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    Cholesterol, Omega-3 Fatty Acids and Celiac Disease by Roy Jamron


    Roy Jamron


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    Celiac.com 09/12/2006 - Symptoms of celiac disease prominently include fat malabsorption. One would expect this to impact levels of essential fatty acids in celiacs. The omega-3 essential fatty acids, especially eicosapentaenoic (EPA) and docosahexaenoic (DHA) acids available in fish oil supplements have been demonstrated to have numerous health benefits. However, there are almost no studies on the effect of celiac disease on essential fatty acid levels. I am currently in the process of writing an article on essential fatty acids that will appear in Celiac.coms Scott-Free Newsletter, so a new study on lipid profiles in celiac disease caught my eye with promise. I was disappointed to find the study only measured cholesterol levels in celiacs, which showed an improvement in the "bad" to "good", LDL to HDL, ratio and an increase in "good" HDL cholesterol in patients on a gluten-free diet. The opportunity to study essential fatty acid levels in celiacs was again missed. However, omega-3 fatty acids have a proven beneficial effect on cholesterol levels, and improved fat absorption of omega-3 fatty acids due to a gluten-free diet may be responsible for the results presented in this new celiac disease lipid profile study.

    Below are the abstract of this study and two studies on the effects of omega-3 fatty acids on cholesterol levels:

    Am J Med. 2006 Sep;119(9):786-90.
    Change in lipid profile in celiac disease: beneficial effect of gluten-free diet.
    Brar P, Kwon GY, Holleran S, Bai D, Tall AR, Ramakrishnan R, Green PH.

    Am J Cardiol. 2006 Aug 21;98(4 Suppl 1):71-6.
    Clinical overview of omacor: a concentrated formulation of omega-3 polyunsaturated Fatty acids.
    Bays H.

    Am J Clin Nutr. 2000 May;71(5):1085-94.
    Purified eicosapentaenoic and docosahexaenoic acids have differential effects on serum lipids and lipoproteins, LDL particle size, glucose, and insulin in mildly hyperlipidemic men.
    Mori TA, Burke V, Puddey IB, Watts gluten-free, ONeal DN, Best JD, Beilin LJ.

    New Fatty Acid Celiac Disease Study

    No sooner do I complain there arent any studies of essential fatty acid levels in celiac disease then, at least, a limited pediatric study of essential fatty acids appears! The results of this study on 7 pediatric patients with active celiac disease, 6 with celiac disease in remission, and 11 controls, show serum levels of fatty acids are similar between celiac disease and control patients, but abnormal fatty acid levels exist in intestinal mucosa tissue of active celiac disease patients. Results suggest an omega-6 fatty acid deficiency, at least in the mucosa. Not too surprising because prostaglandin E2 secretion increases in the intestines of active celiac disease patients, and prostaglandin E2 is produced from omega-6 fatty acids. It should be noted that fatty acid profiles may prove to be different in adult celiac disease patients. Also while omega-6 fatty acids may be deficient, increasing intake of omega-3 fatty acids may help reduce inflammatory processes in celiac disease.

    J Pediatr Gastroenterol Nutr. 2006 Sep;43(3):318-323.
    Abnormal Fatty Acid Pattern in Intestinal Mucosa of Children with Celiac Disease is Not Reflected in Serum Phospholipids.
    Steel DM, Ryd W, Ascher H, Strandvik B.

    Abstract:

    "Objective: Celiac disease (celiac disease) is characterized by chronic inflammation of the small intestinal mucosa with disturbed epithelial transport. The fatty acid (FA) composition of intestinal membranes is important for epithelial function, and disturbances may contribute to the pathophysiology of the disease. We aimed to evaluate whether the intestinal mucosal FA status was reflected in serum phospholipids of patients with celiac disease."

    "Patients and Methods: Samples were obtained from 7 pediatric patients with active celiac disease showing mucosal atrophy, 6 pediatric patients with celiac disease in remission, and 11 control pediatric patients with morphologically healthy intestinal mucosa. Small intestinal biopsies were obtained using a Watson biopsy capsule under fluoroscopic control. Blood samples were collected on the same morning after an overnight fast. Tissue phospholipids were isolated by high-performance liquid chromatography, and FAs were analyzed by capillary gas-liquid chromatography."

    "Results: Serum phospholipid FA showed marginal differences between the patients with celiac disease and the controls. Significant differences were observed in mucosa with active celiac disease compared with controls. Linoleic acid (18:2n-6) level was decreased, whereas those of its derivatives were elevated, indicating increased transformation of n-6 FA. Mead acid (20:3n-9) level was increased, with an increased ratio of Mead acid to arachidonic acid (20:4n-6) levels, suggesting essential fatty acid deficiency. The n-3 FA levels were not significantly changed. During remission, the FA pattern of the intestinal mucosa was mainly similar to that in controls."

    "Conclusions: The FA abnormality of intestinal mucosa in patients with active celiac disease was not reflected in serum values. Altered FA content may contribute to the pathophysiology of the disease because FAs are important for enzymes and for the transport and receptor functions of epithelial membranes."

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    Guest Mrs. Sallly Free

    Posted

    I'm very interested in replacing all the nutrients that I am loosing. Thanks for the useful information!

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    Guest sean clonts

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    Thank you for your dedication to helping others.

    I am of the belief that O3s are key to "curing" many modern ailments. We were made in a certain fashion, and to live outside the original concept is killing us.

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    Scott Adams
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    Jefferson Adams
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    http://www.news-medical.net/news/20120222/BioLineRx-BL-7010-may-reduce-gluten-toxicity-in-patients-with-celiac-disease.aspx

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    American Chemical Society

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  • Recent Articles

    Jefferson Adams
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    Dr. Ron Hoggan, Ed.D.
    Celiac.com 06/15/2018 - There seems to be widespread agreement in the published medical research reports that stuttering is driven by abnormalities in the brain. Sometimes these are the result of brain injuries resulting from a stroke. Other types of brain injuries can also result in stuttering. Patients with Parkinson’s disease who were treated with stimulation of the subthalamic nucleus, an area of the brain that regulates some motor functions, experienced a return or worsening of stuttering that improved when the stimulation was turned off (1). Similarly, stroke has also been reported in association with acquired stuttering (2). While there are some reports of psychological mechanisms underlying stuttering, a majority of reports seem to favor altered brain morphology and/or function as the root of stuttering (3). Reports of structural differences between the brain hemispheres that are absent in those who do not stutter are also common (4). About 5% of children stutter, beginning sometime around age 3, during the phase of speech acquisition. However, about 75% of these cases resolve without intervention, before reaching their teens (5). Some cases of aphasia, a loss of speech production or understanding, have been reported in association with damage or changes to one or more of the language centers of the brain (6). Stuttering may sometimes arise from changes or damage to these same language centers (7). Thus, many stutterers have abnormalities in the same regions of the brain similar to those seen in aphasia.
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    My own experience with stuttering is limited. I stuttered as a child when I became nervous, upset, or self-conscious. Although I have been gluten free for many years, I haven’t noticed any impact on my inclination to stutter when upset. I don’t know if they are related, but I have also had challenges with speaking when distressed and I have noticed a substantial improvement in this area since removing gluten from my diet. Nonetheless, I have long wondered if there is a connection between gluten consumption and stuttering. Having done the research for this article, I would now encourage stutterers to try a gluten free diet for six months to see if it will reduce or eliminate their stutter. Meanwhile, I hope that some investigator out there will research this matter, publish her findings, and start the ball rolling toward getting some definitive answers to this question.
    Sources:
    1. Toft M, Dietrichs E. Aggravated stuttering following subthalamic deep brain stimulation in Parkinson’s disease--two cases. BMC Neurol. 2011 Apr 8;11:44.
    2. Tani T, Sakai Y. Stuttering after right cerebellar infarction: a case study. J Fluency Disord. 2010 Jun;35(2):141-5. Epub 2010 Mar 15.
    3. Lundgren K, Helm-Estabrooks N, Klein R. Stuttering Following Acquired Brain Damage: A Review of the Literature. J Neurolinguistics. 2010 Sep 1;23(5):447-454.
    4. Jäncke L, Hänggi J, Steinmetz H. Morphological brain differences between adult stutterers and non-stutterers. BMC Neurol. 2004 Dec 10;4(1):23.
    5. Kell CA, Neumann K, von Kriegstein K, Posenenske C, von Gudenberg AW, Euler H, Giraud AL. How the brain repairs stuttering. Brain. 2009 Oct;132(Pt 10):2747-60. Epub 2009 Aug 26.
    6. Galantucci S, Tartaglia MC, Wilson SM, Henry ML, Filippi M, Agosta F, Dronkers NF, Henry RG, Ogar JM, Miller BL, Gorno-Tempini ML. White matter damage in primary progressive aphasias: a diffusion tensor tractography study. Brain. 2011 Jun 11.
    7. Lundgren K, Helm-Estabrooks N, Klein R. Stuttering Following Acquired Brain Damage: A Review of the Literature. J Neurolinguistics. 2010 Sep 1;23(5):447-454.
    8. [No authors listed] Case records of the Massachusetts General Hospital. Weekly clinicopathological exercises. Case 43-1988. A 52-year-old man with persistent watery diarrhea and aphasia. N Engl J Med. 1988 Oct 27;319(17):1139-48
    9. Molteni N, Bardella MT, Baldassarri AR, Bianchi PA. Celiac disease associated with epilepsy and intracranial calcifications: report of two patients. Am J Gastroenterol. 1988 Sep;83(9):992-4.
    10. http://ezinearticles.com/?Food-Allergy-and-Stuttering-Link&id=1235725 
    11. http://www.craig.copperleife.com/health/stuttering_allergies.htm 
    12. https://www.celiac.com/forums/topic/73362-any-help-is-appreciated/
    13. Ford RP. The gluten syndrome: a neurological disease. Med Hypotheses. 2009 Sep;73(3):438-40. Epub 2009 Apr 29.
    14. Hadjivassiliou M, Gibson A, Davies-Jones GA, Lobo AJ, Stephenson TJ, Milford-Ward A. Does cryptic gluten sensitivity play a part in neurological illness? Lancet. 1996 Feb 10;347(8998):369-71.

    Jefferson Adams
    Celiac.com 06/14/2018 - Refractory celiac disease type II (RCDII) is a rare complication of celiac disease that has high death rates. To diagnose RCDII, doctors identify a clonal population of phenotypically aberrant intraepithelial lymphocytes (IELs). 
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    Source:
    Journal of Clinical Pathologyhttp://dx.doi.org/10.1136/jclinpath-2018-205023

    Jefferson Adams
    Celiac.com 06/13/2018 - There have been numerous reports that olmesartan, aka Benicar, seems to trigger sprue‐like enteropathy in many patients, but so far, studies have produced mixed results, and there really hasn’t been a rigorous study of the issue. A team of researchers recently set out to assess whether olmesartan is associated with a higher rate of enteropathy compared with other angiotensin II receptor blockers (ARBs).
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    Source:
    Alimentary Pharmacology & Therapeutics