[dropcap]A[/dropcap]ortic vasculitis is an inflammatory disease of the aorta that causes dilation of the aorta wall with narrowing of the inside passageway and results in widespread impairment of blood flow to tissues served by the aorta.
Q: What is the result of inflammatory disease of the aorta?
A: The aorta is the largest artery in the body. It extends from the left ventricle (lower chamber) of the heart and carries blood out of the heart with each beat to rest of the body. Narrowing of the aorta’s inside diameter due to swelling from inflammation causes elevated blood pressure and enlarged heart because of back pressure of blood unable to be fully pumped out of the heart with each beat. The heart enlarges because the difficulty of pumping blood out makes it work harder than normal.
Vasculitis that causes midaortic syndrome is a variety of aortic coarctation (narrowing) located in the lower thoracic aorta, the abdominal aorta or both, involving the intestinal and renal vessels (kidney). It usually presents with arterial hypertension.1
What Is Aortic Vasculitis In Celiac Disease and/or Gluten Sensitivity?
Sources:
Massel D. n-3 polyunsaturated fatty acids reduced mortality and morbidity after recent myocardial infarction. Therapeutics. Jan-Feb 2000:6 [↩]
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).
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:
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. [↩]
Richardson AJ. The importance of omega-3 fatty acids for behavior, cognition, and mood. Scandinavian Journal of Nutrition. 2003;47(2):92-8 [↩]
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. [↩]
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 [↩]
[dropcap]T[/dropcap]hiamin, also called vitamin B1, is an essential vitamin that is required to convert foodstuffs into energy and for the health and proper functioning of the nervous, muscular and cardiovascular systems.
In the bloodstream, 90% of active thiamin (TPP) is carried by red blood cells while 10% is transported in the bloodstream as free thiamin and thiamin monophosphate bound mostly to the protein albumin.
In the diet, animal food sources provide active thiamin while plant food sources provide free thiamin.1
Urinary excretion of thiamin cannot be detected when vitamin intake is below the required levels. On the other hand, when intake exceeds saturation in the body, thiamin and/or its metabolites are actively excreted into urine to prevent excessive toxicity of the vitamins.2
In patients who have thiamin deficiency, the most common conditions that bring them to a clinician include neuropathies, depression, myalgia, cardiomyopathies or takes diuretics and/or eat a high carbohydrate diet.3
What Is Thiamin Deficiency In Celiac Disease and/or Gluten Sensitivity?
Shibata K, Hirose J, Fukuwatari T. Relationship Between Urinary Concentrations of Nine Water-soluble Vitamins and their Vitamin Intakes in Japanese Adult Males. Nutr Metab Insights. 2014 Aug 5;7:61-75. doi: 10.4137/NMI.S17245. [↩]
[dropcap]V[/dropcap]itamin B12, also called cobalamin, is a highly complex vitamin that functions in two coenzyme forms: adenosylcobalamin and methylcobalamin.
These forms of the vitamin play important roles in the physical and chemical processes by which amino acids become proprionate, proprionate that becomes acetate, and single carbons.
Q: Why are these steps important?
A: These steps are essential for normal function in the workings of all cells, especially for those of the digestive tract, bone marrow and nervous tissue.
Vitamin B12 is mainly excreted through bile into the duodenum (first part of the small intestine) for excretion in stool.1 However, if vitamin B12 is needed, it is reabsorbed in the ileum (end of the small intestine) while excess is excreted in stool and very little in urine.2
The blood level of vitamin B12 in healthy people ranges between 140 and 750 pg/ml.
What Is Vitamin B12 Deficiency In Celiac Disease and/or Gluten Sensitivity?
Sources:
Shibata K, Hirose J, Fukuwatari T. Relationship Between Urinary Concentrations of Nine Water-soluble Vitamins and their Vitamin Intakes in Japanese Adult Males. Nutr Metab Insights. 2014 Aug 5;7:61-75. doi: 10.4137/NMI.S17245. [↩]
Shinton N K. Vitamin B 12 and folate metabolism. Br Med J. Feb 26, 1972; 1(5799): 556–559. [↩]
[dropcap]A[/dropcap]rachidonic acid is a major essential (must have/can’t make) omega-6 fatty acid.
Structurally, arachidonic acid is a key component of nerve membranes, together with docosahexaenoic acid (DHA), a major opposing omega-3 fatty acid, making up 15-20% of the brain’s dry mass and more than 30% of the retina.
In healthy human volunteers, positron emission tomography (PET) has shown that the normal human brain consumes 17.8 mg/day of arachidonic acid.1
Arachidonic acid is particularly concentrated in highly active membranes such as nerve synapses (junctions) and in photoreceptors in the eye retina.2
Arachidonic acid is an important building substance for the eicosanoids.
Q: What function do the eicosanoids have that are derived from arachidonic acid?
A: Eicosanoids are a large group of highly bioactive hormone-like substances including prostaglandins, leukotrienes, and thromboxanes that are involved in blood clotting, inflammation, and vasoconstriction. Eicosanoids derived from arachidonic acid are pro-inflammatory, pro-blood clotting, and constrict blood vessels in opposition to those derived from the omega-3 fatty acids which do the opposite in order to keep a balance in the body.
What Is Arachidonic Acid Deficiency In Celiac Disease and/or Gluten Sensitivity?
Sources:
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. [↩]
Richardson AJ. The importance of omega-3 fatty acids for behavior, cognition, and mood. Scandinavian Journal of Nutrition. 2003;47(2):92-8. [↩]
[dropcap]A[/dropcap]ngina pectoris, or simply angina, is a coronary syndrome characterized by an oppressive substernal pain (pain under breastbone) or pressure brought on by exertion and relieved by rest that results from failure of coronary arteries to deliver adequate oxygen to heart tissue due to ischemic heart disease.
Q: Why do coronary arteries fail to deliver adequate oxygen to heart tissue?
A: Coronary arteries are the blood vessels that serve the heart. In angina, these vessels fail to deliver adequate oxygen to heart tissue because they are narrowed or blocked by fatty buildups, called atherosclerotic plaques or by a blood clot which impair their ability to carry adequate blood that carries the oxygen. Diseased coronary arteries cannot deliver adequate oxygenated blood pumped by the heart to its own muscle cells.
The heart is a muscular organ that is working all the time without rest, so it needs a constant supply of oxygen. When heart muscle has to work harder, it needs more oxygen. Lack of oxygen causes pain which makes the affected person stop activity and rest.
Angina can be stable or unstable. Unstable angina is much more serious and can be life-threatening.
Stable angina produces predictable pain and responds to rest and/or medication. It is less serious than unstable angina but can be very painful or uncomfortable. Anything that makes the heart muscle need more oxygen can cause an angina attack in someone with heart disease, including: smoking, cold weather, exercise, emotional stress, obesity, and large meals. Other causes of angina include: abnormal heart rhythms (usually ones that cause the heart to beat quickly), anemia, coronary artery spasm, heart failure, heart valve disease, and hyperthyroidism (overactive thyroid).1
Unstable angina produces unpredictable pain that may occur at rest, lasting more than 20 minutes. It is more severe than stable angina and less responsive to medication. Atherosclerosis is by far the most common cause of unstable angina. Oxidized low-density lipoprotein, so-called bad cholesterol, and oxysterols play an important role in atherogenesis, the development of atherosclerosis. Coronary arteries that are narrowed by atherosclerotic plaques can rupture causing injury to the coronary blood vessel resulting in blood clotting which blocks the flow of blood to the heart muscle. Blood clots may form, partially dissolve, and later form again and angina can occur each time a clot blocks blood flow in an artery. People with unstable angina are at increased risk of having a heart attack.2
What Is Angina In Celiac Disease and/or Gluten Sensitivity?
[dropcap]S[/dropcap]elenium is a mineral that is required by the body in trace amounts for a healthy immune system, normal thyroid function, and antioxidant protection.
Selenium is absolutely required in the production of at least 30 selenoproteins in the body. First, selenium is joined to the amino acids cysteine as selenocysteine and to methionine as selenomethionine before being used as components for selenoproteins. Many selenoproteins are important antioxidant enzymes such as glutathione peroxidase.
Q: How does glutathione peroxidase work?
A: Glutathione peroxidase activity helps the recycling of vitamins C and E in optimizing the performance of the antioxidant system. The antioxidant properties of selenoproteins help prevent cellular damage from free radicals. Free radicals are natural by-products of oxygen metabolism that may contribute to the development of chronic diseases such as cancer and heart disease.
In the immune system, selenium stimulates immune properties of lymphocytes (white blood cells) by contributing to higher natural killer lymphocyte activity. Natural killer lymphocytes have the ability to destroy cancer cells and bacterial and viral agents.
Other selenoproteins help protect the thyroid gland from anti-oxidants and regulate thyroid function. Specifically, selenium plays an integral role in thyroid gland metabolism.1 Functions are more fully described below.
According to the Food and Agriculture Organization, United Nations, approximately 30 percent of tissue selenium is contained in the liver, 15 percent in kidney, 30 percent in muscle, and 10 percent in blood plasma.
What Is Selenium Deficiency In Celiac Disease and/or Gluten Sensitivity?
Sources:
Stazi AV, Trinti B. Selenium status and over-expression of interleukin-15 in celiac disease and autoimmune thyroid diseases. Ann Ist Super Sanita. 2010;46(4):389-99.DOI: 10.4415/ANN_10_04_06. [↩]
Figure on right shows how atherosclerosis impedes blood flow through coronary arteries while blood clots block blood flow. Courtesy Google.
What Is Coronary Artery Disease (CAD)?
[dropcap]C[/dropcap]oronary artery disease (CAD), also called ischemic heart disease, is a gradual narrowing of medium and large arteries of the heart by fatty buildups, called atherosclerotic plaques.
It is characterized by slowly developing interference with blood flow to heart tissue itself, resulting in oppressive chest pain called angina and, ultimately, thrombosis (clot) causing heart attack.
The heart is a muscular organ that is working all the time, so it needs a constant supply of oxygen. Oxygen is brought to the working heart tissue by the coronary arteries with each beat of the heart. When heart muscle has to work harder, it needs more oxygen delivered to itself. Lack of oxygen causes pain.
In fact, failure of diseased coronary arteries to deliver adequate oxygen to heart tissue is the most common cause of angina pectoris – substernal pain (under breastbone) or pressure brought on by exertion and relieved by rest.
Thrombosis, or clot formation, occurs when blood cells within a narrowed artery can no longer get through. Trapped, blood cells pile up and block the artery thus triggering a cascade of events called heart attack. Coronary arteries that are narrowed by atherosclerotic plaques can rupture causing injury to the coronary blood vessel resulting in blood clotting which blocks the flow of blood to the heart muscle. Blood clots may form, partially dissolve, and later form again and angina can occur each time a clot blocks blood flow in an artery.1
Q: How does coronary artery disease develop?
A:Coronary artery disease slowly develops from this combination of events:
Dysfunction of epithelial cells that line the inside of arteries cause the vessels to stiffen, and subsequently
Accumulation of lipid (fat) in smooth muscle cells beneath the inside lining of arteries and in foam cells cause buildup of fatty deposits on the inside walls progressing to fibrous plaque formation.
Oxidized low-density lipoprotein (oxLDL), so-called bad cholesterol, and oxysterols play important roles in the development of atherosclerosis. OxLDL triggers the immune system to produce autoantibodies against oxLDL that are detectable in serum. These antibodies are called anti-oxLDL. Anti-oxLDL antibody and oxysterol concentrations are associated with coronary artery stenosis. Oxidative stress may be greatly increased in unstable angina.2 and Chronic inflammation in the general population is a major risk factor for ischemic heart disease.
The pathophysiology of atherosclerosis is, clearly, different in women when compared to the men. The women have a higher risk of blood coagulability making them at high risk for the blood clot formation. In a large number of women endothelial dysfunction, small vessel size and diffuse atherosclerosis have been identified as causes of ischemia without evidence of blockade in the coronary arteries.3
Also, atherosclerotic plaque in women is less fibrotic and contains more lipid filled foam cells, implying greater potential for reversibility but also potentially greater vulnerability for plaque rupture and thrombosis.4
Who is Affected in the General Population?
Coronary artery disease remains the leading cause of death in developed countries despite significant progress in primary prevention and treatment strategies.
It is the leading cause of death in women, as well as an important cause of disability.
Older patients are at particularly high risk of poor outcomes following acute coronary syndrome.5
What Is Coronary Artery Disease In Celiac Disease and/or Gluten Sensitivity?
Ischemic heart disease is the leading cause of death in the United States, making cardiovascular risk assessments and potential interventions or treatments imperative for patients with celiac disease.6
Yasunobu Y, Hayashi K, Shingu T, Yamagata T, Kajiyama G, Kambe M. Coronary atherosclerosis and oxidative stress as reflected by autoantibodies against oxidized low-density lipoprotein and oxysterosis. Atherosclerosis. Apr 2001;155(2):445-53. [↩]
Kunadian V, Ford GA, Bawamia B, Qiu W, Manson JE. Vitamin D deficiency and coronary artery disease: A review of the evidence. Am Heart J. 2014 Mar;167(3):283-291. doi: 10.1016/j.ahj.2013.11.012. Epub 2013 Dec 19. [↩]
Kunadian V, Ford GA, Bawamia B, Qiu W, Manson JE. Vitamin D deficiency and coronary artery disease: A review of the evidence. Am Heart J. 2014 Mar;167(3):283-291. doi: 10.1016/j.ahj.2013.11.012. Epub 2013 Dec 19. [↩]
Kunadian V, Ford GA, Bawamia B, Qiu W, Manson JE. Vitamin D deficiency and coronary artery disease: A review of the evidence. Am Heart J. 2014 Mar;167(3):283-291. doi: 10.1016/j.ahj.2013.11.012. [↩]
Robinson BL, Davis SC, Vess J, Lebel, J. Primary care management of celiac disease. Nurse Practitioner. February 2015: Vol 40 – Issue 2; 28–34. [↩]
[dropcap]A[/dropcap]therosclerosis is a disease of arteries involving the buildup of fatty material called plaque along the walls of medium and large arteries characterized by patchy subintimal thickening, hardening, and loss of elasticity of blood vessels.
The intima is the innermost layer of an artery, having contact with blood. The subintima is beneath it.
Q: What happens when arteries become narrowed and less flexible?
A: Narrowing of the inside diameter of blood vessels and hardening of their walls reduce or obstruct blood flow through them which impairs their ability to supply tissues of the body with oxygen and nourishment.
When tissues are deprived of oxygen, pain and dysfunction results such as angina pectoris involving heart muscle because the heart continually needs oxygen never being able to rest.
It is thought that atherosclerosis develops from 1) epithelial cell dysfunction of the intima, and 2) lipid (fat) accumulation in smooth muscle cells and in foam cells, causing buildup of fatty deposits on the inside walls progressing to fibrous plaque formation. That is, intimal smooth muscle cells are surrounded by connective tissue and intracellular and extracellular lipids (fat build-up inside and outside of these cells).
What Is Atherosclerosis In Celiac Disease and/or Gluten Sensitivity?
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