The Role of Inflammation
Most responsible physicians take it for granted they need to examine the situation of a patient in holistic terms. Such a clinical and diagnostic framework enables a better understanding not only the disease process but also the cause of the disease.
As it happens, inflammation plays a role in different diseases, most especially neurodegenerative syndromes. Alternative therapeutic options need to be explored in depth not only to manage but possibly prevent the condition.1
Inflammation is considered the cornerstone in many neurodegenerative diseases such as Alzheimer’s, Multiple Sclerosis (MS) and Parkinson’s disease. Unlike the usual forms of inflammation which present with tell-tale signs such as redness, necrosis, swelling and pain, inflammation within the brain manifests none of these. It is difficult to ascertain any inflammation occurring in the brain through physical signs. However, with the use of chemical markers which is used in detecting inflammation of the joints, such as arthritis, inflammation in the brain can easily be identified.
Prevention of Alzheimer’s Disease
Most of the current researches and breakthroughs on Alzheimer’s disease focus on epidemiology, occurrences, trends, and cure rather than prevention. It is quite simply more profitable to discover a cure rather than empirically test preventive measures based on lifestyle, nutrition, etc. According to Lancet Neurology, however, no less than 54% of those afflicted by Alzheimer globally could have been prevented (or onset delayed) by addressing certain lifestyle issues of the patient.2 Currently, 2.6 million people in America have been diagnosed; if the preventive measures were initiated, that would be more than 1.3 million people saved from the effects of early-onset Alzheimer’s disease.
Diabetes and Alzheimer’s disease
The positive correlation between elevated blood sugar levels and Alzheimer’s has been supported by many researches all over the world. These experimenter-teams suggest that even the slightest elevation of blood sugar from the baseline for a sustained period of time correlates with a high risk of developing dementia. Aside from this, elevations of haemoglobin A1c, a marker for elevated blood sugar which lasts much longer and is a reliable marker for diabetes, has a direct correlation to shrinkage of certain parts of the brain, in particular the hippocampal and memory centres.
It is possible to control the inflammation in our body in a way by decreasing carbohydrate intake. This is because a high-carbohydrate diet may lead to the modification of certain proteins in the body, those that stimulate inflammation, and encourage production of free radicals which damage our body at a cellular level.
Fat as Alternative Source of Energy
Some people are health-conscious and refrain from eating the carbs and fats that expand their waistlines. People avoid fat especially because of the belief that they already have enough fat in their body and eating any more will induce unhealthy hypercholesterolemia.
However, people forget that the body requires fats to function properly. Fats are important structural components of the most basic subunit of our body, the cell membranes. More importantly, nerve cells are largely composed of fat and require fats to function properly. However, it must be noted that the body requires healthy fats.
Bad Fat vs. Good Fat
It is important to know alternatives to carbohydrates if a patient is supposed to avoid gluten. This is because gluten-free diet limits the carbohydrates available for consumption.
The classic examples of “dead” or “bad” fats are those fats which are found on processed canned goods. This is because food companies process the fats in such a way that the shelf-life is prolonged. This is to ensure that the food, such as a can of pork and beans, won’t turn rancid after a month of purchase because of its fat content. The fat present in these types of food are damaging fats which could have ill consequences for your body and most especially your brain. These are the types of fats that need to be avoided.
If there are bad fats, there are also good fats which we can enjoy and utilize for maximum benefit. Monounsaturated fats are a classic example of these “good” fats which we can use to replace carbohydrate intake. As an additive to dishes, the examples of oils we can use which are good for the body are olive oil and coconut oil. Avocado is a fruit which is delicious, nutritious and is filled with a good amount of healthy fat. Grass-fed beef and wild fish are meats which we can indulge on based on the protein content. In addition, one serving of each has decent amount of “good” fat.
Increased carbohydrate intake increases the function of Insulin. Basically, insulin promotes the formation of fat in most individuals, which shows that a low-fat and high-carbohydrate diet does not necessarily lead to weight loss.
Wheat is a form of carbohydrate. Wheat represents roughly 20 % of the calories ingested by most humans in the planet today. This percentage of calories ingested comes from pure carbohydrates which does not necessarily equate to a healthy diet. Pastas and breads on the other hand have minimal amounts of fat and proteins, but are still basically carbohydrates. Thus, avoiding wheat helps with gluten sensitivity or intolerance, aids in preventing inflammation and helps with weight loss.
Gluten and Headaches
Headaches can relate to many different disease processes. One consideration should be gluten sensitivity. To test for all the many underlying causes would cost a lot of money. If a person lacks the necessary funds to test for the reason behind persistent headache, one of the easiest and most cost-effective diagnostics to do is to test for gluten sensitivity. It is not suggested to forgo testing for other diseases, but testing for gluten sensitivity can help rule it out as one of the possible causes. How can a person test for gluten sensitivity? One must try a gluten-free diet.
It is necessary to check for gluten sensitivity in patients because this is often found in conjunction with headaches, ADHD, depression, movement disorders, Alzheimer’s and dementia.
Patients with gluten sensitivity do not necessarily have villous atrophy (of or referring to the villi that enable absorption) or the antibodies specific for celiac disease but test positive for gliadin-specific antibodies. Both celiac disease and gluten sensitivity may present with a vast number of neurologic and psychiatric symptoms.
This specific type of ataxia is characterized by positive gliadin-specific antibodies, MRI-detectable changes in the cerebellum and ataxic symptoms (gait ataxia or uncoordinated limb movement, dysarthria and limb ataxia on both upper and lower limbs). Upon autopsy, the cerebellum is found to have a decrease in Purkinje cells, decrease in cerebellar size (cerebellar atrophy) and Bergmann Astrocytosis.3 Patients who are subjected to a gluten-free diet for a period of 1 year after diagnosis, had experienced a significant decrease in ataxic symptoms.4
Epilepsy and Other Seizure Disorders
The prevalence of celiac disease ranges from 1-6% of total cases5 thought to be at risk. The triad of symptoms which compose the clinical picture of these cases are: occipital classifications noted through MRI, seizures which traceable to multiple brain locations, and positive diagnosis of either gluten sensitivity or celiac disease.
Patients experience visual manifestation prior to onset of a seizure. These manifestations include blurred vision as well as seeing coloured dots within the visual field.6 In a study done by Pfaender7, patients who experienced these manifestations were found to have bilateral cortical calcifications within the brain as well as the presence of celiac disease. In still another study, three patients who were noted to have hypodense areas within the white matter surrounding the calcifications manifested a reduction in the affected area after adhering to a gluten-free diet.8 There are also a number of studies which prove that the aforementioned triad of symptoms drastically decrease with the introduction of a gluten-free diet9 10
Other Neurological Manifestations
Celiac disease and gluten sensitivity presents with other symptoms which are not necessarily limited to the brain. Patients with gluten sensitivity may present with peripheral neuropathies or problems with their peripheral nervous system (the nerves found before entering the spine).11
Prolamines are a group of plant proteins which serve as a form of storage protein. Examples of prolamines are gliadin (wheat), secalin (rye), zein (corn), hordein (barley) and avening (oats). Prolamines are characterized by their high glutamine and proline amino acid content. These proteins are soluble in strong alcohol solutions but evidently not in the human digestive tract.
The gluten which causes celiac disease is a type of prolamine which triggers a cross-reaction with other prolamines. This is why it is important to test for the possibility of cross-reactivity in most individuals. By doing this, doctors are able to treat patients effectively and restrict the food types that increase the risk of harmful interactions.14
Sensitization is the process of repeated administration of a stimulus. This results in a gradual amplification of response from the body.15 In Immunology, this means the induction of allergic response based on the introduction of a specific stimulus. In this case the stimulus is gluten. This means that once the body has been sensitized to gluten, it leads to a progressively amplified response.
Increased intake of gluten leads to an amplified response in the form of an increased production of another protein called zonulin. These proteins are produced in the luminal cells of the intestine. This other protein creates a gap within the lining of the small intestine, thus making the lining more permeable. The increase in permeability leads to the entry of a variety of proteins within the gut wall. When this happens, it leads to an interaction with the inflammatory cells within the intestinal wall and an adverse immune reaction from the body.
When the intestinal epithelium becomes more permeable due to the intake of gluten, this allows allied proteins to do more damage to the body. The patient not previously sensitive to the prolamine found in corn, reacts badly to the initial “insult” caused by gluten and become sensitives to zein as well. This means that our immune system is challenged by more substances, which leads to different kinds of autoimmune conditions.
Gluten and Autism
Autism’s exact cause and pathogenesis are poorly understood. Evidence suggests that abnormalities in the immune system are related to symptoms in a number of autism patients.16 Researchers have also studied gastrointestinal symptoms and issues when it comes to barrier function in autistic patients.17 The possibility of an association between patient’s with celiac disease and autistic patients started over 40 years back.18 Studies have shown that there is higher rate of celiac disease or elevated gliadin antibody among children with autism.19 This may explain why a gluten-free diet has become a fad among families with autistic community. However, using a controlled and double-blind study has not yet validated such a cause-effect relationship.20
A recent study showed that a subset of autistic children display an increased immune reactivity to gluten. This mechanism is showed to be distinct from that present in adult celiac disease patients. The increased response of the anti-gliadin antibody and its close association with gastrointestinal symptoms show that there may be a mechanism which involves the immunologic and intestinal abnormalities in autistic children. The study showed that the affected children had higher IgG antibodies directed at gliadin compared to otherwise healthy children. Also it was noted that the antibody response of autistic children was significantly higher if they also present with gastrointestinal symptoms. Unlike the gluten sensitivity found in autistic children, celiac disease shows no association between the anti-gliadin antibody level and HLA-DQ2/DQ8, which is a highly specific serologic marker for celiac disease. This means the mechanism involved in patients with Autism is distinct from those with celiac disease. However, the researchers stated that the observed increase in the IgG antibody levels and response to gliadin does not indicate sensitivity to gluten. Neither should their results be interpreted as anti-gliadin antibodies having a pathogenic role in the development of autism.21
- Thomas, K.E., Sapone, A., Fasano, A., & Vogel, S.N. (2006). Gliadin stimulation of murine macrophage inflammatory gene expression and intestinal permeability are MyD88-dependent: Role of the innate immune response in Celiac disease. Journal of Immunology, 176 :2512–2521. ↩
- Reiman, E. M. (2014). Alzheimer’s disease and other dementias: Advances in 2013. The Lancet Neurology, 13 (1) 9-11. ↩
- Bhatia, K.P., Brown, P., Gregory, R., Lennox, G.G., Manji, H. & Thompson, P.D., et al. (1995). Progressive myoclonic ataxia associated with coeliac disease. The myoclonus is of cortical origin, but the pathology is in the cerebellum. Brain, 118 (5):1087–1093. ↩
- Hadjivassiliou, M., Kandler, R.H., Chattopadhyay, A.K., Davies-Jones, A.G., Jarratt, J.A., Sanders, D.S., et al. (2006). Dietary treatment of gluten neuropathy. Muscle and Nerve, 34:762–766. ↩
- Chin, R.L., Latov, N., Green, P.H., Brannagan, T.H., Alaedini, A. & Sander, H.W. (2004). Neurologic complications of celiac disease. Journal of Clinical Neuromuscular Disease, 5:129–137. ↩
- Pfaender, M., D’Souza, W.J., Trost, N., Litewka, L., Paine, M., & Cook, M. (2004). Visual disturbances representing occipital lobe epilepsy in patients with cerebral calcifications and coeliac disease: A case series. Journal of Neurology, Neurosurgery and Psychiatry, 75:1623–1625. ↩
- Morris, J.S., Ajdukiewicz, A.B., & Read, A.E. (1970). Neurological disorders and adult coeliac disease. Gut, 11:549–554. ↩
- Arroyo, H.A., De Rosa, S., Ruggieri, V., de Davila, M.T., & Fejerman, N. (2002). Epilepsy, occipital calcifications, and oligosymptomatic celiac disease in childhood. Journal of Child Neurology, 17: 800–806. ↩
- Canales, P., Mery, V.P., Larrondo, F.J., Bravo, F.L., & Godoy, J. (2006). Epilepsy and celiac disease: Favorable outcome with a gluten-free diet in a patient refractory to antiepileptic drugs. Neurologist, 12: 318–321. ↩
- Cernibori, A. & Gobbi, G. (1995). Partial seizures, cerebral calcifications and celiac disease. Italian Journal of Neurological Sciences,16:187–191. ↩
- Hadjivassiliou, M., Rao, D.G., Wharton, S.B., Sanders, D.S., Grunewald, R.A., & Davies-Jones, A.G. (2010). Sensory ganglionopathy due to gluten sensitivity. Neurology, 75: 1003–1008. ↩
- Hadjivassiliou, M., Chattopadhyay, A.K., Grunewald, R.A., Jarratt, J.A., Kandler, R.H., Rao, D.G., et al. (2007). Myopathy associated with gluten sensitivity. Muscle and Nerve, 35: 443–450 ↩
- Kieslich, M., Errazuriz, G., Posselt, H.G., Moeller-Hartmann, W., Zanella, F., & Boehles, H. (2001). Brain white-matter lesions in celiac disease: A prospective study of 75 diet-treated patients. Pediatrics, 108: 21. ↩
- Nelson, D.L. & Cox, M.M. (2005). Lehninger’s Principles of Biochemistry. (4th ed.). New York, New York: W. H. Freeman and Company. ↩
- Brown, M.J (1992). Sensitization. Miller-Keane Encyclopedia & Dictionary of Medicine, Nursing, and Allied Health, 5th ed. Philadelphia; London: Saunders, p. 1352. ↩
- Onore, C., Careaga, M. & Ashwood, P. (2012). The role of immune dysfunction in the pathophysiology of autism. Brain Behavior Immunology 26: 383–392. ↩
- Wang, L.W., Tancredi, D.J. & Thomas, D.W. (2011). The prevalence of gastrointestinal problems in children across the United States with autism spectrum disorders from families with multiple affected members. Journal of Developmental Behavioral Pediatrics 32: 351–360. ↩
- Dohan, F.C. (1969). Is celiac disease a clue to the pathogenesis of schizophrenia?. Mental Hygeine 53: 525–529. ↩
- Valicenti-McDermott, M.D., McVicar, K., Cohen, H.J., Wershil, B.K. & Shinnar, S. (2008). Gastrointestinal symptoms in children with an autism spectrum disorder and language regression. Pediatric Neurology 39: 392–398. ↩
- Elder, J.H. (2008). The gluten-free, casein-free diet in autism: an overview with clinical implications. Nutr Clin Pract 23: 583–588. ↩
- Lau, N. M., Green, P.H.R., Taylor, A.K., Hellberg, D., Ajamian, M., Tan, C.Z., Kosofsky, B.E., Higgins, J.J., Rajadhyaksha, A.M. & Alaedini, A. (2013). Markers of celiac disease and gluten sensitivity in children with autism. Retrieved from http://www.plosone.org/article/info%3Adoi%2F10.1371%2Fjournal.pone.0066155 ↩