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Gut and Intestinal Health

Back Clinic Gut and Intestinal Health. The health of an individual’s gut determines what nutrients are absorbed along with what toxins, allergens, and microbes are kept out. It is directly linked to the health of the whole body. Intestinal health could be defined as optimal digestion, absorption, and assimilation of food. But this is a job that depends on many other factors. More than 100 million Americans have digestive problems. Two of the top-selling drugs in America are for digestive problems, and they run in the billions. There are more than 200 over-the-counter (OTC) remedies for digestive disorders. And these can and do create additional digestive problems.

If an individual’s digestion is not working properly, the first thing is to understand what is sending the gut out-of-balance in the first place.

  • A low-fiber, high-sugar, processed, nutrient-poor, high-calorie diet causes all the wrong bacteria and yeast to grow in the gut and damages the delicate ecosystem in your intestines.
  • Overuse of medications that damage the gut or block normal digestive function, i.e., acid blockers (Prilosec, Nexium, etc.), anti-inflammatory medication (aspirin, Advil, and Aleve), antibiotics, steroids, and hormones.
  • Undetected gluten intolerance, celiac disease, or low-grade food allergies to foods such as dairy, eggs, or corn.
  • Chronic low-grade infections or gut imbalances with overgrowth of bacteria in the small intestine, yeast overgrowth, parasites.
  • Toxins like mercury and mold toxins damage the gut.
  • Lack of adequate digestive enzyme function from acid-blocking medications or zinc deficiency.
  • Stress can alter the gut’s nervous system, cause a leaky gut, and change the normal bacteria.

Visits for intestinal disorders are among the most common trips to primary care doctors. Unfortunately, most, which also includes most doctors, do not recognize or know that digestive problems wreak havoc in the entire body. This leads to allergies, arthritis, autoimmune disease, rashes, acne, chronic fatigue, mood disorders, autism, dementia, cancer, and more. Having proper gut and intestinal health is absolutely central to your health. It is connected to everything that happens in the body.


Environmental Factors for Autoimmune Diseases

Environmental Factors for Autoimmune Diseases

It has currently been accepted that the interaction between environmental factors, and that of certain genes, can influence the destructive immune response characterized in many autoimmune diseases. As a matter of fact, approximately less than 10 percent of those people with a higher genetic susceptibility to disease may actually develop autoimmunity. This implies a solid environmental cause behind the beginning of the autoimmune process. Environmental factors have also been believed to likely affect the results of the process as well as the rate of development of autoimmune diseases. One theory is that intestinal luminal antigens absorbed through the gut might be involved in the pathogenesis of autoimmune diseases. The intestinal epithelium is the largest mucosal surface in the human body and it provides a connection between the external environment and the mammalian host.

 

What environmental factors cause autoimmune diseases?

 

Healthy, mature intestinal mucosa with its absolute tight junctions, or TJs, is the most significant barrier for the passage of macromolecules, as seen on Figure 1. In a physiological state, quantitatively small but immunologically active antigens can cross the mucosal barrier. These antigens are absorbed through the mucosa via two practical paths. The massive collection of absorbed proteins, amounting to about 90 percent, cross the intestinal barrier throughout the transcellular pathway followed by lysosomal degradation which converts the proteins into smaller, non-immunogenic peptides. The remaining proteins are then carried as entire proteins, causing antigen-specific immune responses in the body. This occurrence utilizes the Microfold (M) cell pathway or the paracellular pathway, which requires a subtle but complex balance of intercellular TJs that can result in antigenic tolerance.

 

Figure 1 Macroscopic Arrangement and Microscopic Composition of Intercellular Tight Junctions Image 1

Figure 1

 

After the integrity of the intestinal barrier are compromised, best known as TJ disassembly, an immune response to environmental antigens that spanned the gut mucosa can grow, leading to autoimmune diseases or allergies. The cells that play a vital part in this immune response lie in close proximity to the intestinal epithelial barrier. Another critical component for this immune response is the human leukocyte antigen, or HLA, system. HLA class I and II genes encode the antigen presenting cell (APC) glycoprotein receptors that present antigens to T cells in the intestinal mucosa. Susceptibility to up to 50 diseases, such as celiac disease, or CD, and type 1 diabetes, or T1D, has been associated with certain HLA class I or class II alleles. A typical denominator of these diseases is the occurrence of numerous preexisting conditions which can lead to autoimmunity. The first is a hereditary susceptibility for the host immune system to recognize, and potentially misinterpret, an environmental antigen introduced within the gastrointestinal tract, or GI tract. Second, the host needs to be exposed to the antigen. Finally, the antigen needs to be introduced into the gastrointestinal mucosal immune system, following its M-cell passage or paracellular passage, usually blocked by TJ competency, from the intestinal lumen to acquire the intestine submucosa. In most instances, higher intestinal permeability precedes disease and triggers an abnormality in antigen delivery which triggers an immune response, ultimately causing autoimmunity. Researchers have therefore hypothesized that genes, environment, and decreased intestinal barrier function are all critical to develop autoimmune diseases, especially CD and T1D.

 

Gliadin as an Environmental Factor of Autoimmune Diseases

 

Celiac Disease

 

Gluten is a well-known environmental factor that triggers celiac disease. It is the gliadin fraction of wheat germ and equal alcohol-soluble proteins in distinct grains, known as prolamins, which are connected to the growth of intestinal damage. A standard characteristic of the prolamins of wheat, rye, and barley is a greater content of glutamine (>30%) and proline (>15%), whereas the non-toxic prolamins of rice and corn have decreased glutamine and proline content. However, the environmental factor that influenced the development CD is complex and unknown. Some aspects of gluten consumption might help determine the risk of CD incidence, particularly in: the amount of gluten intake, the higher the amount, the larger the risk; the caliber of consumed gluten, a few grains contain more hazardous epitopes than others; and the pattern/timing of infant feeding. Recent research studies suggest that the pattern of infant nutrition might have a very important role on the development of the CD as well as that of other autoimmune diseases. Breastfeeding is believed to delay or reduce the possibility of developing CD. The positive effects of breast milk may be attributed to its influence on the microbial colonization procedure for the own newborn’s intestine. The genus Bifidobacterium is predominant in the feces of breast-fed infants, while a larger variety of bacterial groups, including Bacteroides, Streptococcus, Clostridium, etc., are found in the fecal microbiota of all formula-fed infants. Changes in the composition of the intestinal microbiota also occur as a consequence of the following changes from breastfeeding or formula feeding to weaning and even the introduction of solid food. Alterations in the intestinal balance between favorable and possibly harmful bacteria have also been associated with allergy symptoms, type 1 diabetes and inflammatory bowel diseases, among others.

 

Type 1 Diabetes

 

It is believed that genetically predisposed individuals develop T1D after encountering one or more environmental factors of the disease. Fast improvements could be made in disease prevention and treatment if these environmental factors were identified. Amongst the others, gliadin has only been the subject of a series of research studies that aim at establishing its part in the pathogenesis of type 1 diabetes. Early introduction of gliadin-containing cereals were reported to raise the prospect of islet cell autoimmunity in humans. Gliadin-specific, lamina propria-derived T cells play an important role in the pathogenesis of CD. The same HLA class II haplotype, DQ (? 1 * 0501, �1 * 0201), that can be connected with gliadin peptides in CD is also one of two HLA class II haplotypes inherited most frequently by people with T1D. There are also signs of immunological activity in the intestine of T1D patients: jejunal specimens from T1D patients have been found to consist of much higher doses of interferon gamma (IFN?)- and tumor necrosis factor-alpha (TNF-?) positive cells in contrast to people with healthy controls, suggesting an inflammatory response. Still another study found substantially increased manifestation of HLA-DR and HLA-DP molecules on intestinal villi of jejunal specimens from T1D patients in comparison with specimens from healthy controls. Recent evidence confirmed these findings by assessing the mucosal immune response to gliadin in the jejunum of patients with T1D. Small intestinal biopsies from children with T1D were cultured with gliadin and evaluated for epithelial infiltration and lamina propria T-cell activation. The caliber of intraepithelial CD3+ cells and of lamina propria CD25+ mononuclear cells has been higher in jejunal biopsies from T1D patients versus control subjects. In the patients’ biopsies cultured with enzymatically treated gliadin, there was epithelial infiltration by CD3 cells, a more significant growth in lamina propria CD25+ and CD80+ cells, enhanced manifestation of lamina propria cells favorable into ligand and receptor molecules ?4/?7 and ICAM 1, along with enhanced expression of CD54 and crypt HLA-DR. Also, ?4 positive T cells have been recovered in the pancreatic islets of an T1D person, providing an immediate connection between gliadin-activated T cells and destruction of pancreatic islet cells.

 

Findings from research studies using non-obese diabetic, or NOD, mice in addition to the BioBreeding diabetes-prone, or BBDP, rats have also implicated wheat gliadin as a nutritional supplement diabetogen. In BBDP rats, gliadin vulnerability is accompanied by increased intestinal permeability, and changes in gut microbiota composition, as seen on Figure 2., presumably allow food antigens to grow in contact with all the underlying lamina propria. Feeding NOD mice and BBDP rats a gluten free hydrolyzed casein diet resulted in a delay and decline in T1D development. Interestingly, these T1D animal models additionally demonstrated the moment of exposure to wheat proteins is quite important to the development of T1D. Delaying the vulnerability of diabetogenic wheat proteins by prolonging the breastfeeding period decreased T1D expansion from the BBDP rats. What is more, exposing neonatal rats or mice to diabetogenic wheat components or bacterial antigens diminished T1D incidence, which is perhaps due to the induction of immunological tolerance.

 

Figure 2 Postulated Mechanism of Action of Gluten in T1D Pathogenesis Image 2

Figure 2

 

Rats that were fed corn protein-based diets developed T1D and demonstrated a moderate celiac-like enteropathy. Mesenteric lymph nodes, or MLNs, which drain the gut, are the substantial inductive site where dietary antigens are famous in the gut-associated connective tissue. The authors described an increase in the expression ratio of T-bet:Gata3, master transcription factors for Th1 and Th2 cytokines, respectively, in the MLN by wheat-fed BBDP rats compared to this by BBDR rats, mainly due to diminished Gata3 expression. Also, CD3+CD4+IFN?+ T cells were prevalent in the MLN of wheat-fed BBDP rats, but remained at control levels in BBDP rats fed with a diabetes-retardant wheat-free diet. BioBreeding diabetes-prone MLN cells increased quickly in response to wheat protein antigens in a particular, dose-dependent manner, and 93 percent of cells were CD3+CD4+ T cells. This proliferation was connected using a minimum proportion of CD4+CD25+ T cells and a greater proportion of dendritic cells in the MLN of BBDP rats. These results suggest that, before insulitis is established, the MLNs of wheat-fed BBDP rats contain a remarkably large proportion of Th1 cells that rapidly increased particularly in response to wheat protein antigens. Collectively, these research studies suggest a deranged mucosal immune response to gliadin in T1D and a direct connection between gliadin-induced stimulation of gut mucosal T cells and abuse of pancreatic islet cells, as seen on Figure 2.

 

Link between Gliadin, Zonulin & Increased Intestinal Permeability in Autoimmune Diseases

 

Researchers have generated enough evidence to support that gliadin can induce increased intestinal permeability by releasing preformed zonulin. Intestinal cell lines exposed to gliadin released zonulin from the cell medium with subsequent zonulin binding to the cell surface, rearrangement of the cell cytoskeleton, loss of occludin-ZO1 protein interaction, and increased monolayer permeability. Pre-treatment with all of the zonulin antagonist AT1001 blocked these alterations without affecting zonulin release. When exposed to luminal gliadin, intestinal biopsies from patients with celiac disease in remission expressed a continuous luminal zonulin discharge and increase in intestinal permeability. On the contrary, biopsies from non-CD patients showed a limited, transient zonulin release, which was paralleled by a decline in intestinal permeability that had not reached the level of permeability found in celiac disease cells. As a matter of fact, when gliadin was added to the basolateral side of cell lines or intestinal biopsies, no zonulin release was detected. The latter finding indicates that gliadin interacts using an intestinal luminal receptor, which encouraged researchers to comprehend this issue. In vitro experiments revealed specific colocalization of gliadin along with the chemokine receptor CXCR3 expressed in human and mouse intestinal epithelium and lamina propria. Gliadin vulnerability led to a tangible establishment of CXCR3 and MyD88. Ex vivo experiments revealed that gliadin exposure to intestinal segments from wild-type mice increased zonulin terminal and intestinal permeability, whereas CXCR3 intestinal segments failed to respond to gliadin. The increased intestinal permeability appeared cause a specific impact for gliadin, because the subsequent CXCR3 ligand, IP-10, did not affect intestinal barrier function. Based on these figures, researchers suggested that gliadin contrasts to CXCR3 additionally lead to stimulation of the zonulin pathway and improved intestinal permeability in a MyD88-dependent manner.

 

Conclusive Remarks

 

The classical paradigm of the pathogenesis of autoimmune diseases involving certain receptor makeup and exposure to environmental factors was contested with the addition of a third component, the decrease of intestinal barrier function. Genetic predisposition, miscommunication between innate and adaptive immunity, exposure to environmental factors and loss in intestinal barrier function secondary to the breakdown of intercellular tight junctions, or TJs, seem to be vital components in the pathogenesis of autoimmune disorders. Both in CD and T1D gliadin may play a role in inducing loss of intestinal barrier function or inducing the gastrointestinal response in genetically predisposed individuals. This new hypothesis suggests that after the digestive process is triggered, it is not auto-perpetuating, but rather, it might be balanced or reversed by preventing the continuous interaction between genes and the environment. Since TJ dysfunction allows this interaction, new treatment procedures targeted at re-establishing the intestinal barrier function supply innovative, unexplored procedures for caring for autoimmune diseases. Information referenced from the National Center for Biotechnology Information (NCBI) and the National University of Health Sciences. The scope of our information is limited to chiropractic and spinal injuries and conditions. To discuss the subject matter, please feel free to ask Dr. Jimenez or contact us at 915-850-0900 .

 

By Dr. Alex Jimenez

 

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Additional Topics: Wellness

 

Overall health and wellness are essential towards maintaining the proper mental and physical balance in the body. From eating a balanced nutrition as well as exercising and participating in physical activities, to sleeping a healthy amount of time on a regular basis, following the best health and wellness tips can ultimately help maintain overall well-being. Eating plenty of fruits and vegetables can go a long way towards helping people become healthy.

 

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WELLNESS TOPIC: EXTRA EXTRA: Managing Workplace Stress

 

 

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References
1.�Fasano A.�Tight Junctions.�CRC Press, Inc.; Boca Raton, FL: 2001. Pathological and therapeutic implications of macromolecule passage through the tight junction; pp. 697�722.
2.�Mowat AM. Anatomical basis of tolerance and immunity to intestinal antigens.�Nat. Rev. Immunol.�2003;3:331�341.�[PubMed]
3.�Fasano A. Intestinal zonulin: open sesame!�Gut.�2001;49:159�162.�[PMC free article][PubMed]
4.�Brandtzaeg P, Halstensen TS, Kett K, et al. Immunobiology and immunopathology of human gut mucosa: humoral immunity and intraepithelial lymphocytes.�Gastroenterol.�1989;97:1562�1584.�[PubMed]
5.�Brandtzaeg P. Overview of the mucosal immune system.�Curr. Top. Microbiol. Immunol.�1989;146:13�25.�[PubMed]
6.�Bjorkman PJ, Saper MA, Samraoui B, et al. Structure of the human class I histocompatibility antigen, HLA-A2.�Nature.�1987;329:506�512.�[PubMed]
7.�Bjorkman PJ, Saper MA, Samraoui B, et al. The foreign antigen binding site and T cell recognition regions of class I histocompatibility antigens.�Nature.�1987;329:512�518.�[PubMed]
8.�Cuvelier C, Mielants H, De Vos M, et al. Major histocompatibility complex class II antigen (HLA-DR) expression by ileal epithelial cells in patients with seronegative spondylarthropathy.�Gut.�1990;31:545�549.[PMC free article][PubMed]
9.�Wendling D. Role of the intestine in the physiopathology of inflammatory rheumatism.�Rev. Rhum. Mal. Osteoartic.�1992;59:389�392.�[PubMed]
10.�Bjarnson I, Williams P, Smethurst P, et al. Effect of non-steroidal anti-inflammatory drugs and prostaglandins on the permeability of the human small intestine.�Gut.�1986;27:1292�1297.[PMC free article][PubMed]
11.�Bjarnason I, Peters TJ, Levi AJ. Intestinal permeability: clinical correlates.�Dig. Dis.�1986;4:83�92.[PubMed]
12.�Pratesi R, Gandolfi L, Garcia SG, et al. Prevalence of coeliac disease: unexplained age-related variation in the same population.�Scand. J. Gastroenterol.�2003;38:747�50.�[PubMed]
13.�Fasano A, Berti I, Gerarduzzi T, et al. Prevalence of celiac disease in at-risk and not-at-risk groups in the United States: a large multicenter study.�Arch. Int. Med.�2003;163:286�292.�[PubMed]
14.�Nistico L, Fagnani C, Coto I, et al. Concordance, disease progression, and heritability of coeliac disease in Italian twins.�Gut.�2006;55:803�808.�[PMC free article][PubMed]
15.�Louka AS, Sollid LM. HLA in coeliac disease: unravelling the complex genetics of a complex disorder.�Tissue Antigens.�2003;61:105�117.�[PubMed]
16.�Vader W, Stepniak D, Kooy Y, et al. The HLA-DQ2 gene dose effect in celiac disease is directly related to the magnitude and breadth of gluten-specific T cell responses.�Proc. Natl. Acad. Sci. USA.�2003;100:12390�12395.�[PMC free article][PubMed]
17.�Monsuur AJ, Bakker PI, Alidazeh BZ, et al. Myosin IXB variant increases the risk of celiac disease and points toward a primary intestinal barrier defect.�Nat. Gen.�2005;37:1341�1344.�[PubMed]
18.�Wapenaar MC, Monsuur AJ, van Bodegraven AA, et al. Associations with tight junction genes PARD3 and MAGI2 in Dutch patients point to a common barrier defect for coeliac disease and ulcerative colitis.�Gut.�2008;57:463�467.�[PubMed]
19.�Kelly MA, Rayner ML, Mijovic CH, et al. Molecular aspects of type 1 diabetes.�Mol. Pathol.�2003;56:1�10.�[PMC free article][PubMed]
20.�Santiago JL, Martinez A, Nunez C, et al. Association of MYO9B haplotype with type 1 diabetes.�Hum. Immunol.�2008;69:112�115.�[PubMed]
21.�Sollid LM. Breast milk against celiac disease.�Gut.�2002;51:767�768.�[PMC free article][PubMed]
22.�Gr�nlund M-M, Arvilommi H, Kero P, et al. Importance of intestinal colonization in the maturation of humoral immunity in early infancy: a prospective follow up study of healthy infants aged 0�6 months.�Arch. Dis. Child. Fetal. Neon.�2000;83:F186�F192.�[PMC free article][PubMed]
23.�Kirjavainen PV, Arvola T, Salminen SJ, et al. Aberrant composition of gut microbiota of allergic infants: a target of bifidobacterial therapy at weaning?�Gut.�2002;51:51�55.�[PMC free article][PubMed]
24.�Sartor RB. Therapeutic manipulation of the enteric microflora in inflammatory bowel diseases: antibiotics, probiotics, and prebiotics.�Gastroenterol.�2004;126:1620�1633.�[PubMed]
25.�Lefebvre DE, Powell KL, Strom A, et al. Dietary proteins as environmental modifiers of type 1 diabetes mellitus.�Annu. Rev. Nutr.�2006;26:175�202.�[PubMed]
26.�Ziegler AG, Schmid S, Huber D, et al. Early infant feeding and risk of developing type 1 diabetes-associated autoantibodies.�JAMA.�2003;290:1721�1728.�[PubMed]
27.�Norris JM, Barriga K, Klingensmith G, et al. Timing of initial cereal exposure in infancy and risk of islet autoimmunity.�JAMA.�2003;290:1713�1720.�[PubMed]
28.�Lundin KEA, Scott H, Hansen T, et al. Gliadin-specific, HLA-DQ (?180501,�1 * 0201) restricted T cells isolated from the small intestinal mucosa of celiac patients.�J. Exp. Med.�1993;178:187�196.[PMC free article][PubMed]
29.�Agardh D, Nilsson A, Tuomi T, et al. Prediction of silent celiac disease at diagnosis of childhood type 1 diabetes by tissue transglutaminase autoantibodies and HLA.�Pediatric Diab.�2001;2:58�65.�[PubMed]
30.�Westerholm-Ormio M, Vaarala O, Pihkala P, et al. Imunologic activity in the small intestinal mucosa of pediatric patients with type 1 diabetes.�Diabetes.�2003;52:2287�2295.�[PubMed]
31.�Savilahti E, Ormala T, Saukkonen U, et al. Jejuna of patients with insulin-dependent diabetes mellitus (IDDM) show signs of immune activation.�Clin. Exp. Immunol.�1999;116:70�77.�[PMC free article][PubMed]
32.�Auricchio R, Paparo F, Maglio M, et al. In vitro deranged intestinal immune response to gliadin in type 1 diabetes.�Diabetes.�2004;53:1680�1683.�[PubMed]
33.�Hanninen A, Salmi M, Simell O, et al. Endothelial cell-binding properties of lymphocytes infiltrated into human diabetic pancreas: Implications for pathogenesis in IDDM.�Diabetes.�2003;42:1656�1662.[PubMed]
34.�Chakir H, Lefebvre DE, Wang H, et al. Wheat protein-induced proinflammatory T helper 1 bias in mesenteric lymph nodes of young diabetes-prone rats.�Diabetologia.�2005;48:1576�1584.�[PubMed]
35.�Scott FW, Cloutier HE, Kleeman R, et al. Potential mechanisms by which certain foods promote or inhibit the development of spontaneous diabetes in BB rats. Dose, timing, early effect on islet area, and switch in infiltrate from Th1 to Th2 cells.�Diabetes.�1997;46:589�598.�[PubMed]
36.�Funda DP, Kaas A, Taskalova-Hogenova H, et al. Gluten-free but also gluten-enriched (gluten+) diet prevent diabetes in NOD mice; the gluten enigma in type 1 diabetes.�Diab. Metab. Res. Rev.�2008;24:59�63.�[PubMed]
37.�Meddings JB, Jarand J, Urbanski SJ, et al. Increased gastrointestinal permeability is an early lesion in the spontaneously diabetic BB rat.�Am. J. Physiol.�1999;276:G951�957.�[PubMed]
38.�Visser J, Brugman S, Klatter F, et al. Short-term dietary adjustment with a hydrolyzed casein-based diet postpones diabetes development in the diabetes-prone BB rat.�Metabolism.�2003;52:333�337.�[PubMed]
39.�Brugman S, Klatter F, Visser J, et al. Neonatal oral administration of DiaPep277, combined with hydrolysed casein diet, protects against Type 1 diabetes in BB-DP rats. An experimental study.�Diabetologia.�2004;47:1331�1333.�[PubMed]
40.�Brugman S, Klatter F, Visser J, et al. Antibiotic treatment partially protects against type 1 diabetes in the Bio-Breeding diabetes-prone rat. Is the gut flora involved in the development of type 1 diabetes?�Diabetologia.�2006;49:2105�2108.�[PubMed]
41.�Visser J, Groen H, Klatter F, et al. The diabetes prone BB rat model of IDDM shows duration of breastfeeding to influence Type 1 diabetes development later in life.�Diabetologia.�2003;46:1711�1713.[PubMed]
42.�Scott FW, Rowsell P, Wang GS, et al. Oral exposure to diabetes-promoting food or immunomodulators in neonates alters gut cytokines and diabetes.�Diabetes.�2002;51:73�78.�[PubMed]
43.�Fasano A, Fiorentini C, Donelli G, et al. Zonula occludens toxin modulates tight junctions through protein kinase C-dependent actin reorganization,�in vitro.�J. Clin. Invest.�1995;96:710�720.[PMC free article][PubMed]
44.�Fasano A, Uzzau S, Fiore C, et al. The enterotoxic effect of zonula occludens toxin (Zot) on rabbit small intestine involves the paracellular pathway.�Gastroenterol.�1997;112:839�846.�[PubMed]
45.�Marcial MA, Carlson SL, Madara JL. Partitioning of paracellular conductance along the ileal crypt-villus axis: a hypothesis based on structural analysis with detailed consideration of tight junction structure-function relationships.�J. Membr. Biol.�1984;80:59�70.�[PubMed]
46.�Uzzau S, Lu R, Wang W, et al. Purification and preliminary characterization of the zonula occludens toxin receptor from human (CaCo2) and murine (IEC6) intestinal cell lines.�FEMS Microbiol. Lett.�2001;194:1�5.�[PubMed]
47.�Wang W, Uzzau S, Goldblum SE, et al. Human zonulin, a potential modulator of intestinal tight junctions.�J. Cell Sci.�2000;113:4435�4440.�[PubMed]
48.�Fasano A, Baudry B, Pumplin DW, et al.�Vibrio cholerae�produces a second enterotoxin, which affects intestinal tight junctions.�Proc. Natl. Acad. Sci. USA.�1991;88:5242�5246.�[PMC free article][PubMed]
49.�Baudry B, Fasano A, Ketley JM, et al. Cloning of a gene (zot) encoding a new toxin produced by�Vibrio cholerae.�Infect. Immun.�1992;60:428�434.�[PMC free article][PubMed]
50.�Di Pierro M, Lu R, Uzzau S, et al. Zonula occludens toxin structure-function analysis. Identification of the fragment biologically active on tight junctions and of the zonulin receptor binding domain.�J. Biol. Chem.�2001;276:19160�19165.�[PubMed]
51.�El Asmar R, Panigrahi P, Bamford P, et al. Host-dependent activation of the zonulin system is involved in the impairment of the gut barrier function following bacterial colonization.�Gastroenterol.�2002;123:1607�1615.
52.�Fasano A, Not T, Wang W, et al. Zonulin, a newly discovered modulator of intestinal permeability, and its expression in coeliac disease.�Lancet.�2000;358:1518�1519.�[PubMed]
53.�Watts T, Berti I, Sapone A, et al. Role of the intestinal tight junction modulator zonulin in the pathogenesis of type-I diabetes in BB diabetic prone rats.�Proc. Natl. Acad. Sci. USA.�2005;102:2916�2921.�[PMC free article][PubMed]
54.�Sapone A, de Magistris L, Pietzak M, et al. Zonulin upregulation is associated with increased gut permeability in subjects with type 1 diabetes and their relatives.�Diabetes.�2006;55:1443�1449.�[PubMed]
55.�Clemente MG, Virgiliis S, Kang JS, et al. Early effects of gliadin on enterocyte intracellular signalling involved in intestinal barrier function.�Gut.�2003;52:218�223.�[PMC free article][PubMed]
56.�Drago S, El Asmar R, De Pierro M, et al. Gliadin, zonulin and gut permeability: Effects on celiac and non-celiac intestinal mucosa and intestinal cell lines.�Scand. J. Gastroenterol.�2006;41:408�419.�[PubMed]
57.�Lammers KM, Lu R, Brownley J, et al. Gliadin induces an increase in intestinal permeability and zonulin release by binding to the chemokine receptor CXCR3.�Gastroenterol.�2008;135:194�204.[PMC free article][PubMed]
58.�Barbeau WE, Bassaganya-Riera J, Hontecillas R. Putting the pieces of the puzzle together � a series of hypotheses on the etiology and pathogenesis of type 1 diabetes.�Med. Hypotheses.�2007;68:607�619.[PubMed]
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Junction Complex Structure & Function in the GI Tract

Junction Complex Structure & Function in the GI Tract

Digestive health can be attributed to the optimal function of the gastrointestinal tract. By way of instance, however, if disease affects the structure of the gut, understanding its anatomy and function, can help healthcare specialists conclude a diagnosis outcome. The intestinal epithelium is a single layer of cells found lining the intestinal lumen, which plays the role of carrying out two essential functions in the digestive system. Its first function is to act as a barrier to prevent the passage of harmful intraluminal entities, such as foreign antigens, microorganisms and their toxins. Its second function is to act as a selective filter, allowing the translocation of important dietary nutrients, electrolytes and water from the intestinal lumen to the blood stream. The intestinal epithelium distinguishes selective permeability through two main pathways: the transepithelial/transcellular and paracellular pathways, as seen on Figure 1.

 

Transcellular permeability is generally related with the epithelial cells and is largely regulated by specific transporters in charge of also transferring amino acids, electrolytes, short chain fatty acids and sugars throughout the human body. Paracellular permeability is usually related to the transferring distance between epithelial cells and is greatly regulated by intercellular complexes found in the apical-lateral membrane junction and along the lateral membrane of the gastrointestinal tract, or GI tract. Interaction between the intestinal epithelial cells involves three components which can be identified at the ultrastructural level: desmosomes, adherens junctions, or AJs, and tight junctions, or TJs, as seen on Figure 2. The adhesive junctional complexes are made up of transmembrane proteins which connect adjacent cells to the actin cytoskeleton through cytoplasmic scaffolding proteins. The adherens junctions and desmosomes are believed to be more significant than the mechanical link of adjacent cells. The tight junctions, on the other hand, are the apical-most junctional complex, accountable for closing the intercellular space as well as regulating specific paracellular ionic solute transfer. The AJ and TJ complexes are also essential towards the regulation of cellular proliferation, polarization and distinction.

 

Structural Components of Junctional Complexes

 

Pathways of Epithelial Permeability

Figure 1

 

Overview of Intestinal Epithelial Junction Complexes

Figure 2

 

Adherens Junctions (AJs)

 

The adherens junctions, also known as zonula adherens, are protein complexes located along the lateral membrane which happen in points of cell to cell contact, as seen on Figure 2. They’re shaped by interactions between transmembrane proteins, intracellular adaptor proteins and the cytoskeleton. The major AJs, or adherens junctions are formed by cadherin to catenin interactions. Epithelial (E)-cadherins, or calcium-dependent adhesion molecules, are Type-I single transmembrane spanning glycoproteins that contain an intracellular C-terminus and extracellular N-terminus. The extracellular domain creates homotypical interactions with the cadherins of neighboring cells to develop this cell to cell adhesion. The intracellular domain contains a catenin-binding domain that interacts with members of the armadillo repeat superfamily, ?-, ?- and p120-catenin. The catenins then connect the AJs into the cytoskeletal network through direct binding to the C-terminal domain of F-actin or indirectly through interactions with other adaptor proteins like afadin. Cadherin to catenin complexes are significant not only for connecting adjoining cells, but also for keeping cell polarity and for regulating epithelial migration and proliferation as well as the formation of additional adhesive complexes, such as desmosomes. In order to allow the link of adjoining cells, a decreased regulation of E-cadherin from the intestinal epithelium interrupts cell to cell adhesion which has been associated with affected intestinal epithelial proliferation and migration.

 

Nectin-afadin interactions create another significant AJ complex. Nectins, specificially nectin-1-4, are immunoglobulin-like proteins that withstand homophilic and heterophilic interactions with nectins on adjacent cells. Nectins can interact with the cytoskeleton through afadin, an F-actin binding protein, or rather preferably through interactions with other F- or ?-actin binding proteins including ponsin/SH3P12, vinculin and afadin dil domain-interacting proteins.

 

Tight Junctions (TJs)

 

The tight junctions are the apical-most adhesive junctional complexes in the epithelial cells of mammals which develop a continuous belt-like ring around epithelial cells at the boundary between the apical and lateral membrane regions of the gastrointestinal tract, according to Figure 2. Tight junctions, or TJs, are powerful, multi-protein complexes which serve as a selective/semipermeable paracellular barrier, that eases the passage of ions and solutes through the intercellular space, while also preventing the translocation of luminal antigens, microorganisms and their toxins. The progression of TJ biology began in the 1960’s with the development of electron microscopy. Evaluation and analysis of epithelial cells explained a series of apparent fusions, in which the space between adjacent epithelial cells had been eliminated. These so-called “kissing points” are morphologically different from AJs and desmosomes, where adjoining cell membranes stay approximately 15 to 20nm apart. Since the first observations, TJs have been found to include four families of transmembrane proteins: occludin, claudins, junctional adhesion molecules, or JAMs, and tricellulin.

 

The extracellular domains of transmembrane TJ proteins in adjoining cells anastomose to shape the TJ isolate. These interactions involve those proteins found in the exact same membrane as well as those including proteins in adjacent cells. Additionally, TJ proteins may form homophilic interactions, with the exact same protein, or heterophilic interactions, between non-identical TJ proteins. Like the adherens junctions, the intracellular domains interact with different scaffolding proteins, adaptor proteins and signaling complexes to moderate cytoskeletal attachment, cell polarity, cell signaling and vesicle trafficking, as seen on Figure 3. The intracellular regions of AJs possess PDZ-binding domains, which gather and come in contact with PDZ domain containing proteins. The PDZ domain (Post synaptic density-95/Drosophila disk large/Zonula occludens-1 protein) is a common structural domain of about 80 to 90 amino acids which play the role of anchoring transmembrane proteins to the cytoskeleton. The intracellular domains may also interact with non-PDZ-binding domain including proteins like cingulin, which can interact with junctional membrane proteins, the actin cytoskeleton and signaling proteins. The complex network of intracellular protein interactions can also be known as the “cytoplasmic plaque”.

 

Tight Junctions

Figure 3

 

Tight Junction Formation in the Gastrointestinal Tract

 

The intestinal epithelium shapes the largest and most essential barrier between our external and internal gastrointestinal tract environments. The barrier is preserved by the presence of AJs and TJs, such as cadherins, claudins, occludin and JAM proteins, which isolate groups of adjacent cells and maintains cytoskeletal anchorage, as seen on Figure 3. Expression of junctional proteins in the gut are highly regulated and dependent on both the small and/or large intestine, villus/crypt location and cell membrane specificity; apical, lateral or basolateral. The complex pattern of TJ expression from the gut is related to the particular functions of a distinct intestinal region and location. Expression of adherens junctions and tight junctions proteins can also be controlled by phosphorylation, according to Table 1. Phosphorylation can either promote TJ formation and barrier feature, or alternatively promote TJ protein redistribution and intricate destabilization.

 

Transgenic or Knockout Mice & Effects on Intestinal Barrier Function

 

Occludin

 

One of the first integral membrane proteins belonging specifically to the tight junctions to be recognized is the occludin. Occludin are predominantly found at TJs in the epithelial and endothelial cells but can also be located in astrocytes, neurons and dendritic cells. Occludin (60 to 82 kDa) is a tetraspanning integral membrane protein consisting of two extracellular loops, a short cytoplasmic N-terminus and a long cytoplasmic C-terminus. Analysis and evaluation of the function of these have demonstrated that the extracellular loops and transmembrane domains of occludin manage and maintain selective paracellular permeability. Intracellularly, the C-terminus interacts with the PDZ-domain containing protein ZO-1, which is required to connect occludin into the actin cytoskeleton, according to Figure 3.

 

Several occludin isoforms are characterized and believed to be the result of alternative mRNA splicing. Quite distinctly, many splice variants demonstrate altered subcellular distribution and interaction with other TJ molecules. Evaluation of these splice variants showed that the cytoplasmic C-terminal domain is funcamental for the intracellular exchange of occludin to the lateral cell membrane, which the fourth transmembrane domain name is important for targeting occludin into the TJ as well as for ZO-1 interactions.

 

The role of occludin is not fully outlined; nonetheless, data suggested another function for occludin from the regulation of paracellular permeability. The major allergen of the house dust mite, Der p 1, was determined to proteolyticly disrupt occludin altering this TJ complex and increasing paracellular permeability. In addition, hydrocortisone treatment of bovine retinal endothelial cells improved occludin expression two-fold and enhanced monolayer barrier properties. Though occludin is an important element of TJs, TJ formation and paracellular permeability barrier function are not dependent on occludin. Experimental investigations of occludin on mice demonstrated equivalent numbers and groups of TJs and corresponding paracellular ion passage as wild mice. Furthermore, epithelial transport and barrier function were normal in mice with occludin. Along with regulating paracellular permeability, there is evidence indicating occludin is included in cellular adhesion. Length of occludin at occludin and rat fibroblasts conferred cell to cell adhesion that has formally been interrupted by synthetic peptides associated to the first extracellular loop of occludin, underscoring the significance of the area of occludin in cell adhesion.

 

Evaluations indicated that occludin found along the TJ complex is regulated by phosphorylation. Several potential phosphorylation sites at tyrosine, serine, and threonine residues of occludin have been identified where the regulation of occludin phosphorylation is proposed to happen by kinases, for instance, non-receptor tyrosine kinase c-Yes and protein kinase C (PKC), and phosphatases including the serine/threonine protein phosphatase 2A, according to Figure 3. PKC?, a novel protein kinase predominantly expressed in the intestinal epithelium, was demonstrated to directly phosphorylate occludin in threonine residues (T403 and T404). Blockade of all PKC?-mediated occludin phosphorylation interrupted junctional distribution of occludin and ZO-1 and interrupted epithelial barrier function. The data suggest that occludin phosphorylation modulates occludin-ZO-1 interactions and the maintenance of intact TJ complexes and paracellular barrier function.

 

Claudins

 

Claudins are 20 to 27 kDa integral membrane proteins with four hydrophobic transmembrane domains, two extracellular loops and N- together with C-terminal cytoplasmic domains. The extracellular loops are crucial for homophilic and/or heterophilic TJ protein to protein interactions alongside the creation of ion-selective channels. The intracellular C-terminal domain is included in anchoring claudin into the cytoskeleton through connections with PDZ-binding domain names, such as ZO-1, -2 and -3, according to Figure 3. Presently, 24 distinct claudin family receptor members are identified in those who have a number of orthologues expressed in various species. They exhibit distinct cell, tissue and developmental stage-specific expression routines.

 

Claudin to claudin interactions between adjoining cells might be homophilic or heterophilic. Homophilic interactions have been shown for claudins 1, 2, 3, 5, 6, 9, 11, 14 and 19. On the reverse side, heterophilic interactions are more restricted and largely have been detected with claudin-3, which could interact with claudins-1, -2 and -5. Notably, there’s specificity in heterophilic trans-interactions. By way of instance, transfection of fibroblasts with claudins-1, -2 and -3 led to claudin-3 interactions with claudin-1 and -2; yet no interactions involving claudin-1 and -2 were detected. These discerning interactions are considered to describe the diversity in TJ formations and provide a molecular basis for tissue-specific heterogeneity of barrier function.

 

Recent study, together with claudin-deficient mice also give corroborative information supporting a role for claudins in the law of barrier function. Claudin-1 mice die within a day of birth due to significant transepidermal water loss. Furthermore, transgenic overexpression of both claudin-6 in skin disrupted tight junction formation and increased epithelial permeability. Experimental data indicates that claudins could have differential impacts on paracellular permeability. By way of instance, introduction of claudin-2 to MDCK I cells which state claudin-1 and -4 activates a decrease in transepithelial resistance, or TER; whereas transfection of claudin-3 had no effect indicating that claudin-2 markedly diminished claudin-1/claudin-4 based TJ strand regeneration. In support of the latest experimental evidence indicates that claudins can form measurements and charge-specific paracellular stations. Transfection of claudin-8 into MDCK II cells that lacks endogenous claudin-8 substantially reduced paracellular movement without impacting anion and uncharged solute movement. Experimental investigations suggest that the first extracellular loop of claudins play an essential role in deciding charge selectivity. Interchanging of the earliest or extracellular domains of claudin-4 on claudin-2 profoundly diminished the ion conductance of Na+ relative to Cl? 76. Additionally, substitution of a negatively-charged lysine into some positively charged aspartic acid (K65D) inside the loop of claudin-15 generated an increase in Na+ permeability, whereas mutation in exactly the same place of three positively charged amino acids into negatively charged aspartic acid, arginine and aspartic acid (E46K, D55R and E64K) altered the ion selectivity of claudin-15 in Na+ to Cl? channel. Pore size and density may also impact paracellular movement of non invasive and charged charged solutes.

 

Claudins also play an essential role in epithelial cell invasion and motility. Overexpression of claudins-3 and -4 in human ovarian epithelial cells, which lack the expression of these proteins, has been connected with enhanced epithelial cell survival and enhanced invasion and motility. Consistent with this observation, siRNA-mediated knockdown of the two claudins-3 and -4 in ovarian cancer cell lines diminished intrusion. The outcome of claudin-3 appear to get connected to altered matrix metalloprotease-2 activity, meaning claudin-induced invasion could possibly be regulated by metalloprotease proteins.

 

Similar to occludin, claudin localization to the TJ complex and its function are regulated by post-translational phosphorylation and through connections with PDZ-binding domains. The intracellular C-terminal domain of claudin possesses multiple regulatory sites, such as possible serine and theronine phosphorylation sites and PDZ-binding domain names. Phosphorylation of claudins-3 and -4 in prostate cancer cells is closely connected to the regulation of paracellular permeability. By way of instance, patients with pseudohypoaldosteronism type II (PHA II; or vitamin shunt syndrome) present with hyperkalemic metabolic acidosis, hypertension and dysregulated paracellular ion transport. The molecular basis is connected to some loss-of-function mutation from the serine-threonine kinases, WNK1 and WNK4, which regulate epithelial chloride cotransporters. This also contributes to an increase in the phosphorylation of both claudins-1-4 and an increase in paracellular permeability. A lot of signaling pathways are implicated in the phosphorylation of claudins like PKC, Rho GTPases, mitogen-activated protein kinases (MAPKs) and phosphatases. MAPK phosphorylation of claudin-1 is required for claudin-1-mediated barrier function. Furthermore, claudins-1, -2, -7, -8, -16 and -17 have putative PKC phosphorylation websites.

 

All claudins, except claudin-12, completing from the dipeptide arrangement YV, that’s been shown to interact with PDZ-binding domains comprise ZO-1, -2 and -3, multi-PDZ domain name and PALS1-associated TJ protein, according to Figure 3. Several of those scaffolding proteins contain several PDZ domains, which eases the introduction of dense localized protein complexes, also called “cytoplasmic plaques”. Also, the scaffolding proteins can interact with signaling molecules, such as heterodimeric GTP binding proteins (Rab13 and G?12), transcriptional factors and RNA-processing variables, to connect TJ complexes to the actin-cytoskeleton and modulate aspects of adrenal polarization, differentiation and barrier function.

 

Junctional Adhesion Molecules (JAMs)

 

Junctional adhesion molecules are integral membrane proteins which belong to the immunoglobulin superfamily and have two immunoglobulin folds, the VH- and C2-type, from the extracellular domain. JAMs are expressed by multiple cell types, including epithelial, endothelial and immune cells. They’re subdivided based on the expression of Type I or II PDZ-binding themes in the intracellular C-terminus, which implies that the two types interact with exceptional scaffolding and cytoplasmic proteins. JAM-A, -B and -C (or JAM1-3) have Type II binding subjects, while the atypical JAMs, such as JAM-4, coxsackie and adenovirus receptor (CAR) and endothelial selective adhesion molecule make up Type I PDZ-binding domains. Comparable to additional TJ proteins, these JAM-PDZ interactions provide anchorage to the actin cytoskeleton, according to Figure 3.

 

The extracellular region of JAMs adapting to multiple ligands through homophilic and heterophilic interactions, which can be proposed to regulate the mobile functions and paracellular permeability of JAMs. Homophilic JAM-A or -B interactions govern the creation of operational TJs and cell to cell border formation, while heterophilic JAM interactions play a role in leukocyte-endothelial cell adhesion.

 

Recent studies demonstrate the significance of JAM-A at the formation and assembly of TJs in intestinal epithelial cells. SiRNA downregulation of JAM-A at SK-C015 epithelial cells triggered an increase in permeability. Consistent with this, JAM-A mice had increased mucosal permeability as indicated by enhanced dextran flux and decreased TER. Nonetheless, these mice also had an increase in claudin-10 and -15 expression, which is believed to shape selective pores from the TJ complex, improving paracellular permeability. Interestingly, JAM-A mice have increased susceptibility to chemical-induced colitis. Dextran sodium sulfate administration to JAM-A mice induced more acute colonic injury as compared to WT control animals. These studies imply altered intestinal permeability for a susceptibility factor to autoimmune disorder.

 

The above information is evidence-based. The scope of our information is limited to chiropractic and spinal injuries and conditions. To discuss the subject matter, please feel free to ask Dr. Jimenez or contact us at 915-850-0900 .

 

By Dr. Alex Jimenez

 

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Additional Topics: Wellness

 

Overall health and wellness are essential towards maintaining the proper mental and physical balance in the body. From eating a balanced nutrition as well as exercising and participating in physical activities, to sleeping a healthy amount of time on a regular basis, following the best health and wellness tips can ultimately help maintain overall well-being. Eating plenty of fruits and vegetables can go a long way towards helping people become healthy.

 

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TRENDING TOPIC: EXTRA EXTRA: How to Become a Healthier You!

 

 

How to Ensure a Correct Digestive Health Diagnosis

How to Ensure a Correct Digestive Health Diagnosis

A healthcare professional at a gastroenterology practice, such as a dietitian specializing in gastrointestinal diseases, will often care for a great deal of individuals who walk into their clinic reporting symptoms which haven’t yet been diagnosed to a specific digestive health issue. Because not many primary care physicians are in charge of diagnosing GI diseases nor are they properly aware of their wide array of symptoms, many people with gastrointestinal diseases will often go undiagnosed for years.

 

How can you talk to your doctor about your digestive issues?

 

A healthcare provider specializing in gastrointestinal diseases may look out for certain symptoms, as well as possible dietary triggers, to determine a digestive health issue. Simple lifestyle changes are generally the best treatment method to help improve GI diseases and its symptoms, however, being able to communicate accordingly with your doctor can help them diagnose your problem more accurately in order to begin treatment immediately. By following a few factors the patient can control, they can ensure their medical diagnostic procedure is fast, easy, and correct.

 

Arrive to your Appointment on Time

 

While careful planning and preparations can occasionally be sabotaged by events and situations that are out of our control, it’s essential for you to initially intend to reach your appointment on time. It’s recommended to arrive at least 15 minutes before your original appointment time, especially if you are a new patient as you will need to complete the necessary paperwork on your first visit. If you show up 15 minutes late for a 15 minute appointment, there is a great chance you’ll be hurried through your visit without ample time to go over your issues thoroughly with your doctor.

 

Bring Evaluation Results & Procedure Reports

 

It can’t be emphasized enough how common it is for patients to not know which previous diagnostic tests or even surgeries they’ve gone through for their specific disease and/or condition. If you show up to a healthcare professional’s appointment for further diagnosis and a second opinion regarding your symptoms without being aware of this information, your doctor may waste valuable time and money re-testing you for digestive health issues which may have already been ruled out by another healthcare specialist. Furthermore, without previous evaluation results and/or procedure reports, doctors can miss an obvious diagnosis based on your health history, or worse, they may perform yet another invasive procedure which you no longer needed.

 

If you have had an endoscopy or a colonoscopy, what were the signs? If you’ve had surgery somewhere on your gastrointestinal tract, which process was it? If you have experienced a breath test, what were they checking for and what were the results? If blood has been drawn lately, what was being checked and also what, if anything, has been discovered? Have you had any specialized tests that involved imaging of your gastrointestinal tract? These are all important questions you must know before visiting a doctor’s office.

 

Also, to get to a faster diagnosis, your best option is to bring copies of all relevant tests and reports you have undergone related to your digestive health issues. It may take some effort to collect these results from previous doctors or even hospitals, though medical practices offering online patient portals may make this procedure easier. If you can’t obtain the true exam results, then compiling a summarized “medical resume” may be the next best thing. Just type up a list of all of the test names or procedure reports you’ve had; who ran them (as well as where and when they were performed); and exactly what they discovered, based on those evaluations and procedures. Hand the sheet to your healthcare professional. Their office can then track down copies of any relevant results after you leave from your first appointment.

 

Describe your Symptoms in Detail

 

It can be quite embarrassing to describe your digestive symptoms to a healthcare professional and you might even feel unsure of whether you may actually have a digestive issue based on your “normal” collection of gut sounds, backed up stools and that occasional nausea you experience after eating a heavy meal. You may be tempted to use more conservative, generic phrases to describe your symptoms but healthcare specialists say you don’t have to be considerate. Your doctor has literally heard it all and it is as routine to them as speaking about the weather is to everyone else.

 

If you say that you “get sick to your stomach” when referring to having diarrhea, for instance, the healthcare professional may actually think you are referring to nausea. If you say “constipated” to refer to straining to have a daily bowel movement, your doctor may presume you mean you are unable to move your bowels more than once or twice per week. If you say you get a “stomachache” after eating, it could refer to sharp pain, cramps or dull pain and it doesn’t properly inform your doctor where the pain is located. Tell your doctor exactly what you mean, along with all of the extra descriptive details. What’s happening and where, what it looks like, what it smells like, what it feels like and how frequently it happens. Correctly describing your symptoms is key to a correct diagnosis.

 

Mention When your Symptoms Started

 

At times, telling your healthcare specialist when your symptoms all started can be the clue to your diagnosis. Did you notice your digestive health issues after you recovered from a bout of food poisoning in your holiday? Did things change for you in the bathroom after having your gallbladder removed? Did your digestive discomfort increase after switching to a brand new diet, such as a 30-day cleanse, Weight Watchers or a paleo-style diet? Do your symptoms coincide with starting or stopping a particular drug/medication or supplement? Have you experienced this digestive health issue since you were a child? Did your issue get better or worse during pregnancy? Putting your complaints in context will help your doctor perform a better medical diagnostic procedure.

 

Inform your Doctor of What you Have & Haven’t Tried

 

Doctors often learn just as much out of what hasn’t helped you feel better as they do from what has helped you feel better. If you have already tried a drug/medication, supplement, lifestyle changes, including diet modifications and physical activities, to address your gastrointestinal issues and it has not worked, make sure you incorporate this in your conversation with your healthcare specialist. It will help them narrow down the list of possibilities and help point to more likely gastrointestinal diseases and conditions.

 

Keep an Open Mind

 

Now that we all have access to the internet, we’ll often arrive to a doctor’s appointment with a preconceived notion about what we believe we may have. Because of this, many patients may attempt to steer the conversation toward this self-diagnosis and accidentally leave out important information that could shed light on the correct diagnosis. It is absolutely appropriate to share your own hypothesis about your digestive health issue with your healthcare provider and this can be particularly more important if you’ve got a family medical history which may accurately indicate your problem. But be sure to share all the details of your conclusion, and be open to the possibility that your doctor may see matters in a different light than all the other articles you may have read on the internet. The scope of our information is limited to chiropractic and spinal injuries and conditions. To discuss the subject matter, please feel free to ask Dr. Jimenez or contact us at 915-850-0900 .

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By Dr. Alex Jimenez

Additional Topics: Wellness

 

Overall health and wellness are essential towards maintaining the proper mental and physical balance in the body. From eating a balanced nutrition as well as exercising and participating in physical activities, to sleeping a healthy amount of time on a regular basis, following the best health and wellness tips can ultimately help maintain overall well-being. Eating plenty of fruits and vegetables can go a long way towards helping people become healthy.

 

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TRENDING TOPIC: EXTRA EXTRA: How to Become a Healthier You!

 

 

The Role of Healthcare Professionals for Gastrointestinal Diseases

The Role of Healthcare Professionals for Gastrointestinal Diseases

In the month of October, approximately 50,000 people worldwide gathered in the World Congress of Gastroenterology to discuss different ways in which healthcare professionals could improve care for individuals with gastrointestinal, or GI, diseases, involving the gastrointestinal tract. While these attempts within the GI community are undeniably essential, it’s also fundamental that we teach the broader medical community concerning the growing challenge these gastrointestinal diseases present for the doctors.

 

How can you improve gastrointestinal diseases and its symptoms?

 

As many as 16 million individuals in the United States alone, suffer from irritable bowel syndrome, or IBS, with diarrhea, a gastrointestinal disease which mainly affects the bowel or colon and its symptoms are commonly characterized by abdominal pain and nausea. Constipation is the most common and uncomfortable gastrointestinal, or GI, issue, frequently reported by patients taking opioids. There are over 200 million opioid prescriptions written every year, each of which can lead to GI disease.

 

Inflammatory bowel diseases, such as ulcerative colitis and Crohn’s disease, usually involve severe nausea, abdominal pain, fatigue and weight loss. In 1999, there were 1.8 million cases of inflammatory bowel diseases, or IBD, among Americans. As of 2016, that number has substantially increased up to 3.1 million cases within the American population. When the liver is unable to efficiently eliminate toxins from the bloodstream, it can cause loss of brain function, a condition known as hepatic encephalopathy. The yearly inpatient incidence of hepatic encephalopathy increased from 20,918 from 2005 to 22,931 in 2009, making up approximately 0.33 percent of all hospitalizations from the United States.

 

The Significance of Proper Care for Gastrointestinal Diseases

 

Not only do gastrointestinal, or GI, diseases and their symptoms affect an overwhelmingly big part of our population, these have also become a burden on the federal health care system. In 2013, direct expenses of IBS, or irritable bowel syndrome, had ranged from $1,562 to $7,547 per individual, annually. The total national charges associated with HE, or hepatic encephalopathy, also increased from $4.6 billion in 2005 to $7.2 billion in 2009.

 

The logical question we should ask ourselves regarding the increasing cases of gastrointestinal diseases is: Are patients receiving the proper treatment they need? Let us take a closer look at IBS, as it’s one of the most frequent functional GI diseases. Research published in the American Journal of Gastroenterology in June 2017, demonstrated that there is a greater than 40 percent chance that people who visit a healthcare professional for symptoms of IBS may not receive a proper diagnosis, as it generally takes patients four years to be diagnosed with IBS. It’s no surprise that gastrointestinal healthcare specialists would appreciate it if primary care physicians and nurse practitioners would handle the most common cases. But that may not occur until the wider medical community becomes more comfortable with diagnosing gastrointestinal disorders.

 

Unfortunately for the population of IBS sufferers that go undiagnosed, many resort to searching the internet for the answers themselves, followed by one attempt after another of self-diagnosis and self-treatment for their specific gastrointestinal diseases. A survey by the Pew Internet & American Life Project found that 80 percent of internet users have searched for a health-related topic online, most frequently, for information about a specific disease or medical issue. A Google search for “IBS,” for example, yields approximately 50 million hits. Add direct-to-consumer advertisements into the mix, and the clutter of information may be overwhelming for patients and healthcare professionals alike. Much of the information readily available to anyone with an online connection is evidence-based, however, much is specious and unfounded. Evaluating the information in an effort to self-diagnose and self-treat may be dangerous. What we need is a strategy to help individuals and doctors cut through the clutter and make that information work for them in mutually positive ways.

 

Many healthcare professionals are pledging to invest multimillions to increase awareness of gastrointestinal diseases and their symptoms. Specialist groups are starting a national educational program at the primary care level which will require doctors to take an educational voyage deep within a high-definition, virtual lumen of the small intestine. Through the lens of a virtual reality tool, doctors peruse a swarm of microbiota and various bacteria drifting through the undulating, glistening layers of pinkish gut while a narrator explains how these life forms can potentially create a life of abdominal pain and discomfort. This immersive cartoon is part of a strategy to engage and educate the wider medical community on many leading theories about IBS, including the role gut microbiota can play in generating symptoms as well as that of other GI diseases.

 

Gastrointestinal healthcare specialists are already knowledgeable about the anatomy and function of the digestive system, however a lot of primary care physicians and the broader medical community may not be. By educating the wider medical community about these common digestive health issues, healthcare professionals can begin making a difference towards the overall treatment of gastrointestinal, or GI, diseases. If primary care physicians and nurse practitioners aren’t acutely conscious of the symptoms and possible etiologies that could point a GI� healthcare specialist to the proper treatment, their patient may continue to endure the uncomfortable symptoms for several years before finding an appropriate treatment therapy.

 

The greatest goal for us is to remove any obstacles which may come in between proper GI patient care, especially for the undiagnosed and untreated patient population. If healthcare professionals can diagnose patients earlier, those obstacles may soon disappear altogether. The scope of our information is limited to chiropractic and spinal injuries and conditions. To discuss the subject matter, please feel free to ask Dr. Jimenez or contact us at 915-850-0900 .Green-Call-Now-Button-24H-150x150-2-3.png

 

By Dr. Alex Jimenez

 

Additional Topics: Wellness

 

Overall health and wellness are essential towards maintaining the proper mental and physical balance in the body. From eating a balanced nutrition as well as exercising and participating in physical activities, to sleeping a healthy amount of time on a regular basis, following the best health and wellness tips can ultimately help maintain overall well-being. Eating plenty of fruits and vegetables can go a long way towards helping people become healthy.

 

blog picture of cartoon paperboy big news

 

TRENDING TOPIC: EXTRA EXTRA: How to Become a Healthier You!

 

 

What are Gastrointestinal Diseases?

What are Gastrointestinal Diseases?

The digestive system is largely in charge of providing the body with the essential nutrients needed for all the other systems of the body to function effectively. But, what happens when your digestive health is less than optimal and your overall wellness is affected? Gastrointestinal diseases can wreak havoc on the structure and function of the digestive system, altering its effectiveness when providing the body with essential nutrients, as well as that of other important processes in the human body.

What are Functional Gastrointestinal Diseases?

 

Functional gastrointestinal diseases are those in which the gastrointestinal tract, or GI tract, appear normal but may actually not be functioning properly. They are the most common issues which affect the gastrointestinal tract, including the colon and the rectum. Irritable bowel syndrome, or IBS, and constipation are two of the most commonly reported examples of functional GI diseases. Many factors may affect the gastrointestinal tract’s function, primarily when it involves its motility, or the ability to keep “things” moving, such as:

 

  • Eating an improper diet that is also low in fiber,
  • Not participating in enough physical activity or exercise,
  • Changes in your daily routine due to traveling,
  • Eating large quantities of dairy products,
  • Stress,
  • Resisting the urge to go to the bathroom,
  • Resisting the urge to go to the bathroom due to pain from hemorrhoids
  • Overdoing it on the use of laxatives, or stool softeners, which weaken bowel muscles,
  • Taking antacid medicines, which calcium or aluminum,
  • Using certain drugs and/or medications, especially antidepressants, iron pills, and strong pain medicines such as narcotics,
  • And pregnancy.

 

Irritable Bowel Syndrome, or IBS

 

Irritable bowel syndrome, also known as spastic colon, irritable colon, or nervous stomach, is a gastrointestinal disease in which the colon muscle contracts more frequently than in people without IBS. Certain foods, drugs and medications, and even emotional stress have been identified to be some of the most prevalent aspects which can trigger irritable bowel syndrome and its symptoms. Symptoms of irritable bowel syndrome, or IBS, include:

 

  • Abdominal pain and cramps,
  • Excessive gas,
  • Bloating,
  • Changes in bowel movement habits, such as harder, looser, or more urgent stools than normal,
  • And alternating constipation and diarrhea.

 

Treatment methods for irritable bowel syndrome, or IBS include:

 

  • Avoiding the consumption of caffeine or caffeinated products,
  • Adding more fiber intake to your diet,
  • Monitoring which foods trigger your IBS and taking action to avoid eating these foods,
  • Decreasing stress levels by learning different ways to cope with the stress,
  • And occasionally taking drugs and medications as prescribed by a healthcare professional.

 

Constipation

 

Constipation is a common gastrointestinal disease, described as the inability or struggle to have a regular bowel movement, or move stools, where they’re infrequent, about less than three times a week, or incomplete. Constipation is usually brought on by insufficient fiber in the diet, or due to a disruption in your normal diet or daily routine. Constipation can cause a person to strain during a bowel movement. It may create small, hard stools and can sometimes lead to anal issues, such as hemorrhoids and fissures. Constipation is seldom a sign of a more serious digestive health issue. People with constipation can treat the problem by:

 

  • Increasing fiber intake to your diet,
  • Engaging in regular physical activity or exercise,
  • And by going to the bathroom promptly when you feel the urge to go, as resisting the urge is believed to cause constipation.

 

If these treatment methods are not enough, laxatives can be used but only as a temporary alternative. Be aware that the overuse of laxatives can eventually worsen constipation symptoms. Always follow the advice of your healthcare professional or follow the directions on the laxative medicine, accordingly.

 

What are Structural Gastrointestinal Diseases?

 

Structural gastrointestinal diseases are those in which the bowels themselves look abnormal while also not functioning properly. Occasionally, the structural abnormality may need to be surgically removed to relieve the digestive health issue. Commonly reported examples of structural gastrointestinal diseases, include hemorrhoids, diverticular disease, colon polyps, colon cancer, and inflammatory bowel disease.

 

Anal Disorders

 

Hemorrhoids

 

Hemorrhoids can be characterized as the swollen blood vessels that line the anal opening. They are brought on by chronic, excessive pressure from straining during a bowel movement, persistent diarrhea or even pregnancy. There are two types of hemorrhoids: internal and external.

 

Internal Hemorrhoids

 

Internal hemorrhoids are blood vessels on the interior of the anal opening. When they fall down into the anus as a result of straining, they can become irritated and start to bleed. Ultimately, internal hemorrhoids can fall down enough to prolapse, or sink and/or stick, out from the anus.

 

Treatment methods for internal hemorrhoids include:

 

  • Improving bowel movement habits, such as avoiding constipation, not straining during bowel movements and going to the bathroom when you have the urge to go,
  • Having your doctor use elastic bands to remove the blood vessels,
  • And, having a healthcare professional surgically remove them. Surgical interventions are generally only utilized for patients with painfully large and persistent hemorrhoids.

 

External Hemorrhoids

 

External hemorrhoids are veins that lie just underneath the skin on the outside of the anus. Occasionally, after straining, the external hemorrhoidal veins can burst, forming a blood clot under the skin. This very painful condition is medically referred to as a pile.

 

Treatment methods for external hemorrhoids include removing the clot and vein under local anesthesia and/or removing the hemorrhoid itself.

 

Anal Fissures

 

Anal fissures are splits or cracks which occur in the lining of the anal opening. The most common cause of an anal fissure is the passing of very hard or watery stools. The crack in the anal lining exposes the muscles which control the passage of stool through the anus and out of the body. An anal fissure is considered to be one of the most painful gastrointestinal diseases, or disorders, because the vulnerable muscles can become irritated from exposure to feces, or stool, and/or air, and may lead to intense burning pain, bleeding, or spasm after bowel movements.

 

Initial treatment methods for anal fissures includes pain drugs/medications, the addition of dietary fiber to reduce the incidence of large, bulky stools, and sitz baths, where the individual sits in a few inches of warm water. If these treatments do not relieve the painful symptoms, surgery may be required to repair the sphincter muscle.

 

Perianal Abscesses

 

Perianal abscesses can occur when the tiny anal glands that open on the interior of the anus become obstructed, and the bacteria always present in these glands trigger an infection. When pus develops, it can create the perianal abscess.

 

Treatment involves draining the abscess, usually under local anesthesia by a qualified and experienced healthcare professional.

 

Anal Fistula

 

An anal fistula often follows drainage of an abscess and can be an unnatural tube-like passageway in the anal canal to a hole in the skin near the opening of the anus. Body wastes traveling through the anal canal are redirected through this tiny channel and out through the skin, causing itching and irritation. Anal fistulas also bring about drainage, pain, and bleeding. They rarely heal by themselves and usually require surgery to drain the abscess and “close off” the fistula.

 

Other Perianal Infections

 

Occasionally, the skin glands near the anus become infected and may need to be drained. Just behind the anus, abscesses can form that contain a little tuft of hair at the back of the pelvis, known as a pilonidal cyst. Sexually transmitted diseases which could affect the anus include anal warts, herpes, AIDS, chlamydia, and gonorrhea.

 

Diverticular Disease

 

Diverticulosis is the presence of small outpouchings, known as the diverticula, in the muscular wall of the large intestine which form in weakened areas of the gastrointestinal tract, or GI tract. They usually develop in the sigmoid colon, the high-pressure area of the lower large intestine. Diverticular disease is relatively common and can occur in approximately 10 percent of people over the age of 40 and in 50 percent of people over the age of 60 in Western cultures. It’s frequently caused by too little amounts of fiber in the diet. Diverticulosis rarely causes symptoms.

 

Complications of diverticular disease happen in about 10 percent of people with outpouchings. They include inflammation or infection (diverticulitis), bleeding, and obstruction. Treatment methods for diverticulitis includes antibiotics, increased fluids, along with a specialized diet. Surgical interventions are needed in about half of the patients who have complications to eliminate the involved segment of colon.

 

Colon Polyps and Cancer

 

About 130,000 Americans are diagnosed with colorectal cancer each year, making it the second most common type of cancer in the United States. Fortunately, with medical advances in early detection and treatment method therapies, colorectal cancer is one of the most curable forms of the disease. By utilizing a variety of screening tests, it is possible to prevent, detect, and treat the disease before symptoms begin to appear.

 

The Value of Screening

 

Virtually all colorectal cancers begin as polyps, benign, or non-cancerous, growths in the tissues lining the colon and rectum. Cancer develops when these polyps grow and abnormal cells develop and start to invade surrounding tissues. Removal of polyps can prevent the development of colorectal cancer. Almost all precancerous polyps may be removed painlessly using a flexible, lighted tube called a colonoscope. If not caught in the early stages, colorectal cancer can spread throughout your system. More advanced cancer requires more complex surgical procedures. Most early forms of colorectal cancer do not cause symptoms, making screening an essential part of its diagnosis. When symptoms do occur, the cancer might already be very advanced. Symptoms include, blood mixed in with the stool, a change in normal bowel movement habits, narrowing of the stool, abdominal pain, weight loss, or constant tiredness.

 

Most cases of colorectal cancer are detected in one of four ways:

 

  • By screening people at average risk for colorectal cancer beginning at age 50,
  • By screening people at higher risk for colorectal cancer, for example, those with a family history or a personal history of colon polyps or cancer,
  • By investigating the bowel in patients with symptoms,
  • And through a chance finding at a routine, doctor’s check-up.

 

Early detection is your best opportunity for a cure.

 

Colitis

 

There are several types of colitis, gastrointestinal diseases which can cause an inflammation of the gut. The different types of colitis include:

 

  • Infectious colitis,
  • Ulcerative colitis, where the cause is unknown,
  • Crohn’s disease, where the cause is unknown,
  • Ischemic colitis, caused when not enough blood is going to the colon,
  • And radiation colitis, caused after radiotherapy.

 

Colitis causes diarrhea, rectal bleeding, abdominal cramps, and urgency, or frequent and immediate need to empty the bowels. Treatment methods for colitis depend on the diagnosis, which is made after a colonoscopy and biopsy.

 

Can Gastrointestinal Diseases be Avoided?

 

Many gastrointestinal diseases, or GI diseases, can be prevented or their risk can reduced by managing and maintaining a healthy lifestyle, such as a proper nutrition, exercise, and hydration, among other lifestyle modifications, by practicing good bowel movement habits, and submitting to cancer screening. Colonoscopy is recommended for average risk patients at age 50. When you have a family history of colorectal cancer or polyps, colonoscopy may be recommended at a younger age. Normally, colonoscopy is recommended 10 years younger than the affected relative. For instance, if your brother has been diagnosed with colorectal cancer or polyps at age 45, you should begin screening at age 35. In case you have symptoms of colorectal cancer you should speak to your doctor right away. Common symptoms include:

 

  • A change in normal bowel movement habits,
  • Blood on or in the stool which is either bright or dark,
  • Unusual abdominal or gas pains,
  • Very narrow stool,
  • A feeling that the bowel has not emptied completely after passing stool,
  • Unexplained weight loss,
  • And fatigue.

 

The scope of our information is limited to chiropractic and spinal injuries and conditions. To discuss the subject matter, please feel free to ask Dr. Jimenez or contact us at 915-850-0900 .

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By Dr. Alex Jimenez

 

Additional Topics: Wellness

 

Overall health and wellness are essential towards maintaining the proper mental and physical balance in the body. From eating a balanced nutrition as well as exercising and participating in physical activities, to sleeping a healthy amount of time on a regular basis, following the best health and wellness tips can ultimately help maintain overall well-being. Eating plenty of fruits and vegetables can go a long way towards helping people become healthy.

 

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Important Tips for Good Digestive Health | Wellness Clinic

Important Tips for Good Digestive Health | Wellness Clinic

Several hours after you’ve swallowed that delicious first bite from your breakfast meal, the process of digestion has already started helping you get the most essential nutrients from your food. Your gastrointestinal tract, around 30 feet of prime digestive real estate, has the important function of breaking down food to absorb carbohydrates, proteins and fats, as well as vitamins and minerals, necessary for you to survive. However, your digestive system may not always function seamlessly.

 

Is digestive health important for overall wellness?

 

In fact, approximately 60 percent of adults suffer from gastrointestinal diseases and often experience symptoms such as gas, bloating and constipation. While an occasional abdominal discomfort might appear normal to most people, it could signal the beginning of a much bigger digestive health issue and you may find that it can be quite a relief to know that you can take action to feel your best. Listed below are five digestion health tips everyone can put into practice to achieve optimal gut wellness.

 

Understanding the Gut’s Microbiome

 

One hundred trillion of your body’s greatest allies, bacteria found throughout various areas of the gastrointestinal tract, make up what’s referred to as the microbiome. Researchers believe that digestive health can provide an insight into the well-being of the entire human body and there’s evidence that both the type and amount of bacteria growing on your gut can affect other functions as well, from your immunity to even your mood. The good kinds of bacteria, commonly known as probiotics, also need to eat in order to survive and help control the growth of harmful bacteria in the gastrointestinal tract. Prebiotics are the essential “food” for probiotics. There’s been many discussions regarding those probiotics found in fermented foods such as yogurt, kefir and kimchi, but it should be understood how vital it is to nourish these probiotics with prebiotics. Some prebiotic foods include raw asparagus, cooked onions, bananas and kiwifruit, among others.

 

Understanding How to Maximize Digestion

 

When it comes to achieving optimal digestive health, fiber can promote that sought after, comfortable digestion. The best sources of fiber include plant foods. In addition to enjoying those deliciously, colorful fruits and vegetables, make sure to fill up on whole grain foods to get enough fiber. The 2015-20 Dietary Guidelines recommends making half your plate fruits and vegetables and half of all your grains, whole grains. The United Nations called 2016 the International Year of Pulses, yet another name for beans and lentils, which are also rich in fiber. Some foods have compounds known as proteases which help break down protein, easing digestion when eating a hearty meal with meat. For instance, pineapple has a protease called bromelain, kiwifruit contains actinidin and papaya has papain. Another essential that can help maximize digestion which many people overlook is the simple principle of slowing down when you’re eating to make digestion easier. Taking time to properly chew your food is one of the smartest tricks anyone can do in order to optimize digestion.

 

Understanding How to Get the Gut Back on Track

 

Many of you may well know that sensation when your digestion is thrown out of whack and “things” get backed up a little. Although you may not have constipation, one can experience bloating and discomfort. In order to get your gut back on its regular track, you should maximize three things: water, exercise, and fiber. When that alone isn’t enough, many men and women can turn to fiber supplements such as psyllium and other bulking agents. Preliminary evidence from a study in New Zealand demonstrated that eating two green kiwifruit a day eases constipation as effectively as fiber supplements. Kiwifruit is an excellent source of fiber, like many fruits, but research affirms that kiwifruit fibers have a higher capacity of holding water, helping in laxation in the colon. Research studies are now underway in Italy and Japan to add to the understanding of kiwifruit as a natural remedy for relieving constipation. It’s a pretty exciting notion that using whole foods over supplements can be all that’s needed to get your digestive health back on track.

 

Understanding FODMAPs

 

Irritable bowel syndrome is a gastrointestinal disease estimated to affect 1 in 10 people. In the last few years, those diagnosed with irritable bowel syndrome, or IBS, have found digestive relief following a low FODMAP eating strategy. Certain carbohydrate foods, many of which can be nourishing fruits, vegetables and beans, are saturated in FODMAPs, which stands for Fermentable Oligosaccharides, Disaccharides, Monosaccharides And Polyols, and may not be absorbed by people with sensitive intestines. Subsequently, these can create gas and other uncomfortable symptoms in the colon when bacteria ferment them, triggering irritable bowel syndrome symptoms. To ease IBS symptoms, the FODMAP foods must be removed from the individual’s diet and then later reintroduced in tolerable amounts. Talk to your gastroenterologist or a registered dietitian specializing in the low FODMAP protocol in case you have IBS and are considering trying this diet to improve your digestive health.

 

Understanding the Link Between the Brain and the GI Tract

 

You may also have already heard that stress can ultimately affect your digestive health. When some people feel stressed and anxious, their gastrointestinal tract often goes into hyperdrive. Nevertheless, the link between the brain and the GI tract is more than just that. More than 60 percent of our immune cells call the digestive system home. The gut has its own nervous system as well, frequently referred to as “the second mind,” containing more than a million nerve cells. Additionally, around 95 percent of people with IBS also struggle with depression or other mood disorders.

 

The concept that the gut microbiome can influence mood has become one of the most interesting areas of research today. Studies have revealed that the gut synthesizes significant levels of serotonin, the neurotransmitter that helps calm and relax the body. Adequate vitamin C is required for the gut to turn tryptophan into serotonin.

 

Scientists are analyzing how modifications to our eating patterns may contribute to an improved and diverse microbial community. Those studying kiwifruit have supplied evidence that consuming two kiwifruit per day (200 mg per day of vitamin C) was associated with optimal blood levels of vitamin C to benefit immune function and well-being. One study demonstrated a 35 percent decrease in mood disbalances based on self-reported perception of an improved mood once the participants consumed kiwifruit. While many different foods, such as oranges and strawberries, can provide vitamin C, SunGold kiwifruit is a particularly rich source of the nutrient.

 

Now that you’ve understood how to manage and maintain your digestive health better, you can start to make lifestyle changes that can help you support it. The good news is these changes can be simple, delicious and beneficial to your overall wellness. Whether you begin to eat more slowly, build a balanced plate to get more fiber, be sure to consume probiotics and prebiotics, get sufficient water, exercise, or do a bit of each of the tips mentioned above, you’ll feel the difference with better digestive health. Keep your eyes open for further evidence of what creates a healthy gut microbiome, because we’re just digging into the knowledge base of beneficial bacteria. The scope of our information is limited to chiropractic and spinal injuries and conditions. To discuss the subject matter, please feel free to ask Dr. Jimenez or contact us at 915-850-0900 .

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By Dr. Alex Jimenez

 

Additional Topics: Wellness

 

Overall health and wellness are essential towards maintaining the proper mental and physical balance in the body. From eating a balanced nutrition as well as exercising and participating in physical activities, to sleeping a healthy amount of time on a regular basis, following the best health and wellness tips can ultimately help maintain overall well-being. Eating plenty of fruits and vegetables can go a long way towards helping people become healthy.

 

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TRENDING TOPIC: EXTRA EXTRA: How to Become a Healthier You!

 

 

The 5 Most Common Gastrointestinal Diseases | Wellness Clinic

The 5 Most Common Gastrointestinal Diseases | Wellness Clinic

There’s something about gastrointestinal issues that makes them difficult to talk about in polite company, which unfortunately leaves many of us suffering one problem or another in silence. “What’s more, gastrointestinal, or GI, diseases are putting an increasing weight on Americans, causing an unprecedented number of clinical visits and hospitalizations than ever before”, stated Stephen Bickston, an American Gastroenterological Association professor of internal medicine at Virginia Commonwealth University.

 

What are the most prevalent gastrointestinal diseases?

 

Nevertheless, treatments for gastrointestinal diseases can be as simple as making informed lifestyle modifications or even taking over-the-counter drugs and medications. Peppermint oil and soluble fiber, for instance, has been used to help people with irritable bowel syndrome, or IBS, where a 2008 British Medical Journal study suggested that both of these natural remedies ought to be first-line treatment therapies for IBS. Here’s a rundown of the latest medical knowledge on five of the most common gastrointen.

 

Acid Reflux

 

Symptoms of acid reflux, such as heartburn, are among several of the most common digestive discomforts reported by the general population. In a Swedish study, approximately 6 percent of people reported suffering from acid reflux symptoms daily and 14 percent had them at least weekly. Such frequent symptoms may indicate the presence of gastroesophageal reflux disorder, or GERD. Aside from being painful, GERD, or gastroesophageal reflux disorder can damage the esophagus throughout the years or even lead to esophageal cancer.

 

“Heartburn typically involves a hot or burning sensation which rises up from the center of the abdomen area and to the chest under the breastbone or sternum”, states Michael Gold, a gastroenterologist at MedStar Washington Hospital Center in Washington, D.C. “It might also be accompanied by a sour taste in the mouth, or hypersalivation, in addition to discovering fluid or food out of your mouth, particularly at night time.” Pregnancy, several drugs and medications, as well as consuming alcohol or certain foods can cause heartburn. Children under the age of 12 and a few adults may have GERD without heartburn, instead experiencing asthma-like symptoms, difficulty swallowing, or a dry cough.

 

Treatment options for acid reflux include drugs and medications that reduce acid levels, like the proton pump inhibitors Aciphex, Nexium, Prevacid, Prilosec, and Protonix, along with the H2 blockers Axid, Pepcid, Tagamet, and Zantac. But taking these drugs and/or medications is not without risk. In 2008, a study found that a proton pump inhibitor can weaken the heart-protective impact of the blood thinner Plavix in patients taking the two drugs/medications together. In severe cases of gastroesophageal reflux disorder, surgeons can tighten a loose muscle found between the esophagus and the stomach, to inhibit the upwards flow of gastric acid. Laparoscopic surgery, which involves small incisions, has been proven to reduce scarring and shorten recovery time in comparison with open procedures.

 

Diverticulitis

By one estimate, about 3 in 5 Americans older than 70 years of age have the abnormal lumps called diverticula someplace in the wall of their intestinal tract. However, only 20 percent may experience a complication like diverticulitis, inflammation of a pouch, a tear, or an abscess.

 

Individuals with Crohn’s disease or ulcerative colitis, the two most prevalent inflammatory bowel diseases, complain of abdominal pain and diarrhea and may sometimes experience anemia, rectal bleeding, weight loss and other symptoms. “No definitive tests and evaluations exist for either disease and patients generally endure two primary misdiagnoses”, says R. Balfour Sartor, chief medical adviser to the Crohn’s & Colitis Foundation of America. “With Crohn’s”, he states, “appendicitis, irritable bowel syndrome, an ulcer, or an infection can be incorrectly diagnosed.”

 

In case diverticulitis does develop, symptoms are most likely to manifest through abdominal pain and potentially fever, however, antibiotics can treat the problem. In severe instances, a tear can result in an abscess, which might result in nausea, vomiting, fever, and intense abdominal tenderness which demands surgical repair. Some healthcare specialists consider that a diet too low in fiber could trigger the gastrointestinal disease, which develops growingly common with age and is most widespread in western societies.

 

Inflammatory Bowel Disease

 

Both disorders may emerge from a wayward immune system that leads the body to attack the gastrointestinal tract, or GI tract. Crohn’s disease involves ulcers that could seep deep into the tissue lining at any given section of the GI tract, leading to infection and thickening of the intestinal wall and blockages which may need surgery. Ulcerative colitis, by comparison, interrupts only the colon and rectum, where it also causes ulcers; colitis is characterized by bleeding and pus.

 

Treating either disease requires beating back, then constantly holding in check, the inappropriate inflammatory response. Both steps are accomplished by means of a combination of prescription anti-inflammatories, steroids and immunosuppressants. Crohn’s patients might also be given antibiotics or other specialized drugs and medications. The current debate stands as to whether Crohn’s disease sufferers benefit if given highly potent treatment therapies early in the course of the gastrointestinal disease instead of escalating potency with time from milder initial treatments, as is traditionally done, clarified Themos Dassopoulos, manager of inflammatory bowel diseases at Washington University at St. Louis. Surgery “cures” ulcerative disorders by simply taking away the colon but signifies that patients will need to wear a pouch, internally or externally, for waste. “Inflammatory bowel disease, or IBD, patients must take particular caution when using NSAIDs, such as aspirin, since these painkillers may cause additional gut inflammation in 10 to 20 percent of individuals, ” states Dassopoulos.

 

Constipation

 

The fact that Americans spend $725 million annually on laxatives indicates that trying to unclog the nation’s plumbing, so to speak, is a national pastime. But overuse of stimulant laxatives, which cause the intestines to contract rhythmically, can make the gut more reliant on these, requiring more of them and finally rendering the aid ineffective. First, a little bit of clarification on the frequency of your flushing: “There is no need to worry about having a daily bowel motion; anywhere between three times a day and three times per week is normal”, says Sandler.

 

“However, if you are having discomfort and can not make your bowels move, try out an over-the-counter remedy such as milk of magnesia’,’ he states. And should you have attempted laxatives or not, going a week without a bowel movement is a very good reason to see the doctor, ” says Sandler. Constipation, hard stools, and straining could result in hemorrhoids or an anal fissure. Constipation is best avoided through regular exercise and a diet high in fiber from whole grains, fruits, and vegetables. To elderly folks, that are inclined to become constipated more frequently: Be sure you’re hydrating properly and conscious of any drugs and medications which may be causing your bowel movements to be backed up.

 

Gallstones

 

Just a quarter of people with gallstones typically require treatment. That’s fortunate, because every year nearly 1 million Americans are diagnosed with these small pebbles, which are largely made of cholesterol and bile salts. Eliminating these typically requires removal of the gallbladder, one of the most frequent surgeries in the United States.

 

“Gallstones can get blamed for symptoms caused by other, more elusive culprits, such as irritable bowel syndrome”, states Robert Sandler, chief of the division of gastroenterology and hepatology together with the University of North Carolina School of Medicine. An ultrasound evaluation may pick them up while missing the real issue. “If you’re told you’ve got to have gallstones out however they aren’t bothering you, get a second opinion”, he advises. Removal may be mandatory when the stones instigate infection or inflammation of the gallbladder, pancreas, or liver. This can happen if a stone going out of the intestine becomes trapped, blocking the flow of bile, at the ducts between the liver and the small intestine.

 

The pain of a gallstone lodged at a duct normally comes on quickly at the right upper abdomen, between the shoulder blades, or beneath the right shoulder,� and also means a visit to the ER is necessary, as may fever, vomiting, nausea, or pain lasting more than five hours. Gallbladder removal may be accomplished laparoscopically and more recently has been completed with no external incision by going through your mouth or vagina. Obesity can also be a risk factor for gallstones, and it is theorized that they increase due to a lack of fiber and an excessive amount of fat from the western diet. Losing weight then regaining it also seems to set the stage for the common gastrointestinal disease. In a 2006 study of men, the more frequent the weight cycling and the bigger the amount of pounds fall and are regained, the larger the chances of developing gallstones. Women, in particular those people who are pregnant or using birth control pills, face an increased risk of developing gallstones as well.

 

We will continue to discuss the common issues affecting the gastrointestinal tract, or GI tract, including the colon as well as rectum and anal problems, in the following series of articles. The 5 common gastrointestinal diseases mentioned above can manifest pain and discomfort as well as a variety of other symptoms if left untreated. Be sure to seek proper medical attention. The scope of our information is limited to chiropractic and spinal injuries and conditions. To discuss the subject matter, please feel free to ask Dr. Jimenez or contact us at 915-850-0900 .

Green-Call-Now-Button-24H-150x150-2-3.png

By Dr. Alex Jimenez

 

Additional Topics: Wellness

 

Overall health and wellness are essential towards maintaining the proper mental and physical balance in the body. From eating a balanced nutrition as well as exercising and participating in physical activities, to sleeping a healthy amount of time on a regular basis, following the best health and wellness tips can ultimately help maintain overall well-being. Eating plenty of fruits and vegetables can go a long way towards helping people become healthy.

 

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TRENDING TOPIC: EXTRA EXTRA: How to Become a Healthier You!