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Does ibd run in your family ?

As far as I am aware there are no other relatives in my family currently suffering from any form of IBD or in the past.
What about you ?
Do you believe there is any chance you inherited from some member of your family genetically ?
May we pass it as well to the next generations ?
 
For me there is a definite generic component. My moms mom had crohns. And my dads sister had crohns. My first cousins son also has it. In my family, the pattern is that it seems to skip a generation. For example, it affected my grandmother but one of her children. It affected my aunts grandson but not her children.
 
Hello Everyone,

I got diagnosed in just 4 hours last September in the ER. I was there for hemorrhoids that were bleeding profusely. The good doctor felt my stomach was hardened and a CAT scan showed the Crohn's.

My sister was diagnosed in 1978. She was in the hospital for nearly a month before they were able to figure it out. One of her doctors went to a GI conference in Boston and saw a presentation on Crohn's and came back and got my sister on the treatment using sulfodene. No Remicade or other drugs that we have today. It was the dark ages in many ways.

She has been mostly in remission since with a few flares and having to change meds. She is now on Entivio. She didn't want to get on another med, but the doctor said she would lose her colon if she did not.

She is one of my inspirations and often conferences in with me at my appointments.;););)
 
No one in my family has had Crohns. I heard it could be genetic and possibly environmental.

I didn't get until I was 51. The chances are 16 higher for a sibling, but still great odds in Vegas.

I think mine started as a combination of a vitamin D deficiency, with my compromised biome from a childhood of many, many antibiotics and adult life, and finally the stress of taking care of my mom as she said her long goodbye with Alzheimer Disease. Months before my diagnosis, I felt a twinge in my gut and wrote it off as anxiety for my mom. I juiced for a month until I just got too overwhelmed to take care of myself.

That twinge free month with the extra vitamins of kale, arugula, spinach, fruit juice and flax seed, I had no idea what I was gambling with in my gut. I believe if I would have continued taking better care of myself, juicing and better dealing with the stress, I may not be here. So when I get out of current my flare, back to juicing and stress is now better manged with meditation and soon with exercise.

In developing countries where their diets are not processed food, there are fewer antibiotics and it is not as sterilized and clean as we live, their biomes are significantly more diverse. As countries industrialize the number of auto-immune diseases rise significantly. As well, many of these countries are closer to the equator and get more vitamin D.

It could be diet, processed food and so many other aspects of our lives in concert that gets our TNF cells to battle against us.
 
In my opinion my Crohn's could be related to an over use of antibiotics during my childhood , as I used to get sick often and due to my limited dietary habits as a child (I was too picky with food ).
Also I was never breastfed as an infant.
My vitamin D levels I suppose that are normal as I live in a sunny country.
My first episode of Crohn's occurred at a stressful period of my life.
Some other Crohn's' patients have told me that they feel that stress was the reason they got this diasease
 
In my opinion my Crohn's could be related to an over use of antibiotics during my childhood , as I used to get sick often and due to my limited dietary habits as a child (I was too picky with food ).
Also I was never breastfed as an infant.
My vitamin D levels I suppose that are normal as I live in a sunny country.
My first episode of Crohn's occurred at a stressful period of my life.
Some other Crohn's' patients have told me that they feel that stress was the reason they got this diasease
I wonder about that for myself too.
 

Scipio

Well-known member
Location
San Diego
No family history of IBD for me. I had low level abdominal pain for years. But the Crohn's really bloomed several months after I had received massive IV doses of multiple antibiotics to treat a ruptured appendix. The Crohn's was finally diagnosed one year almost to the day after I had the surgery for the appendicitis.
 

Cross-stitch gal

Moderator
Staff member
Location
Vancouver,
I believe Granny has some form of it. But, she also has Alzheimer's and is in her last stages of it so we really can't tell much about what all she really has.

Mom has diverticulitis and was diagnosed sometime within the last 10 years or so. She's also been hospitalized once or twice from it.

One of my cousins has been diagnosed with Ulcerative Colitis like me. I haven't heard him talk much about it though.

From what I originally understood, IBD ran in every other generation in my family until my mom was diagnosed with Diverticulitis.
 
Hi Lynda,
I don’t mean to change the thread but Have you researched the SCD diet yet. I started the first week of April and can already feel the difference. It is very restrictive but many are able to achieve remission with no meds. I was DX in August of 2017 and doc put me right on Humira. I didn’t know about the diet or the book “breaking the viscous cycle” then. Just wanted to share.
Best wishes to you.
 
On my dad's side of the family, my aunt (his sister) and my neice (my brother's daughter) has Crohns. My sister-in-law, mother to my neice, also has Crohns. On my mother's side, my first cousin has UC. One of my daughters also has bowel issues - not confirmed as Crohns yet, but has been treated for bowel issues. As for me, I am confirmed to have Crohns, UC, Diverticulitis, as well as IBS-D. Having problems now, but UC related and not the Crohns. It is interesting how the deeper one looks into family health, the more you can find.
 
Yes my dad has mild ulcerative colitis and then I have Crohn’s and probably a severe form (based on I’ve had a perforation before) what rubbish luck!! My dad is the only person ion the family we are aware of to get IBD. My brother so far, 27 and healthy.


My Dad was diagnosed when I was 3 . He was 28. I was diagnosed 2 years later when I was 5. Not sure what that says about genetics. I have a friend who has Crohn’s and his sister does as well. At 5, I don’t know what could have triggered it. There is a genetic component but I don’t know what or how serious it is. Ultimately, I can’t worry about it. I already have it. My dr said that chances of my daughter having it were slim. If my wife also had Crohn’s, the chances would be higher.
 
I have a cousin on my mother's side with crohns, and a cousin on my father's side with UC, other than that I believe the rest of the family are all OK
 

emmaaaargh

Moderator
Staff member
Nobody in my family has IBD. I'm the first! I also don't have a particular event or situation that triggered it, it just came on suddenly one fateful day.
 
Brother has Crohn's, Father has Diverticulitis. Maternal grandfather has UC, and a cousin with UC and one with Crohns (father's side). 😬
 

my little penguin

Moderator
Staff member
No known family history for ds
But multiple known genetic snps in his dna associated with high risk of Crohns
So it’s there somewhere in the family
 

my little penguin

Moderator
Staff member
Results
Prevalence of siblings with IBD there were 16 families identified with more than one offspring with IBD. This is a prevalence of 2.5%. Of the 16 families, there were 4 families with three offspring (25%). There was 1 family in which all three siblings had IBD. Amongst the remaining 3 families with three offspring, the third sibling was free of IBD thus far. All of our sibling pairs with IBD were consecutive in birth order.

Birth order of presentation

The second born (youngest) sibling was the first to present with IBD in 11 of the 16 families (69%). In the remaining 5 families, the firstborn (older) sibling presented first (31%) (Table 1).

First to present(%) Second to present (%)
Youngest 11 (69) 5 (31%)
Oldest 5 (31) 11 (69)
Total (33)* 16 16
Table 1: Distribution of sibling’s presentation by birth order. *One family with three effected.

Incidence of parental IBD

In 3 of the 16 families, one parent had IBD (19%). One parent had Ulcerative Colitis (UC) and two had Crohn’s disease (CD).

Gender

Of the total group of siblings with IBD, there were 12 females and 21 males. Seven of the females presented first (58%), whereas 9 males presented first (43%). This difference was not statistically significant (p = 0.39, by the Chi-square test).

Time to presentation between siblings

Overall median time from presentation of the first sibling to the second sibling was 3.9 years (10–19 years of age). Median time of presentation from youngest to oldest was 3.3 years (10–17). Median time of presentation from oldest to youngest was 4.4 years (13–19) (NS).

Concordance

In 6 of the families there were seven siblings with mixed phenotype. Amongst these families, UC presented first in six patients (86%) and CD in 1 (14%). In 10 families there was concordance of phenotype amongst the siblings. Six families were concordant for CD (60%) and four with UC (40%). In the remaining six families the siblings had discordant phenotypes (Table 2).

Phenotype No. Families No. Sibs Sibs with CD Sibs with UC
Concordance 10 20 16 4
Discordance 6 13 6 7
Total 16 33 22 11
Table 2: Distribution of IBD phenotype among siblings.

Discussion
The major finding in this study was that, in the vast majority of cases of pediatric siblings with IBD, the second-born (youngest) sibling presented before the first-born (oldest) sibling. This is not what one would expect if the disease distribution of birth order were random. Hugot et al. studied 10 sibling pairs with IBD using the CAST statistical model and found that the distribution of disease onset was not random and that birth order had an influence on disease. They concluded that environmental factors contribute to the observed familial aggregation of disease [14]. Hampe et al. found that higher birth rank was associated with a lower risk of IBD [15]. Our findings support the existence of environmental factor(s) resulting in the distribution of the birth order of presentation of IBD that we observed. What could be responsible for the distribution we observed in patients who were raised in a very similar milieu? One factor may be an alteration in the gut microbiome. For this to explain our findings, the youngest sibling would have to be affected by factors that would alter the microbiome more frequently than the older sibling. Recently, there has been great interest in the gut microbiome and the role it may play in IBD. It is felt that perturbation of the gut microbiome may, in turn, alter host immunity. When this occurs in the presence of an at-risk genetic host, IBD may follow.

In fact, this dysbiosis in IBD has been described in detail in patients with IBD [16,17]. Ponsonby et al. examined perinatal risk factors and their relationship to the development of IBD and found that delivery by Cesarean (elective or emergent) was associated with a higher risk of developing IBD. The microbiome in newborns differs markedly between those delivered vaginally versus by Cesarean section [18]. Furthermore, the resultant dysbiosis associated with antibiotic treatment may last long after the antibiotics have been discontinued. There is also evidence to support that there may be a slow and incomplete recovery of the microbiome in infants treated with antibiotics [19]. Shaw et al. showed that there is an association between the risk of IBD in children and the occurrence of otitis media prior to age 5 years [20]. Otitis media may indeed represent a proxy for antibiotic use. More specifically, it has been shown that antibiotic use in early childhood is a risk factor for the development of IBD [21-23]. The use of broad-spectrum antibiotics has significantly increased during the last four to five decades. The increased incidence of IBD and other disorders of immune dysregulation has paralleled the increasing use of antibiotics since the first introduction of amoxicillin in the UK in 1972 [24,25]. This trend in aggressive, non-specific antibiotic use has likely caused a perturbation of the intestinal microbiome and hence changes in both the mucosal and systemic immune systems.

Another trend that has become widespread during the past several decades is attendance in some form of “school” at a very early age. The resultant risk of acute illness in daycare attendees is greatest during the first three years of life and decreases with advancing age. In a large Danish cohort, it was shown that the second-born sibling had a greater number of acute illnesses and received a greater number of courses of antibiotics when compared to the first-born sibling [26]. Furthermore, there is a significant increase of antibiotic use among second-born siblings versus first -born siblings that has been confirmed by Koppleman et al. [27]. Our study is notable for describing certain trends. The prevalence of IBD of 2.5% in siblings with IBD in pediatrics is roughly half of that shown in siblings with IBD over a lifetime, which is 4.8% [28,29]. We also found that the onset of IBD in the second-born sibling preceded that of the older siblings in about 70% of the sibling pairs. Our findings are consistent with studies showing that exposure to antibiotics in early childhood is a risk factor for IBD. Furthermore, the younger sibling is more likely to contact common illnesses and receive a course of antibiotics as compared to the older sibling. This may indeed account for our findings. The primary limitations of this study include a relatively small number of pediatric sibling pairs with IBD to power this analysis. This is unavoidable in any one institution given the low prevalence of pediatric siblings with IBD. Furthermore, we did not have access to specific antibiotic regimen(s) amongst our patients. This study is, however, a first step and should be confirmed by other studies.

Conclusion
The more we know about the epidemiology of a disease, the closer we get to elucidating the etiology. The ultimate goal is to find ways to prevent the disease from occurring. This study is the first to examine certain trends in children and adolescents who are siblings and have been diagnosed with IBD. Our most striking finding was that in the majority of cases, the onset of IBD in pediatric sibships occurred in the second-born sibling first. The age of onset for the next sibling to present was approximately four years no matter what combinations of phenotype we examined. Our findings lend support to the potential role of antibiotic use and the potential role in the increasing incidence of disorders of immune dysregulation. Finally, it should add further support to the judicious use of antibiotics in the pediatric age group. This study was approved by the institution’s IRB.

From

https://www.omicsonline.org/open-ac...sease-jibdd-1000103.php?aid=73369&view=mobile
 
I am not officially diagnosed (in the process though) but I do suffer from IBD symptoms (stool problems, weight loss, fistula) and my aunt has the same symptoms but she believes she has simply IBS. I doubt she ever went to a doctor. She plays her own doc apparently. I am of Jewish descent as well.
 

Lynda Lynda

Member
Hi Lynda,
I don’t mean to change the thread but Have you researched the SCD diet yet. I started the first week of April and can already feel the difference. It is very restrictive but many are able to achieve remission with no meds. I was DX in August of 2017 and doc put me right on Humira. I didn’t know about the diet or the book “breaking the viscous cycle” then. Just wanted to share.
Best wishes to you.
Thanks.
I will read up on this.
🐥
 

Lynda Lynda

Member
Were the use of colonoscopies and endoscopies frequent years ago ? Possibly many folks had IBD, but tests we have now were not available then ? Yikes, I recently had a colonoscopy, endoscopy, stool samples, blood draw, CT Scan and X-ray.
Have a good weekend. 🐙
 
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