inflammation was the albumin-to-globulin (A/G) ratio. Albumin is an important protein to remove amyloid, and to carry many other molecules (including drugs and hormones) in the blood. When inflammation occurs, from bacteria, fungi, viruses, harmful microbes or dietary inflammagens (like trans fats or simple carbohydrates) the globulin fraction (from which antibodies are derived) increases at the expense of the albumin fraction. This reduces the A/G ratio. This is associated with reduced cognition.

Hygiene, and the maintenance of intact barriers (gut lining, blood-brain barrier, oral, nasal, integumentary (skin, nails, hair), etc.), play a key role in optimizing the A/G ratio. Oral hygiene with an electric toothbrush, floss, and a water-pressure flosser are all important. Oral microbes have been identified repeatedly in the brain in Alzheimer’s disease. Some like to use nasal washes, as well. Evaluation for MARCoNS (multiple antibiotic resistant coagulase-negative Staphylococcus) is helpful, especially in anyone with type 3 (toxic) Alzheimer’s disease. Furthermore, ensuring good nail and skin hygiene can be helpful.Your Cognitive Health Is Worth The Investment:

In essence physical and mental exercise, sleep, relaxation, auditory physiology, and hygiene are all important factors to consider when supporting your brain health. All six of these lifestyle tips will help to optimize your physical and mental wellbeing.

Please click here to learn more about Happy Health Institute can guide your health and healing. Happy Health Institute Services: http://onnalomd.com/services/. Furthermore, you can click here to book a free discovery call to gain personalized attention: http://onnalomd.com/contact-us/.

If you missed the post from last week, be sure to click here: Guide To Boosting Your Cognitive Health Part 1: Nutrition.

PS: Join our free Facebook Group here to learn more about cognitive health and more happy healthy tips: https://www.facebook.com/groups/happyhealthcommunity/To learn more on this topic please reference our resources below:

Book: The End of Alzheimer’s: The First Program to Prevent and Reverse Cognitive Decline by Dale Bredesen, MD

Website + Research: https://www.drbredesen.com/thebredesenprotocol

Guide To Boosting Your Cognitive Health Part 1: Nutrition

If you want to improve your brain health, at any age and in any condition, this article is a must-read for you.

This article is perfect for four types of people:

A) You are starting to notice the first signs of cognitive decline:

  • Confusion
  • Poor motor coordination
  • Loss of short-term or long-term memory
  • Identity confusion
  • Impaired judgment

B) You simply want the best brain health your whole life through.

C) You are supporting a loved one who has started to lose optimal brain function.

D) All of the above.

Whether you yourself are suffering, your loved one is struggling, or you are an advocate of healthy living- you will want to take note of the 16 tips offered here in this guide.

This guide is based on Dr. Bredesen’s #1 Bestseller, The End of Alzheimer’s: The First Program to Prevent and Reverse Cognitive Decline. His substantial work in the field of reversing cognitive decline is instrumental for anyone suffering from this themselves or supporting a loved one going through this process.  

These tips would truly benefit all of us, especially those of you who are trying to find the right protocol to support your brain health.  Stay tuned next week too when we share part 2 of this special series!

1. Fast for at least 12 hours between the end of dinner and the beginning of breakfast.

This allows autophagy to occur, which helps your brain to destroy aggregated proteins and other unwanted accumulated molecules. It is best to break the fast with water with some lemon, as a detoxifying drink. Please note: It is best to work with your functional medicine doctor to ensure your blood sugar levels are in a safe proper range for fasting.

2. Fast for at least 3 hours prior to going to bed.

This helps to prevent insulin from inhibiting melatonin and growth hormone, and thus improves sleep and immune function. 

3. It is key to minimize simple carbohydrates

Such as sugar, sweet treats, bread (white and brown), white rice, white potatoes (OK to eat sweet potatoes and other colored potatoes in small quantities), soft drinks (both regular and diet, since diet alter microbiome), alcohol, candy, cakes, processed foods, and anything else with simple carbohydrates. The goal is to change from carbohydrate metabolism to lipid metabolism.

4. Make most of your diet from items that have a glycemic index lower than 35.

For a list of glycemic indices for food, see: https://www.health.harvard.edu/diseases-and-conditions/glycemic-index-and-glycemic-load-for-100-foods

5. Vegetables should be the largest part of the diet

Especially non-starchy ones. Include both uncooked (salads) and cooked. Include as many colors as possible.

6. Avoid fruit juices, but eat fruits 

The whole fruit includes the fiber or have smoothies with fruit, but do not make the smoothies too sweet —best with some vegetables.

7. Avoid gluten and dairy as much as possible.

It is recommended that you get Cyrex Arrays 2, 3, 4 and 20 to help guide you: Array 2 is to determine if you have leaky gut; Array 3 is to determine if you have gluten sensitivity; and Array 20 is to determine whether you have a leaky blood-brain barrier.

8. Reduce blood sugar

You can do this by including fiber, both soluble and insoluble. Try this recipe to make your own almond milk.

9. Reduce toxins

Try this by including cilantro, cruciferous vegetables (e.g., broccoli, cauliflower, brussels sprouts).

10. Include good fats

Such as avocado, nuts, olive oil, seeds, etc.

11. Avoid processed foods and instead eat whole foods.

12. Meat is a condiment, not a main course.

If you eat it, fine, but don’t eat too much (2 or 3 ounces, 1-5 nights per week), and eat pastured chicken or grass-fed beef. Fish is fine if wild caught, best to avoid high-mercury fish such as tuna, swordfish, and shark (fish with large mouths and long lifespans are worst). “SMASH” fish are best (salmon, mackerel, anchovies, sardines, and herring).

13. Emphasize foods with high nutrient density

Such as kale and romaine lettuce. Each day, try to eat at least 3 helpings of:

  • Dark leafy greens, such as kale, collards, spinach, or chard.
  • Colored vegetables or fruits, such as berries, carrots, or beets.
  • Sulfur-rich vegetables, such as cabbage, broccoli, cauliflower, or asparagus.
  • Include aromatic herbs such as cilantro, parsley, basil, or mint.

14. Be aware of the “dirty dozen and clean 15” foods.

The Dirty Dozen are foods highest in pesticides, and therefore important to buy as organic: Click here to learn more: https://www.ewg.org/foodnews/dirty-dozen.php The Clean 15 are foods that are not sprayed as heavily, and therefore relatively safe to buy conventionally (non-organically): Click here to learn more: https://www.ewg.org/foodnews/clean-fifteen.php  See: www.fullyraw.com/dirty-dozen-clean-15

15. For grains, legumes, nuts, and seeds, it is helpful to remove the lectins and phytates

Do this by soaking prior to cooking. https://wholelifestylenutrition.com/health/is-soaking-grains-and-legumes-necessary-and-how-to-properly-soak-and-prepare-them/

16. Incorporate pro-biotics and pre-biotics

Do this after determining that you do not have a leaky gut (Cyrex 2). Pro-biotics help to optimize your microbiome, the bacterial population in your gut. Pro-biotic foods include fermented foods such as sauerkraut, kimchi, kombucha, dairy- free yogurt, tempeh, miso, kefir, and coconut water. Pre-biotics help to support the bacteria of the microbiome. Pre-biotic foods include jicama, chicory, Jerusalem artichoke, and others. 

May this guide to boosting your cognitive health be helpful for you.

There are 16 powerful tips here, and starting with just one will make a difference. If you’d like personal support in this process. Please click here to learn more about Happy Health Institute can guide your health and healing. Happy Health Institute Services: http://onnalomd.com/services/. Furthermore, you can click here to book a free discovery call to gain personalized attention: http://onnalomd.com/contact-us/.

Tune in next week when we share Guide To Boosting Your Cognitive Health Part 2: Lifestyle

PS: Join our free Facebook Group here to learn more about cognitive health and more happy healthy tips: https://www.facebook.com/groups/happyhealthcommunity/Image result for facebook group

RESOURCES:

Book: The End of Alzheimer’s: The First Program to Prevent and Reverse Cognitive Decline

by Dale Bredesen, MD

Image result for end of alzheimer's book

5 Best Tips for a Better Sleep

Here are some tips from Sleep specialist Dr. Mathew Walker, PhD in his book: Why We Sleep: Unlock the power of Sleep and Dreams. 

  1. Maintain regularity
    •  Wake up the same time and go to bed the same time, even on weekends. 
  2. Create darkness around our room
    • We are a darkness deprived society.  We need light and dark cycles to create healthy doses of melatonin – A hormone that helps us initiate sleep.  Dim the lights before bed, stay away from LED screens that emit blue light and fool your brain into thinking it’s daytime still.  Use nightshift on your phone, or blue light blocking glasses. Thick curtains.
  3. Keep it cool!  
    • We often sleep in a room too warm.  Keep a room temperature of 68 degrees fahrenheit,  our brain and body need our core body temp to drop down to initiate sleep.
  4. Avoid alcohol and caffeine – 
    • Alcohol is a class of drug that’s called a sedative, it knocks our brain out and does not bring us into a natural sleep.  It also is potent chemical for blocking dream sleep or REM sleep.  Caffeine is a stimulant as a class of drug, you might be able to fall asleep easily  when you drink it, but the depth of your sleep is not as deep as if you didn’t drink it,  so in the morning, you find your self not refreshed and you wake up needing more coffee.
  5. Do not stay in bed if you are awake 
    •  If you can’t call asleep after 20 minutes or wake up for more than 20 min during the middle of the night, then you might associate your bedroom with the behavior of not sleeping, instead, get up and move to another room, read a book.    An alternative is meditation, which has shown to calm down flight or fight response, and that can also help you fall asleep more easily.

 

12 things that you can do immediately to improve your body’s circadian clock

Alignment is the key to health.  One aspect of many people’s lives that is out of alignment is their sleep and wake patterns.  One of the greatest detriments to a person’s health is a poor rest and recovery routine.  This short video will go over some the of the things that you can do to optimize your natural clock.  By doing so, you will have deeper sleep, wake up more refreshed, have better mid-day energy, better mental clarity, and natural weight loss.

Here are 12 things that you can do immediately to improve your body’s circadian clock.

  1. Wake up and go to sleep at the same time every day.  Ideally, asleep by 10 pm and up around 6 am.
  2. Use a salt lamp in your bedroom as a way to reset your circadian clock.  Turn it on in the morning and after the sun sets at night, candles are also an option.  Avoid full spectrum light after sunset.
  3. Be sure to get mid-day sunlight, this will help increase serotonin (happy) and melatonin (sleep).
  4.  Eliminate exposure to phones, tablets, computers, and television 2 hours before designated bedtime
  5. Sleep in completely dark room, you should not be able to see your hand in front of your face
  6. Avoid excessive fluid intake after 8 pm
  7. Avoid opening the mail or watching the news in the evening
  8. Avoid checking and responding to email in the evening
  9. Settle any conflicts before going to bed
  10. Use lavender essential oils to help promote calm
  11. Practice deep breathing exercises before bed to help you relax, click here for more info
  12. If you use a computer, download f.lux at https://justgetflux.com/ as a digital filter for your screen

Electromagnetic Fields and Radiation: A hidden source of stress on the body

Some of the most overlooked stressors are electromagnetic fields (EMF) radiation and radio frequency radiation. On a daily basis, we are bombarded with radio frequencies and EMFs from televisions, computers, Wi-Fi signals, cellular phones and other electronic devices that we carry around like an extra limb. Even when we are travelling, we are exposed through cars, buses, and airplanes. The frightening aspect of EMF and radio frequency radiation is the fact that it simply has not existed long enough to allow us to know what the long term consequences really are. While the research in this area is still young, EMF radiation has been indicated as possible contributor to multiple types of cancer, Alzheimer’s disease, Parkinson’s disease, headaches, low sperm count, impaired immune function, mood disorders, and sleep disorders to name a few. One thing we do know conclusively is if there is EMF near us, our body is completely exposed. At this point in time, the National Institute of Environmental Health Sciences has identified EMF as a possible carcinogen. More information on EMF can be found at World Health Organization EMF Project (http://www.who.int/peh-emf/project/EMF_Project/en/). 

This image below is a great illustration of the power and frequency of different electromagneticspectrums that we all exposed to (Photo courtesy of: http://www.vortexbioshield.com/assets/images/EM-Spectrum-Colour.jpg)

Hans Selye, considered the father of the concept of stress found that our response to stress typically goes one of two ways. The first step is the alarm stage where we perceive the stressor and our sympathetic nervous system (called the “fight or flight” system) gets activated. This phase can be defined by physiologic processes such as an increase in heart rate, inhibition of digestive function, constriction of blood vessels, dilation of the pupils, and dilation of the blood vessels for muscles. The second step is the resistance phase. This phase is characterized by the body adapting to the stressor and using resources such as the body’s natural coping mechanisms to defend off the stressor and move into the recovery phase. However, prolonged exposure to the stressor can deplete our resources and literally exhaust our body to move it into the second pathway: exhaustion. Selye indicated that this stage alone can be a trigger for a myriad of health conditions such as ulcers, gastrointestinal bleeding, and cardiovascular manifestations. If the stressor persists for long enough, it can ultimately lead to death. Since EMFs are all around us, these are stressors that are always there without our awareness and can be a hidden contributor to several pathologic processes.

One key point to remember is that not all stress is bad stress (“distress”). There is also good stress (“eustress”) which we need to move forward in our life and grow physically, mentally, emotionally and spiritually. Examples of eustress include physical exercise (including sports), getting married, watching a horror movie, going shopping, travelling, and getting a promotion at work. However, for individuals with compromised adrenal function (for more on adrenal fatigue visit our more detailed article), even a positive stressor such as physical exercise may be enough to cause distress. This further highlights the importance of minimizing EMF exposure and actively working to avoid this hidden factor can be vital in achieving optimal long-term health. Below I share 10 not-so-common tips to protect you from EMF that are highly effective and easy to implement:

  1. Turn off your Wi-Fi before you go to sleep. We are exposed to Wi-Fi signals on a daily basis, from coffee shops to malls to our own homes. If it is not a life or death situation, your Wi-Fi should be turned off before bed.
  2. Turn off your cell phone or at least put it into airplane mode. This terminates all signals coming and going from your cell phone and allows you to be protected while you sleep. This action step is extremely important as the vast majority of cell phone owners keep their phone near their bed in case of an emergency call or to use the alarm clock feature.
  3. Ditch the alarm clock, especially if it has a bright backlight so you can see the time all through the night. Not only will it interfere with your sleep by constantly reminding you what time it is, the light itself from the alarm clock will inhibit your ability to get deep and efficient sleep. Sleeping in a pitch-black environment is essential to waking up rested.
  4. Switch out your cordless phones for its predecessor. While this may not be the most convenient step, sticking to a landline phone will help limit your EMF exposure.
  5. Use a wired headset for any cell phone conversations. While you can’t always prepare to have a headset plugged in and ready to go, if you know you have a call to make, use a headset. This is an extremely cheap fix with a huge return on your investment.
  6. Buy EMF filters for all your outlets. These can be found online and are relatively cheap way to prevent your outlets from creating EMF.
  7. Unplug all electronics near your bed such as lamps before going to sleep. If you require a bedside light source, I recommend a Himalayan salt lamp which is a far more natural light to get you ready for bed.
  8. Invest in EMF protective clothing, especially if you are pregnant. You can find everything from hats to underwear and maternity clothing that actually blocks EMF.
  9. Move your furniture away from the wall. Even the wiring in your wall emits EMF and this can be dissipated by simply moving your furniture 3-6 inches from the wall. If you are building a new wall (new project or renovation), putting all your wires in piping can permanently block EMF from being created.
  10. The final step is simply to practice awareness. Be aware of how much you are using your cell phone, how close you’re sitting to the router and how much time you spend surrounded by EMF.

Given the fact that we live in a time where electronics have become a requirement for basic day to day requirements such as lighting and heating our homes, complete avoidance is not the goal and that could create another stressor in itself. By practicing awareness, you are protecting yourself from the unnecessary EMF that is completely avoidable.

Phases of Digestion

Phases of Digestion

Your digestive system will process 170,000 pounds of food over the course of your life.  Your digestive system has more nerve endings than your brain.  These facts are amazing and helps us to realize how critical the digestive system is to human health.  One of the most important functions of your digestive system is to physically and chemically break down food to allow for absorption further down the digestive tract.  What is the point of eating all this healthy food if your body cannot break it down properly to get the nutrients that it needs to benefit you?  We feel the digestive system is one of the most important yet overlooked systems in your body.

A simple way to think about digestion is to equate it to a car wash.  Each phase in the car wash is critical and dependent on the previous phase being completed.  These steps must occur in the right order.  You would never dry the car before it’s been soaped.  So let’s break the digestive process down so that you have a better understanding of how this amazing sequence of events takes place and turns your food into nutrition to fuel your body.
Digestive Health

Phase 1 – Food for Thought

Digestion starts in the brain.  The smell and anticipation of food triggers the brain and digestive system to start releasing enzymes and gastric juices to prepare for the incoming meal.  It is important that you are in a calm and stress-free environment when you eat.  This will keep your body in the “rest and digest” mode.

Phase 2 – Chew Your Food: your stomach does not have teeth!

Mom was right, chewing your food is good for you, but she may not have told you why.  Chewing your food is one of the most critical steps to digestion.  The physical crushing of food in your mouth breaks increases the surface  area of your food and unlocks the nutrients in the food for further digestion in the stomach. bigstock-Assorted-metal-gears-on-white-17158397Chewing your food also stimulates stomach secretions and mixes your saliva with your food to start the breakdown of carbohydrates. This critical step is not reproduced anywhere else and therefore is critical to the process.  If you food is not properly chewed it will disrupt the entire process that follows, there is nothing that can replicate this step for you.

Phase 3 – Stomach

When food enters the stomach, your stomach starts to secrete hydrochloric acid and digestive enzymes that work mainly on breaking down protein.  The hydrochloric acid also sterilizes your food stomach to prevent bugs that may be in your food from entering your bloodstream.

A common reason for heartburn is a lack of stomach acid secretion or dilution of enzymes.  This results from not chewing your food, or drinking lots of water with your food.  Food remains partially digested and starts to rot. This rotten food becomes acidic (lactic acid), which is acidic enough to burn your esophagus, but not acidic enough to digest your food properly. For this reason, in our office, we often prescribe digestive enzymes that actually acidify the stomach contents.

Phase 4 – Pancreas

The next step once the food has been sterilized and acidified is to further break down that food via the release of pancreatic enzymes.  The pancreatic enzymes also alter the pH of the food to make it more alkaline in preparation for entry into the jejunum.

bigstock-Car-wash-35801489

Phase 5 – Gallbladder Secretion

The final major step in digestion takes place once bile is released to emulsify fats.  These fats are chemically broken down by bile so that they can be absorbed.  The gallbladder does not make bile, it stores it.  Bile is made from cholesterol and toxins that are neutralized by the liver.  Bile not only digests fats but it further sterilizes the bowel and promotes regularity.

The physical and chemical breakdown of food is critical to proper digestion and absorption. The problem with undigested food is that it is these food particles can leak into the bloodstream. Then the immune system will recognize that food particle as an invader. This is where lots of food sensitivities come from. This immune response can also increase inflammation and raise blood sugars, causing a system-wide reaction.

Woman choosing between healthy food and caloric food

What can you do to help with proper digestion?

  • Choose the right foods
  • Chew your food thoroughly
  • Don’t drink more than 8 oz. of fluid with meals
  • Eat in a relaxing environment
  • Eat fresh fiber first
  • Eliminate food allergens (get tested)
  • Identify and eliminate any microbes or parasites
  • Get a comprehensive stool test to identify digestive system health

At the Onna Lo MD Clinic we help you get to the underlying cause of your digestive issues, instead of just treating the symptoms.  We help you find out WHY you don’t feel well and what you can do about it.

A Functional Medicine Approach to Adrenal Fatigue

Adrenal fatigue is the common name for a set of symptoms that result from the adrenal glands being worked to exhaustion. For the majority of cases, adrenal fatigue is secondary to some other underlying health issue such as chronic, hidden inflammation.  Stress can come in a variety of forms, but your body’s response is the same.  It can take years for your adrenal glands to fail to meet the demands of your daily life, ultimately resulting in adrenal fatigue.

If you’re suspecting that you have adrenal fatigue.  Ask yourself if you suffer from these adrenal fatigue symptoms;

  • get tired for no reason
  • have trouble getting up in the morning
  • need caffeine or energy drinks to keep goingAdrenal Fatigue
  • crave either salty or sweet snacks
  • either have trouble falling asleep or staying asleep
  • chronic allergies
  • never get sick
  • get sick often
  • poor memory
  • poor concentration
  • depression
  • menstrual cycle irregularities
  • chronic pain
  • slow healing from injuries
  • bruise easily
  • inability to handle stress

If you answered yes to any of these questions then consider adrenal fatigue.

The Anatomy of Adrenal Fatigue

The adrenals are two small glands, each about the size of an almond, that are located above the kidneys. The adrenals have one of the highest rates of blood flow per gram of tissue, and the highest content of vitamin C per gram of any tissue in the body. Each adrenal gland is composed of two separate functional entities. The outer zone, or cortex, accounts for 80% to 90% of the gland and secretes adrenal steroids (cortisol, DHEA-S, aldosterone and small amounts of sex hormones). The inner zone, or medulla, comprises 10% to 20% of the gland and secretes the catecholamines (adrenaline and nor-adrenaline). Cortisol, DHEA, and adrenaline are the three main adrenal stress hormones. These hormones help you to buffer stress and adapt to everyday life demands. We’d love to talk to you about natural adrenal supplements.

Under stress, healthy adrenals increase their output of cortisol and DHEA to enable you to preserve health. They also secrete adrenaline, giving you a boost of energy when needed (ie mother lifting car off of a baby). If this becomes chronic, the adrenals can no longer keep up with the demand, and DHEA levels begin to fall, signifying adrenal fatigue.  In addition, the over-secretion of adrenaline can cause you to feel anxious and nervous.  Complaints of insomnia, fatigue, depression, irritability, and digestive difficulties are also common.  As adrenaline surges during stress, digestive enzymes are simultaneously lowered, and blood sugar levels rise.  As this becomes a more chronic occurrence, the results of high cortisol and adrenaline levels from prolonged stress wreak havoc on the body. Essentially under stress all systems that are required for rest, repair, and digestion shut down.

“Adrenal fatigue is the end-stage of a poorly adapted stress response that can take years to break down.”

Below are areas of the body that are negatively impacted by adrenal exhaustion and the chronic stress response that causes it.

Energy Production

Abnormal adrenal function can alter the ability of cells to produce energy for the activities of daily life. People who have a hard time rising in the morning, or who suffer from low energy throughout the day, often have abnormal adrenal rhythms, adrenal fatigue, and poor blood sugar regulation. The maintenance of a stable blood sugar level depends on food choice, lifestyle, adrenal function, and insulin activity.

Muscle and Joint Function

Abnormal adrenal rhythms are known to compromise tissue healing. Reduced tissue repair and increased tissue breakdown can lead to muscle and joint wasting with chronic pain.

Bone Health

The adrenal rhythm determines how well we build bone. If the night and morning cortisol levels are elevated, our bones do not rebuild well, and we are more prone to osteoporosis. Stress is the enemy of the bones. In postmenopausal women, the effect of stress worsens due to female hormone imbalances.

Immune Health

Various immune cells (white blood cells) cycle in and out of the spleen and bone marrow. The immune system trafficking follows the cortisol cycle. If the cycle is disrupted, especially at night, then the immune system is adversely affected. Short- and long-term stress is known to suppress the immune response in the lungs, throat, urinary tract and intestines. With reduction in the surface antibody (called secretory IgA), the resistance to infection is reduced and allergic reactions increase.

Sleep QualityAdrenal fatigue

In sleep-deprived individuals, the mean cortisol levels are elevated, and the quiescent period is shorter. Evening cortisol level is increased in patients with insomnia, affecting the first part of the nocturnal sleep period, increasing risk for depression. Chronic lack of REM sleep can reduce a person’s mental vitality, vigor and induce depression.

Fertility

Couples with high level of stress markers are less likely to succeed in conceiving. Stress alters the brain signals that trigger the ovaries to release eggs each month, so women under non-stop stress ovulate fewer eggs than less stressed women. Stress can also affect testosterone level and sperm production in men. Helping couples to de-stress while trying to conceive can impact their success rate.

Skin Regeneration

Human skin regenerates mostly at night. With higher night cortisol values, less skin regeneration takes place. Thus normal cortisol rhythm is essential for optimal skin health.

Thyroid Function

The level of cortisol at the cellular level controls thyroid hormone production. Often, hypothyroid symptoms such as fatigue and low body temperature are due to a stress or adrenal fatigue.  Chronic stress will convert thyroid hormone to it’s inactive form (reverse T3) and shuts down the production of TSH.

Gluten Sensitivity and Stress Response

Approximately 12-18% of the U.S. population suffers from a genetic intolerance to grains, such as wheat, rye or barley contained in cereals, breads and pasta. A high incidence occurs in people with Celtic, Nordic, non-Caucasian and Mediterranean ethnicity. The gut becomes inflamed within 30 minutes after consuming grains, and this can lead to an adrenal stress response, increased cortisol and reduced DHEA.

Diabetes - BrainMemory

Sustained stress adversely affects brain function and memory processing. Too much cortisol interferes with the functioning chemicals the brain uses for its cellular intercommunication as well as decrease the function of the hippocampus, which is the part of your brain that forms memories. Chronic long term stress, with increased cortisol level at night, makes it perplexing to think, organize, and store new memories or retrieve long-term ones.

Chronic Fatigue Syndrome (CFS)

A common adrenal fatigue issue in CFS is impaired corticotrophin release.  As a result, low cortisol and eventual adrenal atrophy may be observed.  Simultaneous use of several therapies can help improve the debilitating effects of CFS.

Glycemic Dysregulation

Chronic low blood sugars can impair normal adrenal function by repetitive over-stimulation of cortisol production. Recurring exposure to high cortisol will impair insulin activity, and invariably lead to insulin resistance and beta-cell exhaustion (diabetes).

Allergies/Autoimmune Disorders

More than fifty years ago, Dr. W. Jefferies (author of Safe Uses of Cortisol) discovered that patients with environmentally triggered allergies and autoimmune diseases dramatically benefited when given cortisol for other purposes. More recently, German researchers reported that disruption of the adrenal axis and cytokine relationships lead to predisposition and aggravation of autoimmune diseases.

Depression/ADD

Several recent publications report a hyperactive HPA axis in depressed patients. Elevated midnight salivary cortisol is now considered one of the best tests in diagnosing endogenous depression. Other anomalies in cortisol rhythm usually accompany the midnight elevation. On the other hand, cortisol elevations and rhythm disruptions throughout the day are typical of attention deficit disorders (ADD).

 

Our Clinic’s Approach to Adrenal Fatigue

As you can see, a chronic stress response that eventually develops into adrenal fatigue has a negative impact on virtually every aspect of health. Stress is reaching an epidemic proportion due to our fast-paced lifestyle and is at the heart of virtually all chronic disease.  As mentioned earlier, adrenal fatigue is secondary to a chronic stress stimulus. These stressors can be in the form of:

  • Dysbiosis (bacterial imbalance in the gut)
  • Food Sensitivities
  • Chemical Sensitivities
  • Chronic Pain
  • Blood Sugar issues such as reactive hypoglycemia and diabetes
  • Environmental factors such as quality of air, food, and water, as well as toxin exposure
  • Fast-paced lifestyle
  • Poor relationships

As Functional Medicine Providers, it is our job to dig through the dirt to find the underlying cause of your stress response gone awry.  Not only do we tell you WHY you don’t feel well, but teach you what YOU can do about it.  Let us help you develop a strategy to conquer adrenal fatigue and restore your vitality and quality of life.

Let us help navigate you towards better health!

Gluten Sensitivity

It is almost impossible to discuss health and nutrition these days without discussing the topic of gluten with our patients. Are food companies merely taking advantage of vulnerable consumers looking for the latest fad or is there merit to “going gluten-free”? With all the questions that we get surrounding gluten, we at the Living Proof Institute think that it is necessary to set the record straight. By now, many of you have certainly heard of celebrities following a gluten free diet, or have heard of someone’s health turning around as a result of gluten elimination. This report will give you a deeper understanding of what gluten is, where it is found, and the implications to your health.

The Gluten Free Industry

In the last few years, sales of gluten-free food has grown 27% and is estimated at being a $4.2 billion market in 2012. To say this is an exploding market is an understatement. Many foods have always been gluten free, but are now being labelled as such. Gluten free foods include nuts, seeds, dairy, meats, eggs, vegetables, fruits and several grains. To be considered Gluten-free typically means that a food must be processed in a separate plant that is certified Gluten-free. Technically, gluten-free means that a food has less than 30 parts per million (ppm) of gluten. Those with Celiac disease and severe reactivities to gluten can react at 3 ppm. Often the certification process is what accounts for the increased cost of gluten free foods. Also keep in mind that wheat is heavily subsidized unlike other gluten-free grains such as amaranth.

As consumer demand grows there will be more and more gluten-free products coming to the market. Our position on these foods is to consume them in extreme moderation. Replacing one grain with another will still have a negative impact on blood sugar, insulin and weight. Gluten free items should be used as a last solution, not a staple in your diet. You can find hundreds of recipes that are all gluten free at www.drpatelsdiet.com

What is Gluten?

Gluten is a protein molecule found in wheat, barley, rye, spelt, kamut, and 98% of oats (due to cross-contamination). Gluten literally means “glue”. Gluten is what gives bread its elasticity and texture. Modern wheat has been cultivated to contain higher amounts of gluten. This is great for manufacturers, at the price of your health. Until recently, there was no genetically modified (GM) wheat on the market. GM wheat was modified to “turn off” the gene that is responsible for the immune system response in a person with Celiac’s Disease. The problem with this is that that particular gene is also responsible for expressing other genetic traits. So the effects on a genetic level are unknown. Some animals that have consumed GM wheat have been reported to develop liver failure.

Hidden Sources of Gluten

Some hidden or unknown sources of gluten are soy sauce, food starches, food emulsifiers, food stabilizers, artificial food coloring, malt extract, beer, some red wines, seasonings and sauces. When in doubt, call the manufacturer or look for the gluten free label. Products that are manufactured in a plant that processes gluten may also be contaminated due to shared equipment.

Gluten Sensitivity and Chronic Illness

It is estimated that there are at at least 18 million Americans that have a gluten sensitivity. We feel that number is grossly underestimated, but it is difficult to estimate the breadth of the problem since many people are misdiagnosed and never receive the right treatment.

Celiac’s disease gets the lions share of attention when talking about gluten, we will discuss the many spin-off conditions that arise from gluten exposure later. To date, research indicates that over 200 diseases are associated with gluten sensitivity. These can range from seizures to skin conditions. The list would surprise you.

What is Gluten Sensitivity?

Gluten sensitivity can often be challenging for an untrained practitioner to identify. A sensitivity can cause subtle to severe symptoms depending on the patient. Another unfortunate fact regarding sensitivities is that they often occur outside of the digestive system, such as, joints, skin and nervous system. These reactions may also be delayed (30 minutes – 4 days), making it challenging for one to recognize gluten as the offending agent.

Once ingested the gluten molecule is particularly difficult for your body to digest. This undigested gluten can wreak havoc on the immune system all the way from the mouth to the anus. When ingested, anti-bodies to gluten are produced and gluten is “tagged” by the immune system as a foreign invader. This type of subtle and delayed reaction is known as an IGG response, much different than a IGE response often associated with foods like peanuts.

My Parents ate wheat and They seemed Fine

We have been eating wheat for generations, but not the commercial wheat that is grown today. By modifying wheat to contain more gluten than it originally did, the agriculture business has vastly increased our exposure. Also, the wheat a person eats today goes through a process called de-amidation, which your immune system happens to not like and it causes more of an immune reaction. The Standard American Diet (SAD) has very little nutritional value and our society is much more stressful, which contributes to the breakdown of our immune tolerance for substances like gluten. Lastly, without proper nutrition, our bodies have a tendency to make less of the enzymes required to digest and break down gluten particles. Chronic exposure combined with a compromised nutritional status and immune health seem the be the perfect storm for chronic illness related to gluten.

My doctor told me I Do Not Have Celiac Disease

As mentioned earlier, when a person hears the word gluten it is synonymous with Celiac’s Disease. However, the research clearly states that gluten sensitivity being regarded principally as a disease of the small bowel is a historical misconception. The research also demonstrates that for every gluten sensitive patient with symptoms of an enteropathy (Classic Celiac Disease), there are 8 people with no GI symptoms!

Thinking beyond the Gut

Other organs and areas that have been demonstrated to be involved in gluten sensitivity are the joints (Rheumatoid Arthritis and Ankylosing Spondylitis), the heart, thyroid, bone, and most notably the brain, cerebellum, and neuronal synapsins (think Multiple Sclerosis and Cerebellar Ataxia). There is a connection with gluten sensitivity and type 1 diabetes, osteoporosis, Addison’s disease, and ADHD. Gluten sensitivity has also been demonstrated to play a critical role in infertility and stillbirths. Lastly, people with a gluten sensitivity are 10 times more likely to develop an autoimmune disease. As you can see, the notion that gluten only affects the small bowel is archaic to say the least, it is time for a radical paradigm shift.

Gluten Sensitivity and Autism

80% of children diagnosed with autism not only produce antibodies to gluten, they also produce antibodies to their brain. This is a mind blowing number of children that are being mismanaged, misdiagnosed, and mistreated. How can a solution so simple, so effective and so cheap be ignored? At The Living Proof Institute going gluten free is our first line of therapy for our autistic patients.

Why has my doctor Never Mentioned Gluten Sensitivity? What shall I do?

The answer is easy, most clinicians are not trained to look at a gluten sensitivity when areas other than the GI tract are affected. Also, when most clinicians run an antibody test they are only looking for the alpha-gliadin marker. The problem with that is that only around 50% of celiac patients have antibodies to the alpha-gliadin portion of wheat, the other half are sensitive to a different portion.

What type of testing is best for Gluten Sensitivity?

The blood test that we recommend looks at 12 different peptides of gluten. Luckily, there is testing out there that is not only more accurate than the traditional blood test, but also easier to administer because it is done through saliva. This can be an excellent screen for people suspecting gluten sensitivity.

Despite advanced testing, it should be noted that the gold standard for any type of allergy or sensitivity is complete elimination for up to 6 months.

When going Gluten-free goes wrong

In rare instances patients may report that their symptoms worsen when going on a gluten free diet. There are three possible explanation for this. Firstly, gluten binds to opioid receptors in the brain and literally acts like a drug. Similar to coming off of any addictive substance there will be a withdrawal period. This may last a few days.

Secondly, around 36% of people that go gluten free are still getting accidental exposure. This exposure may be from cross contamination, poor technique at restaurants, lack of due diligence and the occasional ingestion such as at birthdays and celebrations.

Lastly, when people go gluten-free, they usually start ingesting other grains in place of gluten. In some cases, this may initiate an immune response very similar to eating gluten. This is a notion called cross-reactivity. Cross-reactivity is the ability of an antibody to bind with similar-looking parts on different proteins called epitopes. This phenomenon is also known as molecular mimicry. Up to 82% of gluten sensitive patients have antibodies to other foods including rice, milk, beef, sheep, and eggs. Other studies have identified cross-reactivity with chocolate, sesame, hemp, rye, kamut, buckwheat, sorghum, millet, spelt, amaranth, quinoa, yeast, tapioca, oats, coffee, corn, and potatoes. As you can see, a lot of the foods that people use to replace gluten in their diet are on this list. Luckily, there is a test that we recommend that looks at these cross-reactivities as well as other common food sensitivities in those that are unresponsive to gluten elimination.

Our Approach to Gluten Sensitivity

In the face of so much research and empirical data it is difficult to ignore the elephant in the room. Going gluten free can be an extremely easy dietary change with the right guidance and by taking small efforts to read food labels more closely. When in doubt stick to a whole food diet that excludes processed and packaged foods. Refer to our recipe website for food options if you have a gluten sensitivity.

By listening to your unique story, we help you uncover why you don’t fell well and what you can do about it. Call us today to schedule a personal health consultation.

References:

  1. Vojdani A, O’Bryan T, Green J, McCandless J, Woeller K, Vojdani E, Nourian E, Cooper E, Immune Response to Dietary Proteins, Gliadin and Cerebellar Peptides in Children with Autism, Nutritional Neuroscience, Volume 7 Number 3 (June 2004), pp. 151–161.
  2. Marks J, Shuster S, Watson AJ. Small bowel changes in dermatitis herpetiformis. Lancet 1966; 2:1280- 1282.
  3. Cooke WT, Thomas-Smith W. Neurological disorders associated with adult celiac disease. Brain 1966; 89:683-722.
  4. Hvatut M, Kanerud L, Hällgren R, Brandtzaeg P. The gut-joint axis: cross-reactive food antibodies in rheumatoid arthritis. Gut 2006; 55:1240-1247.
  5. Kjeldsen-Kragh J, Hvatum M, Haugen M, Forre O, Scott H. Antibodies against dietary antigens in rheumatoid arthritis patients treated with fasting and a one-year vegetarian diet. Clin Exp Rheumatol 1995; 13:167-172.
  6. Koot VC, Van Straaten M, Hekkens WT, Collee G, Dijkmans BA. Elevated level of IgA gliadin antibodies in patients with rheumatoid arthritis. Clin Exp Rheumatol 1989; 7:623-626.
  7. O’Farelly C, Marten D, Melcher D, McDougall B, Price R, Goldstein AJ, Sherwood R, Fernandes L.A. VOJDANI ET AL.Association between villous atrophy in rheumatoid arthritis and a rheumatoid factor and gliadin-specific IgG. Lancet 1988; 2:819-822.
  8. Quan CP, Berneman A, Pires R, Avrameas S, Bouvet JP. Natural polyreactive secretory immunoglobulin A autoantibodies as a possible barrier to infection in humans. Infect Immun 1997; 65:3997-4004.
  9. Frustaci A, Cuoco L, Chimenti C, Pieroni M, Fioravanti G, Gentiloni N, Maseri A, Gasbarrini G. Celiac disease associated with autoimmune myocarditis. Circulation 2002; 105:2611-1618.
  10. Chimenti C, Pieroni M, Frustac IA. Celiac disease in idiopathic dilated cardiomyopathy. Ital Heart J 2001; 2:658-659.
  11. Counsell CE, Taha A, Ruddell WS. Coeliac disease and autoimmune thyroid disease. Gut 1994; 35:844- 846.
  12. Natter S, Granditsch G, Reichel GL, Baghestanian M, Valent P, Elfman L, Gronlund H, Kraft D, Valenta R. IgA cross-reactivity between a nuclear autoantigen and wheat proteins suggests molecular mimicry as a possible pathomechanism in celiac disease. Eur J Immunol 2001; 31:918-928.
  13. Pedeira S, Vazquez H, Sugai E, Niveloni S, Smecuol E, Mazure R, Flores D, Maurino E, Bai JC. Clinical significance of anti-smooth muscle antibody (SMA) fluorescence in patients with celiac disease. Gastroenterol 2000; 118:A363.
  14. Sugai E, Cherñavsky A, Pedreira S, Smecuol E, Vazquez H, Niveloni S, Mazure R, Mauriño E, Rabinovich GA, Bai JC. Bone-specific antibodies in sera from patients with celiac disease: characterization and implications in osteoporosis. J Clin Immunol 2002; 22:353-362.
  15. Vazquez H, Mazure R, Gonzalez D, Flores D, Pedreira S, Niveloni S, Smecuol E, Mauriño E, Bai JC. Risk of fractures in celiac disease patients: A cross-sectional, case-control study. Am J Gastroentero1 2000; 95:183-189.
  16. Pratesi R, Gandolfi L, Friedman H, Farage L, De Castro CAM, Catassi C. Serum IgA antibodies from patients with coeliac disease react strongly with human brain blood-vessel structures. Scand J Gastroenterol 1998; 33:817- 821.
  17. Volta U, De Giorgio R, Petrolini N, Stangbellini V, Barbara G, Granito A, De Ponti F, Corinaldesi R, Bianchi FB. Clinical findings and anti-neuronal antibodies in celiac disease with neurological disorders. Scand J Gastroenterol 2002; 137: 1276- 1281.
  18. Hadjivassiliou M, Grünewald R, Sharrack B, Sanders D, Lobo A, Williamson C, Woodroofe N, Wood N, Davies-Jones A. Gluten ataxia in perspective: epidemiology, genetic susceptibility and clinical characteristics. Brain 2003; 126:685-691.
  19. Abele M, Schöls L, Schwartz S, Klockgether T. Prevalence of antigliadin antibodies in ataxia patients. Neurology 2003; 60:1674-1675.
  20. Hadjivassiliou M, Boscolo S, Davies-Jones GA, Grünewald RA, Not T, Sanders DS, Simpson JE, Tongiorgi E, Williamson CA, Woodroofe NM. The humoral response in the pathogenesis of gluten ataxia. Neurology 2002; 58:1221-1226.
  21. Hadjivassiliou M, Davies-Jones GAB, Sanders DS, Grünewald RA. Dietary treatment of gluten ataxia. J Neurol Neurosurg Psychiatry 2003; 74:1221-1224.
  22. Vojdani A, O’Bryan T, Green JA, McCandless J, Woeller KN, Vojdani E, Nourian AA, Cooper EL. Immune response to dietary proteins, gliadin and cerebellar peptides in children with autism. Nutritional Neurosciences 2004; 7(3):151-161.
  23. Alaedini A, Okamoto H, Briani C, Wollenberg K, Shill HA, Bushara KO, Sander HW, Green PH, Hallett M, Latov N. Immune cross-reactivity in celiac disease: anti-gliadin antibodies bind to neuronal synapsin I. J Immunol 2007; 178:6590- 6595.
  24. Green PH, Alaedini A, Sander HW, Brannagan TH III, Latov N, Chin RL. Mechanisms underlying celiac disease and its neurologic manifestations. Cell Mol Life Sci 2005; 62:191-199.
  25. Hilfiker S, Benfenati F, Doussau F, Nairn AC, Czernik AJ, Augustine GJ, Greengard P. Structural domains involved in the regulation of transmitter release by synapsins. J Neurosci 2005; 25:2658- 2669.
  26. Sommer C, Weishaupt A, Brinkhoff J, Biko L, Wessig C, Gold R, Toyka KV. Paraneoplastic stiff- person syndrome: passive transfer to rats by means of IgG antibodies to amphiphysin. Lancet 2005; 365: 1406-1411.
  27. Takenoshita HM, Shizuka-Ikeda M, Mitoma H, SongS-Y, Harigaya Y, Igeta Y, Yaguchi M, Ishida K, Shoji M, Tanaka M, Mizusawa H, Okamoto K. Presynaptic inhibition of cerebellar GABAergic transmission by glutamate decarboxylase autoantibodies in progressive cerebellar ataxia. J Neural Neurosurg Psychiatry 2001; 70:386-389.
  28. Zelnick N, Pacht A, Obeid R, Lerner A. Range of neurologic disorders in patients with celiac disease. Pediatr 2004; 113:1672-1676.
  29. Hadjivassiliou M, Williamson CA, Woodroofe N. The immunology of gluten sensitivity beyond the gut. Trends Immunol 2004; 25:578-582.
  30. Kumar V, Rajadhyaksha M, Wortsman J. Celiac disease associated autoimmune endocrinopathies. Clin Diag Lab Immunol 2001; 8:678-685.
  31. Funda DP, Kaas A, Bock T, Tlaskalová-Hogenová H, Buschard K. Gluten-free diet prevents diabetes in NOD mice. Diabetes Metab Res Rev 1999; 15:323-327.
  32. Westman E, Ambler GR, Royle M, Peat J, Chan A. Children with coeliac disease and insulin-dependent diabetes mellitus-growth, diabetes control dietary intake. J Pediatr Endocrinol Metab 1999; 12:433-37.
  33. Cronin CC, Shanahan F. Insulin-dependent diabetes
mellitus and coeliac disease. Lancet 1997; 349:1096- 442.
  34. Lorini R, Scotta MS, Cortona L, Avanzini MA, Vitali 
L, De Giacomo C, Scaramuzza A, Severi F. Celiac disease and type I (insulin-dependent) diabetes mellitus in childhood: follow-up study. J Diabetes Complications 1996; 10:154-159.
  35. Velluzzi F, Caradonna A, Boy MF, Mossa P, Corda G, Pinna MA, Cabula R, Lai MA, Piras E, Atzeni F, Loviselli A, Usai P, Mariotti S. Thyroid and celiac disease: clinical, serologic and echographic study. Am J Gastroenterol 1998; 93:976-979.
  36. Sategna-Guidetti C, Bruno M, Mazza E, Carlino A, Predebon S, Tagliabue M, Brossa C. Autoimmune thyroid disease and coeliac disease. Eur J Gastroenterol Hepatol 1998; 10:927-931.
  37. Venture A, Neri E, Ughi C, Leopaldi A, Citta A, Not T. Gluten-dependent diabetes-related and thyroid- related antibodies in patients with celiac disease. J Pediatr 2000; 137:263-265.
  38. Valentino R, Savastano S, Tommaselli AP, Dorato M, Scarpitta MT, Gigante M, Lombardi G, Troncone R. Unusual association of thyroiditis, Addison’s disease, ovarian failure and celiac disease in a young woman. J Endocrinol Investig 1999; 22:390-394.
  39. Selby P. Bone loss in celiac disease is related to secondary hyperparathyroidism. J Bone Mineral Res 1999; 14:652-657.
  40. Iafusco D, Rea F, Chiarelli F, Mohn A, Prisco F. Effect of gluten-free diet on the metabolic control of type I diabetes in patients with diabetes and celiac disease. Diabetes Care 2000; 23:712-713.
  41. Hadjavassilios, M., Gluten Sensitivity as a Neurological illness, J Neurol Neurosurg Psychiatry 2002;72:560–563.
  42. van Heel D., West J, Recent Advances in Coeliac Disease, Gut 2006;55:1037–1046.
  43. Fasano A, Catassi C., Current Approaches to Diagnosis and Treatment of Celiac Disease: An Evolving Spectrum Gastroenterology 2001;120:636-651.
  44. Goddard CJ., Gillett H R., Complications of coeliac disease: are all patients at risk? Postgrad. Med. J. 2006;82;705-712.
  45. Green PHR, Stavropoulos SN, Panagi SG, et al. Characteristics of adult celiac disease in the USA: results of a national survey. Am J Gasroenterol 2001;96:126–31.
  46. Olesen M, Eriksson S, Bohr J, Jarnerot G, Tysk C. Microscopic colitis: a common diarrhoeal disease. An epidemiological study in Orebro, Sweden, 1993-1998. Gut, 2004; 53:346-350.
  47. Gillet HR, Freeman HJ. Prevalence of celiac disease in collagenous and lymphocytic colitis. Can J Gastroenterol, 2000; 14: 919-921.
  48. Koskela RM, Niemelä SE, Karttunen TJ, Lehtola JK. Clinical characteristics of collagenous and lymphocytic colitis. Scand J Gastroenterol, 2004;39: 837-845.
  49. Corrao G, Corrazza GR, Bagnardi V, et al. Mortality in patients with coeliac disease and their relatives: a cohort study. Lancet 2001;358:356–61.
  50. Hill I Salem W, Dirks M, Liptak G, Colletti R , Fasano A, Guandalini S, Hoffenberg E, Horvath K, Murray J, Pivor M, Salem W, Seidman E, Guideline for the Diagnosis and Treatment of Celiac Disease in Children: Recommendations of the North American Society for Pediatric Gastroenterology, Hepatology and Nutrition, J Pediatr Gastroenterol Nutr, Vol. 40, No. 1, January 2005.
  51. Hadjavassilios, M, Gluten Sensitivity: from Gut to Brain. Lancet Neurol 2010; 9: 318–30.
  52. Fasano, A, Celiac Disease-How to handle a Clinical Chameleon, NEJM 348;25 June 19,2003.
  53. Arnson Y, Amital H, and Shoenfeld Y, Vitamin D and autoimmunity: new aetiological and therapeutic considerations, J of Immunology, 2005, 175: 4119–4126.
  54. Alaedini A, Okamoto H, Briani, C, Wollenberg K, Shill H, Bushara K, Sander H, Green P, Hallett M, Latov N, Immune Cross-Reactivity in Celiac Disease: Anti-Gliadin Antibodies Bind to Neuronal Synapsin I, The Journal of Immunology, 2007, 178: 6590– 6595.
  55. Bland J., Understanding the Origins and Applying Advanced Nutritional Strategies for Autoimmune Disease, Metagenics Seminar Series, 2006.
  56. Green P, Alaedini A, Sander HW, Brannagan III TH, Latov N, Chin R, Mechanisms underlying celiac disease and its Neurologic Manifestations Cell. Mol. Life Sci. 62 (2005) 791–799.
  57. Marietta E, Black K, Camilleri M, Krause P, Rogers RS 3rd, David C, Pittelkow MR, Murray JA., A new model for dermatitis herpetiformis that uses HLA-DQ8 transgenic NOD mice, J Clin Invest. 2004 Oct;114(8):1090-7.
  58. Lindqvist U, Rudsander A, Boström A, Nilsson B, Michaëlsson G., IgA antibodies to gliadin and coeliac disease in psoriatic arthritis, Rheumatology (Oxford). 2002 Jan;41(1):31-7.
  59. Humbert P, Pelletier F, Dreno B, Puzenat E, Aubin F, Gluten intolerance and skin diseases, Eur J Dermatol 2006; 16 (1): 4-11.
  60. Selva-O’Callaghan A, Casellas F, de Torres I, Palou E, Grau-Junyent JM, Vilardell- Tarrés M., CELIAC DISEASE AND ANTIBODIES ASSOCIATED WITH CELIAC DISEASE IN PATIENTS WITH INFLAMMATORY MYOPATHY, Muscle Nerve. 2007 Jan;35(1):49-54.
  61. Hadjivassiliou M, Grünewald R, Sharrack B, Sanders D, Lobo A, Williamson C, Woodroofe N, Wood N, Davies-Jones A., Gluten ataxia in perspective: epidemiology, genetic susceptibility and clinical characteristics, Brain. 2003 Mar;126(Pt 3):685-91.
  62. Hadjivassiliou M, Aeschlimann D, Grünewald RA, Sanders DS, Sharrack B, Woodroofe N, GAD antibody-associated neurological illness and its relationship to gluten sensitivity, Acta Neurol Scand. 2010 Apr 15.
  63. Eaton W, Mortensen PB, Agerbo E, Byrne M, Mors O, Ewald H., Coeliac disease and schizophrenia: population based case control study with linkage of Danish national registers, BMJ. 2004 Feb 21;328(7437):438-9.
  64. Hadjivassiliou M, Grünewald RA, Chattopadhyay AK, Davies-Jones GAB, Gibson A, Jarratt JA, et al. Clinical, radiological, neurophysiological and neuropathological characteristics of gluten ataxia. Lancet 1998;352:1582-5.
  65. J Neurol Neurosurg Psychiatry. 2006 Nov;77(11):1262-6., Hadjivassiliou M, Grünewald RA, Kandler RH, Chattopadhyay AK, Jarratt JA, Sanders DS, Sharrack B, Wharton SB, Davies-Jones GA, Neuropathy associated with gluten sensitivity.
  66. Gluten sensitivity: from gut to brain., Hadjivassiliou M, Sanders DS, Grünewald RA, Woodroofe N, Boscolo S, Aeschlimann D, Lancet Neurol. 2010 Mar;9(3):318-30.
  67. Hopper A., et.al., Pre-endoscopy serological testing for coeliac disease:evaluation of a clinical decision tool, BMJ. 2007 Apr 7;334(7596):729.
  68. Hill ID., What are the sensitivity and specificity of serologic tests for celiac disease? Do sensitivity and specificity vary in different populations? Gastroenterology. 2005 Apr;128(4 Suppl 1):S25-32.
  69. Memeo L, Jhang J, Hibshoosh H, Green PH, Rotterdam H, Bhagat G., Duodenal intraepithelial lymphocytosis with normal villous architecture: common occurrence in H. pylori gastritis, Mod Pathol. 2005 Aug;18(8):1134-44.
  70. Abrams JA, Diamond B, Rotterdam H, Green PH. Seronegative celiac disease: increased prevalence with lesser degrees of villous atrophy, Dig Dis Sci. 2004 Apr;49(4):546-50.
  71. Tursi A., Seronegative Coeliac Disease: a Clinical Challenge. BMJ 26 April, 2005.
  72. Rostami, K., Unforgiving Master of Non-Specificity and Disguise, BMJ 27, April 2005.
  73. Lebwold, Green P., Screening for Celiac Disease. N Engl J Med Oct.23 2003,1673-4.
  74. Freeman HJ., Pearls and pitfalls in the diagnosis of adult celiac disease. Can J Gastroenterol 2008;22(3):273-280.
  75. Bonamico M., Serologic and Genetic Markers of Celiac Disease: A Sequential Study in the Screening of First Degree Relatives, Journal of Pediatric Gastroenterology and Nutrition 42:150–154.
  76. Fasano A., Catassi C., Current Approaches to Diagnosis and Treatment of Celiac Disease: An Evolving Spectrum, GASTROENTEROLOGY 2001;120:636–651.
  77. Hadjavassiliou M., Grunewald R., The Neurology of Gluten Sensitivity:Science vs. Conviction Practical Neurology, 2004, 4, 124–126.
  78. Camarca, A., et.al., Intestinal T Cell Responses to Gluten Peptides Are Largely Heterogeneous: Implications for a Peptide-Based Therapy in Celiac Disease, J. Immunol. 2009;182;4158-4166.
  79. Meresse B., , Ripoche J., Heyman M., Cerf-Bensussan N., Celiac disease: from oral tolerance to intestinal inflammation, autoimmunity and lymphomagenesis, Nature Vol 2 No 1, JANUARY 2009.
  80. Bethune M.,Parallels Between Pathogens and Gluten Peptides in Celiac Sprue, Plos Pathogens Feb 2008 Vol 4: 2;e34.
  81. Ehrhardt G., et.al. Discriminating gene expression profiles of memory B cell subpopulations JEM VOL. 205, August 4, 2008.
  82. Martucci S., Corazza G., Spreading and Focusing of Gluten Epitopes in Celiac Disease GASTROENTEROLOGY Vol. 122, No. 7, 2002.
  83. Pastore L., et.al., Orally Based Diagnosis of Celiac Disease: Current Perspectives, J Dent Res 87(12):1100-1107, 2008.
  84. Vader W., et.al., The Gluten Response in Children With Celiac Disease Is Directed Toward Multiple Gliadin and Glutenin Peptides, GASTROENTEROLOGY 2002;122 :1729–1737.
  85. Green P, Cellier C, Celiac Disease NEJM 357;17 Oct 25, 2007.
  86. Leffler DA, Dennis M, Hyett B, Kelly E, Schuppan D, Kelly CP., Etiologies and predictors of diagnosis in nonresponsive celiac disease, Clin Gastroenterol Hepatol. 2007 Apr;5(4):445-50.
  87. Sicherer SH., Clinical implications of cross-reactive food allergens, J Allergy Clin Immunol. 2001 Dec;108(6):881-90.
  88. Kristjánsson G, Venge P, Hällgren R., Mucosal reactivity to cow’s milk protein in coeliac disease, Clin Exp Immunol. 2007 Mar;147(3):449-55.
  89. Bürgin-Wolff A, Hernandez R, Just M, Signer E., Immunofluorescent antibodies against gliadin: a screening test for coeliac disease, Helv Paediatr Acta. 1976 Dec;31(4-5):375-80.
  90. Ferguson A, Carswell F, Precipitins to dietary proteins in serum and upper intestinal secretions of coeliac children, Br Med J. 1972 Jan 8;1(5792):75-7.
  91. Becker CG, Van Hamont N, Wagner M. Tobacco, cocoa, coffee, and ragweed: cross-reacting allergens that activate factor-XII-dependent pathways. Blood, 1981; 58(5):861-867.
  92. Gangur V, Kelly C, Navuluri L. Sesame allergy: a growing food allergy of global proportions? Ann Allergy Asthma Immunol, 2005; 95:4-11.
  93. Kagi Mk, Wuthrich B. Falafel burger anaphylaxis due to sesame seed allergy. Ann Allergy, 1993; 71(2):127-129.
  94. Keskinen H, Ostman P, Vaheria E, et al. A case of occupational asthma, rhinitis and urticaria due to sesame seed. Clin Exp Allergy, 1991; 21:623-624.
  95. Pecquet C, Leynadier F, SaÏag P. Immediate hypersensitivity to sesame in foods and cosmetics. Contact Dermatitis, 1998; 39:313.
  96. Perkins MS. Raising awareness of sesame allergy. Pharma J, 2001; 267:757-758.
  97. Popa V, Gavrilescu N, Preda N, et al. an investigation of allergy in byssinosis: sensitization to cotton, hemp, flax and jute antigens. Brit J Industr Med, 1969; 26:101-108.
  98. Ciclitiera PJ and Ellis HJ. Relation of antigenic structure of cereal proteins to their toxicity in coeliac patients. Brit J Nutr, 1985; 53:39-45.
  99. Kasarda DD. Grains in relation to celiac disease. Cereal Foods World, 2001; 46:209-210.
  100. Simonato B, Pasini G, Giannattasio M, Curioni A. Allergenic potential of Kamut® wheat. Allergy, 2002; 57:653-654.
  101. Göhte C-J, Wislander G, Ancker K, Forsbeck M. bucksheat allergy: health food, an inhalation health risk. Allergy, 2007; 38(3):155-159.
  102. Hekkens WT. The determination of prolamins in gluten-free food. Introductory remarks. Panminerva Med, 1991; 33(2):61-64.
  103. Kim J-L, Wieslander G, Norbäck D. Allergy/Intolerance to buckwheat and other food products among Swedish subjects with celiac disease. Proc. 9th Int’l Symp Buckwheat, Prague, 2004:705-709.
  104. Lee SY, Lee KS, Hong CH, Lee KY. Three cases of childhood nocturnal asthma due to buckwheat allergy. Allergy, 2001; 56:763-766.
  105. Pomeranz Y, Marshall HG, Robbins Gs, Gilbertson JT. Protein contect and amino acid composition of maturing buckwheat (Fagopyrum esculentim moench). Cereal Chem, 1975; 52:479-484.
  106. De Maat-Bleeker F, Stapel SO. Cross-reactivity between buckwheat and latex. Allergy, 1998; 53:538-539.
  107. Sdepanian VL, Scaletsky ICA, Fagundes-Neto U, de Morais MB. Assessment of gliadin in supposedly gluten-free foods prepared and purchased by celiac patients. J Ped Gastroenterol Nutr, 2001; 32:65-70.
  108. Skerritt JH, Devery JM, Hill AS. Chemistry, coeliac-toxicity and detection of gluten and related prolamins in foods. Panminerva Med, 1991; 33(2):65-74.
  109. Wieslander G, Norbäck D. Buckwheat allergy. Allergy, 2001; 56:703-704.
  110. Bietz JA. Cereal prolamin evolution and homology revealed by sequence analysis. Biochm Gentics, 1982; 20(11/12):1039-1053.
  111. Cicek M and Esen A. Stucture and expression of a dhurrinase (-glucosidase) from sorghum. Plant Physiol, 1998; 116:1469-1478.
  112. Mazhar H, Chandrashekar A, Shetty HS. Isolation and immunochemical characterization of the alcohol-extractabel proteins (kafirins) of Sorghum bicolor (L.) Moench. J Cereal Sci, 1993; 17(1):83-93.
  113. Gaitan E, Cooksey RC, Legan J, Lindsay RH. Antithyroid effects invivo and invitro of vitexin: a C-glucosylflavone in millet. J Clin Endocrinol Metab, 1995; 80(4):114-1147.
  114. Monteiro PV, Virupaksha TK, Rao DR. Proteins of Italian millet: amino acid composition, solubility fractionation and electrophoresis of protein fractions. J Sci Food Agric, 1982; 33(11):1072-1079.
  115. Monteiro PV, Sudharhsna L, Ramachandra G. Japanese barnyard millet (Echinochloa frumentacea): protein content, quality and SDS-PAGE of protein fractions. J Sci Food Agric, 1988; 43(1):17-25.
  116. Parameswaran KP and Thayumanavan B. Homologies between prolamins of different minor millets. Plant Foods Human Nutr, 1995; 48:119-126.
  117. Parameswaran KP and Thayumanavan B. Isolation and characterization of a 20 kD prolamin from kodo millet (Paspalum scrobiculatum) (L.): homology with other millets and cereals.. Plant Foods Human Nutr, 1997; 50:359-373.
  118. Grela ER. Nutrient composition and content of antinutritional factors in spelt (Triticum spelta L.) cultivars. J Sci Food Agric, 1996; 71(3):399-404.
  119. Jones SM, Megnolfi CG, Cooke SK, Sampson HA. Allergens, IgE, mediators, inflammatory mechanisms: immunologic cross-reactivity among cereal grains and grasses in children with food hypersensitivity. J Allergy Clin Immunol, 1995; 96:341-351.
  120. Pastorello EA, Farioli L, Robino A, et al. A lipid transfer protein involved in occupational sensitization to spelt. J Allergy Clin Immunol, 2001; 108(1):145-146.
  121. Skrabaqnja V, Kovac B, Golob T, et al. Effect of spelt wheat flour and kernel on bread composition and nutritional characteristics. J Agric Food Chem, 2001; 49:497-500.
  122. Aphalo P, Castellani OF, Martinez EN, Anón MC. Surface phyusicochemical properties of globulin-P amaranth protein. J Agric Food Chem, 2004; 52:616-622.
  123. Gorinstein S, Delgado-Licon E, Pawelzik E, et al. Characterization of soluble amaranth and soybean proteins based on fluorescence, hydrophobicity, electrophoresis, amino acid analysis, circular dichroism, and differential scanning calorimetry measurements. J Agric Food Chem, 2001; 49:5595-5601.
  124. Vasco-Méndez NL and Paredes-López O. antigenic homology between amaranth glutelins and other storage proteins. J Food Biochem, 1995; 18(4):227-238.
  125. Aluko RE and Monu E. Functional and bioactive properties of quinoa seed protein hydrolysates. J Food Sci, 2003; 68(4):1254-1258.
  126. Lee AR, Ng DL, Dave E, et al. The effect of substituting alternative grains in the diet on the nutritional profile of the gluten-free diet. J Hum Nutr Diet, 2009; 22:359-363.
  127. Wright KH, Huber KC, Fairbanks DJ, Huber CS. Isolation and characterization of Atriplex hortensis and sweet Chenopodium quinoa starches. Cereal Chem, 2002; 79(5):715-719.
  128. Heelan Bt, Allan S, Barnes RMR. Identification of a 200-kDa glycoprotein antigen of Saccharomyces cerevisiae. Immunol Lett, 1991; 28:181-186.
  129. Oshitani N, Hato F, Kenishi S, et al. Cross-reactivity of yeast antigens in human colon and peripheral leukocytes. J Pathol, 2003; 199:361-367.
  130. Sendid B, Quinton JF, Charrier G, et al. Anti-Saccharomycies cerevisiae mannan antibodies in familial Crohn’s disease. Am J Gastroenterol, 2001; 93(8):1306-1310.
  131. Vojdani A, Rahimian P, Kalhor H, Mordechai E. Immunological cross reactivity between candida albicans and human tissue. J Clin Lab Immunol, 1996; 48:1-15.
  132. Young Ca, Sonnenberg A, Berns EA. Lymphocyte proliferation response to baker’s yeast in Crohn’s disease. Digestion; 1994:55(1):40-43.
  133. Beezhold DH, Sussman GL, Liss GM, Chang NS. Latex allergy can induce clinical reactions to specific foods. Clin Exp Allergy, 1996; 26(4):416-422.
  134. Brehler R, Theissen U, Hohr C, Luger T. “Latex-fruit syndrome”: frequency of cross-reacting IgE antibodies. Allergy, 1997; 52:404-410.
  135. Ibero M, Castillo MJ, Pineda F. Allergy to cassava: a new allergenic food with cross-reactivity to latex. J Investig Allergol Clin Immunol, 2007; 17(6):409-412.
  136. Mikkola JH, Alenius H, Kalkkinen N, et al. Hevein-like protein domains as a possible cause for allergen cross-reactivity between latex and banana. J Allergy Clin Immunol, 1998; 102:1005- 1012.
  137. Arentz-Hansen H, Fleckenstein B, Molberg Ø, et al. The molecular basis for oat intolerance in patients with celiac disease. PLoS Med, 2004 1(1):084-092.
  138. Janatuinen EK, Pekka HP, Kemppainen TA, et al. A comparison of diets with and without oats in adults with celiac disease. N Engl J Med, 1995; 333:1033-1037.
  139. Reunala T, Collin P, Holm K, et al. Tolerance to oats in dermatitis herpetiformis. Gut, 1998; 43:490-493.
  140. Silano M, Dessì M, De Vincenzi M, Cornell H. In Vitro tests indicate that certain varieties of oats may be harmful to patients with coeliac disease. J Gastroenterol Hematol, 2007; 22:528-531.
  141. Srinivasan U, Jones E, Carolan J, Feighery C. Immunohistochemical analysis of coeliac mucosa following ingestion of oats. Clin Exp Immunol, 2006; 144:197-203.
  142. Thompson T. Gluten contamination of commercial oat products in the United States. N Engl J Med. 2004; 351(19):2021-2022.
  143. Axelsson IG. Allergy to the coffee plant. Allergy, 1994; 49(10):885-887.
  144. Caballero Tm, Garcia-Ara C, Pascual C, et al. Urticaria induced by caffeine. J Investig Allergol Clin Immunol, 1993; 3(3):160-162.
  145. Moneret-Vautrin DA, Kanny G, Faller JP, et al. [Severe anaphylactic shock with heart arrest caused by coffee and gum Arabic, potentiated by beta-blocking eyedrops]. Rev Med Interne, 1993; 14(2):107-111.
  146. Osterman K, Johansson SG, Zetterström O. Diagnostic tests in allergy to green coffee. Allergy, 1995; 40(5):336-343.
  147. Treudler R, Tebbe B, Orfanos CE. Coexistence of type I and type IV sensitization in occupational coffee allergy. Contact Dermatitis, 1997; 36:109.
  148. Davidson IW, Lloyd RS, Whorwell PJ, Wright R. Antibodies to maize in patients with Crohn’s disease, ulcerative colitis and coelic disease. Clin Exp Immunol, 1979, 35:147-148 lxvi Lehrer SB, Reese G, Malo J-L, et al. Corn Allergens: IgE antibody reactivity and cross- reactivity with rice, soy, and peanut. Int Arch Allergy Immunol, 1999; 118:298-299.
  149. Paulis JW and Bietz JA. Separation of alcohol-soluble maize proteins by reversed-phase high performance liquid chromatography. J Cereal Sci, 4986; 4:205-216.
  150. Asero R, Amato S, Alfieri B, et al. Rice: another potential cause of food allergy in patients sensitized to lipid transfer protein. Int Arch Allergy Immunol, 2007; 143:69-74.
  151. Horikoshi M, Kobayashi H, Yamazoe Y, et al. Purification and complete amino acid sequence of a major prolamin of rice endosperm. J Cereal Sci, 1991; 14(1):1-14.
  152. Urisu A, Yamada K, Masuda S, et al. 16-kilodalton rice protein is one of the major allergens in rice grain extract and responsible for cross-allergenicity between cereal grains in the poaceae family. Int Arch Allergy Immunol, 1991; 96(3):244-252.
  153. Wen T-N and Luthe DS. Biochemical characterization of rice glutelin. Plant Physiol, 1985; 78:172-177.
  154. Yamada K, Urisu A, Komada H, et al. [Involvement of rice protein 16KD in cross- allergenicity between antigens in rice, wheat, corn, Japanese millet, Italian millet]. Arerugi, 1991; 40(12):1485-1495.
  155. Racusen D and Foote M. A major soluble glycoprotein of potato tubers. J Food Biochem, 1980; 4(1):43-52.
  156. Vos-Scheperkeuter GH, De Boer W, Visser RGF, et al. Identification of granule-bound starch synthase in potato tubers. Plant Physiol, 1986; 82:411-416.
  157. Vos-Scheperkeuter GH, de Wit JG, Ponstein AS, et al. Immunological comparison of the starch branching enzymes from potato tubers and maize kernels. Plant Physiol, 1989; 90:75-84.
  158. Hvatum M, Scott H, Brandtzaeg P., Serum IgG subclass antibodies to a variety of food antigens in patients with coeliac disease, Gut. 1992 May;33(5):632-8.
  159. Husby S, Foged N, Oxelius VA, Svehag SE,Serum IgG subclass antibodies to gliadin and other dietary antigens in children with coeliac disease,Clin Exp Immunol. 1986 Jun;64(3):526-35.
  160. Breiteneder H, Ebner C., Molecular and biochemical classification of plant-derived food allergens, J Allergy Clin Immunol. 2000 Jul;106(1 Pt 1):27-36. Review
  161. Scott H, Fausa O, Ek J, Brandtzaeg P., Immune response patterns in coeliac disease. Serum antibodies to dietary antigens measured by an enzyme linked immunosorbent assay (ELISA), Clin Exp Immunol. 1984 Jul;57(1):25-32.
  162. Farthing M, Rees L, Edwards C, Dawson A. Male gonadal func- tion in coeliac disease: 2. Sex hormones. Gut, 1983; 24, 127-135. 26. Betterle C, Zanchetta R. Update on autoimmune polyendocrine syndromes (APS). Acta Bio Medica, 2003; 74; 9-33.
  163. F, Facciuto E, Migliaccio S, Bardella MT, Dubini A, Borghi MO, Saraifoger S, Teti A, Bianchi ML. Imbalance of osteoclastogene- sis-regulating factors in patients with celiac disease. J Bone Miner Res, 2004; 19: 1112-1121.
  164. da Silva K, Kotze L, Nishihara R, daRosa U, Piovezan G, Kotze L. Thyroid disorders in Brazilian patients with celiac disease. J Clin Gastroenterol, 2006; 40(1):33-36.
  165. Stone S, Khamashta MA, Poston L. Placentation, antiphospholipid syndrome and pregnancy outcome. Lupus, 2001;10:67-74.
  166. Shamir R, Shoenfeld Y, Blank M, Eliakim R, Lahat N, Sobel E, Shinar E, Lerner A. The prevalence of coeliac disease antibodies in patients with the antiphospholipid syndrome. Lupus, 2003;12;394.
  167. La Villa G, Pantaleo P, Tarquini R, Cirami L, Perfetto F, Man- cuso F, Laffi G. Multiple immune disorders in unrecognized celiac disease: a case report. World J Gastroenterol, 2003;9(6): 1377-1380.
  168. Sategna-Guidetti C,V olta U, Ciacci C, Usai P , Carlino A, De Franceschi L, Camera A, Pelli A, Brossa C. Prevalence of Thy- roid Disorders in Untreated Adult Celiac Disease Patients and Effect of Gluten Withdrawal: An Italian Multicenter Study. AJG, 2001;Vol. 96, No. 3: 751-757.
  169. Levine JS, Branch DW, Rauch J. The antiphospholipid sindrome. NEJM, 2002; 346: 752-763.
  170. Djuric Z, Zivic S, Katic V. Coeliac disease with diffuse cutaneous Vitamin K deficiency bleeding. Adv Ther, 2007;24(6):1286- 1289.
  171. Rujner J. Age at menarche in girls with celiac disease. Ginekol Pol, 1999;70:359-362.
  172. Sher KS, Mayberry JF. Female fertility, obstetric and gynaeco- logical history in coeliac disease: a case control study. Acta Pae- diatr Suppl, 1996;412:76-77.
  173. Martinelli P, Troncone R, Paparo F, Torre P, Trapanese E, Fasano C, et al. Coeliac disease and unfavourable outcome of pregnancy. Gut, 2000;46(3):332-335.
  174. http://www.greenmedinfo.com/blog/200-clinically-confirmed-reasons-not-eat-wheat
  175. http://www.naturalnews.com/037170_gm_wheat_liver_failure_gmo.html

A fizzy gut healing surprise: Beet Kvass

Fermented food has been known to help rebuild our gut flora and support immune response along with digestion in our gut. This year, in supporting my own gut healing journey, I set the intention to learn the art of all things fermented. We had all these excess beets from our CSA veggie box, so we started making this simple refreshing, fermented drink. A nice alternative to kombucha.

Beet Kvass

Ingredients:

  • 3 medium beets cut into small chunks
  • 2 – 3 slices of ginger
  • 4 tsp salt
  • Filtered water
  • 1 large glass jar

Instructions:

  1. Place beets in a bowl and sprinkle with salt. Combine the mixture and place into the glass container and fill with filtered water. Cover container.
  2. Keep at room temperature for 3 to 6 days until it starts tasting tart. I like mine tart, so I keep it for 5-6 days. Then transfer liquid into container to be refrigerated.
  3. You can keep some left over Kvass as inoculant for the next batch.
  4. Recommend 1/2 cup per day. I use the leftover beet chunks as pickles for a side dish or in salads. You can add them to soups, but heating will kill the beneficial bacteria.

***It is always important to keep the liquid covering the food that’s fermenting to prevent mold from growing.

ENJOY!!!