Symptoms of Crohn’s disease, LRRK2 genes , Parkinson and nutrition

ulcerative and chrons.JPGSymptoms of Crohn’s Disease

The most common symptoms of Crohn’s disease are abdominal pain and diarrhea. Other signs of inflammation frequently are present including fever and abdominal tenderness. Because symptoms can be worsened by eating, the intake of food is reduced, and this leads to loss of weight, and, less commonly, nutritional deficiencies. Slow continuous loss of blood into the intestine that may not even be recognizable in the stool can lead to iron deficiency anemia.

Complications of Crohn’s Disease

Several complications of Crohn’s disease have already been mentioned, including nutritional deficiencies, loss of weight, anemia, growth retardation, and delayed puberty. Two more serious complications also mentioned previously are strictures or narrowing of the intestine due to scarring and the formation of fistulas. Massive intestinal bleeding and perforation are unusual.

Other Complications of Crohn’s Disease

There are also extraintestinal manifestations of Crohn’s disease, some of which may be debilitating. These include arthritis, inflammation of the eye that can impair vision, skin diseases that vary from mild (erythema nodosum) to severe (pyoderma gangrenosum) gallstones, and loss of bone due to nutritional deficiencies. Most of these manifestations are believed to be due to inflammation that is occurring outside of the intestine.

Variants of LRRK2 gene are associated with an increased risk of Parkinson’s and Crohn’s disease

Leucine-rich repeat kinase 2 (LRRK2), also known as dardarin (from the Basque word “dardara” which means trembling), is an enzyme that in humans is encoded by the PARK8 gene.[5] LRRK2 is a member of the leucine-rich repeat kinase family. Variants of this gene are associated with an increased risk of Parkinson’s disease and also Crohn’s disease.[5][6]

The LRRK2 gene encodes a protein with an armadillo repeats (ARM) region, an ankyrin repeat (ANK) region, a leucine-rich repeat (LRR) domain, a kinase domain, a RAS domain, a GTPase domain, and a WD40 domain. The protein is present largely in the cytoplasm but also associates with the mitochondrial outer membrane.

LRRK2 interacts with the C-terminal R2 RING finger domain of parkin, and parkin interacted with the COR domain of LRRK2. Expression of mutant LRRK2 induced apoptotic cell death in neuroblastoma cells and in mouse cortical neurons.[7]

Expression of LRRK2 mutants implicated in autosomal dominant Parkinson’s disease causes shortening and simplification of the dendritic tree in vivo and in cultured neurons.[8] This is mediated in part by alterations in macroautophagy,[9][10][11][12][13] and can be prevented by protein kinase A regulation of the autophagy protein LC3.[14] The G2019S and R1441C mutations elicit post-synaptic calcium imbalance, leading to excess mitochondrial clearance from dendrites by mitophagy.[15] LRRK2 is also a substrate for chaperone-mediated autophagy.[16]

Clinical significance

Mutations in this gene have been associated with Parkinson’s disease type 8.[17]

The Gly2019Ser mutation in LRRK2 is a relatively common cause of familial Parkinson’s Disease in Caucasians.[18] It may also cause sporadic Parkinson’s Disease. The mutated Gly amino acid is conserved in all kinase domains of all species.

The Gly2019Ser mutation is one of a small number of LRRK2 mutations proven to cause Parkinson’s disease. Of these, Gly2019Ser is the most common in the Western World, accounting for ~2% of all Parkinson’s disease cases in North American Caucasians. This mutation is enriched in certain populations, being found in approximately 20% of all Ashkenazi Jewish Parkinson’s disease patients and in approximately 40% of all Parkinson’s disease patients of North African Berber Arab ancestry.[citation needed]

Unexpectedly, genomewide association studies have found an association between LRRK2 and Crohn’s disease as well as with Parkinson’s disease, suggesting that the two diseases share common pathways.

Connie’s comments: AGELOC family of supplementation reset your genes to a younger you. When taking calcium, it must have magnesium in 60:40 ratio. Vitamin C is necessary for absorption. Eat iron rich food in the morning and calcium and magnesium supplementation at night.

Supplements can be found here:


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Inflamm Bowel Dis. 2016 May;22(5):1049-55. doi: 10.1097/MIB.0000000000000735.

Association Between Parkinson’s Disease and Inflammatory Bowel Disease: a Nationwide Taiwanese Retrospective Cohort Study.



Inflammatory bowel disease (IBD) is a chronic inflammatory disorder. Previous studies have suggested that chronic systemic inflammation increases the risk of Parkinson’s disease (PD). This study examined the effects of IBD on the development of PD.


In a nationwide population-based cohort of 23.22 million insured residents of Taiwan aged ≥ 20 years, we compared people diagnosed with IBD during 2000 to 2011 (n = 8373) with IBD-free individuals. Patients with PD were identified in the National Health Insurance Research Database. Using univariable and multivariable Cox proportion hazard regression models, we estimated the adjusted hazard ratio (aHR) for PD with a 95% confidence interval (CI) with adjustment for age, sex, and comorbidities.


In the cohort, IBD was associated with an increased incidence of PD (crude hazard ratio = 1.43, 95% CI = 1.15-1.79). The risk was highest among individuals with Crohn’s disease (aHR = 1.40, 95% CI = 1.11-1.77). In the multivariable model, the risk of PD was increased for men (aHR = 1.28, 95% CI = 1.05-1.56) and higher for patients with hypertension (aHR = 1.72, 95% CI = 1.33-2.24), coronary artery disease (aHR = 1.31, 95% CI = 1.04-1.66), or depression (aHR = 2.51, 95% CI = 1.82-3.46).


We suggest that IBD is associated with an increased risk of PD. Patients with IBD should be aware of the potential risk for PD development.


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