Celiac.com 05/30/2020 - Recently, I posted a query to ICORS Listserv’s celiac email group listing the following symptoms of hypochondria as found on the Mayo Clinic website:

1. Excessive fear or anxiety about having a particular disease or condition.
2. Worry that minor symptoms mean you have a serious illness.
3. Seeking repeated medical exams or consultations.
4. “Doctor shopping,” or frequently switching doctors.
5. Frustration with doctors or medical care.
6. Strained social relationships.
7. Obsessive medical research.
8. Emotional distress.
9. Frequent checking of your body for problems, such as lumps or sores.
10. Frequent checking of vital signs, such as pulse or blood pressure.
11. Inability to be reassured by medical exams.
12. Thinking you have a disease after reading or hearing about it.
13. Avoidance of situations that make you feel anxious, such as being in a hospital.

The response from people on the Listserv was immediate and most of them reflected my own experience on the long road to diagnosis.  Some responded with gratitude and relief that they were not alone and named their “symptoms” by number.

“I too am guilty of 1, 2, 3, 4 sort of, 5 still am, 6-even my friends thought I was a little over the top, 7-still to this day, 8 never goes away, 11 wondering if the doctors actually have the right diagnosis.  After all it took them this long to come up with it.”

“As far as the hypochondria list—I’m guilty of:  3 4 5 6 11 & 13.” 

“I have not been treated for hypochondria, but I know people who were beginning to say it was all in my head.  I suffered from 3, 5, 11 and 12.  It took me nearly 8-10 years before they finally diagnosed me with celiac disease.  My mother-in-law went through the same thing until they diagnosed her thyroid condition.  After awhile, you’re afraid the doctors are going to see and think, “Oh, no! Not her again! What does she think she might have now?” ”

There were many others who listed numbers or told their story.  This is my story about the long road to a celiac disease diagnosis:

I was 42 years old and had been incapacitated for thirteen years by the time I was diagnosed with celiac disease.  My husband’s jobs in retail moved us so often (eight cities in thirteen years) that I had seen nearly two dozen doctors including a gynecologist, a rheumatologist and at least one family doctor in each city.  At the time of my diagnosis, I’d suffered over a decade from pain, severe fatigue, and anxiety as well as cognitive trouble that made me unemployable.  The question of digestive irregularity was sometimes brought up and dismissed as a nervous reaction.  My biggest concern, though, by far, was the drastic loss of cognitive function.  After I’d seen about a dozen doctors, I became savvy enough to quit bringing up my fibromyalgia and chronic fatigue diagnoses (the mention of which garnered responses anywhere from lip-tightening to eye-rolling, followed by anti-depressant prescriptions).  I never admitted to my first diagnosis which was hypochondria.

After the birth of my last child, I began my quest for relief.  I saw a neurologist first, with the following complaints: My short-term memory was non-existent; I had severe fatigue; I had a severely impaired sense of direction, and; my reading and comprehension had slowed markedly.  Attending art school had become difficult because my visual memory seemed to have gone missing.  I could no longer hold a picture in my head between viewing the object and turning back to the paper to draw it.  The bonus of a tremor made my line-quality suffer which was extremely disheartening.  I couldn’t control line-width by subtle variation of pressure of the chalk on paper.  

At home, completing mundane tasks required an outsized effort and was extremely frustrating.  I couldn’t remember a phone number long enough to dial it without referring back to it two or three times.  More often than not, I became confused and had to start dialing all over.  I frequently got lost in my own town while driving, and I began stammering in stressful situations.  

At the neurologist’s office, I was given an EEG which showed no indication of nerve impairment.  Although my quality of life was annihilated, my neurologist was not impressed with my symptoms.  I was a 27-year-old mother of two small children, he said, as he looked at his watch and suggested that I get some rest and a psychiatric evaluation.

I was naïve.  I thought that by getting an evaluation I would prove that I was earnestly looking for an answer.  I made an appointment with a psychiatrist to give me the exam.  The test was exhausting; it went on for hours.  There was a long questionnaire that asked, several times in different ways, whether I ever heard voices or believed people were following me.  I was asked many times, each time in slightly different way, what my most fervent desire was.  My answer was always that I wanted to get well.  

After the questionnaire, I was given a round of verbal tests, that involved word recall and some non verbal tests that involved drawing pictures and assembling puzzles.  I had a very hard time finding synonyms and naming objects, but my puzzles went together very quickly, I was told.  

When I went back to the neurologist he said that because of the psychiatric report, diagnosing hypochondria, I wasn’t a suitable patient and he could do nothing for me.  

I tried to believe in the possibility that I did, indeed, have hypochondria.  At least that was something I could be responsible for; something over which I could take control.  Raised with a belief in the ability of the mind to affect the body, I looked into the disease of hypochondriasis.  I was desperate to help myself so I researched our home medical encyclopedia (this was a while before the Internet) and bought a book on the subject of hypochondria.  I learned that it was then considered a fairly rare illness, and that real hypochondriacs drew some benefit from the sympathy they received due to the perception they are ill.  That was far from the case with me.

On the verge of a divorce because my husband hadn’t yet come around to believing that I was actually ill, I was getting no sympathy from him or his family.  My siblings found it more convenient to believe I was either lazy or exaggerating my complaints than to do anything to help with my two small boys.  My parents, who believed me, were too elderly and ill to help much, but my mother would send over the occasional roast beef dinner which I received with tears of gratitude.  I rejected the concept of hypochondria when I saw that there was absolutely nothing in it for me, and wondered who in the world could possibly benefit from such a mindset.  

When I received a bill from the psychiatrist, I wrote him to insist on a copy of my test results.  He was very reluctant, and told me I might not like what I found.  I told him he might not get paid if I didn’t have the access to my file.  His one-paragraph evaluation stated that although there was a big discrepancy between my verbal skills and sorting tests, and although I did seem to want to get well, since I still complained and nothing was found, I was a hypochondriac.  In other words, the results of the hours of expensive testing were discounted and he made a diagnosis based on the fact that I had no other diagnosis.  I, too, discounted the value of the test by refusing to pay for it.

The weeks dragged into years.  Many days I was so weak that I could only lock myself and my toddlers in my bedroom with diapers, baby food and formula and lie on the floor with them.  Just trying to stay conscious to make sure they didn’t hurt themselves required a monumental effort.  Often, I was too ill to prepare even a sandwich for myself.  Periods lost in this type of exhaustion continued on and off for over a decade until my eighth gynecologist discovered the pain in my outer abdomen.  I admitted to having long bouts of diarrhea that I had sometimes been unable to control.  

He insisted that before I leave the exam room that I get an appointment with a gastroenterologist whom he knew to be very competent.  Before I left, I had an appointment in hand, written on a prescription sheet.  I can’t express the warmth and gratitude I still feel toward this doctor who took my health so seriously when I’d come to feel so disposable.  

A few weeks later, I was diagnosed with celiac disease and started the arduous journey toward a completely gluten-free diet, the only treatment yet available.  I saw a significant improvement just 12 hours into the diet, and thought my suffering was over.

It wasn’t.  I had become ill with Graves’ disease which my family doctor was unwilling to diagnose.  After a few weeks with a heartbeat at 144 beats per minute, I asked to be referred to an endocrinologist who ordered new labs.  I put my arm out for another prick, tried to breathe slowly, and decided to stop at Barnes and Noble on the way home to buy a book so I could read up on diagnostic criteria.  By this time in my life, I’d become quite unwilling to trust my health to any one person.

It may well be that I am here today because I took the initiative to do a little of my own research.  My first endocrinologist misread my lab results and declared that I was getting better and suggested a “wait and see” approach.  While I was on the phone, I tried to remain calm despite the hammering in my chest and the excruciating sense of urgency spreading across my throat.  I calmly, if haltingly, asked for the numbers of my new test results.  

The man had read the results wrong.  He thought they were getting better, but because he compared results from two different labs, he hadn’t perceived that both sets of lab results showed a non-existent production of thyroid stimulating hormone, a sure sign that my thyroid was in overdrive.  

After asking for a second opinion, I was diagnosed with Graves’ disease and finally, after four months of agony, put on anti-thyroid drugs which returned me to a state of relative normalcy.  Graves’ disease, before the invention of these drugs, by the way, had a 50% survival rate.  I could just as easily be dead today.

Naturally, when I consider the years I lost when my boys were small, I still get angry.  I wonder if my physically talented son, Patrick, would have been a baseball star had I been able to cheer him on at his games.  I wonder whether more time with Stevie puttering in the garden and encouraging his extraordinary love of natural science would have invested him with more self-confidence.  Perhaps that would have made his middle school years less excruciating.  I would have loved to visit my older daughter in Manhattan and taken in a show once in a while, but was always too weak when it came time to live up to my plans.  I wish I had been able to finish my schooling and get a job to help take the load off my husband who has been the sole breadwinner for all of our marriage.  

I carry all of these regrets in the pain in my back, I believe, and still look forward to the day I can lay them down.

In the early stages, after the Graves’ diagnosis, a rage ran through me that burned like poison in my veins.  The tens of thousands of dollars that were wasted on tests, the snide comments and the derisive looks from medical professionals, friends, neighbors and family still boil in the back of my consciousness.  I started to write to every doctor that had failed me, then threw the letters away, knowing they’d just take me for a hysteric, and simply consider my case anecdotal.  I started goading my friends into questioning their doctors and getting second opinions.  I saw undiagnosed celiac disease or Graves’ disease in nearly everyone I met.

Then something, something beyond will or intent, something deep within me broke.  I realized that my trials, my ill health, my burdenhood were really not my fault.  Yes, yes, all this time I’d been telling myself this truth, but now the clouds of recrimination and responsibility were actually parting.  Finally, after several years of righteous anger and indignation, for the first time, I allowed myself to grieve over my lost years of health.  I began to realize how, even though I fought tooth and nail against the idea that my illness was all in my head, that the very perception of me as weak-minded had the power to alter my perception of myself.  This was a true epiphany.  My mother had taught me that if I was doing the right thing, that the opinions of other people meant nothing, but after being told so many times that it was normal to be tired, or that I had occult depression, or lectured that I should not let myself get stressed out, I had begun to feel like someone who couldn’t be trusted no matter how trustworthy I was.  I had become the mythical Cassandra’s twin sister.

My story is far from unique.  When the dozens of people who responded to my inquiry on the Listserv shared their stories, I began to see a pattern of systemic failure in our medical system.  Some of these stories can only be described as horrific.

Kat Fury, who responded with a thoughtful email, told me how she suffered agony for years before she was finally diagnosed with celiac disease and Ehlers-Danlos Syndrome type 3.  She had this to say:

By the time I was five I had learned to not complain about things hurting me or the dislocation of my limbs.  My parents didn’t believe in doctors, but having enough of my being “lazy, depressed, and bulimic” they had me hospitalized in a psychiatric ward for said symptoms.  This confirmed my worst fear, that I was crazy and that everyone felt this kind of daily pain.  Even though I couldn’t keep my food down sometimes, and the pain of both disorders was unbearable, I rarely complained.  During my stay in the psychiatric facility I met a girl with a diagnosis of Reynaud’s Syndrome, a circulatory disorder.  When I learned about it I discovered I also had all of her symptoms, usually worse.  I made the mistake of saying something and was punished by being put into solitary confinement for a week.

Kat was eventually diagnosed with Ehlers-Danlos Syndrome, a rare genetic mutation that causes her to have inadequate collagen and be overly flexible.  Before her diagnosis she once got dismissed from work after being caught trying to put her shoulder back into its socket.  She was told not to come back without a doctor’s note.  Because of her intense guilt over not being able to handle her aches and pains, she misunderstood.  She thought she had been fired and she never returned to her job.  The incompetent treatment she received as a medical patient left her with psychological wounds so severe she couldn’t even take her own dislocated shoulder seriously.

She went on to describe how her EDS diagnosis made doctors reluctant to treat her broken back after a car accident.  She is now permanently unable to walk unassisted.  Her mistreatment defies comprehension.  She related this insight “…my body has many things considered rare, but the more I investigate my genetic propensity for these diseases, the more I learn they are only rare because of a systemic failure to diagnose.” … If my doctors had stopped using the saying ‘When you hear hoof beats think horses not zebras’ I would’ve had a better childhood.”

Unfortunately, those who have celiac disease, thyroid disease and Ehlers Danlos syndrome are not alone.  Patients with difficult to diagnose autoimmune disease are all at terrible risk of permanent damage to their health because of delays in diagnosis and treatment.  There seems to be no standard of care in place to look beyond the horses to find the zebras.  Drug companies, who have made themselves the physicians’ source of new information and medical advancement, have no interest in talking about diseases for which there is no drug currently under patent.  The current practice of confining office visits to eight-minutes, along with insurance company pressure to limit testing, it is likely that anyone who doesn’t have a popular illness with textbook symptoms is going to get shunted aside and labeled “hypochondriac.”  

This label serves many functions.  It aids in the loss of family support, replacing it with disgust, which makes it more difficult for the patient to believe in herself, or continue to bother her doctor with her concerns.  Labeling a complaining patient as a hypochondriac allows the doctor to feel antipathy instead of sympathy, which is efficient and cost-effective because it releases the doctor from any obligation to do the time-consuming research needed to follow up on her case.  In the big picture, creating a culture that makes this apocryphal diagnosis so very pervasive makes patients more likely to change doctors, which results in more first-visit charges, which are usually more than double the price of a regular office visit.  Hence, every doctor’s coffers are fortified.  

We like to think that our doctors think like Dr. House on the TV series…that they won’t give up on us until they figure out what is really wrong, that when they rule out the common diseases, they will follow the trail to the less common sources of symptoms, but this is rarely the case.  Any time a patient is given a diagnosis of exclusion, that ends in the word “syndrome,” that means your doctor has given up.  Fibromyalgia syndrome is one of these.  No known etiology, a vague collection of symptoms, no further need to research once cancer and Crohn’s disease are ruled out.  The same goes for “irritable bowel syndrome.” Although there are plenty of expensive drugs to treat it, it isn’t an actual disease, it’s a medical stalemate.  Perhaps you actually have small intestinal bacterial overgrowth or an intestinal yeast infection, or God forbid, celiac disease.  Most patients will never know, because there are plenty of expensive new drugs on the market that treat and mask only the symptoms.

Hypochondria may be a real psychiatric condition, but its diagnosis depends on the black and white determination that there really is nothing physically wrong with the patient.  Otherwise, it is perfectly understandable that a curious, pro-active person would try again and again to get help, and investigate her symptoms.  To tell a patient conclusively that there is nothing wrong with her requires a burden of proof that is insurmountable, since not every disease is immediately diagnosable and not every disease is well-known.  The fair thing to say would be something along the lines of: “I’m at the limits of my capability to help you,” or, more honestly, “Digging any deeper into the cause of your malaise is more than I care to do.”

The cracks in the system are becoming more noticeable.  Because of patient awareness and activism, conditions once thought to be rare, such as celiac disease, are now known to be common.  When I was diagnosed with celiac disease in 2002, it was thought to have a prevalence of one in 4200 people in the general population.  It is now known to affect around one in a hundred.  Other recent examples are the greatly increased prevalence of thyroid disease, vitamin D and vitamin B12 deficiencies.  Any of these can cause an array of vague but debilitating symptoms, such as generalized pain and chronic fatigue.  Yet the suspicion of hypochondria is always at the forefront.  This should not be the case.  Such a diagnosis has a terrible impact on the patient’s mental and physical health.  It should be considered with the greatest of caution instead of flung, like monkey-product, in arrogance.  This egregious mistake violates both the spirit and the letter of the Hippocratic Oath, “First, do no harm.”

If, as the Mayo site suggests, hypochondria diagnoses occur at a rate of between one and five percent of all patients, consider this: Celiac disease and thyroid diseases occur at rates of one percent and at least five percent respectively.  These two severely under-diagnosed conditions alone pretty much take care of the alleged prevalence of hypochondria in the general population.  Add to those patients anyone else with difficult-to-diagnose ailments such as lupus, multiple sclerosis or any of the dozens of other autoimmune diseases less familiar to the family practitioner, and we are easily past the full suspected five percent.  For these reasons, it is high time we sent the diagnosis of hypochondria to the dust-bin of history.  

Celiac.com 05/16/2020 - Yes, I’m “just a vet,” but I have realized something very important.  If MDs studied veterinary medicine like I have studied human medicine, we would be a lot further down the road toward solving many medical puzzles.

For instance, dogs get multiple sclerosis (MS).  We call it degenerative myelopathy.  It occurs primarily in large breed dogs, with German Shepherds being the number one victim.  In fact, the condition in the dog is so similar to that in people that it was once thought that humans may have contracted it from dogs.  (As canine distemper virus is a paramyxovirus, and with measles and mumps being paramyxoviruses, such transmission may be possible, especially when we see that many viruses that afflict humans are harbored in animals).  If the distemper virus is causing it, why do such a small, select number of dogs get it?  Why don’t we see it across the board in all breeds?  If it were a parasite (which is highly unlikely), then the same would be true...  it should not select the specific breeds.  Thus, since genetic traits are specific to breeds, we have to look at “genetics”.

But what are “genetics”?  They are basically two things- Gene sequences that determine traits and body functions and sequences derived from viruses.  Yes, approximately 45% of the genetic information in our DNA is from viruses.  This is a very important “fun fact”.  The DNA IS “command central.” It contains both the information for normal development and the potential for things to go wrong.  Researchers have tried to nail down the “genetics” of MS for a long time but it just doesn’t seem to be working out for them.  That’s because MS is complicated and multiple factors have to come together to make it happen.  

What do we know, other than it happens in select breeds of dogs and that MDs think there is a hereditary link but can’t seem to prove it?  M.S. occurs most prevalently in northern climates, above the 33rd parallel.  Why?  Relative lack of vitamin D, with the consequent lack of sunlight exposure being the main culprit, is the accepted theory.  I think they are right.  Vitamin D is crucial for the immune system to function properly.  A recent medical study boldly proclaimed that if all Americans took an effective vitamin D supplement, we would cut the cancer risks by over a 1/3.  Air pollution, which is horribly neurotoxic and immune suppressive, also has a major detrimental effect on MS patients.  It does sound like an immune system problem (weakness) doesn’t it?

So, what is being unleashed by this weakened immune system?  A parasite?  (Not likely...we would have SEEN that microscopically long ago.  Also, parasites would not be nearly so selective.).  A bacteria?  ( For the same reasons, this isn’t likely either.  A virus?  Ahhh...maybe.  But why haven’t researchers been able to culture it or at least identify it yet?  Perhaps because it is already in the DNA, as is suggested by the limited number of breeds of dogs that are afflicted?  We know this happens in the case of retroviruses and cancer.

What we also know is that there are some viruses that require “helper” viruses that provide essential amino acid sequences that are missing in the genetic make-up of the primary virus or segment already in place in the DNA.  This is well established.  Imagine someone who has that incomplete sequence in their DNA then contracts a virus that supplies the missing information.  It is like someone putting the right code into a stalled computer....suddenly it starts running.  This would help explain the relatively uncommon incidence of MS in both species as well as the “genetic” tendency that investigators just can’t seem to find.  It would also explain the demise of the immune system, nutrition, the northern climate prevalence (the vitamin D connection), and just about every other loose end that we have before us right now.  

With this kind of “idiopathic condition” (MS, epilepsy, Alzheimer’s, Parkinson’s, etc.) we should be looking for a “syndrome”...a number of factors that come together that produce a particular range of results.  

The really cool thing to see is the role that the big “4” foods play in all of this.  Just add the potentially cataclysmic effects of the malabsorption syndrome that goes along with the intolerance (to gluten, casein, soy, corn, which dominate our diet) the direct effect of lectins on cellular function, and the role of viruses, both overt and those whose information is already embedded in our very genome.  

We need to study all we can about these three things: food intolerance; lectins, and; viruses.  If we do, the world of medicine will open up before us.  It becomes readily apparent that bacteria, parasites, and fungi/yeast are secondary players.  They are opportunists that arise and cause problems as this process unfolds.  In fact, I look at them as the clues that can help us understand what is missing - our immune system and microscopic damage done to our tissues.  Once we examine them in this way, then we can see them as warning signs to go along with the other signs that preceded their arrival, such as heartburn, IBS, allergies, asthma, chronic fatigue, insomnia, etc.  etc.

Celiac.com 04/17/2020 - In 1992, the U.S.  Department of Agriculture published a food pyramid, recommending the following servings per day: 

• 6-11 servings per day of bread, cereal, rice, and pasta
• 2-3 servings of meat, poultry, fish, dry beans, eggs, and nuts

For many years, this pyramid was considered almost holy by many nutritionists and dieters.  

A few years ago, the government revised the food pyramid, only to confuse all of us with its uneven pie wedge shapes and staircase on the side.  According to Dr.  Walter Willett, a leading U.S.  nutrition researcher at Harvard Medical School, this new pyramid is simply wrong.

Willett claims that the job of the U.S.  Department of Agriculture is to promote American agriculture.  “What’s good for some agricultural interests isn’t necessarily good for people who eat their products.”  It would have been better (healthier) if the Department of Health or National Institutes of Health had created the new pyramid.

According to Willett, the USDA pyramid puts too much emphasis on red meat and lumps too many types of carbohydrates together.  All carbohydrates are not created equal.  There is too little emphasis on nuts, beans, and healthy oils, all of which have positive health effects.

So Dr.  Walter Willett devised his own pyramid.  It looks like the original one, with a wide horizontal base that slowly builds upwards toward the pinnacle, with a total of 7 layers.  

At the wide base of the pyramid is exercise (to stress its importance) along with a bottle of Vitamin D.  Layer two, the second largest section, is devoted to whole grains and plant oils (primarily olive, avocado, and grapeseed).  The third most important layer is vegetables (in abundance) and fruits (2-3 times a day).  Level four is devoted to nuts and legumes (1-2 times a day).  Level five lists fish, poultry, and eggs.  Dairy (1-2 times a day) is on level six.  At the uppermost tip of the pyramid, labeled “Use sparingly,” are red meat, butter, salt, pasta, rice, potatoes, refined grains and sweets.  (This is a major deviation from the original pyramid that listed 2-3 servings of meat, poultry, fish, and eggs per day and 6-11 servings per day of processed bread, cereal, rice and pasta.)

Many people struggle with their weight.  You are what you eat.  So how can you eat healthier?

There are many “faux” foods on the market today -- imitation sugar, imitation soda, imitation chocolate, imitation-almost-everything.  No matter how closely you look at the Harvard Pyramid, there are no artificial foods listed there.  This sobering reality suggests that we are better off eating real food.  

Get in the habit of buying fresh foods when possible, shopping the inside perimeter of the store where fresh produce, fresh meats, and fresh dairy are sold.  Weigh the value of what you prepare-- Alfredo sauce, while it may taste delicious, has no redeeming nutritional value, whereas marinara sauce made from fresh, crushed tomatoes is a healthier alternative.

Even as celiacs, there are viable ways to consume whole grains.  For side dishes, make brown rice or quinoa instead of white rice.  Add flaxseed meal to baked products.  Enjoy buckwheat or cornmeal pancakes instead of pancakes made with white rice flour.  

The pyramid suggests “an abundance” of vegetables, so add veggies to everything.  Thin slices of cucumber, avocado, and tomatoes, along with leaf lettuce, are perfect to add to sandwiches.  Julienned slices of zucchini, red pepper, and onions can be added to turkey wraps.  Scramble chopped green pepper, onions, mushrooms, and zucchini into your morning eggs.  Rice (brown rice) can be enhanced by adding drained garbanzo or black beans, peas, and thinly-sliced carrots and celery.  

If you are preparing your weekly ration of red meat for dinner by grilling a 4-ounce (not an 8- ounce or a 12 ounce) steak, heap piles of sautéed onion, green pepper, and mushrooms on top of the steak.  When making meatloaf, shred carrots, zucchini, onion, celery and green pepper into the mix.  Serve more stews, cutting back on the amount of meat and increasing the amount of vegetables and beans used to prepare the dish.  Stir-fries can be made with very little meat (or better yet, use seafood or chicken breast in place of beef or pork), adding more veggies and stirring in cashews and sesame seeds.  It’s doubtful that the fish shown in the pyramid is meant to be deep fried; instead, stew fish with lots of veggies (onions, celery, carrots, spinach) in a seasoned tomato sauce or brush lightly with oil, sprinkle with seasonings, and broil.

Olive oil is a good fat.  Drizzle olive oil over hot, steamed beets, adding a touch of cider vinegar.  Stir-fry in olive oil.  Brush your pan with olive oil when scrambling eggs or making pancakes (preferable buckwheat pumpkin pancakes with shredded apples and cinnamon added).  

Eating healthier is 25% knowing the right foods to eat and 75% making up your mind that you WANT to eat healthier-- not because someone told you to, but because you want to put the very best food into your body for your own good health.

Gluten-Free Tuna Fish Sandwich Recipe Like No Other

This recipe is from Gluten-Free Cooking for Dummies.

Ingredients:

• 4 slices high fiber gluten-free bread
• 1/4 green pepper, cut into thin julienne strips
• 1/8 red onion, sliced thin
• 1/2 cup baby spinach leaves
• 2 small plum tomatoes, sliced thin
• 8 artichoke hearts, drained
• 1/8 teaspoon pepper
• 1/4 teaspoon Italian seasoning
• 1 can (6.5 ounces) water-pack chunk tuna, drained
• 2 teaspoons Italian dressing
• 4 slices low fat pepper cheese

Directions:
Preheat broiler.  Place the bread slices in a 9 X 13 inch baking pan.  On each of the slices, layer the green pepper, onion, spinach leaves, and tomatoes, dividing evenly.  Cut the artichoke hearts into quarters.  Lay 4 quarters on each sandwich.  In a small bowl, stir together the pepper, Italian seasoning, tuna, and Italian dressing.  Spoon the tuna mixture over the top of each sandwich then top each with a slice of cheese.  Broil the sandwiches for about 2 minutes or just until the cheese is melted.  Serves 4.

Celiac.com 04/10/2020 - There is a growing epidemic of obesity, type II diabetes, cardiovascular disease, and predictions that 15,000,000 people in the United States alone will have Alzheimer’s Disease by the year 2050.

In 2001, Dr.  Richard L.  Veech of the NIH, and others, published an article entitled, “Ketone bodies, potential therapeutic uses.”(1)  In 2003, George F.  Cahill, Jr. and Richard Veech authored, “Ketoacids?  Good Medicine?”(2) and in 2004, Richard Veech published a review of the therapeutic implications of ketone bodies.(3)  These articles are not found in journals that the average physician would read, much less the lay public.  Unless you are researching the topic, it is unlikely that you would ever randomly come across this information.

My husband Steve, age 58, has had progressive dementia for at least five years.  He had an MRI in May 2008 showing a diffuse involutional change of the frontal and parietal lobes and moderate left-sided and severe right-sided amygdala and hippocampal atrophy with no ischemic change, which would support a clinical diagnosis of Alzheimer’s Disease.  For non-medical people, this means that he has shrunken areas of the brain.  Many days, often for several days in a row, he was in a fog; couldn’t find a spoon or remember how to get water out of the refrigerator.  Some days were not so bad; he almost seemed like his former self, happy, with his unique sense of humor, creative, full of ideas.  One day I would ask if a certain call came that I was expecting and he would say, “No.” Two days later he would remember the message from so-and-so from a couple of days earlier and what they said.  Strange to have no short-term memory and yet the information was filed somewhere in his brain.  My gut feeling is that diet has something to do with the fluctuation, but what.  I knew that he was locked up in there somewhere, if only there was a key to open up the areas of his brain that he didn’t have access to.

Steve has a BSBA in accounting, and did billing, bookkeeping and accounting for my neonatology practice from home, so that he could stay with our girls.  He loved computers and was a fast typist.  He could open computers up to repair them and fix practically anything else without ever having instruction.  If he did not have a tool to do something he would “invent” it and make a usable prototype.  He loved to kayak and made an attachment to keep his kayak moving in a straight line.  About five years ago he began to have trouble organizing to do his accounting work.  He would procrastinate as much as possible.  He made mistakes with the payroll and I began to sit with him to help him get it right.  I thought it was just that our practice had gotten more complicated with more employees.  He knew that something was wrong and depression set in.  We took him to a neurologist about 4 years ago, who did a Mini Mental Status Exam (MMSE,) and Steve scored a 23 out of 30, putting him into the mild range of dementia.  On this test, the lower the score is, the worse the dementia.  His MRI was reported as normal at that time.

About three years ago, Steve started taking Aricept and two years ago Namenda.  We were hopeful that, if we could slow his decline enough, a treatment would come along that would turn things around for him.  He was changed over from Aricept to Exelon in August 2007 after losing ten pounds over several weeks.  In the past 12 months there was a noticeable change.  He can no longer cook for himself, remember to eat a good meal, use a calculator or even perform the simplest addition, however he still keeps busy all day working in the yard or in his garage and he is still in good physical condition.  I now do all the cooking for a man who used to cook for his family regularly.  I give him the medications because he can’t remember to take them, much less take the right pills.  Every night, we hold each other before we go to sleep and I wonder how many more times we will get to do this.  It has been a nightmare to watch his decline and feel helpless to do anything but watch it happen.  He is fully aware of his dementia, and we talk about it frequently.  He is no longer depressed, probably with the help of counseling, Lexipro and Wellbutrin, or maybe worsening of his disease.

I subscribe to various alerts and check the website clinicaltrials.gov periodically to look for drug studies that he may qualify for.  Two years ago we tried to get him into a study for a promising anti-inflammatory drug, Flurizan, but he did not qualify because he had a history of depression within the previous two years.  Wouldn’t you be depressed if you knew you had Alzheimer’s?  In fact, depression may be a symptom or precursor of Alzheimer’s.

Until very recently, I didn’t see anything regarding the potential use of medium chain triglycerides (MCT oil), or ketone bodies (also called ketoacids,) the end product of their metabolism, which may not only treat, but also prevent Alzheimer’s disease.  Further, this is a potential treatment for Parkinson’s disease, Huntington’s disease, multiple sclerosis and amyotrophic lateral sclerosis (ALS or Lou Gehrig’s disease), drug resistant epilepsy, brittle type I diabetes, and diabetes type II, where there is insulin resistance.  Ketone bodies may help the brain recover after a loss of oxygen in newborns through adults, may help the heart recover after an acute attack, and may shrink cancerous tumors.  Children with drug resistant epilepsy sometimes respond to an extremely low carbohydrate ketogenic diet.  MCT oil appears to be useful as an aid in weight loss and body builders use it already to improve their lean body mass (MCT oil can be easily purchased on the internet.) Athletes and soldiers could use MCT oil as a source of fuel when the body runs out of carbohydrates, which occurs rather quickly when food is not readily available.

What do these entities have in common?  Our cells can use ketone bodies as an alternative fuel when glucose is not available.  Brain cells, specifically neurons, are very limited, more limited than other cells, in what kinds of fuel they can use to function and to stay alive.  Normally, they require glucose (sugar), but they can also use ketone bodies. Humans do not normally have ketone bodies circulating and available to the brain unless they have been starving for a couple of days or longer, or are consuming a ketogenic (very low carbohydrate) diet, such as Atkins.  In Alzheimer’s disease, the neurons in certain areas of the brain are unable to take in glucose (4), (5) due to insulin resistance and slowly die off, a process that appears to happen one or more decades before the symptoms become apparent.  If these cells had access to ketone bodies, they could potentially stay alive and continue to function.  It appears that persons with Parkinson’s disease, (6) Huntington’s disease, (7) multiple and ALS (9) have a similar defect in utilizing glucose but in different areas of the brain or spinal cord.

MCT oil is digested differently by the body than other fats. Instead of storing all MCTs as fat, the liver converts them directly to ketone bodies, which are then available for use as energy. Oral and intravenous administration of MCT oil produces hyperketonemia, (10) or circulating ketone bodies, which are then available to the brain for energy, in the absence of glucose (19) and even in the presence of glucose. (22)  In addition, hyperketonemia results in a substantial (39%) increase in cerebral blood flow, (18) and appears to reduce cognitive dysfunction associated with systemic hypoglycemia in normal humans. (19)

About 2 months ago, we took Steve to the Johnny B. Byrd, Jr. Alzheimer’s Institute at University of South Florida (USF) in Tampa, Florida for an annual evaluation and screening for a vaccine study (Elan).  He was fasting for blood work and had an MMSE of 12, much too low to qualify for the vaccine study – a minimum score of 16 was required. We were very disappointed, but were advised that we could come back another time to try again, since he met all of the other criteria.

We made an appointment in mid-May 2008 in St. Petersburg, Florida to screen Steve for an Eli Lilly gamma-secretase inhibitor and made another appointment for Steve to be screened for entry into the Elan study at USF the following day. The evening before the first screening in St. Pete, I researched the two drugs to help us decide which drug to choose, should he qualify for both studies. I came across another drug, Ketasyn, or AC-1202, that was also recruiting healthy older people to test the tolerability of three different formulations.  Investigating further, I learned that this treatment brought about significant improvement over a 90-day period in about half of the subjects who had a certain genetic profile (APOE2 or APOE3.) The APOE4 group remained about the same, whereas the controls (people taking the placebo) continued to show decline. The results were even more impressive for people who were already taking certain Alzheimer’s medications.  In a pilot study, some people improved on memory testing with the very first dose.  Upon doing an internet search for Ketasyn,  I found a January 2008 patent application (see freepatentsonline.com) (10) a continuation of a 2000 application, 75 pages long, with a well-written and thorough description of the science of Alzheimer’s disease and description of the “invention,” including these study results and numerous potential formulations in combination with other substances that may enhance its effect.

I learned that the promising “ingredient” in Ketasyn is simply MCT oil, and that a dose of 20 grams (about 20 ml or 4 teaspoons) was used to produce these results. The MCT oil that these researchers used was obtained from Stepan Company and consists of primarily 6 and 8 carbon chains, however they state that MCT of any combination of medium chains (6 to 12 carbon chains are medium chain) would also be effective. Just once in this application, the author mentions that MCT oil is derived from coconut or palm oil (this is incorrect, the author should have stated palm kernel oil.)

I didn’t know at that point that I could easily purchase MCT oil online, so I researched coconut oil and found out that coconut oil is about 60% medium chain fatty acids (MCFA), contains no cholesterol and also contains omega-6 fatty acids and some other short and long chain fatty acids of up to 18 carbon chains. (11)  Coconut oil can be found in many health food stores and even some grocery stores.  Wal-Mart sells a non-hydrogenated (no transfat) brand of coconut oil in a one-liter size (almost 32 ounce containers) for about $7 in our area of Florida.  It can be purchased in quantities as small as a pint and up to five gallons online. It is important to use coconut oil that is non-hydrogenated and contains no transfat.  There is a widely held misconception that coconut oil is the “artery clogging oil,” a term coined in the mid-1900’s by the president of Proctor and Gamble, the manufacturer of Crisco and other hydrogenated vegetable oils. The early studies in animals used hydrogenated coconut oil, which we now know produces the notorious trans-fats, and the essential fatty acids were excluded from the diet. (13)  

The largest producer of coconut oil is the Philippines, where coconut and its oil are food staples, and it is also produced in India, Thailand and other parts of Southeast Asia, the Caribbean islands and even in south Florida. The Philippines has one of the lowest incidences of cardiovascular disease in the world. Studies have shown that total cholesterol to HDL ratio improves with non-hydrogenated coconut oil. (14, 15, 16, 17)  The people in this part of the world also eat fish regularly, providing them with omega-3 fatty acids, which probably contributes as well to the lack of cardiovascular disease. My nurse friends from the Philippines tell me that many of their relatives back home cook everything in coconut oil and have coconut in one form or another at nearly every meal.

I have also learned that after coconut and palm kernel oil, the food that medium chain triglycerides are most concentrated in is human breast milk. (12)  It is also found in smaller concentrations in goat and cow’s milk, as well as the butters from these milks. In fact, we used to add MCT oil 20-25 years ago to premature formulas to add calories, and MCT, coconut and palm oils are currently added to premature and full term infant formulas, along with ARA and DHA to mimic breast milk.

Back to Steve, it was too late to find coconut oil before the first screening. On the way, I reminded him repeatedly that we were in St. Petersburg, in Pinellas County.  On the MMSE, he remembered the city but not the county, and he couldn’t remember the season, the month or day of the week, much less the date, even though he had to initial and date numerous pages of consent forms before the MMSE. He had to be reminded on every single page where to initial and what the date was and even how to write out the date.  He scored a 14, too low for entry into the study.  Dr. Margarita Nunez spent considerable time with us and asked Steve to draw a clock (see clock #1), which she said was a specific test for Alzheimer’s.  She took me aside and told me that his “clock” indicated he was leaning more towards severe than moderate AD, a devastating, but not surprising revelation to me, considering that I am his wife of 36 years and now his caretaker.

Thinking, what have we got to lose, we stopped at a health food store on the way home and picked up a quart of 100% “virgin” coconut oil.  I calculated that in order to provide 20 gm of MCT, he would need to take 35 grams or just over two tablespoons (about 35 ml or 7 level teaspoons) of coconut oil.  The following morning, around 9 A.M., I made oatmeal for breakfast and stirred two tablespoons, plus more for “good luck,” into his portion.  I had some as well, since I cannot expect him to eat something that I won’t eat. 

On the way to the 1:00 P.M. screening, I tried to prepare Steve by asking him the season, the month, the day of the week, reminding him that we were going to Tampa, in Hillsborough county. He couldn’t remember the word “spring,” came up with April instead of May for the month every time I asked him and he couldn’t remember it was Wednesday.  During the hour-long drive, we went through these facts at least 10 times, but he still couldn’t remember.  Shortly after we arrived he was whisked away for the test, about 4 ½ hours after consuming the coconut oil.  When he returned, he was very unhappy about his performance.  Laura, the research coordinator, returned shortly thereafter and began to take his vital signs and blood pressure, and, suspecting that we were continuing with the screening process, I asked her if she could share his score with us.  She said, “Didn’t he tell you? He scored an 18!” more than he needed to qualify for the vaccine study. He remembered it was spring, it was May, it was Wednesday, that he was in Tampa, in Hillsborough County and that we were at the Byrd Institute, all points that he missed on the previous attempt at USF. As a result of the screening, we learned that he is positive for APOE4, but do not know at this time if he has one or two copies.

According to the Ketasyn studies, Steve should not have improved, but rather he should have stayed about the same.  Since then he has retested for the Eli Lilly study drug, now available closer to home and scored an MMSE of 17 - he even remembered the date of July 2, 2008 this time.  We have decided, after looking at the potential side effects of the vaccine for APOE4+ people, to go with the Eli Lilly drug.

At the time of this writing it has been 60 days since he started taking coconut oil (May 21, 2008.) He walks into the kitchen every morning alert and happy, talkative, making jokes. His gait is still a little weird. His tremor is no longer very noticeable. He is able to concentrate on things that he wants to do around the house and in the yard and stay on task, whereas before coconut oil he was easily distractible and rarely accomplished anything unless I supervised him directly, a source of some contention between us!

After about two weeks, and again at 37 days, after starting the coconut oil, I asked him to draw a clock (see Clocks #2 and #3.) There is an obvious marked improvement. I promise that I did not help him.  He tells me that he could not even picture a clock at the St. Pete screening, but with the last two attempts, he was very concerned that the 6 was opposite the 12 and the 9 opposite the 3 on the face of the clock.  He drew “spokes” to help them line up.  I did not ask him to try to put in a time, the next part of that test.

Steve has not been able to type for at least two years, but he feels that he can picture the position of the letters on the keyboard. At this point he is afraid to sit down and try to type, worried that he will be discouraged if it doesn’t come back right away. We are considering trying occupational therapy to see if he can relearn some of the skills he has lost. I cannot explain why he has improved, except that perhaps the 10 and 12 carbon chains are important, or the APOE4 people in the Ketasyn studies were not taking omega-3 fatty acids.  We eat salmon at least twice a week and take fish oil supplements twice a day and have for at least the past two years.

I have been researching on the internet everything I can find about coconut oil, MCT oil, fatty acids, ketone bodies, fatty acid composition of breast milk, ketones and various disease states.  When I researched ketone bodies, I came across the name of Dr. Richard Veech of the National Institutes of Health.  I contacted him to ask questions about all of this and he very kindly spoke with me and emailed me articles he had written on the subject.  I have had numerous questions and ideas, and he has continued to provide me with answers and more papers to read.  I am thinking not only about people with neurodegenerative diseases like my husband, but also the sick and premature newborns that I take care of, and potential uses for those at both ends of the spectrum of life and everyone in between.  I wonder about autism and whether something very important is missing in infant formulas and in the diets of women who are breastfeeding. (23)  

Beta-hydroxybutyrate is the primary ketone body that is the end product of fatty acid metabolism and appears to protect neurons when glucose is not available. (20)  Dr. Veech can make an ester form of beta-hydroxybutyrate in his lab from MCT oil that can be taken orally and converted to energy by neurons and other cells.  Potentially, higher levels of ketone bodies could be obtained by ingesting beta-hydroxybutyrate directly. He has done studies on animals, but needs to produce this in quantity to be able to do human studies.  He could start testing this year, if only he had the funding.  He needs $15 million to build a plant to produce his beta-hydroxybutyrate.  That is a lot of money, but not so much if you consider that it is $1.00 for every person that is expected to have Alzheimer’s disease by the year 2050. 

We visited Cincinnati at the end of June and all of my family and Steve’s family noticed a very significant difference in how he interacted with them socially compared to a year ago.  Instead of looking lost, he was involved and interested in what they had to say.  He recognized relatives (brothers-in-law, nieces and nephews) by name immediately that were unfamiliar to him a year ago.  His facial expression was more animated.  He participated actively in conversations, understood jokes immediately and even came up with his own humorous comments.  He still had difficulty finding some words, but he was talking in sentences and even stringing sentences together.  In the morning he would come to the kitchen and ask me to walk the “big hill” with him before breakfast to get some exercise.  He is a very different person than he was a year ago and perhaps even two or three years ago. He has serious atrophy of his brain and will never be “normal,” but for now we are very pleased with where he is at and, should coconut oil stop or slow down the progress of his disease, it will be worth every drop that he takes.

My sister Lois told a lady she works with about the coconut oil and Steve’s response to it.  Her father began to give this to her mother, who has Alzheimer’s and she has had a similar response, with more alertness, conversation and sense of humor.

On July 9, 2008, Steve had blood samples drawn at various times before and following breakfast and dinner.  He received 35 ml of coconut oil at each of those meals.  He did not receive any other coconut oil or other coconut products during the rest of that day.  Normally, he receives more coconut oil than that on the average day.  Steve’s ketone body levels began to increase after breakfast over 3 hours, but at relatively low levels, dropped again before dinner and were steadily rising about 3 hours after dinner.  We do not know when his levels peaked because we did not draw any further levels thereafter.  Dr. Veech stated that it is surprising that Steve would improve with these relatively low levels of ketones.  This study reaffirms his belief that it is necessary to go forward with the production and testing of his ketone body b-hydroxy butyrate esters, since considerably higher levels of ketone bodies, timed and controlled could be achieved, and more ketones would be available for the neurons to use, and therefore greater improvement could be expected.

It is urgent that funding become available to move forward for the sake of the millions who currently suffer, and will in the future suffer, from Alzheimer’s disease, Parkinson’s disease, Huntington’s chorea, multiple sclerosis, ALS, type I and type II diabetes, as well as any number of other conditions that involve a defect in transport of glucose into neurons and other cells.

Until Dr. Veech’s beta-hydroxybutyrate is tested and available for use, a simple dietary change to coconut oil could make a difference for people who believe they are at risk and for those who already have one of these diseases.

To duplicate the dose of MCT taken in the Ketasyn study, about 7 level teaspoons should be taken at one time, once a day, which should circulate ketone bodies for about 24 hours. I do not know if it is necessary to take this much at one time or if the dosage could be spread out over the course of the day. Studies obviously need to be done to determine this.  We actually give this amount to Steve at least twice a day to make sure that there are no periods without ketone bodies circulating. Many days he receives at least 50% more than this.  The amounts we are taking would not be excessive in areas of the world where coconut is a staple. If a person can tolerate more, or can work up to tolerating more, it may be a good idea to do so. As an alternative, one could take 4 teaspoons of MCT oil once or twice a day, or more often as tolerated.

Some people may experience a sense of “fullness” or even have diarrhea after taking this much to start, but this problem can be reduced by starting with one or two teaspoons and increasing over a week or so to the full amount.  We put it in oatmeal, combine it with salad dressings, use it to cook with, and put it on anything that one would normally put butter on, such as potatoes, sweet potatoes, rice, pasta or noodles.  Coconut ice cream can be purchased at Asian stores, contains coconut oil and is the most pleasant way I can think of to make ketone bodies.  Likewise, coconut milk is a combination of coconut oil and coconut water and can be found in the Asian and condensed milk sections of many grocery stores. It is a pleasant substitute for milk, and can be added instead of milk, for example, to make scrambled eggs, French toast and mashed potatoes.  You can figure out portion sizes of various combinations of foods containing coconut and coconut oil equivalent to at least 35 grams of fat from coconut oil.

If you are using any type of hydrogenated vegetable oil or any oil with transfat, do not use any more and get rid of it!  Extra virgin olive oil, butter and other natural, non-hydrogenated oils are okay to use along with the coconut oil.  It is possible to use coconut oil in place of all other oils, however, since it contains no omega-3 fatty acids, it is very important to eat salmon twice a week or get enough omega-3 fatty acid from other rich sources such as fish oil capsules, flax meal, flax oil (not for cooking) or walnuts.

It is inconceivable that a potential dietary prevention and cure for Alzheimer’s disease, and other neurodegenerative diseases, has been out there for so many years, and yet has gone unnoticed.  It is very likely that these diseases are becoming more prevalent due our current diet. The American diet has changed drastically from what it was before the 1950’s, when our parents and grandparents used lard and coconut oil to cook. Cardiovascular disease was rare at the beginning of the 20th century, and has skyrocketed, along with other devastating diseases, such as Alzheimer’s, diabetes type II, obesity, since mass produced hydrogenated vegetable oils containing trans fats were introduced into our diets and replaced these other natural fats. Sadly, the incidences of cardiovascular and other serious diseases are becoming more and more common among people in other areas of the world who have changed over from their indigenous foods to the “western” diet.

I plan to tell everyone I can and get this information to persons in positions to investigate this with the hope that Dr. Veech and other MCT oil and ketone body researchers get the funding they need.  Feel free to make copies and pass this write-up on.

If you have a loved one or a patient with Alzheimer’s or one of these other degenerative neurologic diseases, consider trying coconut oil.  Dr. Veech suggests that, if possible, a videotape of the person before starting and at various points after starting the coconut oil would be very useful to document change. He suggests including segments of the persons face, speech and gait (walking).  He also advises to have ketone bodies
measured.  What have you got to lose?

References:

1. “Ketone bodies, potential therapeutic uses,” RL Veech, B Chance, Y Kashiwaya, HA Lardy, GC Cahill, Jr., IUBMB Life, 2001, Vol.  51 No.4, 241-247
2. “Ketoacids?  Good Medicine?” George F.  Cahill, Jr., Richard L.  Veech, Transactions of the American Clinical and Climatological Association, Vol.  114, 2003.
3. “The therapaeutic implications of ketone bodies: the effects of ketone bodies in pathological conditions: ketosis, ketogenic diet, redox states, insulin resistance, and mitochondrial metabolism,” Richard L. Veech, Prostaglandins, Leukotrienes and Essential Fatty Acids, 70 (2004) 309-319.
4. "Diminished glucose transport and phosphorylation in Alzheimer’s Disease determined by dynamic FDG-PET,” M Piert, et.al., The Journal of Nuclear Medicine, Vol.37 No.2, February 1996, 201-208.
5. “Glucose metabolism in early onset versus late onset Alzheimer’s Disease: an SPM analysis of 120 patients,” EJ Kim, et.  al., Brain, 2005, Vol.  128, 1790-1801.
6. “Cerebral glucose metabolism in Parkinson’s disease with and without dementia,” RF Peppard, et.al., Archives of Neurology, Vol.  49 No.12, December 1992.
7. “Cortical and subcortical glucose consumption measured by PET in patients with Huntington’s disease,” Brain, October 1990, Vol 113, part 5, 1405-23.
8. “Reduced glucose metabolism in the frontal cortex and basal ganglia of multiple sclerosis patients with fatigue: a 18F-fluorodeoxyglucose positron emission tomography study,” U Roelcke, et.  al., Neurology, 1997, Vol.  48, Issue 6, 1566-1571.
9. “ALS-linked Cu/Zn-SOD mutation impairs cerebral synaptic glucose and glutamate transport and exacerbates ischemic brain injury,” Z Guo, et.  al., Journal of Cerebral Blood Flow Metabolism, March 2000, Vol.  20 No.  3, 463-8.
10. “Combinations of medium chain triglycerides and therapeutic agents for the treatment and prevention of Alzheimer’s disease and other diseases resulting from reduced neuronal metabolism,” United States Patent 20080009467, Inventor Samuel T.  Henderson, Accera, Inc., Broomfield, Colorado (Ketasyn).
11. Nutrient analysis of coconut oil (vegetable), NDB No: 04047 – www.nal.usda.gov/fnic/foodcomp .
12. “Lipids in (human) milk and the first steps in their digestion,” M Hamosh, et.  al., Pediatrics, 1985, Vol.  75, 146-150.
13. “Nutritional factors and serum lipid levels,” EH Ahrens, American Journal of Medicine, 1957, vol.  23, 928 (used hydrogenated coconut oil).
14. “Trans fatty acids and coronary artery disease,” NEJM, 1999, Vol.  340, 1994-1998.
15. “Effect of mixed fat formula feeding on serum cholesterol level in man,” SA Hashim, American Journal of Clinical Nutrition, 1959, Vol.  7, 30-34.
16. “Modified-fat dietary management of the young male with coronary disease: a five-year report,” JL Bierenbaum, JAMA, 1967, Vol.  202, 1119-1123.
17. “Cholesterol, coconuts and diet in Polynesian atolls-a natural experiment; the Pukapuka and Toklau island studies,” IA Prior, American Journal of Clinical Nutrition, 1981, Vol.  34, 1552-1561.
18. “Changes in cerebral blood flow and carbohydrate metabolism during acute hyperketonemia,” S.G.  Hasselbalch, et.al, Am J Physiol, 1996, Vol.  270, E746-51.
19. “Effect of hyperketonemia and hyperlacticacidemia on symptoms, cognitive dysfunction, and counterregulatory hormone responses during hypoglycemia in normal humans,” T.  Veneman, et.  al., Diabetes 43:1311-7 (1994).
20. “D-b-Hydroxybutyrate protects neurons in models of Alzheimer’s and Parkinson’s disease,” Y Kashiwaya, et.  al.  including RL Veech, PNAS, May 9, 2000, Vol.  97 No.  10, 5440-5444.
21. “High carbohydrate diets and Alzheimer’s disease,” Samuel T.  Henderson, Medical Hypotheses, 2004, Vol 62, 689-700 (Another article of interest).
22. “Effects of b-Hydroxybutyrate on cognition in memory-impaired adults,” MA Reger, ST Henderson, et.  al., Neurobiology of Aging, 2004, Vol.  25, 311-314.
23. “Breastfeeding, infant formula supplementation, and Autistic Disorder: the results of a parent survey,” ST Schultz, et.  al., International Breastfeeding Journal, 2006, Vol.  1 No.  16.

Other Important Resources

•  “Ketones: Metabolism’s Ugly Duckling,” TB VanItallie, TH Nufert, Nutrition Reviews, Vol 61, No 10, 327-341.
• • “Fuel Metabolism in Starvation,” GF Cahill, Jr., Annual Reviews in Nutrition, 2006, 26:1-22. “Ketone Bodies as a Therapeutic for Alzheimer’s Disease,” ST Henderson, Journal of the American Society for Experimental NeuroTherapeutics, Vol 5, 470-480, July 2008.

Celiac.com 04/03/2020 - I don’t recall ever hearing of celiac disease before I diagnosed myself 7 years go, at age 75.  When my doctors found no answer to my disabling colitis, I turned to a surprising wealth of universal web-site information about healing my microscopic-colitis, about gluten sensitivity, and its wide range of toxic possibilities.  This is but one of the numerous articles that was vital to my education in ‘02:

• The neurology of gluten sensitivity: separating the wheat from the chaff. LLWonline 2002 Dept.of Neurology,Queen’s Medical Centre, Nottingham, UK.  "Clinocopathological features heal on a gluten-free diet and relapse when gluten is reintroduced...A number of neurological syndromes may be associated with celiac disease...This is an exciting hypothesis because it offers new therapeutic possibilities including simple exclusion diets...”

Little did I realize that the disease, being genetic, would cause a revolution in my life, reaching far beyond my own illness.  My gene test results with Dr.  Kenneth Fine, (www.enterolab.com) indicated that I had two identical genes for gluten-sensitivity.  His report explained, “Having two copies of a gluten-sensitive or celiac gene means that each of your parents, & all of their children will possess at least one copy of the gene."

This startling information seemed to present the first opportunity to identify the causes of numerous mysterious and tragic illnesses and deaths in both of my parents’ families.  One by one I was shocked to discover or recall illnesses that could probably be linked to parents and grandparents now known to be gluten-sensitive.  

My test result became the nucleus of my discoveries.  Although my research and writing have been limited by concerns for the privacy of family and friends, as well as by the comparatively small number of family members with whom I have been in touch on a regular basis, I suspect that my summary of newly discovered and recalled family history can be a vital addition to the growing technical research on gluten toxicity.  Everyone who is referenced here has a direct familial-link to my mother or my father.  As each of my parents had 5 siblings, these are large families, but replies to my suppositions have been rare; of the twelve relatives who decided to be tested so far, five results have been positive for celiac or gluten-sensitivity.  

Aside from the startling reports linking dietary-gluten and dementia, perhaps even more shocking is the possibility that gluten may provide answers concerning the mysterious deaths of my younger brother and my two young adult nieces by cancer.  My gene test indicates, in addition to my brother’s link, that each of my nieces had at least one parent and two grandparents with at least one gluten-intolerant gene (Increased Cancer Risk Associated With Delayed Diagnosis of Celiac Disease).

The following summary of the generation-statistics available to me, of family-members who have a probable link to this genetic-sensitivity, may simplify my report:

1. In our oldest generation, my maternal grandmother was reported to have critical “senile-dementia” ; and my paternal grandfather was a victim of Parkinson’s disease.  
2. Of their offspring, the deaths of my mother and her three sisters were all attributed to Alzheimer’s disease (my mother’s 1980 autopsy specifies this finding).   Her brother was a cancer-victim, with possible dementia; and my father’s sister inherited my grandfather’s Parkinson’s disease.
3. In my generation there are 4 relatives who have succumbed to Alzheimer’s; three first-cousins and my sister who is in the last-stages.  My youngest brother was a victim of cancer and bi-polar disease.  Another cousin and I have tested positive for gluten-sensitivity; while two additional cousins are victims of Parkinson’s—one in each family; while one of these cousins was a cancer victim as well.  
4. In my children’s generation, my daughter and a cousin have been diagnosed with gluten-sensitivity, and two of my  young-adult nieces died of cancer.  
5. In this youngest generation, my grand-nephew has tested positive for celiac disease, and at least three young relatives have exhibited commonly-reported signs of Asperger’s (on the Autism-spectrum) and one of them has been diagnosed with this condition.  

Some new genetic discoveries concerning Parkinson’s explain the inclusion of this disease in my summary.  (From “Psychiatric News, Sept.17, ‘04,Volume 39 #18 ) “Could it be that the two most common neurdegenerative disorders—Parkinson’s disease and Alzheimer’s disease—share the same common origins?” 

I have also included Asperger’s and  bi-polar disease, two additional alterations to brain function that are possible results of gluten-toxicity.  (“Gluten Causes Brain Disease” by Prof.  Rodney Ford M.D.)

My own brain-condition, at age 82, may present a wider view of “cognition”, as the Alzheimer’s disease literature seems to focus primarily on memory.  As most of my family resides in another city, I have been far more educated about senior-issues in the six years I have been a tenant in a large senior-housing facility.  My mysterious life-long memory-disability, which I now recognize to be celiac-induced, has progressed in its severity to match the disappearing memories of several current neighbors, who are exhibiting obvious or diagnosed dementia, along with several more who have moved to full-care facilities.

It has been of particular importance to me, to be able to study the differences in our “cognition”.  At some point these friends have eventually required daily aid for household tasks they can no longer perform.  But, in spite of my severe memory-loss, the aspects of my cognition for reasoning, awareness, and especially (as an artist), my creativity, have not been affected.  If I am correct, that this is probably due to my seven years of being gluten-free, this may be of great importance, proving that under similar circumstances dementia may be avoided, even as a senior.  

I have also learned that although these seven years of being gluten-free have resulted in a few welcome changes, the previous 75 years of ingesting gluten have probably resulted in the limited healing of most of my other symptoms.  These include ataxia (loss of balance) chronic migraines, permanent dermatitis herpetiformis (that is about 50% improved) and minor but continuing colon damage.  The celiac factor in my degenerating osteoporosis and widespread arthritis has gradually necessitated the use of a walker for at least two years—yet one more obvious consideration for testing of gluten-sensitivity at the earliest possible age.  

There are some reports now estimating that approximately 1 in 100 persons have celiac disease and approximately 1 in 10 people are gluten-sensitive.  The results of the chance union of my two genetic, gluten-affected families, has created circumstances that far transcend coincidence, and should not be ignored.

Celiac.com 03/28/2020 - Were you thinking that there wasn't much gluten in your medicine?  Had you read that less than 1% of drugs were made with it?  Think again, because while pharmaceutical manufacturers don't actually add gluten to drugs in most instances, they very frequently cannot say that their products are gluten free.  That's because before some ingredients get into a manufacturing facility, they are purchased from suppliers that are not controlled by the drug maker.  Let me explain.  

When you take a drug, most of what you are swallowing is filler.  This is called an excipient in the trade.  Excipients are inert stuff that the actual drug is mixed with, and it influences the rate the drug enters your blood.  For people with celiac disease, the problem is that the excipient is often made from starches derived from corn, rice, tapioca, etc.  If you're reading this, you probably just recognized how gluten could be getting into your medicine even when a drug maker did not intentionally use gluten as the excipient.

Drug companies affirm that even when they have not added gluten to a particular drug, there could be gluten in that drug, and they won't say the drug is gluten free.  Here is where Sister Jeanne Patricia Crowe Pharm.D. (no relation to the actor) comes into the picture.  About ten years ago Sister Jeanne Patricia did a study which established just how much trouble drug makers had even knowing when there was gluten in their products.  Working with her research partner Nancy Patin Falini M.A., R.D., Crowe sent out questionnaires to about 170 drug makers asking each what the gluten content of their medicine was.  Their results were published in the American Journal of Health-System Pharmacy in 2001 (1).  In their peer reviewed article titled Gluten in Pharmaceutical Products, the two researchers were able to conclude the following:

Only 5 of 100 pharmaceutical companies that responded to a survey reported having a policy of producing gluten-free products.  Many companies believed their products were gluten-free but could not guarantee it.

But what Crowe and Falini's results also showed was that drug makers themselves had a hard time making sure that when they bought an ingredient from an outside supplier, that they were not letting gluten get into their manufacturing facility.  Two other studies support the Crowe and Falini findings, so they are pretty convincing.  Simply put, gluten can be making its way into your drugs, and you can't find out about it because the drug manufacturer also doesn't know it's there.  And if the drug maker doesn't know, then when your pharmacist helps you to read the package insert, it really won't matter much what it says on the label.

This chaotic situation is not acceptable for the manufacture of medication.  At the least, a company that makes drugs needs to determine whether they are making their product with an excipient like corn starch,  and whether that the corn starch is gluten-free.  Either the excipient is gluten-free or it isn't.  Even when a consumer goes to buy a gluten-free food like Cheese Curls, the manufacturer at least has a letter from its raw ingredient suppliers, stating that the ingredients are gluten-free.  Some food makers will even test every batch of raw ingredient before it enters their own facility.  It isn't too much to ask that drug makers learn what's in their products.

The FDA is currently looking at how to address the issue of gluten in medications.  One approach is to require that drug makers disclose when a particular drug is gluten-free.  At the other extreme, as a petitioner, I have argued that because gluten is toxic, the law of the United States should be satisfied, and gluten should be taken off the list of allowed excipients.  But the work of Sister Crowe and Nancy Falini has demonstrated just why the FDA must take a step back and first require drug makers themselves to know exactly what's inside that pill or capsule.  

I hope that I've gotten at least a few of you wound up.  I'm a bit surprised that drug makers would put themselves in a position where they sometimes don't know what's in any given pill they make.  Don't they see the liability issues?  Where are their lawyers, anyway?  In the first article I wrote for celiac.com, I asked readers to let the FDA know that they wanted to get gluten out of drugs, and many people did exactly that.  And those comments do get read.  Now I am going to make sure that the FDA takes into account the work of Sister Crowe and Nancy Falini.  Tell the FDA what you think.

Maybe next time you fill a prescription for whatever ails you, it will be possible for you and your pharmacist to determine whether gluten is present in your medication.

Michael Weber lives in New York and can still remember what pizza tastes like.

References:
1. Crowe, JP, Falini, NP Gluten in pharmaceutical products Am J Health Syst Pharm 2001 58: 396-401 

Celiac.com 03/14/2020 - Dr. Mary Newport reported that, in the U.S. alone, up to 15,000,000 people will have Alzheimer’s disease by the year 2020 (1).  Dementia is a growing problem that threatens the very fabric of most advanced nations with their aging populations.  Many consider dementia to be an inevitable part of aging, and hopelessly irreversible.  However, gluten-induced dementia may be changing the way physicians and members of the general populace see dementia, as well as offering new hope for effective treatment of early stage dementias.  In previous issues I have discussed gluten induced psychiatric and neurological conditions ranging from attention deficit disorders, to schizophrenia, to epilepsy.  The connections are clear for anyone who will look at the relevant peer reviewed research reports with an open mind.  Dementia is another issue.  

Dementia is commonly recognized, in the peer reviewed literature, as one manifestation of untreated celiac disease.  One research report indicates that the cognitive decline of two subjects was “attributed to Alzheimer’s dementia but ameliorated after the initiation of gluten-free diet” (2).  Another group has identified gluten as the causative agent in some cases of moderate to severe dementia but these subjects did not experience intellectual recovery following institution of a gluten free diet (3).  This group also suggested that gluten induced dementia may be driven by immunological mechanisms (3).  Further, a highly regarded researcher and celiac disease sub-specialist, Dr.  Joseph Murray, M.D., Ph.D., along with several other investigators, also at the Mayo Clinic, recently reported several cases of dementia in the context of celiac disease.  They went on to indicate that a gluten-free diet halted the progression of dementia in some cases, while it even brought about improvements in other patients.  This group concluded their report by saying that their work “has the potential of expanding the narrow spectrum of the treatable dementia” (4) So we have a mixed picture in which early detection and treatment of celiac disease may stave off cognitive decline or halt the progression of this insidious condition.  However, if diagnosis of celiac disease is delayed, and dementia becomes severe, there is little hope for recovery.  

Although cognitive decline among the elderly is one of the manifestations of untreated celiac disease, making gluten a direct cause or contributor to dementia in the above reports, it can also contribute to cognitive decline in other, more subtle ways.  For instance, vascular dementia can be caused by reductions in the supply of nutrients to certain parts of the brain, leading to the cell death in those “starved” areas.  This might occur if regions of the brain develop insulin resistance, blocking nutrients from moving into the cells.  Gluten grains have a very large glycemic load, causing considerable insulin production over lengthy periods.  It might also result from inadequate circulating insulin, which softens cell walls to aid in their absorption of glucose from the bloodstream.  Similarly, another type of cognitive decline is called vascular dementia.  The latter is characterized by multiple small strokes and is called multiple infarct dementia or MID (5) causing cells to die due to insufficient oxygen.  Over time, any of these dynamics will cause brain shrinkage and compromise cognitive function.  

After more than 50 years of intensive research, we still don’t know the specific cause of plaques that form on the walls of blood vessels, resulting in an array of cardio-vascular ailments and incidents, including some forms of vascular dementia.  However, we do know that carbohydrates contribute to insulin spikes, and hence, fat storage.  These fats can then be mobilized into the circulation, ultimately binding to vessel walls or completely blocking smaller blood vessels with fatty plaques.  

Current conventional wisdom suggests that the location of these plaques is determined by lesions that occur on blood vessel walls.  Some of the well documented toxic and allergenic dynamics, driven by inappropriate absorption of undigested and partly digested dietary proteins into the bloodstream, commonly occur in the context of celiac disease and gluten sensitivity.  Such foreign substances circulating in the blood could well contribute to the formation of these lesions on blood vessel walls.  This, in combination with the heavy glycemic load imposed by gluten consumption, could contribute to dementia both through helping to create the lesions where plaques can accumulate fats from the circulation, as well as through inciting extended periods of insulin production by the pancreas.  This excessive insulin production can facilitate the development of insulin resistance.  Whether the lipoproteins that aggregate at these lesions block or only impede blood flow, the death of brain cells could well be the result.  Whether from oxygen starvation, nutrient starvation, or both, these data support the suggestion that such starvation may cause the regional brain cell death that typifies dementia. 

While we’re on the topic of excessive insulin production contributing to fats circulating in the bloodstream, it may be instructive to point out that diabetic patients have an increased risk of developing dementia (6).  Since the risk of type 2 diabetes increases with age, some researchers have asserted the value of glycemic control to stave off a range of geriatric syndromes, including dementia (7).  Further, current research is suggesting that the risk of vascular dementia is elevated among those with insulin resistance, while insufficient insulin production may be related to an increased likelihood of developing Alzheimer’s (8).  

Thus, whether there is insufficient insulin production to move nutrients into brain cells, insulin resistance in some of the brain cells blocking glucose from entering (perhaps due to excessive insulin production) vascular damage due to a leaky gut, or gluten-induced alterations to blood flow patterns in the brain, gluten grains are likely a large contributor to dementia in many of its forms.  

It is also worth pointing out that statins, a class of drugs that lower cholesterol have, in the past, sometimes been touted, both in peer reviewed and promotional literature,  as a means of reducing the incidence of various dementias by reducing serum cholesterol, and hence, reducing plaques on vessel walls that feed the brain.  However, randomized controlled trials have repeatedly shown that these drugs either have no effect on the risk of dementia (9, 10) or, in rare cases they can induce memory losses or exacerbate pre-existing memory disturbances (11).  All of the preceding suggests the need for particular caution when prescribing statins to elderly individuals (12).  It has also been asserted that physician awareness is quite low regarding even the most common adverse reactions to these lipid lowering drugs (13).  

Hunting and gathering societies do not experience such ailments.  Just as schizophrenia is rare in primitive cultures (14) diabetes and strokes are also rare (15).  Perhaps dementia is another set of diseases of modernity.  In other words, they result from eating modern diets which are laden with sugar, allergenic grain/flour products, and a wide range of chemicals that are added to processed food to improve its shelf life, enhance its flavor, or otherwise improve its marketability.  

I’m not suggesting that we can return to a hunter-gatherer lifestyle.  The planet would only be able to support a tiny fraction of its current population if we undertook such a shift in our eating habits.  However, our governmental position on the nature of healthful foods and agricultural production should undergo dramatic revision to bring it into line with current research which would remove two dramatic causes of illness and delayed sensitivities, dairy and gluten, from their current, highly vaunted positions on government dietary recommendations.  

Further research is needed to determine if a leaky gut is a common factor in the formation of plaques on blood vessel walls.  It might also be useful to determine whether the capillary leakage associated with celiac disease has implications for gluten-associated dementia.  Finally, we must wonder if Zonulin (a messenger that increases the spaces between epithelial barrier cells) is playing a role in dementias, either through compromising the blood brain barrier or through compromising the integrity of blood vessel walls, or both.  Zonulin production is increased in response to certain infectious agents, or gluten, when eaten by gluten sensitive individuals (16).  

Clearly, we need to increase our understanding of the many facets of all forms of dementia.  We need to bring a critical eye to bear on the prescription of statins for elderly patients, and we need to reduce the 13 year delays to diagnosis of celiac disease (17).  If our physicians are not familiar with the range of adverse events associated with Statins or the protean manifestations of celiac disease, we must either educate them, or seek out physicians who are knowledgeable in these areas.  

References: 
1. Newport M, http://www.tampabay.com/news/aging/article879333.ece
2. Lurie Y, Landau DA, Pfeffer J, Oren R.  Celiac disease diagnosed in the elderly.  J Clin Gastroenterol.  2008 Jan;42(1):59-61.  
3. Collin P, Pirttilä T, Nurmikko T, Somer H, Erilä T, Keyriläinen O.  Celiac disease, brain atrophy, and dementia.  Neurology.  1991 Mar;41(3):372-5.
4. Hu WT, Murray JA, Greenaway MC, Parisi JE, Josephs KA.  Cognitive impairment and celiac disease.Arch Neurol.  2006 Oct;63(10):1440-6.  
5. Kantarci K, Weigand SD, Przybelski SA, Shiung MM, Whitwell JL, Negash S, Knopman DS, Boeve BF, O’Brien PC, Petersen RC, Jack CR Jr.Risk of dementia in MCI: combined effect of cerebrovascular disease, volumetric MRI, and 1H MRS.  Neurology.  2009 Apr 28;72(17):1519-25.  
6. Bruehl H, Wolf OT, Sweat V, Tirsi A, Richardson S, Convit A.  Modifiers of cognitive function and brain structure in middle-aged and elderly individuals with type 2 diabetes mellitus.  Brain Res.  2009 May 19.
7.    Vischer UM, Bauduceau B, Bourdel-Marchasson I, Blickle JF, Constans T, Fagot-Campagna A, Kaloustian E, Lassman-Vague V, Lecomte P, Simon D, Tessier D, Verny C, Doucet J A call to incorporate the prevention and treatment of geriatric disorders in the management of diabetes in the elderly.  Diabetes Metab.  2009 May 13.  
8.     Rönnemaa E, Zethelius B, Sundelöf J, Sundström J, Degerman-Gunnarsson M, Lannfelt L, Berne C, Kilander L.  Glucose metabolism and the risk of Alzheimer’s disease and dementia: a population-based 12 year follow-up study in 71-year-old men.  Diabetologia.  2009 May 20.
9.    McGuinness B, Craig D, Bullock R, Passmore P.  Statins for the prevention of dementia.  Cochrane Database Syst Rev.  2001;(4)
10.    Carlsson CM, Nondahl DM, Klein BE, McBride PE, Sager MA, Schubert CR, Klein R, Cruickshanks KJ.Increased atherogenic lipoproteins are associated with cognitive impairment: effects of statins and subclinical atherosclerosis.  Alzheimer Dis Assoc Disord.  2009 Jan-Mar;23(1):11-7.
11.     Golomb BA, Implications of statin adverse effects in the elderly.  Expert Opinion on Drug Safety May 2005, Vol.  4, No.  3, Pages 389-397.  
12.    Padala KP, Padala PR, Potter JF.  Simvastatin-induced decline in cognition.  Ann Pharmacother.  2006 Oct;40(10):1880-3.  Epub 2006 Aug 29.
13.    Golomb BA, Evans MA.  Statin adverse effects : a review of the literature and evidence for a mitochondrial mechanism.  Am J Cardiovasc Drugs.  2008;8(6):373-418.  
14.    Dohan FC, Harper EH, Clark MH, Rodrigue RB, Zigas V.  Is schizophrenia rare if grain is rare?  Biol Psychiatry.  1984 Mar;19(3):385-99.
15.    Collins C.  Said another way: stroke, evolution, and the rainforests: an ancient approach to modern health care.Nurs Forum.  2007 Jan-Mar;42(1):39-44.
16.    Fasano A, Physiological, Pathological, and Therapeutic Implications of Zonulin-Mediated Intestinal Barrier Modulation.  American Journal of Pathology.  2008;173:1243-1252.
17.    Kostopoulou O, Devereaux-Walsh C, Delaney BC.  Missing Celiac Disease in Family Medicine: The Importance of Hypothesis Generation.  Med Decis Making.  2009 Apr 10.
 

Celiac.com 08/03/2009 - We have a set of glands in our body that are specifically designed to help us adapt successfully to life’s stressors.

Need to move quickly? This gland will increase your heart rate and bring more blood to your muscles, making you faster and stronger.

Stressed?  This gland will produce hormones to help you deal with that stress so seems less overwhelming.

Immune system under attack? This gland will increase immunity, and hence, your potential to better “fight off” the infectious agent.

In menopause, but still want to produce hormones to keep your heart healthy, your mind sharp. and your bones strong?  This gland does the job.

Tired?  This gland will produce extra adrenaline to give you a boost.

Want to burn the calories you eat?  This gland will do that too.

Sound too good to be true?  Not at all – Let me introduce you to your adrenal glands.  They’re not very big, they sit on top of your kidneys, and they are VERY busy performing many vital functions for you.

Would you like to know if yours are functioning optimally?  Take the self-test below:

Symptoms of Adrenal Gland Malfunction

If you have 3 or more of these symptoms, you may be suffering from adrenal fatigue.

• Fatigue
• Interruption in sleep
• Difficulty waking in morning
• Joint and muscle aches
• Weight gain that is resistant to diet or exercise
• Frequent infections
• Fertility problems
• PMS
• Poor concentration/memory
• Migraines Depression/mood swings
• Low blood sugar
• Allergies
• Light headedness/ fainting
• Asthma
• Skin conditions
• Thyroid imbalances

What does adrenal fatigue have to do with gluten sensitivity?  The adrenal glands are very sensitive to blood sugar levels.  When blood sugar is unstable it puts a lot of stress on the adrenal glands and they’re unable to do their many jobs effectively.

When individuals suffer from gluten sensitivity they concurrently malabsorb some critical nutrients, thereby causing blood sugar instability.  Such instability can result in cravings for sugar, salt, or simple carbohydrates. It can also cause symptoms such as fatigue, brain fog, headaches, irritability, light-headedness, etc.

With stressed adrenal glands the body has to make a decision.  It’s the same decision you make when you have too many things to do but not enough energy to do them all.  How do you prioritize?  You undertake the most critical tasks and leave the others undone.

Similarly the adrenal glands, when overstressed, are unable to complete all the vital activities for which they are designed.  Think about it: the adrenal glands make adrenaline to provide good energy; they support your immune system to successfully fight off infections; they work in tandem with the thyroid, pituitary and hypothalamus glands to keep the endocrine system stable and functioning; they dictate your metabolic rate so you maintain an ideal weight; they make precursor sex hormones so you have a stable mood and hormonal balance; they make natural anti-inflammatories and natural antihistamines – and that’s not even a complete list!

Where does this leave us?  With a host of possible symptoms and one key root cause!  This is significant because many people are suffering from adrenal fatigue due to blood sugar instability secondary to gluten sensitivity.

When a person discovers their gluten sensitivity and removes it from their diet one of two things may happen.  They feel fantastic and all their symptoms are resolved or they feel much better but are still suffering from some problems.  It’s to this latter group that I am speaking. Sometimes when patients’ symptoms are not completely resolved, they are convinced that they have more food sensitivities or they are somehow stumbling onto some hidden gluten in their diet.  While it’s important to be diligent in this regard, more often than not in my clinic we discover adrenal fatigue to be the culprit behind these lingering symptoms.

The good news?  Adrenal fatigue is not difficult to handle.  It is a drug-free, surgery-free program that is entirely natural.

One does need to find a clinician who is familiar with diagnosing and treating this condition.  Lab tests exist to assess the functional status of the adrenals. With some nutritional and lifestyle changes, you’ll be on your way to healthy adrenal glands.  

By the way, did I mention that one of the adrenal glands’ jobs is anti-aging?  They are well worth taking care of for that reason alone.