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    How a Gluten-free Diet Helps to Reverse Some Cases of Recent-onset Dementia


    Dr. Ron Hoggan, Ed.D.


    • Journal of Gluten Sensitivity Spring 2016 Issue - Originally published April 14, 2016


    Image Caption: Photo: CC--Todd Huffman

    Celiac.com 04/26/2016 - Vice President Dan Quayle famously stated: "what a waste it is to lose one's mind, or not to have a mind is being very wasteful, how true that is," when speaking to people involved in the United Negro College Fund (1). While it is entertaining to read and ponder, this statement evokes some ideas I have about senility, which is increasing, along with many other modern diseases, at a frightening speed. The prospect of losing my mind, my memory, my sense of connection with friends and loved-ones, and even my sense of identity and personal hygiene is a frightening spectre. Can you separate your memories and experiences, along with what you think and feel, from who you are? I can't. I'm not sure I would want to be able to do so. My identity is tied to my memories, experiences, and how I responded and continue to respond to them. I remember looking at my son's tiny hands and feet when we first brought him home from the hospital. My daughter, born prematurely, had even smaller digits. They seemed impossibly tiny yet they were all perfectly formed and quite beautiful. It seemed miraculous to me. It still does. I can't imagine anything that I'd be willing to accept in exchange for those memories. Neither would I willingly surrender my memory of the joy I felt at my first convocation or my first car. Yet those lost memories form the prison in which many people already find themselves. It appears that many more will follow.


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    Photo: CC--Todd HuffmanOne segment of this problem, the epidemic of Alzheimer's disease (AD), already effects 5.4 million Americans and 30 million people throughout the world (2). Parkinson's disease, which is a neurological ailment that, in its later stages is often accompanied by dementia, is a similar ailment that is rapidly increasing both in absolute numbers and as a percentage of the population (3). Vascular dementia is yet another condition in which brain mass and mental acuity wane with advancing years (4). Perhaps this trend is partly due to the large number of aging baby boomers from the World War II era. But the relevant research suggests otherwise. Although we may be living longer and that may contribute to a small part of the growth of these devastating ailments, the biggest contributors appear to be lifestyle choices that include low daily activity levels, consumption of highly glycemic and inflammation-promoting refined carbohydrates and grain products, inadequate sleep duration, and exposure to toxic substances.

    As most students of celiac disease have long been aware, there is a powerful and potentially devastating component of brain and neurological damage associated with this ailment as a result of gluten grain consumption. In addition to the behavioral changes identified by Gibbons in 1889 (5), attention deficits identified by Reichelt (6), Neiderhofer (7, 8), and others (9 - 11), subsequent reports have connected increased incidence of seizure disorders(12-17), reductions of brain size (17 -20), a variety of neurological movement disorders (21 -23), a range of mood disorders (24, 25), and several psychiatric ailments (26, 27) including schizophrenia (28, 29), and signs of learning disabilities have been reported to improve quite dramatically and quickly on a gluten-free diet (30). Sleep disorders are also common among people with celiac disease (31). With emerging research into non-celiac gluten sensitivity over the last two decades, we have also begun to see evidence of similar connections between gluten consumption and most of these neurological/brain ailments. This added dimension of non celiac gluten sensitivity and its impact on human neurological health, were previously obscure and, in the case of amyotrophic lateral sclerosis (ALS) (26, 32), was thought to be rapidly deadly and incurable (33). Most recently, Bredesen reported that the gluten-free diet, or a low grain diet, forms one significant part of their multi-modal protocol for reversing several dementias among a small group of those who experienced recent symptom onset, including Alzheimer's disease, objectively identified disruptions in memory function or subjective, self-reported symptoms of dementia (2). Of the ten subjects studied in this latter investigation, nine showed substantial recovery in the form of symptom reversal along with either a return to work or improved performance at work (2).

    Harnessing the gluten-free diet makes sense, of course, because of the many neurological dimensions of gluten's harmful impact on human neurological tissues. Over the last 20 years, Dr. Marios Hadjivassiliou and colleagues, at the University of Sheffield and the Royal Hallamshire Hospital, have been reporting a wide range of neurological ailments in association with elevated anti-gliadin antibodies ( both with and without celiac disease) afflicting a large portion of their patients with neurological diseases of unknown origin (34 -37). Further, Dr. Joe Murray and colleagues have also reported on a group of thirteen patients experiencing moderate cognitive decline, three of whom experienced stabilized or improved cognitive function on a gluten-free diet alone (38). However, the protocol reported by Bredesen is aimed at correcting a greater number and broader spectrum of converging metabolic processes that are shaped, in large part, by our modern lifestyle, and are increasingly thought to be at the root of the current epidemic of dementias, including Alzheimer's disease (2). Gluten is only an important part of the overall picture. Dr. Suzanne de la Monte and colleagues have also identified a dynamic which they call type 3 diabetes at work in the brains of many patients with Alzheimer's disease (39). Insulin resistance, in the brain and elsewhere, is also a multi-factorial condition (40) which mostly involves disrupted metabolic processes, either through depletion of insulin production or, more likely, increased cellular resistance to insulin's movement of glucose into the cell.

    Dr. Dale Bredesen has argued that "in the past decade alone, hundreds of clinical trials have been conducted for AD, at an aggregate cost of billions of dollars, without success. This has led some to question whether the approach taken to drug development for AD is an optimal one" (2) This is the rationale that underlies his enormously broad therapeutic approach employed in his protocol.

    Please consider each of the following facets of Bredesen's therapeutic protocol:

    1. Serum testing was conducted and subsequent supplement recommendations were made, aimed at improving vitamin, mineral, amino acid, and herb supplements to achieve optimal values. All of the foregoing is aimed at harnessing their putative anti-oxidant function, supporting various facets of metabolism, and making use of their reported anti-inflammatory properties. Chelation therapy was also used to correct heavy metal (mercury, lead, cadmium) toxicity. Non-farmed fish, vegetables, and fruits were emphasized, while meat consumption was either discouraged or patients were encouraged to eat only organic and free range meat.

    2. Patients were given their choice of several low glycemic, low inflammatory, low grain diets. By this description, such a diet would exclude or severely limit gluten consumption.

    3. Patients were encouraged to engage daily in strategies, including meditation and listening to music, toward reducing their stress levels, which would reduce their cortisol production. Cortisol is a hormone that triggers increased release of glucose into the bloodstream, suppresses the immune system, and inhibits bone formation. In addition to excluding or treating sleep apnea, patients were prescribed melatonin at 0.5 mg daily, toward achieving at least eight hours of sleep each night, thereby reducing production of hunger-inducing ghrelin hormones in the stomach and increasing hunger-suppressing leptin hormones which are produced in the fat cells. Each carries its message to the brain.

    Reductions in cortisol and ghrelin secretion in combination with increasing leptin production would have a net effect of reducing inflammation while aiding weight loss and reducing blood glucose levels to normal fasting levels and targeting reduction of hemoglobin A1c levels to below 5.5, further reducing inflammation. Optimum levels of thyroid hormones, along with progesterone and pregnenolone were also pursued, along with reductions of free homocysteine to below 7 mg/L by prescription of vitamin B6, B12, and folic acid supplements, to reduce vascular damage and blockage that can be caused by elevated free homocysteine levels.

    Twice daily dietary supplementation with medium chain triglycerides (MCTs) also provides strategy for altering hormone production aimed at improved cognitive function. In humans, medium chain fatty acids resist storage. They must either be converted to ketone bodies in the liver, or rapidly utilized for energy. Because MCTs can induce the liver to increase ketone production, it provides an alternative energy source for many of the brain's cells, without requiring insulin to usher these ketones into the cells, as glucose does. In essence, adequate ketone production provides an alternative fuel both for many brain and other cells throughout the body. The liver mostly produces the ketone called beta-hydroxybutyrate. This acts not only as a fuel source, but is also a powerful anti-oxidant that does not require insulin to enter the cell, unlike vitamin C, which does require insulin to enter cells.

    4. To further promote these values and other facets of wellness arising out of regular activity, patients were asked to exercise for 30 to 60 minutes per day, 4 to 6 days each week.

    Each and all of the above have been reported somewhere in the literature as valid and valuable as part of reversing dementias, which Bredesen's list of citations supports (2). However, while significant improvements in the dementia symptoms of nine of the ten subjects does argue for the validity of this protocol, wholesale acceptance of all of the concepts here would fail to narrow our focus on those factors that are most likely to contribute to causing the vast majority of the various dementias that are contributing to the emerging epidemic. Bredesen also acknowledges that study participants were encouraged to follow as many instructions as they could. They were not asked or expected to be fully compliant with the instructions they were given. Nonetheless, I would probably err on the side of caution, by implementing as many of these strategies as possible, were I dealing with a loved-one who struggled with dementia.
    Conversely, I would be most reluctant to accept the interdiction of meats, organic or otherwise. On the other hand, growth promotion using low doses of anti-biotics can result in delivering anti-biotic resistant microbes. Poultry, hogs, and cattle are all high risk meats. Further, grains, especially gluten grains and corn, combine to form the mainstay of feeds used to fatten these animals and birds for market, where weight is the determining factor in the price paid for these meats.

    Bredesen also pointed, quite rightly, to the small number of subjects as a weakness in his study. However, when 9 of their 10 subjects achieved such remarkable results, especially in the context of the common belief that dementia, at any stage, is irreversible, this study certainly suggests that exploring dementias as a group of metabolic illnesses is a potentially fruitful path.

    This is a perspective that is enjoying considerable support from a variety of sources. Many researchers have, for the past decade or so, thought of many dementias as type 3 diabetes, with a growing body of support for this perspective amassing in the peer reviewed literature (41). More recently, chronic sleep deprivation has been similarly implicated in several ways. The first is specific to Alzheimer's disease, where beta amyloid deposits or plaques characterize this ailment. New research has shown that during sleep, brain tissues shrink, while the fluids that surround the brain permeate these tissues and inter-cellular structures, assimilating amyloid, which is a group of protein fragments (peptides) that are waste products of daytime brain cell activities (42). Because there is no lymphatic system in the brain, it has long been believed that the brain did not dispose of its waste products. However, another field of brain research has shown that conduits of these fluids form surrounding the blood vessels, carrying waste products into the bloodstream and, ultimately, out of the brain for disposal (42). Since average nightly sleep duration has shortened from nine hours to seven hours, given the above research findings, this reduction in sleep decreases our nightly capacity to remove waste amyloid and other detritus, leading to the formation and growth of amyloid deposits, which characterize at least one form of dementia.

    This same culture-wide sleep deprivation also induces memory disturbances and memory losses. It does so by a circuitous route. Throughout the day, each of us encodes memories through our hippocampus, a small region of the brain that is also involved in spatial navigation and contributes, with other parts of the lymbic system, to the regulation of many body functions. During sleep, the day's memories are thought to be processed and integrated with prior knowledge, emotions, and impressions in the neo-cortex. Some researchers are now postulating that this integration process is what results in our dreams (43-45). Regardless of whether it is the author of our dreams, Dr. Robert Stickgold and colleagues have shown that sleep helps us to consolidate the day's learning experiences, thus improving our memory retention. He has also shown that inadequate sleep compromises learning (43). The net result is that we not only need sleep to permit the brain to clean out the day's wastes, we also need it to form and preserve learning.

    Although Bredesen made no mention of it, there is another complicating factor here. Statin drugs are aimed at reducing cholesterol. However, they have also been shown to induce memory problems. One friend of mine was prescribed a statin drug, and he stopped being able to recognize me. After discontinuing this medication, he told me that I looked familiar, but he couldn't even guess at my name or where he knew me from. He waves hello to me from across the street, but doesn't cross it to visit anymore. And that seems to be where the recovery of his memory is stalled. It is with heart-rending sadness that I occasionally see him in passing. I say hello. But if he doesn't notice me waving or hear me shouting, there isn't even an exchange of greetings. He seems happy enough. So perhaps the loss is mostly mine. But I don't imagine that he would willingly have chosen this "new" world of his.

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    What a great article. It gives me some hope.

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    I have been gluten free for over 10 years due to the diagnosis of celiac disease. I don't cheat because.....well, I just don't. I have recently been diagnosed with Primary Progressive Aphasia, which is a type of dementia that starts by affecting speech. Maybe I'm one of the exceptions to the article.

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    Guest corine peck

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    What a great article. It gives me some hope.

    Great.

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  • About Me

    As co-author of "Dangerous Grains" and "Cereal Killers", the study of the impact of gluten continues to be a driving passion in my life. I am fascinated by the way that gluten induces illness and impedes learning while it alters mood, behavior, and a host of other facets of our existence. Sure, the impact of gluten on health is an important issue, but that is only the most obvious area of impact. Mood disturbances, learning disabilities, and the loss of quality of life due to psychiatric and neurological illness are even more tragic than the plethora of physical ailments that are caused or worsened by gluten. The further I go down this rabbit hole, the more I realize that grains are a good food for ruminants - not people. I am a retired school teacher. Over the last decade, I have done some college and university level teaching, but the bulk of my teaching career was spent working with high school students. My Web page is: www.DangerousGrains.com

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    Did you know that decreased calcium levels and osteoporosis, specifically calcium and vitamin D (which are lost in the stool instead of being absorbed into the body) are leading to rickets in children, a type of kidney stone called an oxalate stone, as well as osteomalacia (softening of the bone), osteopenia and osteoporosis? Those of you who have been diagnosed as having gluten sensitivity are not left out because bone diseases can occur in people with milder forms who do not appear to have malabsorption. In such people bone density can actually improve once the gluten-free diet is started.
    Did you know that many celiac patients on the gluten-free diet find that once their intestines have healed, lactase (which helps us digest the lactose in dairy products and is produced in the cells that line the surface of the villi in the small intestine) production
    The cancer concern, according to most studies, is most prevalent in long-standing UNTREATED celiac disease. Gastrointestinal cancer, such as lymphoma, even with this increased risk, is still noted as relatively rare according to Nancy Lepid, celiac disease and gluten sensitivity Expert. Yet people with celiac disease may have a near two-fold increased risk of coronary artery disease compared with the general population, according to research to be presented at the American College of Cardiology's 63rd Annual Scientific Session. This study is the first to look at the association between celiac disease and coronary artery disease and adds to the evolving understanding of how systemic inflammation and autoimmune processes might influence cardiovascular disease development. Data also showed a slightly higher risk of stroke among people with celiac disease compared to controls. Time and time again it is repeated that celiac disease is a chronic inflammatory condition of the digestive system that can damage the small intestine, eventually interfering with the absorption of key nutrients. People with celiac disease are unable to tolerate gluten because gluten is thought to trigger an immune and inflammatory response in the gut.
    Did you know that researchers found a significantly higher prevalence of coronary artery disease among patients with celiac disease compared to the control population (90.5 percent compared to 5.6 percent, respectively)? Data showed a similar trend among younger patients those under age 65, (WOW!) That is younger!?!) Compared to those without celiac disease (4.5 percent compared to 2.4 percent). This is an important study because it highlights a specific patient population who might be at higher risk for coronary artery disease, even in the absence of traditional cardiovascular risk factors, according to R.D. Gajulapelli, M.D. , clinical associate at the Cleveland Clinic and co-investigator of the study. "Our findings reinforce the idea that chronic inflammation, whether it's from an infection or a disease, can have an adverse role in coronary artery disease and heart health in general."
    I was urged to have bowel scopes every five years when I was diagnosed with celiac disease and dermatitis herpetiformis, but I was never informed of the increased risk of coronary artery disease, or that people with celiac disease were slightly more likely to have high cholesterol. Dr. Gajulapelli himself said: "We were surprised by the strength of the association of the high prevalence of coronary artery disease, "Especially" in younger people. Patients and doctors should be aware of this association. If celiac disease affects an estimated 1 in 133 Americans, but experts believe upwards of 80 percent of people with celiac disease are under-diagnosed or misdiagnosed with conditions such as lactose intolerance and irritable bowel (often called the "Catch-all" diagnoses when a physician does not know what is wrong with a patient). Previous research shows celiac disease has been on the rise and is four times more common now than it was 50 years ago. The only treatment for celiac disease is adopting a gluten-free diet.
    So you believe that these rapidly growing numbers are directly related to earlier or better diagnosis, or the education of physicians today? I prefer to believe that it is the better education of the family physician with regard to the signs of celiac disease.
    To close I wanted to surprise you with some statistics with regards to the sales of gluten-free products, which in 2010 reached $2.6 billion, and were expected to exceed more than $5 billion in 2015. This year, with the increase in prepackaged gluten-free foods and the marketing restaurant guidelines one could estimate that it will be well over $15 billion. Celiac patients used to have to prepare everything from scratch, but we are quickly buying into the boxed fast-food "celiac generation".

    Dr. Ron Hoggan, Ed.D.
    Celiac.com 10/04/2016 - Several years ago, Dr. Levinovitz contacted me by telephone, asking if he could interview me then, and in subsequent calls, for a book he was writing about gluten consumption. Assuming he, as an academic employed by a university, had an open mind, I was happy to share my own anti-gluten paradigm and the sources of my angst about these harmful foods. Dr. Levinovitz mentioned that he was involved in religious studies, but since I had earned my doctorate in the field of Education, I didn't feel any particular concern about answering his questions or his qualifications to write about gluten. As the interviews proceeded (he called back for further information and/or clarification at least once more but I think it was twice) I was most anxious to help with his project as I see gluten as a food source that fosters a great deal of illness. Because he used a poor, static laden Internet phone (VOIP) for these interviews, I missed much of what he was saying, but when I got the gist of his questions, I did my best to answer as fully and honestly as I could.
    However, when I mentioned that several of my former students had benefitted academically from excluding gluten from their diets, he wanted their names and contact information. That is when I began to feel uneasy. I told him that I would get back to him with that information if my former students were willing to be interviewed. After some thought, I decided that I would not expose these people to Dr. Levinovitz's questions without their prior permission and without a clear understanding of what he was trying to accomplish. He was quite forthcoming when I asked for some specifics about his book project. He said that he planned to attack the whole gluten-free "fad". He said that he saw it as silly and unscientific. Please remember that I'm paraphrasing something that was said several years ago, over a poor telephone connection, so I am open to correction on the specific words he used, although his meaning was crystal clear.
    I realized that he was determined to undermine much of the work I had done to sound the alarm about the human health hazards posed by gluten consumption. I speculated aloud that he had used the VOIP to make it more difficult for me to detect his duplicity when not telling me what his book project was about during that first call when he asked to interview me. I ended the call and did not respond to the two phone messages he subsequently left for me. He hadn't lied. He just hadn't told the whole truth. He claims, in his book, that exaggeration or distortion is a lie when it comes to science (p. 18). What is it when the distortion is aimed at getting an interview? Is that a lie too? I don't know.
    On the other hand, readers of his book will not suffer any confusion about its author's bias. The title gives adequate forewarning. He begins with the anti-MSG movement, which he describes in detail, beginning in 1968 and extending to a 2013 edition of a reference book where MSG is exonerated as a harmful additive, except in "rare" cases. The implication is clear. Americans condemned and avoided this Japanese flavor enhance for a period of 45 years without what Dr. Levinovitz considers to be good reason. Perhaps some Americans continue to avoid MSG. Dr. Levinovitz says that "Today, food allergy experts believe the overwhelming majority of reactions to MSG are psychological, not physiological." (1 p. 4) I saw this type of statement repeatedly when reading his book. Dr. Levinovitz makes sweeping generalizations for experts in "food allergy" and other such specialist practitioners without any apparent desire to provide a source for these statements of opinion. If his approach is correct, my training has me suffering under the faulty illusion that citing sources is a very important part of science.
    But "what," you may ask, "does MSG have to do with gluten?" Well, it seems that Dr. Levinovitz wants us to conclude that the anti-MSG fad is the same as the shift away from eating gluten grains. He also tells his readers a story about Horace Fletcher and his "theory of mastication," in which a low protein diet is consumed, chewing the food hundreds of times. This, according to Levinovitz, was what led Fletcher to make claims of weight loss and improved health. Levinovitz names several prominent individuals who followed Fletcher's prescription. Then, Dr. Levinovitz discusses epidemiology. Quoting an authority on the subject, who attributes the causal connection of lung cancer to smoking to this type of study. This authority also states that it is exceedingly difficult to establish "credible linkages" in these studies. There is a very good reason for that. Epidemiology may have pointed researchers at smoking as a candidate for causing lung cancer, but this kind of study cannot be used to establish causal relationships. That approach to dietary research is a major source of the many dietary misconceptions that Dr. Levinovitz decries.
    Levinovitz fails to explain just what epidemiology is. It is the study of correlations. During my first year of university, in the 1960s, I was taught that "correlation ‰ causation". This means that simply because two things happen at the same time and place does not mean that they are linked in a causal relationship. For example, drowning deaths can be shown to rise and fall with ice cream sales, and victims of auto accidents usually wear white underwear. Does that mean that ice cream causes drowning deaths? Or that white underwear causes car accidents? Most of us recognize these as foolish claims. Yet that is the type of study that is at the very heart of the epidemiology or "science" that Dr. Levinovitz offers his readers under the heading of "What Real Experts Say about Gluten".
    He claims that "..... after I reveal the myths and superstitions behind fears of gluten, fat, sugar, and salt, you will be less afraid of these vilified foods - and food in general." (1 p.22) He also says that: "..... exaggeration in science is nothing less than a lie" (1 p. 18).
    Lest you begin to fear that Dr. Levinovitz becomes more timid as the book progresses, the first sub-heading in chapter two is "The Gluten Liars" (1 p. 23). He very briefly explains that there are about one percent of Americans, or about 3 million have celiac disease and only 17% have been diagnosed. Thus, 2 and 1/2 million Americans with active celiac disease are, as yet, undiagnosed.
    He goes on to say that "a slightly larger number of Americans" have a condition called non celiac gluten sensitivity, but says that this malady or set of maladies is a "matter of considerable debate". Yet some of the world's foremost experts in gluten sensitivity research (2, 3) publishing in a wide array of journals, have estimated that between 0.5% and 6% of Americans have non celiac gluten sensitivity (2, 3). They define it as a condition in which the person's innate immune system reacts to gluten and causes symptoms similar to those seen in celiac disease. Although it defines a range, it is a number that could stretch to something north of 18 million individuals in the USA alone. Where I come from, that's more than just "a slightly larger number". As Dr. Levinovitz repeatedly admonishes, 'remember, in science, any exaggeration is a lie' (1 p 18).
    But there's more. Levinovitz acknowledges celiac disease (he is unclear about the diagnostic criteria) and non celiac gluten sensitivity (NCGS) diagnosed on the basis of innate immune reactions to gluten, but he really is missing quite a few people who are gluten sensitive and would, and sometimes do, benefit from a gluten free diet. For instance, when IgG antibodies against gliadin are measured, they show that 10% to 12% of the population is mounting an identifiable, measurable immune reaction to gluten grains. However, these findings are non-specific, so they are not popular with doctrinaire writers such as Dr. Levinovitz. There is also a sub-group of people with schizophrenia who show an immune reaction to transglutaminase 6, another grain-related reaction that is also implicated in some brain disorders (3).
    Dr. Levinovitz presents both Grain Brain by David Perlmutter, M.D., and Wheat Belly, by William Davis, M.D., as irresponsible and alarmist. He then claims that reading such books can "make people physically and mentally ill". That claim falls well short of the scientific standards set by these two anti-grain authors. Levinovitz apparently doesn't see any harm in his sensationalist rhetoric attacking these two physicians for writing within their areas of specialty, yet Dr. Levinovitz's field quite far removed from the laboratory. There is something terribly incongruent here. But what, exactly, does Levinovitz have to teach us about science?
    He wants us to listen to statements he attributes to several authorities. For instance, he quotes Dr. Stefano Guandalini, as an expert in nutrition, saying that the gluten free diet "is not a healthier diet for those who don't need it" p. 29 and later in the same paragraph, Guandalini is quoted as saying "these people are following a fad, essentially" but the reader is left wondering if Dr. Guandalini defined who does or does not need the diet? Such selected quotes can sometimes fail to accurately communicate the meaning of the speaker's comment.
    When I conducted an Internet search for this statement along with Dr. Guandalini's name, I found an article from the New York Times in 2013. The statement appeared to be exactly the one Dr. Levinovitz attributed to Guandalini (p. 29). However, in the NYT article, Dr. Guandalini goes on to say "And that's my biased opinion." That small addition makes a huge difference to the meaning of Dr. Guandalini's statement. I had only read to page 29 of The Gluten Lie when I discovered this deception. And Dr. Levinovitz has the nerve to go around calling others liars? He deliberately withheld the part of Dr. Guandalini's statement that qualified it as his own bias.
    Dr. Levinovitz is certainly teaching us something about gluten lies, but his lessons may not carry the message he wants to disseminate. Levinovitz mentions me in his acknowledgements. At the time of the interview, I told him repeatedly that I had earned a doctoral degree in Education, shortly after the publication of Dangerous Grains. Yet he represents me as having gone back to university to get a Master's degree. I had already accomplished that well before the time Dangerous Grains was published. I now wonder if he made this omission intentionally, especially given his other "oversights" outlined above.
    He also mentions me at several points in his book. He does grant that undiagnosed celiac disease in connection with fibromyalgia, irritable bowel syndrome, diabetes, atopic eczema, and "other related conditions." p. 43 But he insists that only those with these conditions in the context of undiagnosed celiac disease will benefit from a gluten free diet. That's a pretty strong statement. It appears that Dr. Levinovitz has not experienced the challenges of getting appropriate testing for celiac disease, so he doesn't understand.
    Perhaps he missed all the twists and turns that researchers have experienced on their way to choosing villous atrophy as the defining characteristic of celiac disease? He may not realize that the "gold standard" intestinal biopsy was a retrofit added to the diagnostic criteria for celiac disease to counter the widespread resistance to Dr. Dicke's claim that dietary gluten was the cause of celiac disease. Gastroenterologists simply wouldn't believe that gluten could cause celiac disease without some rigorous testing that ultimately excluded many of the folks who were previously diagnosable with this ailment, many of whom died from it. So the diagnostic criteria began with a constellation of gut symptoms, then it relied on an intestinal biopsy showing damage that was reversed by a gluten free diet. Now, those who have the same symptoms, which also respond to a gluten free diet, and who might previously been diagnosed with celiac disease, are now thought to have non-celiac gluten sensitivity.
    The rude dismissal of Dr. Dickie's ideas by American gastroenterologists, signals a dynamic in science that was originally outlined by Thomas S. Kuhn, which Dr. Levinovitz seems to have overlooked. Kuhn's book, The Structure of Scientific Revolutions (7) outlines the process by which scientific revolutions take place. To oversimplify and paraphrase the process, it begins with scientists in that field ignoring the new idea. Then, as it gains credence, the scientists laugh at it. With gaining momentum, the new idea is vigorously opposed. Finally, once widespread acceptance has been gained, the scientists give the impression that they had known this all along.
    Apparently, Elaine Gottshall wrote two books about gluten. I haven't read them. I have heard of them, and some folks swear by them. I don't know about the quality of information she provides. But I know that the information I provided in Dangerous Grains was accurate and it was mostly drawn from the peer reviewed medical and scientific literature, and supported by personal anecdotes from individuals on the celiac listserv. Further, every one of the more than 200 correlations between celiac disease and other ailments was drawn directly from the peer reviewed medical literature. Yet, Dr. Levinovitz lumps us together, saying that "Gottshall and Hoggan deserve our sympathy....." and in the next paragraph: "Sure, they distort the evidence and overstate the dangers of gluten. But is there any harm in that? You bet there is" (1 p. 48).
    So what did I distort? What did I overstate? Does he base his refutation of our ideas on science? His evidence looks a lot less scientific to me. For instance, he claims that "rumors of illness can make you sick" (1 p.50). So it isn't much of a stretch for him to depict specialist physicians such as William Davis, MD, David Perlmutter, MD, and myself (not a physician) as purveyors of illness. Dr. Levinovitz's "science" is made up of the personal bias of Dr. Guandalini, as quoted in the New York Times, gossip from an endocrinologist, more personal opinions from scientists, consensus opinions, and even some opinion statements published in medical journals. For instance, he quotes Jennifer Thomas, a professor of psychology at Harvard Medical School as saying "There are no studies, but anecdotally we see this all the time". She is then quoted as saying "Of course most of my patients are reading these types of books and it definitely concerns me. People can't typically stick to these rigid diets" (1 p. 54). So, if there aren't any studies are we supposed to accept her pronouncements instead? And what harm do these rigid diets do if people can't stick to them?
    Dr. Thomas does grant that "Eating disorders have been around, with or without these food fads, But I still believe that these diets can be a gateway to an eating disorder, and that they can help you maintain it" (1 p. 55). If there aren't any studies, what does she base this belief on? Isn't this the very heart of Levinovitz's argument? Doesn't he say that we should use science, not personal beliefs, to inform our views about diet?
    Then Dr. Levinovitz attacks Dr. Robert Lustig, MD, an endocrinologist. Levinovitz quotes, in his chapter about sugar, gossip from another, nameless endocrinologist who calls Lustig "extreme and opinionated" (1 p.94). Perhaps he is. I don't know Dr. Lustig. However, I do know that Dr. Levinovitz has presented this gossip as "evidence" to further his attack on a group of not just physicians, but specialist physicians who have conducted studies and have done extensive work in their specialty fields. Levinovitz relies primarily on epidemiological studies (the ones that can be used to blame drowning on ice cream sales) expressions of personal bias, published opinion statements, and consensus opinions.
    I believe that Dr. Levinovitz should attack any idea that he believes to be faulty. I believe that he is entitled to believe whatever he believes and shout it from the rooftops if he wishes. But I hope that his readers recognize that he needs more than personal opinions, gossip, sweeping generalizations, and the hyperbole he accuses others of wielding to effectively counter the work of dedicated people who have found answers for themselves and are trying to share them with others.
    His attack on salt misses the more important point that we should be consuming sea salt, not just sodium chloride, to get the salt taste and the nutritional benefits of salt without the possible hazards of too much sodium for those who are sodium sensitive.
    Are there other deceptions in The Gluten Lie? Perhaps. Is there anything of value here? I don't know. I think that we all need to take more responsibility for our own health. I don't know how most of us can do it through reading peer reviewed research articles. They are available but difficult to read without a strong educational background, especially in statistics. Dr. Levinovitz seems like a nice enough fellow except for his tendency to do exactly what he criticizes me and others for... hyperbolizing and twisting the facts to fit his own narrative. He may even have good intentions. It's hard to say. Although his omissions are misleading, I'm not sure whether he really means to mislead, or if his personal bias is so powerful that he is confused about the difference between gossip and evidence; the difference between opinion and data, and; the difference between epidemiology and the various other forms of research designs that can be brought to bear on questions about human nutrition. Whatever the source of his views on the gluten free diet, there doesn't seem to be much actual scientific insight there.
    Sources:
    Levinovitz A. The Gluten Lie And other myths about what you eat. Regan Arts, 65 Bleeker Street, NY, NY 2015. Catassi C, Bai JC, Bonaz B, Bouma G, Calabrò A, Carroccio A, Castillejo G, Ciacci C, Cristofori F, Dolinsek J, Francavilla R, Elli L, Green P, Holtmeier W, Koehler P, Koletzko S, Meinhold C, Sanders D, Schumann M, Schuppan D, Ullrich R, Vécsei A, Volta U, Zevallos V, Sapone A, Fasano A. Non-Celiac Gluten sensitivity: the new frontier of gluten related disorders. Nutrients. 2013 Sep 26;5(10):3839-53. Lebwohl B, Ludvigsson JF, Green PH. Celiac disease and non-celiac gluten sensitivity. BMJ. 2015 Oct 5;351:h4347 Cascella NG, Santora D, Gregory P, Kelly DL, Fasano A, Eaton WW. increased prevalence of transglutaminase 6 antibodies in sera from schizophrenia patients. Schizophr Bull. 2013 Jul;39(4):867-71. Leonard MM, Vasagar B. US perspective on gluten-related diseases. Clin Exp Gastroenterol. 2014 Jan 24;7:25-37. http://well.blogs.nytimes.com/2013/02/04/gluten-free-whether-you-need-it-or-not/?_r=0 Kuhn Thomas S. The Structu5re of Scientific Revolutions. University of Chicago. 1962. Aziz I, Lewis NR, Hadjivassiliou M, et al. A UK study assessing the population prevalence of self-reported gluten sensitivity and referral characteristics to secondary care. Eur J Gastroenterol Hepatol 2014;26:33-9.

    Jefferson Adams
    Celiac.com 12/01/2016 - Alcohol-related cerebellar degeneration is one of the most common forms of acquired cerebellar ataxia. Researchers still do not understand the exactly how alcohol damages the cerebellum. Very little study has been done on auto-reactive immune mediated mechanisms as a possible contributor.
    Recently, a team of researchers set out to investigate the potential role of alcohol-induced immune mediated cerebellar degeneration. The research team included Priya D. Shanmugarajah, Nigel Hoggard, Stuart Currie, Daniel P. Aeschlimann, Pascale C. Aeschlimann, Dermot C. Gleeson, Mohammed Karajeh, Nicola Woodroofe, Richard A. Grünewald and Marios Hadjivassiliou. They are variously associated with the National Blood Service Sheffield, UK; Department of Immunology, Northern General Hospital, Sheffield, UK and Academic Unit of Radiology, University of Sheffield, UK.
    For their study, the team recruited patients with ataxia and a history of heavy alcohol use from the Ataxia and Hepatology tertiary clinics at Sheffield Teaching Hospitals NHS Trust. The team determined the pattern of cerebellar involvement both on clinical (SARA score) and imaging (MRI volumetry and MR spectroscopy) parameters. They also evaluated HLA genotyping, serological markers for gluten-related disorders and serological reactivity on rat cerebellar tissue using indirect immunohistochemistry.
    In all, the team studied thirty-eight patients with ataxia, which negatively impacted the gait in 97% of patients, and stance and heel-shin slide in 89% of patients. The team used MRI volumetric and spectroscopy techniques to show significant structural, volumetric and functional deficiencies of the cerebellum with particular involvement of the cerebellar vermis.
    They found circulating anti-gliadin antibodies in 34% of patients, compared with 12% of healthy controls. They found antibodies to transglutaminase 6 (TG6) in 39% of patients, but only in 4% of healthy control subjects. Using immunohistochemistry, they found Purkinje cell and/or granular layer reactivity in 71% of patient sera.
    Alcohol induced tissue injury to the CNS leading to cerebellar degeneration may also involve immune mediated mechanisms, including sensitization to gluten. The team is calling for role of gluten in ataxia to be studied further, to determine the exact mechanism, and the extent of gluten's impact on ataxia patients.
    Source:
    Cerebellum & Ataxias 2016, 3:17. DOI: 10.1186/s40673-016-0055-1

    Jefferson Adams
    Celiac.com 04/13/2017 - A team of researchers recently set out to determine whether hospital admission for autoimmune disease is associated with an elevated risk of future admission for dementia.
    The research team included Clare J Wotton, and Michael J Goldacre, both affiliated with the Unit of Health-Care Epidemiology, Nuffield Department of Population Health, University of Oxford, Oxford, UK.
    The pair set up their retrospective, record-linkage cohort study using national hospital care and mortality administrative data from 1999–2012. From that patient data, they assembled a study group of people admitted to hospital with a range of autoimmune diseases, along with a control group, and followed forward in time to see if how many patients eventually developed dementia.
    Data revealed a total of 1,833,827 people admitted to hospital with an autoimmune disease. The number of patients for each autoimmune disease group ranged from 1,019 patients in the Goodpasture's syndrome group, to 316,043 people in the rheumatoid arthritis group.
    The researchers found that the rate ratio for dementia after admission for an autoimmune disease, compared with the control cohort, was 1.20 (95% CI 1.19 to 1.21). For patients whose dementia type was specified, the rate ratio ranged from 1.04 to 1.08 for Alzheimer's disease, and 1.26 to 1.31 for vascular dementia.
    Of the 25 autoimmune diseases studied, 18 showed significant positive associations with dementia, 14 of which were statistically significant. Significant associations include Addison's disease (1.48, 1.34 to 1.64), multiple sclerosis (1.97, 1.88 to 2.07), psoriasis (1.29, 1.25 to 1.34) and systemic lupus erythematosus (1.46, 1.32 to 1.61).
    The connections with vascular dementia may be one aspect of a wider connection between autoimmune diseases and vascular damage. Though findings were significant, effect sizes were small. Researchers advise clinicians to note the possibility of dementia in patients with autoimmune disease.
    The researchers are calling for further studies to assess their findings and to explore possible ways to reduce any increased risk.
    Source:
    BMJ

  • Recent Articles

    Christina Kantzavelos
    Celiac.com 07/20/2018 - During my Vipassana retreat, I wasn’t left with much to eat during breakfast, at least in terms of gluten free options. Even with gluten free bread, the toasters weren’t separated to prevent cross contamination. All of my other options were full of sugar (cereals, fruits), which I try to avoid, especially for breakfast. I had to come up with something that did not have sugar, was tasty, salty, and gave me some form of protein. After about four days of mixing and matching, I was finally able to come up with the strangest concoction, that may not look the prettiest, but sure tastes delicious. Actually, if you squint your eyes just enough, it tastes like buttery popcorn. I now can’t stop eating it as a snack at home, and would like to share it with others who are looking for a yummy nutritious snack. 
    Ingredients:
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    Jefferson Adams
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    Jefferson Adams
    Celiac.com 07/18/2018 - Despite many studies on immune development in children, there still isn’t much good data on how a mother’s diet during pregnancy and infancy influences a child’s immune development.  A team of researchers recently set out to assess whether changes in maternal or infant diet might influence the risk of allergies or autoimmune disease.
    The team included Vanessa Garcia-Larsen, Despo Ierodiakonou, Katharine Jarrold, Sergio Cunha,  Jennifer Chivinge, Zoe Robinson, Natalie Geoghegan, Alisha Ruparelia, Pooja Devani, Marialena Trivella, Jo Leonardi-Bee, and Robert J. Boyle.
    They are variously associated with the Department of Undiagnosed Celiac Disease More Common in Women and Girls International Health, Johns Hopkins School of Public Health, Baltimore, Maryland, United States of America; the Respiratory Epidemiology, Occupational Medicine and Public Health, National Heart and Lung Institute, Imperial College London, London, United Kingdom; the Section of Paediatrics, Department of Medicine, Imperial College London, London, United Kingdom; the Centre for Statistics in Medicine, University of Oxford, Oxford, United Kingdom; the Division of Epidemiology and Public Health, University of Nottingham, Nottingham, United Kingdom; the Centre of Evidence Based Dermatology, University of Nottingham, Nottingham, United Kingdom; and Stanford University in the USA.
    Team members searched MEDLINE, Excerpta Medica dataBASE (EMBASE), Web of Science, Central Register of Controlled Trials (CENTRAL), and Literatura Latino Americana em Ciências da Saúde (LILACS) for observational studies conducted between January 1946 and July 2013, and interventional studies conducted through December 2017, that evaluated the relationship between diet during pregnancy, lactation, or the first year of life, and future risk of allergic or autoimmune disease. 
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    They found a high bias risk in nearly half of the more than 250 milk feeding studies and in about one-quarter of studies of other dietary exposures. Evidence from 19 intervention trials suggests that oral supplementation with probiotics during late pregnancy and lactation may reduce risk of eczema. 44 cases per 1,000; 95% CI 20–64), and 6 trials, suggest that fish oil supplementation during pregnancy and lactation may reduce risk of allergic sensitization to egg. GRADE certainty of these findings was moderate. 
    The team found less evidence, and low GRADE certainty, for claims that breastfeeding reduces eczema risk during infancy, that longer exclusive breastfeeding is associated with reduced type 1 diabetes mellitus, and that probiotics reduce risk of infants developing allergies to cow’s milk. 
    They found no evidence that dietary exposure to other factors, including prebiotic supplements, maternal allergenic food avoidance, and vitamin, mineral, fruit, and vegetable intake, influence risk of allergic or autoimmune disease. 
    Overall, the team’s findings support a connection between the mother’s diet and risk of immune-mediated diseases in the child. Maternal probiotic and fish oil supplementation may reduce risk of eczema and allergic sensitization to food, respectively.
    Stay tuned for more on diet during pregnancy and its role in celiac disease.
    Source:
    PLoS Med. 2018 Feb; 15(2): e1002507. doi:  10.1371/journal.pmed.1002507

    Jefferson Adams
    Celiac.com 07/17/2018 - What can fat soluble vitamin levels in newly diagnosed children tell us about celiac disease? A team of researchers recently assessed fat soluble vitamin levels in children diagnosed with newly celiac disease to determine whether vitamin levels needed to be assessed routinely in these patients during diagnosis.
    The researchers evaluated the symptoms of celiac patients in a newly diagnosed pediatric group and evaluated their fat soluble vitamin levels and intestinal biopsies, and then compared their vitamin levels with those of a healthy control group.
    The research team included Yavuz Tokgöz, Semiha Terlemez and Aslıhan Karul. They are variously affiliated with the Department of Pediatric Gastroenterology, Hepatology and Nutrition, the Department of Pediatrics, and the Department of Biochemistry at Adnan Menderes University Medical Faculty in Aydın, Turkey.
    The team evaluated 27 female, 25 male celiac patients, and an evenly divided group of 50 healthy control subjects. Patients averaged 9 years, and weighed 16.2 kg. The most common symptom in celiac patients was growth retardation, which was seen in 61.5%, with  abdominal pain next at 51.9%, and diarrhea, seen in 11.5%. Histological examination showed nearly half of the patients at grade Marsh 3B. 
    Vitamin A and vitamin D levels for celiac patients were significantly lower than the control group. Vitamin A and vitamin D deficiencies were significantly more common compared to healthy subjects. Nearly all of the celiac patients showed vitamin D insufficiency, while nearly 62% showed vitamin D deficiency. Nearly 33% of celiac patients showed vitamin A deficiency. 
    The team saw no deficiencies in vitamin E or vitamin K1 among celiac patients. In the healthy control group, vitamin D deficiency was seen in 2 (4%) patients, vitamin D insufficiency was determined in 9 (18%) patients. The team found normal levels of all other vitamins in the healthy group.
    Children with newly diagnosed celiac disease showed significantly reduced levels of vitamin D and A. The team recommends screening of vitamin A and D levels during diagnosis of these patients.
    Source:
    BMC Pediatrics

    Jefferson Adams
    Celiac.com 07/16/2018 - Did weak public oversight leave Arizonans ripe for Theranos’ faulty blood tests scam? Scandal-plagued blood-testing company Theranos deceived Arizona officials and patients by selling unproven, unreliable products that produced faulty medical results, according to a new book by Wall Street Journal reporter, whose in-depth, comprehensive investigation of the company uncovered deceit, abuse, and potential fraud.
    Moreover, Arizona government officials facilitated the deception by providing weak regulatory oversight that essentially left patients as guinea pigs, said the book’s author, investigative reporter John Carreyrou. 
    In the newly released "Bad Blood: Secrets and Lies in a Silicon Valley Startup," Carreyrou documents how Theranos and its upstart founder, Elizabeth Holmes, used overblown marketing claims and questionable sales tactics to push faulty products that resulted in consistently faulty blood tests results. Flawed results included tests for celiac disease and numerous other serious, and potentially life-threatening, conditions.
    According to Carreyrou, Theranos’ lies and deceit made Arizonans into guinea pigs in what amounted to a "big, unauthorized medical experiment.” Even though founder Elizabeth Holmes and Theranos duped numerous people, including seemingly savvy investors, Carreyrou points out that there were public facts available to elected officials back then, like a complete lack of clinical data on the company's testing and no approvals from the Food and Drug Administration for any of its tests.
    SEC recently charged the now disgraced Holmes with what it called a 'years-long fraud.’ The company’s value has plummeted, and it is now nearly worthless, and facing dozens, and possibly hundreds of lawsuits from angry investors. Meantime, Theranos will pay Arizona consumers $4.65 million under a consumer-fraud settlement Arizona Attorney General Mark Brnovich negotiated with the embattled blood-testing company.
    Both investors and Arizona officials, “could have picked up on those things or asked more questions or kicked the tires more," Carreyrou said. Unlike other states, such as New York, Arizona lacks robust laboratory oversight that would likely have prevented Theranos from operating in those places, he added.
    Stay tuned for more new on how the Theranos fraud story plays out.
    Read more at azcentral.com.