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Dementia

DementiaWhat Is Dementia?

[dropcap]D[/dropcap]ementia is the term used to describe a group of symptoms that show significant deterioration of an individual’s intellectual and social abilities.

The deterioration in intellectual function is progressive and is characterized by memory and cognitive impairment involving deficits in reasoning, judgment, abstract thought, comprehension, learning, use of language, and task execution.

Some types of dementia can be reversed,  while most types of dementia are degenerative or nonreversible.

Q: What causes dementia?

A: There are  many differing causes of dementia.  Here are some causes according to nonreversible and reversible:

  • Nonreversible dementia may not be turned back due to these conditions:
  • Alzheimer’s disease is the most common type of degenerative dementia caused by abnormal protein structures in certain areas of the brain. 
  • Lewy body disease is a leading cause of dementia in elderly adults.
  • Vascular dementia due to many small strokes.
  • Medical conditions: Huntington’s disease, multiple sclerosis, infections that can affect the brain, such as HIV/AIDS and Lyme disease, Parkinson’s disease, Pick’s disease, and progressive supranuclear palsy.
  • Reversible dementia may be stopped or reversed if these conditions are found soon enough:
  • Brain injury.
  • Brain tumors.
  • Chronic alcohol abuse.
  • Changes in blood sugar, sodium, and calcium levels.
  • Changes that can occur with celiac disease, diabetes, thyroid disease, and other metabolic disorders.
  • Nutritional deficiencies.
  • Use of certain medications, including cimetadine and some cholesterol-lowering medications.1

What Is Dementia In Celiac Disease and/or Gluten Sensitivity?

Sources:
  1. http://www.ncbi.nlm.nih.gov/pubmedhealth/PMH0001748/ []

Depression

Depression and glutenWhat Is Depression?

[dropcap]D[/dropcap]epression is a mood disorder characterized by absence of cheerfulness, dejection, and loss of interest or pleasure in living, making the person dysfunctional and unable to cope with or perform tasks of daily living.

More than a feeling, this negative psychological status can range from mild to profound and can involve other parts of the body, causing physical problems such as poor digestion, constipation, weight gain or weight loss, mentrual irregularities in females, and impotence in males.

Q: How is depression identified?

A: According to the American Psychiatric Association, depression is a psychic condition that lasts for more than a month and involves four or more of these symptoms:

  • Abnormal appetite.
  • Diminished ability to concentrate or think properly.
  • Feelings of worthlessness.
  • Low energy or fatigue.
  • Physical inactivity or hyperactivity.
  • Sleep disturbances.
  • Thoughts of death.

Grief or sadness at the loss of a loved one or a similar event or remorse for sin is normal. However, depression that is prolonged usually involves imbalances of nerve chemicals called neurotransmitters. Imbalances can result from health disorders such as hormonal imbalances, low blood sugar, stress, drug side effects, or nutrient deficiencies.

What Is Depression In Celiac Disease and/or Gluten Sensitivity?

Headache (Emicrania)

headache gluten celiac disease symptomWhat Is Headache Or Emicrania?

[dropcap]E[/dropcap]micrania is a headache resulting from stimulation of, or traction of, or pressure on any of the pain sensitive structures of the head characterized by pain felt anywhere in the head.

In addition to gluten sensitivity and nutritional deficiencies, there are many causes of headache including cardiac, cerebral, vascular, psychiatric, metabolic, and neurologic diseases. Recent studies have highlighted that obesity is significantly associated with headache and disability in adults. This rule also applies to children.1

What Is Headache In Celiac Disease and/or Gluten Sensitivity?

Sources:
  1. Laino D, Vitaliti G, Parisi P,   et. al. Headache, migraine and obesity: an overview on plausible links. J Biol Regul Homeost Agents. 2016 Apr-Jun;30(2):333-8. []

Chronic Fatigue / Lassitude / Tiredness

Chronic FatigueWhat Is Chronic Fatigue?

[dropcap]C[/dropcap]hronic fatigue or lassitude is a state of weariness not relieved by rest and the inability to do normal physical or mental work.

Q: What are causes of chronic fatigue?

A: Chronic fatigue can be a feature of many disorders including nutritional problems like poor diet or malabsorption, sleep problems, systemic conditions like anemia or heart disease, respiratory disorders like COPD or asthma, infectious disease like tuberculosis, endocrine disorders like diabetes, autoimmune disease like thyroid disease, and cancer.

Fatigue greatly reduces quality of life in all aspects including the desire and ability to socialize and find fullfillment in new and interesting ways.

What Is Chronic Fatigue In Celiac Disease and/or Gluten Sensitivity?

Chronic Fatigue Syndrome 

What Is Chronic Syndrome Fatigue? [dropcap]C[/dropcap]hronic fatigue syndrome is a debilitating illness characterized by persistent or relapsing overwhelming and incapacitating fatigue not relieved by rest, having a definite onset and often accompanied by numerous symptoms… 

DHA (Docosahexaenoic Acid) Deficiency

Smoked Salmon...Brain Food that's Good for the Eyes!
Salmon…Brain Food That’s Good for Your Eyes, Heart, Blood Vessels, Blood Sugar, Liver, Muscles, and Fights Inflammation!

What Is DHA?

[dropcap]D[/dropcap]ocosahexaenoic acid (DHA) is an essential omega-3 fatty acid that is abundant in the brain, being crucial in brain structure. As such DHA is a key component of neuronal membranes together with arachidonic acid (a major opposing omega-6 fatty acid), making up 15-20% of the brain’s dry mass.

This polyunsaturated fatty acid is obtained from fish sources of food.

In healthy human volunteers, positron emission tomography (PET) has shown that the normal human brain consumes 4.6 mg/day of DHA.1

DHA is particularly concentrated in highly active membranes such as nerve synapses (junctions) and photoreceptors in the eye (retina).

Q: How much DHA is in the retina?

A: DHA makes up more than 30% of the retina.2

In other roles, DHA is an  important building material for the eicosanoids, a large group of highly bioactive hormone-like substances including prostaglandins, leukotrienes, and thromboxanes that are involved in blood clotting, inflammation, and vasoconstriction.

DHA has been shown to increase insulin sensitivity as opposed to the opposite problem of insulin resistance, to improve muscle mass, and protect against non-alcoholic fatty liver disease.3

Egert et al. in a study of people aged 19 to 43 years with normal cholesterol showed that DHA intake significantly increased serum HDL (good) cholesterol. Also, DHA significantly decreased fasting serum triglycerides.4

What Is DHA Deficiency In Celiac Disease and/or Gluten Sensitivity?

Sources:
  1. Rapoport SI. Brain arachidonic and docosahexaenoic acid cascades are selectively altered by drugs, diet and disease. Prostaglandins Leukot Essent Fatty Acids. 2008 Sep-Nov;79(3-5):153-6. Epub 2008 Oct 29. []
  2. Richardson AJ. The importance of omega-3 fatty acids for behavior, cognition, and mood. Scandinavian Journal of Nutrition. 2003;47(2):92-8 []
  3. Espinosa A, Valenzuela R, González-Mañán D, D’Espessailles A, Guillermo Gormaz J, Barrera C, Tapia G. Prevention of liver steatosis through fish oil supplementation: correlation of oxidative stress with insulin resistance and liver fatty acid content. Arch Latinoam Nutr. 2013 Mar;63(1):29-36. []
  4. Egert S, Kannenberg F, Somoza V, et al. Dietary alpha-linolenic acid, EPA, and DHA have differential effects on LDL fatty acid composition but similar effects on serum lipid profiles in normolipidemic humans. J Nutr. 2009;139:861–868. doi: 10.3945/jn.108.103861 []

Stroke in Childhood 

e4789565d1b49c3541a6a51b31ab8b30What Is Stroke In Childhood?

[dropcap]S[/dropcap]troke in childhood is a medical emergency during which blood flow to an area of the brain is stopped, causing infarction or death of the area of cells in the brain fed by the blocked artery. Stroke is characterized by loss of muscle and brain function according to the location of the lost cells.

The brain is a highly active metabolic and complex organ of our body that performs important functions, therefore, any disruption in its normal functioning can have devastating effects on whole body.

After stroke, an immune response is initiated that leads to production of proinflammatory cytokines (chemicals) and gathering of various inflammatory cells like neutrophils, T-cells, macrophage, and monocytes to the affected area that exacerbate or worsen the ischemic (oxygen starved) injury.1

Arterial ischemic stroke is an important cause of acquired brain injury in children.2 This stroke results from loss of adequate blood flow through an artery that supplies the affected area of the brain with oxygen and nutrients.

A recent study found the majority of  children (85%) had focal features (most commonly one sided weakness or paralysis) at presentation to their medical practitioner. Seizures were more common in younger children a year old or younger and headache was more common in children 5 years or older.3

Who is at Risk in the General Population?

  • A British study in 2014 found the crude incidence of childhood arterial ischemic stroke was 1.60 per 100,000 per year.
  • The incidence of arterial ischemic stroke was highest in children aged under 1 year (4.14 per 100,000 per year).
  • There was no difference in the risk of arterial ischemic stroke between sexes.
  • Asian and black children were at higher risk than were white children.3

What Is Stroke in Childhood In Celiac Disease and/or Gluten Sensitivity?

Sources:
  1. Andrabi SS, Parvez S, Tabassum H. Melatonin and Ischemic Stroke: Mechanistic Roles and Action. Adv Pharmacol Sci. 2015;2015:384750. doi: 10.1155/2015/384750. Epub 2015 Sep 7. []
  2. Mallick AA, Ganesan V, Kirkham FJ, et al. Childhood arterial ischaemic stroke incidence, presenting features, and risk factors: a prospective population-based study. Lancet Neurol. 2014 Jan;13(1):35-43. doi: 10.1016/S1474-4422(13)70290-4. Epub 2013 Dec 2. []
  3. Mallick AA, Ganesan V, Kirkham FJ, et al. Childhood arterial ischaemic stroke incidence, presenting features, and risk factors: a prospective population-based study. Lancet Neurol. 2014 Jan;13(1):35-43. doi: 10.1016/S1474-4422(13)70290-4. Epub 2013 Dec 2. [] []

Autism and Learning Disabilities

Child with autism stacking cans. Courtesy Wikimedia.
Child with autism stacking cans. Courtesy Wikimedia.

What Is Autism and Learning Disabilities?

[dropcap]A[/dropcap]utism and learning disabilities constititute a non-progressive psychiatric syndrome appearing in childhood characterized by withdrawal from communication with others often accompanied by repetitive or primitive behaviors.

Primary gastrointestinal pathology may play an important role in the inception and clinical expression of autism.

Autistic children often manifest complex biochemical and immunological abnormalities.1 Following are four  main features involving the digestive tract:

1) Brain dysfunction from an abnormal gut. Common characteristics of hepatic encephalopathy (brain dysfunction caused by liver disease) and a form of autism associated with developmental regression and immune caused gastrointestinal pathology (abnormal) in an apparently healthy child, have led to the proposal that there may be similar mechanisms of toxic brain dysfunction caused by gluten and casein proteins.

Gluten in wheat and casein in cow milk are called exomorphines because they act like morphine (opioid) in the brain. Aberrations in opioid biochemistry are common in autism.

2) Characteristic intestinal pathology. Many autistic children with gut symptoms have ileocolonoic lymphoid nodular hyperplasia and inflammation of the intestinal lining. The colon lesion consisting of a mucosal infiltrate of yo T cells and Celiac Disease8+ T cells and crypt cell proliferation is enhanced significantly, and the basement membrane is thicker than in normal or disease groups. Neutrophil and eosinophil mucosal infiltration and absence on colonic epithelium of HLA-DR antigen suggests a T-helper -2 dominated immune response.

The corresponding small intestinal lesion also shows a distinct inflammatory reaction in which immune-mediated epithelial cell damage is predominant and blood anitibodies of the IgG type colonizes with complement. 

3) Intestinal permeability abnormalities. A subset of children with autism were found to display increased immune reactivity to gluten, the mechanism of which appears to be distinct from that in celiac disease. The increased anti-gliadin antibody response and its association with gastrointestinal symptoms points to a potential mechanism involving immunologic and/or intestinal permeability abnormalities in affected children.2

4) Secondary dysbiosis. Anaerobic dysbiosis develops in the colon caused by fermentation of the overload of undigested food arriving from the small intestine. Billions of microbes in the colon normally breakdown undigested food, however,  in autism, the process is dysfunctional and produces byproducts that are toxic to the brain resulting in encephalopathy.

What Is Autism and Learning Disabilities In Celiac Disease and/or Gluten Sensitivity?

Sources:
  1. Wakefield AJ, Puleston M, Montgomery SM, Anthony A, O’Leary JJ, Murch SH. Review Article: the concept of entero-colonic encephalopathy, autism, and opioid receptor ligands. Aliment Parmacol Ther. 2002; 16:663-674. []
  2. Lau NM, Green PH, Taylor AK, Hellberg D, Ajamian M, Tan CZ, Kosofsky BE, Higgins JJ, Rajadhyaksha AM, Alaedini A. Markers of Celiac Disease and Gluten Sensitivity in Children with Autism. PLoS One. 2013 Jun 18;8(6):e66155. Print 2013. []

Multiple Sclerosis

Brain scan showing changes in multiple sclerosis over a month. Courtesy Wikimedia
Brain scan showing changes in multiple sclerosis by month over a year’s time. Courtesy Wikimedia

What Is Multiple Sclerosis?

[dropcap]M[/dropcap]ultiple sclerosis is an autoimmune disease of the central nervous system characterized by patchy inflammation of the myelin sheath surrounding nerve cells that produces multiple and varied neurologic symptoms and signs due to demyelination.

Q: What does demyelination mean.

A: Demyelination means there is damage to the myelin sheath which is a fatty substance that surrounds and protects nerve cells much like a the covering of a lamp cord keeps the electricity flowing within it from the plug to the light bulb. This damage impairs transmission of nerve impulses between the brain and body.

In the process of demyelination, T-lymphocyte cells that are activated and potentially autoimmune cross the blood-brain barrier and produce inflammatory plaques and axonal tissue loss in the brain, spinal cord or optic (vision) nerves. The end result is the accumulation of gliosis (scarring) and demyelination of areas in the central nervous system.1

The course of multiple sclerosis is unpredictable and slowly progressive, usually with  exacerbations (worse symptoms) and remissions (relief of symptoms).

Multiple sclerosis affects about 1 ‰ of the population worldwide.

What Is Multiple Sclerosis In Celiac Disease and/or Gluten Sensitivity?

Sources:
  1. Rodrigo L, Hernández-Lahoz C, Fuentes D, Alvarez N, López-Vázquez A, González S. Prevalence of celiac disease in multiple sclerosis. BMC Neurol. 2011 Mar 7;11:31. doi: 10.1186/1471-2377-11-31. []

Developmental Delay

developmental delay gluten celiac diseaseWhat Is Developmental Delay?

[dropcap]D[/dropcap]evelopmental delay is failure in infants and young children to meet expected milestones, such as smiling for the first time or taking the first steps, due to an impairment in physical, learning, language, or behavior areas.

These conditions begin during the developmental period, may impact day-to-day functioning, and usually last throughout a person’s lifetime.1

What Is Developmental Delay In Celiac Disease and/or Gluten Sensitivity?

Sources:
  1. Developmental Disabilities: Delivery of Medical Care for Children and Adults. I. Leslie Rubin and Allen C. Crocker. Philadelphia, Pa, Lea & Febiger, 1989. []