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  • Dr. Ron Hoggan, Ed.D.
    Dr. Ron Hoggan, Ed.D.
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    Type 1 Diabetes - A Case Study Supporting Integration of Existing Hypotheses

      Journal of Gluten Sensitivity Autumn 2013 Issue

    Caption: Image: CC--Jill Brown

    Celiac.com 01/24/2017 - Diabetes is a condition in which blood glucose rises high enough to cause: damage to blood vessel walls, neurological injury, vision loss, and a host of other maladies. Most currently recognized cases of diabetes fall into one of two categories which are identified as type 1 and type 2 diabetes. While these two types of diabetes share many symptoms, the underlying causes are, in most cases, quite distinct, although there is also some overlap which will be explored shortly. There are also cases of gestational diabetes and some researchers are now suggesting that type 3 diabetes may be yet another entity that causes accelerating cell death in the brain, resulting dementia (1) but these latter two types of this condition are not included in the current discussion.

    All but one of these forms of diabetes involves cellular resistance to the action of insulin, although there is some gray area between type 1 and type 2 diabetes. Type 1 diabetes is the result of an autoimmune attack on a specific group of pancreatic cells called islets of Langerhans. These are the cells that produce insulin, a hormone that moves glucose out of the bloodstream and into various cells. About 14% of type 2 diabetics are also thought to experience a late-onset, slowly developing damage to pancreatic islet cells, which results in reduced insulin production in combination with their insulin resistance(2). This may be caused by autoimmunity, similar to type 1 diabetes, or it may be damage induced by other factors. Nonetheless, while type 2 diabetes can often be controlled either during weight loss or by reduced carbohydrate consumption alone, type 1 diabetes is not typically viewed as a condition that can be remedied by a change in eating habits. Yet there are some hints in the literature suggesting that dietary interventions may be therapeutically useful, especially if begun early enough in the disease process.

    Researchers Amanda MacFarlane and Fraser Scott report that there are several environmental factors, including specific foods, as well as viral, bacterial, and chemical agents that have been hypothesized to incite an autoimmune attack on the islet cells (2). They also report that about half of the animals that develop type 1 diabetes are mounting an immune response to wheat, which may also be involved in the attack on the insulin producing cells of the pancreas by either or both of two pathways they outline (2, 3). These hypothesized biological processes are identified as molecular mimicry or bystander activation and cell death. While these authors favor bystander activation, either or both of these pathways may lead to an autoimmune attack on pancreatic islet cells. Regardless of the specific biological route, type 1 diabetes can be induced in a significant portion of genetically susceptible rats and mice, simply by feeding them a diet dominated by wheat gluten. Further, the severity of their disease varies directly with the proportion of wheat gluten in the diet (2). These investigators go on to say that "These similarities between coeliac disease in humans and diabetes in BB rats, NOD mice and type 1 diabetic patients are consistent with the idea that wheat is involved in diabetes pathogenesis, possibly by inducing a subclinical, gut inflammation in many individuals that develop this form of diabetes" (2).

    They go on to report that: "Our data suggest that dietary modulation has effects at two (or more) levels:
    At the target cells before classic insulitis, changing the growth pattern of insulin-producing cells, enhancing islet mass and changing metabolism and insulin reserves . Dampening an ongoing inflammatory condition in the gut." (2)

    Scott's work (4, 5) along with investigations conducted by several groups of his colleagues (6-10) indicate that significant numbers of diabetes patients show immune reactions to the prolamins which are storage proteins in wheat, rye, and barley. Further, investigators have long understood that there is significant overlap between celiac disease and type 1 diabetes, with estimates ranging between 5% and 12% in each disease group (2, 11). MacFarlane and Scott point out that 33% to 40% of patients with type 1 diabetes show transglutaminase autoantibodies which are similar to those found in celiac patients but usually at lower levels (2).

    Low concordance rates in monozygotic (identical) twins also suggest that environmental factors play a large role in causing type 1 diabetes (2). Again, the most compelling evidence indicates that dietary consumption of wheat gluten and similar prolamins is an important factor in the autoimmune attack that destroys the pancreatic capacity to produce insulin, in genetically susceptible individuals.

    Indirect support for this perspective is offered by animal research published in July of 2011. It shows that gamma-Aminobutryic acid (GABA) supplements not only inhibit the autoimmune attack on islet cells, GABA also incites regeneration of insulin producing cells (12). GABA is a non-toxic substance that is produced by the beta cells of the pancreas (13). It plays an inhibitory role throughout the nervous system which may be significant when taken in conjunction with Rodney Ford's identification of gluten as the agent which, directly and indirectly, induces neurological damage in those with celiac disease and those with non-celiac gluten sensitivity. One pathway Ford identifies is gluten-induced neuronal excitation leading to cellular self-destruction. In light of Ford's hypothesis, the inhibitory role of GABA on neuronal tissues, both at and near synapses, offers an inviting new window for envisioning the process that incites, and therefore may reverse, type 1 diabetes.

    Clearly there is considerable cause to suspect gluten grain consumption as an important factor in the onset and perpetuation of many cases of type 1 diabetes. While genetically coded HLA markers predispose to the disease, and a number of other environmental factors may play a role in its pathogenesis, prolamins from wheat and its close relatives are clearly a frequent and important contributor to this life-long condition in which exogenous insulin (injection with hypodermic needles) is necessary for maintaining optimal health (12) while living with this malady. However, given the insights offered by the above, the following case history may offer insights that might otherwise incite only scepticism. MacFarlane and Scott suggest the following: "One approach to achieving this [prevention] is to understand and modify the environmental factors that induce disease or equip those at risk with better means of avoiding or handling these agents"(2).

    Case Study:
    On January 18, 2008, three year old K and her anxious mother were taken to a hospital emergency department in Gilbert, AZ, where the attending physician concluded that the child had experienced a febrile seizure of about 5 minutes' duration. At examination, she had a 102.5 degree temperature. In addition to fevers, K complained of abdominal pain and showed abdominal bloating. During this examination of K, she vomited. Laboratory tests showed elevated glucose (133 mg/dl) and an elevated white blood cell count (19,000). Tylenol was used to bring K's temperature down and she was discharged with instructions for the parents to administer more Tylenol as needed, and to follow up with her regular health care provider within two days.

    By February 29, K experienced more fevers, ranging between 101 and 104, intermittently over 24 hours. Every four hours, when the effects of the previous dose of Tylenol wore off, the fever would, again, spike to 103-104. K was taken to see her regular physician the following day and urinalysis revealed ketone bodies. K and her parents were then sent to the emergency department of Banner Children's Hospital.

    At the hospital, testing showed elevated urinary ketone bodies in the Large category, and blood showed elevated glucose at 193 mg/dL. Type 1 diabetes was diagnosed and K was admitted to hospital where she stayed for four days. Her condition was stabilized with ½ unit of Novalog and 4 units of Lantus. Meanwhile parents were educated about type 1 diabetes, insulin measurement and injection. They were taught to inject 1 unit of insulin for every 20 grams of carbohydrates consumed (20:1 ratio). K's parents repeatedly wondered, in the presence of the diagnosing endocrinologist, just how much insulin K was producing and how many carbohydrates a thirty pound child needed to be healthy? *

    K's father has a history of joint pain when consuming gluten grains. K was still experiencing abdominal bloating and because of the overlap between type 1 diabetes and celiac disease (2) serum IgA antibody tests were undertaken and both transglutaminase and gliadin antibody tests were negative. However, the parents observed that variations in the types of food K ate seemed to have a greater impact on blood glucose than a specific food's putative sugar content.

    In keeping with their observations that different foods, despite their equal sugar content, produced different blood glucose results, the father's history of joint pain when eating gluten, K's abdominal bloating, and the widely documented connection between gluten grains and type 1 diabetes, these foods and several others were eliminated from her diet.

    K's parents were quickly able to adjust the insulin therapy to a 40:1 ratio while K typically maintained a blood glucose range of between 80 and 95 mg/dl, which is well within the reference range for a healthy, non-diabetic person. In fact, this is a far narrower range than is prescribed by the American Diabetes Association which is 70-120 mg/dl for diabetic patients. K's family continued to target and achieve the 80-95 mg/dl range.

    After a few months of lower than normal blood sugars, still on insulin therapy, with the carbohydrate ratio now 40/1, the parents sought permission from the endocrinologist to take K off insulin completely, on the condition that her blood sugar continued within the normal range of 85-95 mg/dl. This was monitored on a daily basis. The first 24 hours were a success and another day was granted.
    After six months of following a strict and intense food therapy diet for K, the family started reintroducing foods. Some foods were reintroduced without a rise in blood sugar. She was also able to eat a larger amount of carbohydrate each meal with the same blood sugar control. Clearly, the pancreas was producing increasing quantities of insulin.

    On August 21, 2008, six months into this intensive and individualized food therapy, the patient's blood test results indicated a regeneration of the pancreas and a complete reversal of her type 1 diabetes. Her A1C was 4.8, well within the normal range for a non-diabetic person.

    Today, more than three years later, the patient is still insulin free and is using food therapy alone to maintain healthy and normal glucose control. Signs of pancreatic inflammation were also absent. Each of these findings echo MacFarlane and Scott on the issue of dietary intervention in animal studies.

    The intensive food therapy has now been replaced with a maintenance program. The variety of foods the patient can eat is vast. However, grain and casein continue to be avoided. It appears that, in this case, these foods may have contributed to K's Type 1 diabetes. It may also be that the underlying cause of the fever K experienced early in this process was a factor in the onset of her type 1diabetes, and the transient nature of this fever, and its cause, may be at the root of her recovery from this ailment. Nonetheless, given the many converging research findings indicting grains and dairy proteins, along with K's suggestive signs and symptoms, and her father's reactions to gluten, continued avoidance of these foods seems a more likely explanation.

    Thoughtful readers may also wonder just how much insulin K was producing, at the time of her diagnosis, and just how many carbohydrates a thirty pound child needs to be healthy? It may be that GABA supplements and other chemical miracles will be unnecessary for large numbers of children who suffer from type 1 diabetes. Perhaps early diagnosis and permanent dietary adjustments will be what is needed to facilitate complete recovery for many, perhaps most, children afflicted by this insidious condition. Perhaps this case history will provide the necessary impetus to encourage undertaking controlled studies of dietary factors early in the disease process of type 1 diabetes.
    * While there are no carbohydrates that are essential to good health, there are essential amino acids and essential fats.

    Sources:

    1. de la Monte SM, Wands JR. Alzheimer's disease is type 3 diabetes-evidence reviewed. J Diabetes Sci Technol. 2008 Nov;2(6):1101-13.
    2. http://www.medicine.uottawa.ca/Students/MD/BlockOrientation/assets/documents/e_inf_week05.pdf
    3. http://www.elements4health.com/type-1-diabetes-patients-have-immune-response-to-wheat-proteins.html
    4. Scott FW, Sarwar G, Cloutier HE. Diabetogenicity of various protein sources in the diet of the diabetes-prone BB rat. Adv Exp Med Biol 1988; 246: 277–85.
    5. Scott F. Dietary initiators and modifiers of BB rat diabetes. In:Shafrir E, Renold AE, eds. Frontiers in Diabetes Research:Lessons from Animal Diabetes. London: Libbey, 1988: 34–9.
    6. Hoorfar J, Buschard K, Dagnaes-Hansen F. Prophylactic nutritional modification of the incidence of diabetes in autoimmune non-obese diabetic (NOD) mice. Br J Nutr 1993; 69: 597–607.
    7. Funda DP, Kaas A, Bock T, Tlaskalova-Hogenov H, Buschard K. Gluten-free diet prevents diabetes in NOD mice. Diabetes Metab Res Rev 1999; 15: 323–7.
    8. Bao F, Yu L, Babu S et al. One third of HLA DQ2 homozygous patients with type 1 diabetes express celiac disease-associated transglutaminase autoantibodies. J Autoimmun 1999; 13:143–8.
    9. Lampasona V, Bonfanti R, Bazzigaluppi E et al. Antibodies to tissue transglutaminase C in type I diabetes. Diabetologia 1999; 42: 1195–8.
    10. Pocecco M, Ventura A. Coeliac disease and insulin-dependent diabetes mellitus: a causal association? Acta Paediatr 1995; 84: 1432–3.
    11. Hansen D, Brock-Jacobsen B, Lund E, Bjørn C, Hansen LP, Nielsen C, Fenger C, Lillevang ST, Husby S. Clinical Benefit of a Gluten-Free Diet in Type 1 Diabetic Children With Screening-Detected Celiac Disease A population-based screening study with 2 years' follow-up Diabetes Care 29:2452-2456, 2006
    12. Soltani N, Qiu H, Aleksic M, Glinka Y, Zhao F, Liu R, Li Y, Zhang N, Chakrabarti R, Ng T, Jin T, Zhang H, Lu WY, Feng ZP, Prud'homme GJ, Wang Q. GABA exerts protective and regenerative effects on islet beta cells and reverses diabetes.Proc Natl Acad Sci U S A. 2011 Jul 12;108(28):11692-7. Epub 2011 Jun 27.
    13. Bouzane B, Postmedia News June 28, 2011
    14. Ford RP. The gluten syndrome: a neurological disease. Med Hypotheses. 2009 Sep;73(3):438-40. Epub 2009 Apr 29.

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    That's lovely for K and I hope she remains free of diabetes. My son was diagnosed with type 1 diabetes - 6.5 years after his celiac diagnosis. Doctors said it's usually the opposite (diabetes then celiac). Oh well. I find that gluten free baked goods really mess with his blood sugar - take it up and keep it up.

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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

  • Related Articles

    Dr. Ron Hoggan, Ed.D.
    Beware the Gluten-Free Diet
    Celiac.com 10/16/2015 - Y Net News, under their "Health & Science" banner, published an article titled "Israeli researchers propose link between gluten and ALS", on April 17, 2015 (1). ALS refers to amyotrophic lateral sclerosis, or Lou Gehrig's disease, also known as motor neuron disease. Authorship of this article is attributed to the news agency, Reuters. The article refers to a study in which the investigators identify an autoimmune dynamic in the brain (2). The Y Net News article quotes one of these investigators as warning ALS patients against experimenting with a gluten-free diet: "Patients should not be tempted to use a gluten-free diet without clear evidence for antibodies, because an unbalanced diet might harm"(1). This is the kind of advice that frequently appears in the popular media. There can be little doubt that a gluten-free can be unhealthy, just as gluten containing diets can be unhealthy. When contacted on this issue, Dr. Drory said that "Patients with ALS tend to lose weight due to symptoms of their disease and it is well known that weight loss has a negative influence on disease progression and survival. Therefore it is very important for these patients not to lose weight" (3). Although Dr. Drory did not mean to impugn the gluten-free diet for the general population, she is legitimately concerned about the longevity and health of ALS patients, so she believes that only those with positive antibody tests should try the diet, and then only under the supervision of a dietitian. Reuters, on the other hand, have not responded to my request, through Y Net News, to contact the author of this article.
    While Dr. Drory's concerns are reasonable, I think that she has missed an important feature of the gluten-free diet and she puts too much faith in the connection between TG6 and ALS [an abbreviation for a recently discovered enzyme named tissue transglutaminase six] apparently believing that it will identify all ALS patients who might benefit from avoiding gluten. However, if we can judge based on those who have celiac disease, it is a diet that is more likely to increase the body mass of someone who is underweight. Dr. Drory also seems to have missed the sentiment expressed in the abstract of her own report. It says: "The data from this study indicate that, in certain cases, an ALS syndrome might be associated with autoimmunity and gluten sensitivity. Although the data are preliminary and need replication, gluten sensitivity is potentially treatable; therefore, this diagnostic challenge should not be overlooked" (1). Thus, when dealing with an otherwise irreversible and unstoppable disease, patients are cautioned not to try the diet without these marker antibodies which the authors identify as "preliminary" findings.
    Dr. Drory's caution also assumes that dietitians will generally be competent to guide the ALS patient in their gluten-free diet. However, it is important to recognize that the neurological patient needs to be even more strict with the diet than a person with celiac disease, and there are many uncertainties and debates around this diet. The average dietitian may not be up to date with the application of the gluten-free diet for such conditions, or the relevant controversies, or their application. Also, the beneficial results of a gluten-free diet are widespread across so many ailments and much medical research currently lags well behind patients' positive experiences. This is what has led to the continuing debate about the frequency and importance of non-celiac gluten sensitivity. Until very recently, it was usually given no attention at all. Further, since "gluten sensitivity is potentially treatable," and the current life expectancy for an ALS patient is about 2 years, it seems irresponsible to warn patients to wait for further research results before trying a gluten-free diet.
    This latter sentiment captures the essence of my current view of the gluten-free diet. Until I was diagnosed with celiac disease, more than twenty years ago, I would have ignored Dr. Drory, and subscribed to the bias inherent in the Y Net News article. Sadly, I used to dismiss people who talked about diet in the same way that I responded to those who talked about "astro travel" and Astrology. I viewed them as foolish concepts that were popular fads among drug-crazed hippies of the 1960s and 1970s, and other similarly deranged individuals. I still question many other diets, astro travel, and Astrology, but hope I do not do so with the same arrogant certitude of my youth.
    You see, I experienced a startling change of perspective shortly after I was diagnosed with celiac disease. Just three days after beginning the gluten-free diet, I awoke to an altered state of consciousness. The closest I can get to describing it is that I felt somewhat like I remember feeling as a kid when I awoke on Christmas morning. I felt optimistic, hopeful, and I looked forward to the day ahead. That was a big change. I was used to waking up feeling tired, depressed, and usually with a sense of foreboding about the coming day. I also found, after about the first six months or so of avoiding gluten, that my mind was becoming sharper, I was more aware of my surroundings, and my memory seemed to improve. My reflexes also seemed quicker. My sense of balance got better and my reaction time was faster. When I looked at others, I saw that many people were similarly challenged and didn't seem to be aware of their limitations—or perhaps they had just become used to them. Thus, I now believe that many people unknowingly suffer from the myriad harms induced or facilitated by gluten consumption. I also see, given the many venues in which the diet made a difference for me, why others might be skeptical.
    But how did Dr. Drory get from the notion that since gluten sensitivity is treatable, and should therefore be investigated as a potential factor in some cases of ALS, to the notion that ALS patients should be cautioned against experimenting with a gluten-free diet because it can cause weight loss? The gluten-free diet can be an effective weight loss strategy for some people. As I have mentioned in previous columns, the gluten-free diet seems to reduce the appetites of overweight individuals with celiac disease by about 400 calories per day. Equally, underweight celiac patients usually gain weight. Dr. Drory's concern about weight loss for those with ALS might be well founded if it was a universally good weight loss strategy. But it isn't. The data regarding weight loss on a gluten-free diet are only available, to my knowledge, with regard to celiac patients, where underweight patients almost always gain weight and about half of overweight patients lose weight. She also thinks that experimentation without a positive antibody test and the oversight of a dietitian might be risky. So her concerns may not be as valid as they first appear. If those ALS patients are gluten sensitive, then they might behave similarly to those with celiac disease, at least with regard to weight gain and loss. Further, how can anyone say, without trying it, that a gluten-free diet would not benefit those ALS patients who do not show TG6 antibodies?
    The Reuters article goes on from there to state: "It’s also worth remembering that an association is not the same as a cause. At least one earlier study concluded that there was no association between TG6 antibodies and either neurological disease or gluten itself" (1). The preceding comment refers to a retrospective research report in which the records of patients, on a Swedish data-base, who had been diagnosed with celiac disease, were further examined for an additional diagnosis of ALS (4). This is more than a little strange, since the very study the Reuters journalist used to distinguish between associations and causality, seeks only evidence of an association between the ALS and celiac disease. The notion that correlation is not causation is valid. However, using a study that looks for a correlation between celiac disease and ALS is not a reasonable basis for differentiating between correlation and causation. Neither is it a valid example of a causal relationship.
    Further, it is difficult to imagine a study design that would be less likely to reveal an association between transglutaminase TG6 and any other ailment, than one based on recorded data from a large number of patients who were diagnosed with celiac disease between 1969 and 2008. All, or almost all of these patients were diagnosed prior to the first published report of the discovery and diagnostic utility of transglutaminase 6 (5). So if one looks through records that predate the discovery of TG6 to find evidence of a connection between TG6 and any other disease, one is highly unlikely to find it.
    The abstract of the study that asserts there is no association between these ailments is based on a very weak design. It also ends with the statement: "Earlier reports of a positive association may be due to surveillance bias just after celiac disease diagnosis or expedited diagnostic work-up of ALS" (4). They are so confident of their own findings that they suggest that contrary findings are either due to bias or fast, careless work. I will leave it to the reader to infer whether there is bias among the authors of this report. Additionally, the Y Net News article, by one or more journalists at the Reuters News Agency, reports that this study found no association between TG6 antibodies and ALS, even though the study in question examines data that predates the use of TG6 antibody testing. While the study in question does appear to claim that there is no connection between celiac disease and ALS, the mention of TG6 and whether there is a connection between these antibodies and ALS appears to be information added by Reuters.
    Regardless of this possibly 'added' information, it really is quite a stretch to warn the public or ALS patients of the dangers of a gluten-free diet in reporting about research that has found evidence of a possible connection between ALS and gluten consumption. In a balanced report, the Reuters journalist would have mentioned the seven other research publications that have reported associations, and/or cause to suspect such associations, between gluten and ALS (5-11). It really isn't rocket science. It is just ethical, balanced reporting, which should serve as a minimum standard for an organization that is engaged in reporting the news. Since there are always at least two sides to almost any argument, both sides should at least have been acknowledged. Thus, in addition to the weak study reporting that they didn't find an association, the seven other reports of possible associations really should have been mentioned.
    It would also have been informative to their readers to mention Stephen Hawking, the longest living patient who was diagnosed with ALS. Dr. Hawking is still alive and has been on a gluten-free diet for the last 40+ years (12). He had already lived well beyond the two year life expectancy predicted by his doctors when, in 1963, Hawking's ALS had progressed to the point where he had begun to choke on his food. That is when he eliminated gluten, sugar, and plant oils from his diet. He has continued to avoid gluten for all these years and has also added several vitamins and supplements to his diet. Whether any or all of these measures have made "the" life extending difference, or if it is all of these measures combined that have allowed him to continue for so long, we can't know. Nonetheless, it may be that the gluten-free diet has been a determining factor in Dr. Hawking's longevity in the context of ALS. We also don't know if he would have tested positive for TG6 back when he was first diagnosed. However, he might not still be with us if he had opted to wait for this research to emerge and be confirmed.
    Since Hawking began his self-directed dietary experiment, researchers at the Royal Hallamshire Hospital in Sheffield, UK, have shown that the TG6 antibodies, while present in some celiac patients, are also found in some patients with non celiac gluten sensitivity and either neurological disease or an increased risk of developing one (5).
    Others, reporting a case study, had diagnosed ALS, then identified, diagnosed, and treated co-existing celiac disease with a gluten-free diet. They then retracted their ALS diagnosis saying: "Ultimately, improvement in the patient’s symptoms following treatment for celiac disease rendered the diagnosis of ALS untenable" (6). It would appear that any improvement in ALS symptoms obviates a diagnosis of ALS. It also raises the possibility that some cases of ALS can be effectively treated with a gluten-free diet.
    Similarly, in another case study report, the authors state: "ALS is a condition with relentless progression; for this reason, the simple observation of an improvement in symptoms is most pertinent in rendering the diagnosis of ALS untenable" (7). Again, the patient's ALS symptoms regressed following institution of a gluten-free diet.
    Yet another report that connects ALS with autoimmunity in general states: "The significance of increased premorbid celiac disease in those with ALS, and in family members of patients with MMN [multifocal motor neuropathy] remains unclear at present."(9). Still others have offered genetic evidence of connections between gluten sensitivity and ALS (10).
    Thus, the Reuters article raises an important question. Why are we seeing so many media attacks on those who are taking responsibility for their own health and experimenting with a gluten-free diet? It might come as a surprise to the Reuters journalist to learn that we humans had evolved and spread into most habitable areas of the world long before a few farmers began cultivating grains in regions of what are now known as Iraq and Iran. She/he might also be surprised to learn that we have known, for decades, that variants of wheat, rye, and barley have a deleterious impact on human neurological tissues (13, 14, 15) and that a variety of neurological ailments arise both in the context of celiac disease and non-celiac gluten sensitivity (14).
    The conclusion in the abstract of the 'no relationship' study dismisses reports of opposing findings as either due to "surveillance bias" or "expedited diagnostic work-up" (4). (This latter is a euphemistic statement suggesting that the work that led to these other reports was conducted too quickly and errors resulted.) Whatever your personal view of the attitude expressed there, the greater concern may be that the media continue to identify the gluten-free diet as potentially harmful (1) while researchers and individuals experimenting with a gluten-free diet have found evidence connecting gluten sensitivity with, at least, some cases of ALS (2).
    Over the years, I have heard many reasons for resisting this diet, but the one that is probably the least defensible is the assertion that it is potentially harmful. Almost any dietary regimen can be hazardous, of course, but the assertion that it might cause a harmful dietary imbalance fails to recognize that gluten has only been part of the Human experience for a very short time, in evolutionary terms. The simple fact is that we humans have spent far more of our evolutionary past eating a gluten-free diet than we have spent eating gluten. Some populations have only been eating these grains since European incursions over the last several hundred years. Some of these populations have only been eating it for less than one hundred years. Still others have been eating gluten for a few thousand years. In Israel, where Dr. Drory's study originated, grains were probably incorporated into the diet much earlier than in most of the rest of Europe, probably sometime between 15,000 and 10,000 years ago. It is difficult to imagine that after hundreds of thousands of years of eating a gluten-free diet, that avoiding gluten can pose a health hazard. The Reuters journalist appears to have another axe to grind, but I continue to wonder why we are seeing so many journalists on the attack against the gluten-free lifestyle?
    The driving force behind these journalists' attacks may well be similar to the perspective that I experienced before my diagnosis with celiac disease. Perhaps they suspect, whatever their reasons, that the gluten-free diet has little or no merit, and their only concession is to grudgingly allow that it may be helpful to those with celiac disease. My suspicion is that this attitude is driven by an insecurity. We want to believe conventional wisdom that gluten grains are healthy and that our medical professionals, and the institutions in which they serve, are above reproach. Nobel Laureate, Kary Mullis, is one highly vaunted physician's voice, among many, who dismiss most diets as fads, arguing that we are omnivores whose secret of successful adaptation to a wide variety of environments is the result of our flexibility in sources of nourishment (18). Many of us want to be able to rely on our physicians. We don't want the insecurity of knowing that our medical establishment is a flawed, human institution. The self-directed experimentation with a gluten-free diet poses a threat to that credibility, and hence, our sense of security, especially when it results in improved health. We don't want to feel the resulting uncertainty that comes from doubting the medical cornerstone of our civilization.
    It is not long ago that Don Wiss, myself, and others, argued extensively with physicians and researchers who insisted that the rate of celiac disease in the USA was variously one in 12,000 persons or one in 25,000 people. Sometimes these discussions became quite heated. Some of the people posting to these newsgroups were asking for suggestions for how they might proceed with various health complaints. When Don or I saw a post asking about symptoms that had been reported in the peer reviewed literature, in association with untreated celiac disease, we suggested a trial of a gluten-free diet. Some of the physicians and researchers contacted these individuals privately, saying things to discredit us. It seems doubtful that they would not have said such things where they were likely to be held accountable for what they said. Their reactions, I suspect, were driven by a sense of feeling threatened. As soon as controlled testing was done, it became clear that the rate of celiac disease, among Americans, is at least 1 in 133 Americans, and many of those individuals we advised to try a gluten-free diet might well have had celiac disease. Yet many journalists, physicians, and researchers have a great deal invested in the current status quo. Any threat to the established order is likely to incite the ire of many members of these groups.
    Thus, while others may consider it prudent to await the end of the current debate about ALS and a gluten-free diet, the ALS patient might be better advised to take dietary steps to ensure against weight loss, while trying a strict gluten-free diet. I know what I would do if were diagnosed with ALS...on second thought, since I've been gluten-free for more than twenty years, maybe I won't ever be diagnosed with ALS. I will continue to hope. In the meantime, Thomas Kuhn clearly outlined this stage of acceptance of new ideas in science (19). We appear to be in the "denial" stage, which is the last one before we can expect the emergence of widespread claims that 'we knew it all along'. If so, then broad acceptance is in the offing, and these nay-saying journalists will move on to some other controversial new discovery, and we can be spared the condescending remarks suggesting that the gluten-free diet is a mere placebo and a 'fad diet' for most of those who follow it.
    Sources:
    http://www.ynetnews.com/articles/0,7340,L-4647994,00.html Gadoth A, Nefussy B, Bleiberg M, Klein T, Artman I, Drory VE. Transglutaminase 6 Antibodies in the Serum of Patients With Amyotrophic Lateral Sclerosis. JAMA Neurol. 2015 Apr 13. Drory V. Personal communication via email Ludvigsson JF, Mariosa D, Lebwohl B, Fang F. No association between biopsy-verified celiac disease and subsequent amyotrophic lateral sclerosis--a population-based cohort study. Eur J Neurol. 2014 Jul;21(7):976-82. Hadjivassiliou M, Aeschlimann P, Strigun A, Sanders D, Woodroofe N, Aeschlimann D. Autoantibodies in gluten ataxia recognize a novel neuronal transglutaminase. Ann Neurol 2008;64:332-343 Brown KJ, Jewells V, Herfarth H, Castillo M. White matter lesions suggestive of amyotrophic lateral sclerosis attributed to celiac disease. AJNR Am J Neuroradiol. 2010 May;31(5):880-1. Turner MR, Chohan G, Quaghebeur G, Greenhall RC, Hadjivassiliou M, Talbot K. A case of celiac disease mimicking amyotrophic lateral sclerosis. Nat Clin Pract Neurol. 2007 Oct;3(10):581-4. Ihara M, Makino F, Sawada H, Mezaki T, Mizutani K, Nakase H, Matsui M, Tomimoto H, Shimohama S. Gluten sensitivity in Japanese patients with adult-onset cerebellar ataxia. Intern Med. 2006;45(3):135-40. Turner MR, Goldacre R, Ramagopalan S, Talbot K, Goldacre MJ. Autoimmune disease preceding amyotrophic lateral sclerosis: an epidemiologic study. Neurology. 2013 Oct 1;81(14):1222-5. Auburger G, Gispert S, Lahut S, Omür O, Damrath E, Heck M, BaÅŸak N. 12q24 locus association with type 1 diabetes: SH2B3 or ATXN2? World J Diabetes. 2014 Jun 15;5(3):316-27. Bersano E, Stecco A, D'Alfonso S, Corrado L, Sarnelli MF, Solara V, Cantello R, Mazzini L. Coeliac disease mimicking Amyotrophic Lateral Sclerosis. Amyotroph Lateral Scler Frontotemporal Degener. 2015 Feb 3:1-3. Hawking J. Travelling to Infinity: My Life with Stephen. Alma Books, Richmond, UK. 2014.

    Tina Turbin
    Is a Low-Glycemic Paleo Diet Beneficial for Celiacs?
    Celiac.com 06/11/2016 - It's never become so clear to me how much our health and quality of life are dependent upon the food we eat since seeing myself, my family and more than my share of celiac friends and acquaintances make the transition to grain-free from gluten-free. This is evident in witnessing such positive results just from eating a biologically appropriate diet, the paleo diet, which is grain-free and thus gluten-free. Some have this simple diet termed as the caveman diet, the paleolithic diet and what-have you, but in essence it has been deemed "man's original" diet.
    In my approaches to the topics of the paleo diet, I discovered the affects this diet has on man's health as a low glycemic alternative to man's diet, aiding ills and physical betterment through glycemic control. In my research and through working with many professionals over the years I've explored a variety of diet, health and lifestyle regimens and looked in depth into the prevailing topic of non-responsive celiacs, also known as refractory celiac disease.
    The paleo gluten-free diet is based on the premise that humans do best eating the foods our ancestors ate prior to the advent of agriculture and animal husbandry around 10,000 B.C. This proven theory is that modern humans do best on paleolithic nutrition because human genetics have largely remained the same since the pre-agricultural era, and thus our genetic makeup is best suited to the ancestral human diet—no grains at all. Taking our current bodies and then applying how man ate back in the day has been having profound effects on the general health and well-being within research and study results.
    According to research, pre-agricultural humans were free of the diseases of the civilized world such as cardiovascular disease, cancer, obesity, and autoimmune diseases. Modern studies, including clinical studies, have shown as well that eating paleo gluten-free can help or reduce risks of a variety of serious health conditions. This includes issues associated with high insulin and blood sugar levels, which can lead to a variety of diseases and health conditions such as hypertension, high cholesterol levels, obesity, type 2 diabetes and gout. That's because many foods on the paleo gluten-free diet are low-glycemic, which is evidenced in the ills they are void of, which we now classify as "normal" or aging, or an aging "disease".
    Grains are biologically similar to table sugar, causing an unhealthy spike in insulin upon consumption. Most of the carbohydrates consumed on the paleo gluten-free diet, consisting of a variety of vegetables, fruits, proteins and healthy fats are low-glycemic. Honey, maple syrups, etc. are currently debatable and this is another topic all together.
    What's the big deal about the Glycemic Index? According to studies, a low-glycemic diet can help with obesity, type 2 diabetes, polycystic ovarian syndrome, cardiovascular disease, as well as other conditions such as Alzheimer's, depression and non-responsive celiac disease. Some of the benefits of low glycemic eating include: improved weight loss, decreased hypoglycemia, steadier moods, mental clarity, sleep improvement, and reduced food cravings, which means less binge eating. This also means less overweight children with early onset diabetes, which is truly a rapidly growing concern.
    It is to our benefit that we all take a good look at our diets and the effects that the carbohydrate intake of the currently prevailing "standard" gluten-free diet has on our bodies. Let's determine if what we are eating could be causing health conditions that could possibly be reversed or avoided. Should we be willing to entertain the idea of change? The change could be as simple as taking a sincere look at man's original diet, the diet we were biologically designed to live on.
    Could our original diet of no grains, low carbohydrates and high "good" fats be a door we need to open, step through with our eyes wide open and be willing to learn about? I truly believe this topic answers many mysteries and unresolved diagnoses.

    Dr. Ron Hoggan, Ed.D.
    Doctor, How Do I Feel?
    Celiac.com 09/20/2016 - A surprising research report from Australia that explores non celiac gluten sensitivity (1) has given rise to a number of journalistic offerings that range between offensive and downright silly, while the reporters who wrote them appear to have somewhat compromised reading skills (3, 4). That is not to say that the research report is without problems. However, at least that report requires a close reading to identify its most troubling elements (1). Specifically, it suggests that patients who claim to feel better on a gluten free diet are either deluded or confused. The research implies that these patients may actually feel better because they have reduced their consumption of the starch in the gluten grains they are avoiding. That doesn't qualify as justification for either "fake" or "b$#@@#$$" (2, 3) as stated in the titles of the above journalistic offerings. The central thrust of the research report is that their investigations showed no evidence of benefits for patients who follow a gluten free diet due to the patients' belief that they are sensitive to gluten. These researchers could have said something indicating that a low FODMAPs diet might work better to help the person with NCGS [non celiac gluten sensitivity], as it not only eliminates gluten, but it also eliminates the associated starches, and a host of other sugars and starches that may also be contributing to their digestive symptoms. But they didn't. They said, instead, that they found ".....no evidence of specific or dose-dependent effects of gluten in patients with NCGS placed on a low FODMAPs diet" (1).
    First, let's be clear about what the acronym FODMAP means. It stands for fermentable, oligosaccharides, disaccharides, monosaccharides, and polyols. They are groups of sugars and starches that can induce or exacerbate gastrointestinal symptoms. But most of the gluten grains are made up of such starches (which are quickly turned to sugar as soon as we ingest them). The protein content is relatively small. Flours made from all forms of wheat and rye are high in FODMAPs (4). These people were not masquerading as having celiac disease. Neither were they trying to mislead anyone. They simply found that they feel better when avoiding gluten grains. So why the profanity and accusations embedded in the headlines of these articles (2, 3)?
    Avoidance of these foods will often help those with digestive problems. But this can happen for a variety of reasons. For instance, in a person with lactose intolerance, that individual has stopped or reduced production of the brush border enzymes (lactase) that are needed to break apart the two constituent sugars that form lactose (galactose and glucose) the sugar found in milk. The lactose molecule, a disaccharide (di = two and saccharide = sugar) is too large to be absorbed through the cells (enterocytes) that line the intestinal wall, and then into the bloodstream. While humans may not be able to digest these larger molecules of lactose, many of the bacteria that live in our intestines do so with little problem. These microscopic residents of our GI tracts multiply rapidly in the presence of so much available food. The enormous and growing numbers of these microbes, combined with their rapid digestion of lactose, produces considerable quantities of methane gas. The resulting symptoms we experience include gut pain, flatulence, smelly stools, and diarrhea. The low FODMAP diet excludes or limits oligosaccharides (from 3 to 6 units of simple sugars) disaccharides, and monosaccharides. It also excludes sugar alcohols and fermentable foods which can produce acids, gases and/or alcohols.
    Thus, only the gluten family of proteins should have been used to "challenge" the research subjects in this study (1) that is causing all the fuss. But that wasn't done.
    As may be very quickly ascertained from the interview with Sachin Rustgi, in the spring issue of this journal, there are many structural variations in each of the families of glutens and in specific gluten structures of each strain of each of the gluten-containing grains (5). In fact, Biesiekierski et al openly acknowledge that they purchased the refined gluten they used in their study from a different supplier than was used in a previous study, conducted by some of the same researchers, that confirmed the presence of non celiac gluten sensitivity (6). The later study used a form of gluten that may not have diverged much from the original, as the research group was able to state that the glutens from both studies were similar. However, they also acknowledged that they did not characterize the other, non-gluten components of the gluten they used, either. Thus, there are two possible confounding factors just in the gluten component used in this study. Small differences in the gluten protein structures may have been sufficient to cause the dramatically different result, or some added or missing non-gluten component of the gluten purchased may have caused the different result. We have no way of telling if, or to what extent, either of these factors may have played in the different findings. Without more careful work, neither could the Biesiekierski et al research group (1).
    It is not news to many of us who are gluten sensitive that differing families of gluten can produce differing symptoms and will sometimes elicit no symptoms at all. Some of us, including those with celiac disease, also react to corn and/or rice glutens, despite very clear medical statements that this is not part of our gluten-induced disease. So some of us have a more generalized reaction to gluten, while others are reacting only to sub-groups of gluten. Still others may cross react with similar proteins from other foods. Yet I can't help but believe that when such foods cause virtually identical digestive symptoms, there is some kind of connection to our problem with digesting and metabolizing gluten. Narrow medical definitions notwithstanding, each individual who struggles with this digestive issue must find her or his best answers through trial and error. Rigid journalists who genuflect at the altar of allopathic medicine will be unable to help us navigate this hazardous swamp. Neither will researchers with pre-conceived notions, who try to conduct dietary studies in a manner developed for pharmaceutical trials.
    For instance, Sachin Rustgi acknowledged that some biopsy-diagnosed celiacs will not react to a given strain of gluten grains while others with celiac disease will mount an immune reaction against the same strain (5). So each of us may be sensitized to different short strings of amino acids that form part of one or more of the family of gluten proteins or one or more of its sub-groups. This is wholly congruent with the science that explains and depicts selective antibody formation and activation.
    And that is only one part of the complexity here. Research that tries to formulate a strain of wheat that will not trigger gluten-induced illnesses must eliminate all sensitizing agents that each person with celiac disease may respond to with selective antibody production, while trying to retain the characteristics that produce the desired taste, smell, and nutrient content. Also, few of us with gluten issues need to be told that other foods can cause us to experience similar symptoms, or exacerbate, or vary, our symptoms. It can sometimes be a very confusing quagmire where it is difficult to identify the source of our symptoms.
    Further, Biesiekierski and colleagues overtly acknowledge that their focus on fatigue might have produced better insight into NCGS by revealing "why those who follow a GFD feel better" if they had asked their question differently (1). They also acknowledge the possibilities that gluten may only cause symptoms in combination with FODMAPs, or that FODMAPs cause gut problems which result in a gluten-induced loss of a sense of wellness. Their comments in this regard commendably reflect a willingness to look beyond the surface in this matter. I would go further, based on Scott Adams' interview of Sachin Rustgi (5) and assert that not all genetic strains of wheat gluten will elicit symptoms of celiac disease in a given individual with biopsy-proven celiac disease, never mind those with NCGS. So the researchers' failure to account for patient-to-patient variability, as is seen in celiac disease, along with specific wording of questions about symptoms are yet two more confounding factors in this study. Perhaps a mixture of several forms of gluten, bereft of contaminants, would have been a better choice for Biesiekierski's group. And other precautions in formulating their questions might have been useful. But there are many more problems with this report.
    Extensive Review by Expert Panel
    Dr. Carlo Catassi and a large group of widely recognized celiac experts published a comprehensive review of the medical literature on the topic of non-celiac gluten sensitivity in September of last year. Therein, they state that: " Lack of biomarkers is still a major limitation of clinical studies, making it difficult to differentiate NCGS from other gluten related disorders" (7). Conversely, the Australian group led by Biesiekierski, asserts in their report which was published the previous month, that "Generally, NCGS is viewed as a defined illness, much like celiac disease, where gluten is the cause and trigger for symptoms" (6). At least one of these groups is confused about whether or not non celiac gluten sensitivity is well defined and well understood.
    As a student of this literature myself, I would assert that the consensus view is that this form of gluten sensitivity is far from being either well defined or well understood. In fact, there is still a great deal that is not understood even about celiac disease. Non celiac gluten sensitivity has only recently begun to be widely recognized in circles of gastrointestinal researchers. Further, the Biesiekierski group's extensive use of celiac-related antibody tests appears to ignore the widely held view that biomarkers are one of the great impediments to understanding non celiac gluten sensitivity. I would also add that while I have often argued for the use of IgG class anti-gliadin antibodies as a marker of many cases gluten sensitivity (also see Jean Duane's article in this issue) with or without symptoms, I have also maintained that there are many cases in which these antibodies are not found, yet the patient will frequently benefit from removal of gluten from her/his diet.
    A further weakness of the Biesiekierski et al study is that each of the intervals during which the low FODMAP diet (2 weeks), the gluten-containing diet at 16 grams/day (for 1 week), the low gluten diet at 2 grams /day (for 1 week), and the whey-containing diet 16 grams/day ( for 1 week) all ran for periods of time that were just too short to produce measurable serological findings in people with celiac disease. Even the washout period of 2 weeks was a minimal duration. Also, the three days allotted for the re-challenge trial was certainly too brief to produce meaningful results. Some celiac disease researchers report that only about 50% of their research subjects, all of whom had biopsy diagnosed celiac disease, produced celiac-associated antibodies after a two week challenge: "Antibody titres increased slightly from baseline to day 14 of GC [gluten challenge] but markedly by day 28" (8). This puts the one week duration of the Biesiekierski study into perspective - it is a choice that may have been directed at a specific research result. By day 28 of the Leffler et al study, 75% of the celiac patients showed markedly increased celiac associated antibodies. Thus, a single week of gluten challenge, as was used in the Biesiekierski et al study would be unlikely to produce any measureable changes in serum antibodies, even among people with celiac disease, who should reasonably be expected to react most quickly and strongly to gluten ingestion. Those with biopsy diagnosed celiac disease form the group that is currently thought to mount a much more serious and vigorous immune reaction to gluten than that seen in those with non celiac gluten sensitivity. While I do not necessarily agree with that perspective, it is wholly unreasonable to expect a reaction from a group of NCGS patients in one quarter of the time it is seen in only 75% of celiac patients.
    This Leffler et al study (8) also indicates that these celiac patients were reporting symptoms within three days of beginning the gluten challenge. Thus, it seems especially surprising that self-diagnosed gluten sensitivity would be such a contentious issue that would incite such rancorous responses as those mentioned earlier (2, 3). Because NCGS is not well characterized or understood, allowing only one week for gluten ingestion to cause symptoms, if that is our only measurement of gluten's impact on their health, might work with about three quarters of celiac patients, if antibodies are measured after 28 days, but how can anyone say that it is appropriate for NCGS? Further, the use of tests, especially serological antibodies, takes the focus off of symptoms and undermines the patients' reports of symptoms, suggesting that their claims of gluten sensitivity are either misguided or duplicitous. Meanwhile, the ~25% of those with biopsy diagnosed celiac disease had not yet produced celiac associated serum antibodies, even after four weeks of gluten challenge.
    We do not need physicians to tell us how we feel.
    While most of the limitations to the Biesiekierski et al study were actually mentioned in their report, those journalists who formulated articles and inflammatory titles that included the terms "fake" (2) and "b$#@@#$$" (3) seem to have missed reading those parts of this report. Further, they took such statements as "These data suggest that NCGS, as currently defined, might not be a discrete entity or that this entity might be confounded by FODMAP restriction" to mean that there is no such thing as NCGS. However, those of us with reading skills above the middle-school level will recognize that Biesiekierski and colleagues qualified their statement in several important ways, suggesting that FODMAP restriction could be a confounding variable or that the current definition of NCGS may need to be adjusted, or the possibility that the gluten they used may not have been appropriate. One must wonder whether these journalists are that challenged when it comes to reading? Or are they trying to raise readership? Perhaps their ads sell according to how many hits and responses their websites garner. Thus, it may make sense to offend groups that are likely to post responses to their site, as a strategy aimed at raising their advertising revenue. I can't see what other limitation or motivation there might be to so dramatize these research findings with little regard for what the researchers actually said. On another level, I hope that the field of Journalism has not become so crass that they don't bother to exercise even a modicum of critical thought when reading reports of research results. That, after all, is their function in democratic societies. They are supposed to offer insightful commentaries on current trends in politics, science, education, law enforcement, and various other facets of our democratic cultures. It is difficult to find thoughtfulness or insight in the terms "fake" and "b$#@@#$$". It is also difficult to see such reports being published when a retrospective study I was involved in remains unpublished. Perhaps that is due to the finding that the gluten free diet had a very positive impact on the behavior and scholastic performance of many children.
    The gluten sensitive community has come a long way, but many biased journalists, physicians, and researchers continue to resist the notion that gluten is a food that harms many people.
    Sources:
    Biesiekierski JR, Peters SL, Newnham ED, Rosella O, Muir JG, Gibson PR. No effects of gluten in patients with self-reported non-celiac gluten sensitivity after dietary reduction of fermentable, poorly absorbed, short-chain carbohydrates. Gastroenterology. 2013 Aug;145(2):320-8.e1-3. https://ca.shine.yahoo.com/gluten-intolerance-is-fake-093131285.html http://kitchenette.jezebel.com/gluten-sensitivity-is-apparently-b$#@@#$$-1577905069 http://stanfordhospital.org/digestivehealth/nutrition/DH-Low-FODMAP-Diet-Handout.pdf Adams S. Discussion with Assistant Resident Research Professor Sachin Rustgi on the Genetic Modification of Wheat to Make it Safe for Celiacs. Jrnl Glut Sens. 2014. Spring; 13 (2): 11-13. Biesiekierski JR, Newnham ED, Irving PM, Barrett JS, Haines M, Doecke JD,Shepherd SJ, Muir JG, Gibson PR. Gluten causes gastrointestinal symptoms in subjects without celiac disease: a double-blind randomized placebo-controlled trial. Am J Gastroenterol. 2011 Mar;106(3):508-514. 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. Leffler D, et al. (2013) Kinetics of the histological, serological and symptomatic responses to gluten challenge in adults with coeliac disease. Gut 62(7):996–1004.

    Dr. Ron Hoggan, Ed.D.
    Parkinson's Disease, Seizures, Slow Recovery from Concussion
    Celiac.com 11/10/2016 - So far, 2014 has been a challenging new year for me. I was reminded of some events that happened almost fifty years ago. Based on that reminder, I resolved to contact a former girlfriend, both to suggest that she get testing for celiac disease, and to apologize for some insensitive things I said and did when I was 17. She was a year younger than me and one grade behind me in school. She was very slender and exceedingly self-conscious about having what she called "a chest like a boy". (She may have been experiencing delayed development, as is sometimes seen in celiac disease.) Every new place we visited, she went looking for the washroom as soon as she could. Movie theatres, restaurants, libraries, everywhere we went, she found the washroom first. She even did that the first time she was at my mother's house, which occasioned an uncharitable comment from my mom.
    Pat was also troubled by some microscopic hair that was growing on her upper lip. It sounds silly now, but these things were important to her at the time. I remember telling her that nobody could see her "moustache" without a magnifying glass. Nonetheless, she put Nair on it and, for at least one day, had the brightest red upper lip I have ever seen. She said it was too sore to put makeup on, so it really drew a lot of unwanted attention. Until meeting my wife, I never knew anyone who was as honest about who she was. I regret that I didn't appreciate her as much as I should have, but that was partly due to my age.
    Time passed, way led onto way, and life happened. Forty nine years later, there I was, looking for her on Facebook and other social media. I tracked her through old phone numbers, family members, and I even searched the title on her parents' home. I was full of excitement about re-connecting with my old friend, a person with whom I had shared those last innocent days of adolescence. Our friendship had been cut short because her dad was transferred to a city more than 600 miles away, and she was annoyed with me because I had said and done some insensitive things. We never even wrote to each other. I used to talk about her with my students, explaining our mutual fascination with literature. I thought about her often, but never, until this year, considered contacting her.
    After about a month of searching, I eventually found her. Much to my dismay, I was almost a year too late. She had passed away on March 10th of 2013, at the age of 64. At the time of her death, she was in the process of being evaluated for Parkinson's disease. She was at home when she experienced her last, massive seizure, which resulted in brain death. Both of her daughters are heartbroken over Pat's sudden, unexpected passing. Already a widow, Pat had left this world before I took the time and made the effort to be in touch with her again. I was filled with sadness, disappointment, and regret when I first reached one of her daughters and confirmed that she was the person I had known. I still wonder, if I had gotten in touch a decade earlier, would she still be alive? Would a gluten-free diet have helped her? I'll never know, but the relevant literature does seem to suggest that a gluten-free diet may have helped (1, 2).
    Then, a week or so ago, I received an email from a concerned mom. Her athletic, teen-aged son was recovering from a brain concussion he had sustained. His friends who had sustained similar concussions, at other times, reported having recovered more quickly. His mom began to wonder if her son's slow recovery could be the result of his celiac disease, despite more than a decade of strict compliance with the diet. I didn't know. I could only offer the suggestions that he try daily supplementation with medium chain triglycerides, and a ketogenic diet, as they seem to have stopped my life-long tremors. I also suggested that he try avoiding dairy and soy as well, based on research I did 14 years ago for my grandson.
    This concerned mom also mentioned, "I generally find doctors are dismissive of the idea that celiac is linked to any issues outside the digestive tract, unless it's malnutrition-related, and they tend to think everything should be hunky-dory if you just follow the gluten-free diet." She went on to say that "It gets kind of old being thought of as the silly, overprotective mom."
    Neurological researchers have long known about a correlation between a variety of neurological ailments and gluten sensitivity, with or without celiac disease (3). We also know that neurological symptoms are commonly found among more than half of patients with celiac disease (4). Also, despite modern diagnostic protocols and technology, we are still seeing some overlap between celiac disease and both amyotrophic lateral sclerosis (5) and multiple sclerosis (6) as well as other neurological illnesses. For instance, the increased presence of the gene named Parkinson's disease 7 (PARK7) has been found in the duodenal mucosa of untreated children with celiac disease and may be implicated in the alteration of the permeability of their intestinal barriers (7). This further suggests an important link between gluten sensitivity and Parkinson's disease. This gene may predispose to the appearance of this most distressing disease later in life.
    Many people with celiac disease continue to experience neurological symptoms, despite compliance with a gluten-free diet. This may suggest that the neurodegenerative dynamics, once initiated by gluten ingestion, may continue, either in the absence of gluten or in response to trace amounts of gluten (10). I also started to wonder if the cellular and immune system clean-up processes that follow brain injuries might initiate some of the same damaging autoimmune processes in the brain? They might also occur in response to other dietary factors which may trigger autoimmune dynamics that mimic reactions to gluten, or maybe there is some other, unknown factor that triggers the brain damage.
    One research group on the leading edge of the investigation of gluten sensitivity in relation to neurological illnesses reports that, "Incomplete elimination of gluten from the diet may be enough to abolish gastrointestinal symptoms with recovery of the small bowel mucosa but is insufficient to arrest the state of heightened immunological responsiveness resulting in neuronal injury" (10). So, when it comes to even tiny amounts of gluten, they may be enough to perpetuate gluten induced neurological illnesses. There may also an agent in the environment that is causing a cross reaction. This area really needs more investigation, as baby boomers threaten alarmingly increased rates of all forms of dementia.
    We already know that people with celiac disease are at much greater risk of developing neurological diseases than the general population (13). These ailments range from headaches to learning disabilities to movement disorders to tic disorders, to seizures, to sensory disorders (4) and many who have non-celiac gluten sensitivity also experience a high rate of neurological disease (3). Does that also mean that young athletes with celiac disease will take longer to recover from head injuries?
    Does it also mean, given the slow acceptance of gluten as a factor in many common neurological illnesses (11) that people like my former high school flame will never be told about the neuro-protective benefits of a gluten-free diet or a ketogenic diet? Surely, resistance to the well established data showing neurological manifestations of gluten sensitivity as a scientific fact (12) is more emotional than rational. A gluten-free diet and/or a ketogenic diet should be offered to those people regardless of whether their neurologist is either resistant to, or not staying current with, his/her professional literature. But they cannot offer what they do not know or have developed some bias against. Dr. David Perlmutter has done an excellent job of getting the word out to the general public, with his recent book titled Grain Brain, but there is much more work to do.
    People who are gluten sensitive, and are therefore at greater risk of developing neurological disease, might be well advised to look carefully at the benefits of a high fat, ketogenic diet, and the benefits of supplementing with medium chain triglycerides and Omega 3 fatty acids (14). Equally, they might be well advised to avoid the pro-inflammatory omega 6 and omega 9 fatty acids, as well as limiting the amounts of polyunsaturated fats they eat, which are also pro-inflammatory 14). I find that I feel my best when I am in mild, diet-induced ketosis (about 15 mg/dl as measured in morning urine, with Ketostix, which are inexpensive and available at most drug stores). There are a number of good books that explore the fine points of a high fat, ketogenic diet. These include The Art and Science of Low Carbohydrate Living by Volek and Phinney, The Ketogenic Diet by Lyle McDonald, and many others.
    Finally, when considering a gluten-free diet for neurological ailments, it is important to recognize that 20 parts per million may be far too much gluten to consume. The maximum threshold to qualify as gluten-free under the United Nations Codex Alimentarius Commission and many other regulatory agencies, including the FDA, is 20 parts per million. Without further research, especially in the field of neurology and gluten sensitivity, we will never know what, if any, levels of gluten are safe to consume.
    Regardless of the nature of your neurological ailment, whether it is Parkinson's disease, or seizures, or multiple sclerosis, or amyotrophic lateral sclerosis, or brain cancer, or almost any other kind of cancer (15), or even if you are just slow recovering from a neurological injury, the positive results of dietary interventions might offer you a whole new lease on life.
    Sources:
    http://www.medscape.com/viewarticle/770593 Currie S, Hadjivassiliou M, Clark MJ, Sanders DS, Wilkinson ID, Griffiths PD, Hoggard N. Should we be ‘nervous' about coeliac disease? Brain abnormalities in patients with coeliac disease referred for neurological opinion. J Neurol Neurosurg Psychiatry. 2012 Dec;83(12):1216-21. Matheson NA. Letter: Food faddism. Am J Clin Nutr. 1975 Oct;28(10):1083. Zelnik N, Pacht A, Obeid R, Lerner A. Range of neurologic disorders in patients with celiac disease. Pediatrics. 2004 Jun;113(6):1672-6. Brown KJ, Jewells V, Herfarth H, Castillo M, White matter lesions suggestive of amyotrophic lateral sclerosis attributed to celiac disease. AJNR Am J Neuroradiol. 2010 May;31(5):880-1 Batur-Caglayan HZ, Irkec C, Yildirim-Capraz I, Atalay-Akyurek N, Dumlu S. A case of multiple sclerosis and celiac disease. Case Rep Neurol Med. 2013;2013:576921. Vörös P, Sziksz E, Himer L, Onody A, Pap D, Frivolt K, Szebeni B, Lippai R, GyÅ‘rffy H, Fekete A, Brandt F, Molnár K, Veres G, Arató A, Tulassay T, Vannay A. Expression of PARK7 is increased in celiac disease. Virchows Arch. 2013 Sep;463(3):401-8. Hadjivassiliou M, Grünewald RA, Lawden M, Davies-Jones GA, Powell T, Smith CM. Headache and CNS white matter abnormalities associated with gluten sensitivity. Neurology. 2001 Feb 13;56(3):385-8. Hadjivassiliou M, Sanders DS, Grünewald RA, Woodroofe N, Boscolo S, Aeschlimann D. Gluten sensitivity: from gut to brain. Lancet Neurol. 2010 Mar;9(3):318-30 Hadjivassiliou M, Grünewald RA, Davies-Jones GA. Gluten sensitivity as a neurological illness. J Neurol Neurosurg Psychiatry. 2002 May;72(5):560-3. Tengah P, AJ Wills. Questions and Answers About the Neurology of Gluten Sensitivity. Pract Neurol 2003;3:354-357 Hadjivassiliou M, Grünewald R. The Neurology of Gluten Sensitivity: science Vs conviction. Pract Neurol 2004;3:4, 124-126. Hadjivassiliou M, Grünewald R. Gluten sensitivity as a neurological illness. Neurol Neurosurg Psychiatry. May 2002; 72(5): 560–563. http://www.omegascience.org/product_ingredients/coconut_oil.aspx Paoli A, Rubini A, Volek JS, Grimaldi KA. Beyond weight loss: a review of the therapeutic uses of very-low-carbohydrate (ketogenic) diets. Eur J Clin Nutr. 2013 Aug;67(8):789-96

    Jefferson Adams
    People with Type 1 Diabetes Show Distinct Gut Inflammation and Microbiota
    Celiac.com 02/01/2017 - More and more evidence shows a connection between gut inflammation and type 1 diabetes (T1D). A team of researchers recently set out to assess gut inflammatory profiles and microbiota in patients with T1D, and to compare them with healthy controls (CTRL) and with celiac disease patients as gut inflammatory disease controls.
    The research team included Silvia Pellegrini, Valeria Sordi, Andrea Mario Bolla, Diego Saita Roberto Ferrarese, Filippo Canducci, Massimo Clementi, Francesca Invernizzi, Alberto Mariani, Riccardo Bonfanti, Graziano Barera, Pier Alberto Testoni, Claudio Doglioni, Emanuele Bosi, and Lorenzo Piemonti. They are affiliated with the Diabetes Research Institute at the IRCCS San Raffaele Scientific Institute in Milan, Italy.
    The team evaluated inflammatory status and microbiome composition in biopsies of the duodenal mucosa from 19 patients with T1D, 19 with celiac disease, and 16 healthy control subjects, recruited at San Raffaele Scientific Institute, in Milan, Italy, between 2009 and 2015. They assessed inflammation by gene expression study and immunohistochemistry and used 16S rRNA gene sequencing to analyze microbiome composition.
    Compared to CTRL and celiac disease patients, the team found an increased expression of CCL13, CCL19, CCL22, CCR2, COX2, IL4R, CD68, PTX3, TNFα and VEGFA genes in T1D patients. The immunohistochemical analysis confirmed T1D specific inflammatory status was mainly marked by increased monocyte/macrophage lineage infiltration, compared to healthy and celiac disease control tissues.
    The T1D duodenal mucosal microbiome also proved to be different from the control groups. This was mainly marked by increased Firmicutes, and Firmicutes/Bacteroidetes ratio and a reduction in Proteobacteria and Bacteroidetes.
    The expression of genes specific for T1D inflammation was associated with the excess of specific bacteria in duodenum. This study shows that patients with T1D show specific abnormalities in gut inflammation and microbiota.
    Greater knowledge of the complex pathogenesis of T1D will likely provide new directions for therapies targeting the gut. Look for more studies in this area in the near future, as scientists look to nail down specific treatments to prevent gut inflammation.
    Source:
    The Journal of Clinical Endocrinology & Metabolism. DOI: https://doi.org/10.1210/jc.2016-3222

    Jefferson Adams
    Are People With Diabetes and Celiac Disease Doomed to Worse Health?
    Celiac.com 02/22/2017 - Type 1 diabetes mellitus (T1DM) and celiac disease (celiac disease) are autoimmune diseases that share similar genetic patterns. T1DM treatment is based on diet, physical activity and insulin therapy, whereas celiac disease treatment is based on a gluten-free diet.
    A research team recently set out to evaluate the quality of life (QoL) of individuals with the association of T1DM and celiac disease, to characterize their nutritional status and to compare it with those with only one disease and to healthier control subjects. The research team included JG Nunes-Silva, VS Nunes, RP Schwartz, S1 Mlss Trecco, D Evazian, ML Correa-Giannella, M Nery, and MS Queiroz. The are variously affiliated with the Nutrition and Dietetics Division, Central Institute of Clinics Hospital, the Lipids Laboratory (LIM-10), Endocrinology and Metabolism Division of Hospital das Clinicas, Faculty of Medical Sciences, the Radiology Institute of Clinics Hospital, the Cellular and Molecular Endocrinology Laboratory (LIM-18), and the Endocrinology Division, Internal Medicine Department, all at the University of São Paulo Medical School, São Paulo, Brazil.
    The researchers evaluated sixty patients controlled by sex, age and body mass index (BMI). Patients were further divided into the following groups based on previous diagnosis: DMCD group (T1DM and celiac disease); DM group (T1DM); celiac disease group (celiac disease); or HC (healthy control subjects). They used the SF-36 questionnaire to assess psychological well-being, and compared the results with glycemic control, presence of complications related to diabetes, and adhesion to gluten-free diet (GFD).
    Using BMI, waist circumference, bio-impedance, general laboratory tests and whole-body densitometry, they determined nutritional status and body mass composition.
    Both the DMCD and DM groups had similar times of diagnosis, but the duration of celiac disease was significantly higher in the celiac disease group compared with DMCD. The SF-36 analysis revealed statistically significant differences between DM and HC groups in two domains: general health (P=0.042) and energy/vitality (P=0.012).
    QoL was also correlated with compliance to a GFD, and scores were similar in both groups: DMCD and celiac disease. Forty percent of individuals in the celiac disease group had visceral fat area above 100 cm2, compared with just 20% in the other groups.
    So, are people with both Type 1 diabetes and celiac disease automatically doomed to worse health? It seems not. To be sure, they are generally less healthy than control subjects, but the study found that the DMCD group had similar scores to DM, celiac disease and HC on QoL, as well as on their nutritional status and bone metabolism. The researchers conclude from this that the association of T1DM and celiac disease did not deteriorate the health status of the individuals with both Type 1 diabetes and celiac disease.
    So, it seems that having both Type 1 diabetes and celiac disease dose not automatically mean having worse health, nutrition and well-being.
    Source:
    Nutr Diabetes. 2017 Jan 9;7(1):e239. doi: 10.1038/nutd.2016.43.

    Jefferson Adams
    Study Tracks Rates of Celiac and Type 1 Diabetes in Youth on Three Continents
    Celiac.com 07/05/2017 - Numerous researchers have documented a connection between celiac disease and type 1 diabetes.
    One team of researchers recently set out to examine international differences in celiac disease rates and clinical characteristics of youth with coexisting type 1 diabetes and celiac disease compared with type 1 diabetes only.
    The research team included Maria E. Craig, Nicole Prinz, Claire T. Boyle, Fiona M. Campbell, Timothy W. Jones, Sabine E. Hofer, Jill H.Simmons, Naomi Holman, Elaine Tham, Elke Fröhlich-Reiterer, Stephanie DuBose, Helen Thornton, Bruce King, David M. Maahs, Reinhard W. Holl and Justin T. Warner.
    To analyze the relationship between outcomes, including HbA1c, height-standard deviation score [sDS], overweight/obesity, and type 1 diabetes with celiac disease versus type 1 diabetes alone, adjusting for sex, age, and diabetes duration, the team created multivariable linear and logistic regression models.
    The analysis included 52,721 people under 18 years of age with a clinic visit between April 2013 and March 2014. The team used the following data sources: the Prospective Diabetes Follow-up registry (Germany/Austria); the T1D Exchange Clinic Network (T1DX) (U.S.); the National Paediatric Diabetes Audit (U.K. [England/Wales]); and the Australasian Diabetes Data Network (ADDN) (Australia).
    The researchers found biopsy-confirmed celiac disease in 1,835 young people, or 3.5%. These patients were diagnosed on average at age 8.1 years, with a range of 5.3 to 11.2 years.
    Most young people (37%) with diabetes upon celiac disease diagnosis had it for less than one year. Eighteen percent with diabetes had it for 1-2 years at celiac diagnosis, 23% had diabetes between 3 and 5 years at celiac diagnosis, while 17% had diabetes for more than 5 years at celiac diagnosis. Celiac disease rates ranged from 1.9% in the T1DX to 7.7% in the ADDN and were higher in girls than boys (4.3% vs. 2.7%, P < 0.001).
    Children with coexisting celiac disease were diagnosed with diabetes at 5.4 years on average, compared with those with type 1 diabetes only, who were diagnosed at 7.0 years of age, on average. Also, fewer children with both conditions were non-white, 15 vs. 18%.
    Height-SDS was lower in those with celiac disease (0.36 vs. 0.48) and fewer were overweight/obese (34 vs. 37%, adjusted P < 0.001), whereas average HbA1c values were comparable: 8.3 ± 1.5% (67 ± 17 mmol/mol) versus 8.4 ± 1.6% (68 ± 17 mmol/mol).
    This study clearly documented that celiac disease is not uncommon in young people with type 1 diabetes. Differences in disease rates may be due to variations in screening and diagnostic practices, and/or risk levels.
    Although the groups showed similar glycemic control, the research team encourages close monitoring of growth and nutrition in this population, due to the lower height-SDS.
    Source:
    Diabetes Care 2017 May; dc162508.  
    The researchers in this study are variously affiliated with the Children’s Hospital at Westmead, Sydney, New South Wales, Australia; University of New South Wales, Sydney, New South Wales, Australia; Charles Perkins Centre Westmead, University of Sydney, Sydney, New South Wales, Australia; Institute of Epidemiology and Medical Biometry, University of Ulm, Ulm, Germany; German Center for Diabetes Research, Munich-Neuherberg, Germany; Jaeb Center for Health Research, Tampa, FL; Leeds Children’s Hospital, Leeds, U.K.; The University of Western Australia, Perth, Western Australia, Australia; Telethon Kids Institute, Perth, Australia; Department of Pediatrics, Medical University of Innsbruck, Innsbruck, Austria; Vanderbilt University Medical Center, Nashville, TN; Institute of Cardiovascular and Medical Sciences, University of Glasgow, Glasgow, U.K.; Women’s and Children’s Hospital, Adelaide, South Australia, Australia; Department of Pediatrics, Medical University of Graz, Graz, Austria; St. Helens and Knowsley Teaching Hospitals NHS Trust, St. Helens, U.K.; John Hunter Children’s Hospital, Hunter Medical Research Institute, University of Newcastle, Callaghan, New South Wales, Australia; Lucile Salter Packard Children's Hospital Stanford, Stanford University Medical Center, Palo Alto, CA; and the Children's Hospital for Wales, Cardiff, U.K.

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    Rinsing it off under running water real good, this is to get any CC off. Examples, if there is a open air bakery some flour might have settled on your produce at the grocery store. OR if they are giving out samples some person might have been handling a dounut and touched your produce. Rinsing it off under running water works to remove any trace amounts normally.

    Organic. some people in general react to stuff used in growing produce, IE glyphostphate, or like me I have a issue with the wax they coat them with to keep the fresh. Going organic or farmers market fresh helps some with these. I think your nutritionist is covering all the bases.
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