what really works for IBS?

[Guest guest]

Just how long an answer do you want? Oh, Pat covered it well. I have

worked with many, many IBS patients that didn't get symptom free until they

tried the LEAP/MRT protocol.

Many IBS patients get " better " on other protocols, and of course, I tend to

get the ones where everything else failed.

It's also important to be sure the IBS was adequately/properly diagnosed.

Frequently, people are diagnosed with IBS but they actually have Small

Intestinal Bacterial Overgrowth (SIBO), celiac disease, gluten intolerance or

candida.

Jan Patenaude, RD, CLT

Co-author of the Certified LEAP Therapist Training program (only because it

wasn't cost/time effective for me to keep training other RDs one-on-one as

I did for a few years!)

In a message dated 8/19/2009 2:47:44 P.M. Mountain Daylight Time,

c.clark1@... writes:

Hi all!

We have heard all the advice on what works for IBS but does anyone know

first hand what really works?

Jan Patenaude, RD, CLT

Director of Medical Nutrition

Signet Diagnostic Corporation

Fax:

DineRight4@...

[Guest guest]

Just how long an answer do you want? Oh, Pat covered it well. I have

worked with many, many IBS patients that didn't get symptom free until they

tried the LEAP/MRT protocol.

Many IBS patients get " better " on other protocols, and of course, I tend to

get the ones where everything else failed.

It's also important to be sure the IBS was adequately/properly diagnosed.

Frequently, people are diagnosed with IBS but they actually have Small

Intestinal Bacterial Overgrowth (SIBO), celiac disease, gluten intolerance or

candida.

Jan Patenaude, RD, CLT

Co-author of the Certified LEAP Therapist Training program (only because it

wasn't cost/time effective for me to keep training other RDs one-on-one as

I did for a few years!)

In a message dated 8/19/2009 2:47:44 P.M. Mountain Daylight Time,

c.clark1@... writes:

Hi all!

We have heard all the advice on what works for IBS but does anyone know

first hand what really works?

Jan Patenaude, RD, CLT

Director of Medical Nutrition

Signet Diagnostic Corporation

Fax:

DineRight4@...

[Guest guest]

Just how long an answer do you want? Oh, Pat covered it well. I have

worked with many, many IBS patients that didn't get symptom free until they

tried the LEAP/MRT protocol.

Many IBS patients get " better " on other protocols, and of course, I tend to

get the ones where everything else failed.

It's also important to be sure the IBS was adequately/properly diagnosed.

Frequently, people are diagnosed with IBS but they actually have Small

Intestinal Bacterial Overgrowth (SIBO), celiac disease, gluten intolerance or

candida.

Jan Patenaude, RD, CLT

Co-author of the Certified LEAP Therapist Training program (only because it

wasn't cost/time effective for me to keep training other RDs one-on-one as

I did for a few years!)

In a message dated 8/19/2009 2:47:44 P.M. Mountain Daylight Time,

c.clark1@... writes:

Hi all!

We have heard all the advice on what works for IBS but does anyone know

first hand what really works?

Jan Patenaude, RD, CLT

Director of Medical Nutrition

Signet Diagnostic Corporation

Fax:

DineRight4@...

[Guest guest]

Hi all!

We have heard all the advice on what works for IBS but does anyone know first

hand what really works?

[Guest guest]

Colleen,

Here is some information on what DOES work for most IBS.

Most cases of IBS (diarrhea predominant or cyclic) involve delayed type

hypersensitivities to foods and food chemicals, therefore having a

strong immune component. An elimination diet would work; blood

testing to identify both type III and type IV delayed hypersensitivities

works faster to identify those foods that are activating the immune

response. I use Mediator Release Testing (MRT) aka LEAP testing. I

have used LEAP personally, though am new at working with clients and

not yet certified. Many RD LEAP therapists who have had hundreds of

patients see 50-80% improvement in sx within 7-10 days with continuing

improvement in the ensuing days/weeks. I can send you information on

MRT testing if you'd like. Below are some research articles on the

role of the immune system in IBS below.

Pat Bollinger, MS RD

Helena, MT

Gastroenterology. 2007 Mar;132(3):913- 20. Epub 2007 Jan 26.

Immune activation in patients with irritable bowel syndrome.

*Liebregts T*

</sites/entrez?Db=pubmed & Cmd=Search & Term=%22Liebregts%20T%22%5BAuthor%5D & itool=E\

ntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_DiscoveryPanel.Pubmed_RVA\

bstractPlus>,

*Adam B*

</sites/entrez?Db=pubmed & Cmd=Search & Term=%22Adam%20B%22%5BAuthor%5D & itool=Entrez\

System2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_DiscoveryPanel.Pubmed_RVAbstra\

ctPlus>,

*Bredack C*

</sites/entrez?Db=pubmed & Cmd=Search & Term=%22Bredack%20C%22%5BAuthor%5D & itool=Ent\

rezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_DiscoveryPanel.Pubmed_RVAbs\

tractPlus>,

*Röth A*

</sites/entrez?Db=pubmed & Cmd=Search & Term=%22R%C3%B6th%20A%22%5BAuthor%5D & itool=E\

ntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_DiscoveryPanel.Pubmed_RVA\

bstractPlus>,

*Heinzel S*

</sites/entrez?Db=pubmed & Cmd=Search & Term=%22Heinzel%20S%22%5BAuthor%5D & itool=Ent\

rezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_DiscoveryPanel.Pubmed_RVAbs\

tractPlus>,

*Lester S*

</sites/entrez?Db=pubmed & Cmd=Search & Term=%22Lester%20S%22%5BAuthor%5D & itool=Entr\

ezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_DiscoveryPanel.Pubmed_RVAbst\

ractPlus>,

*Downie-Doyle S*

</sites/entrez?Db=pubmed & Cmd=Search & Term=%22Downie-Doyle%20S%22%5BAuthor%5D & itoo\

l=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_DiscoveryPanel.Pubmed_\

RVAbstractPlus>,

* E*

</sites/entrez?Db=pubmed & Cmd=Search & Term=%22%20E%22%5BAuthor%5D & itool=Entre\

zSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_DiscoveryPanel.Pubmed_RVAbstr\

actPlus>,

*Drew P*

</sites/entrez?Db=pubmed & Cmd=Search & Term=%22Drew%20P%22%5BAuthor%5D & itool=Entrez\

System2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_DiscoveryPanel.Pubmed_RVAbstra\

ctPlus>,

*Talley NJ*

</sites/entrez?Db=pubmed & Cmd=Search & Term=%22Talley%20NJ%22%5BAuthor%5D & itool=Ent\

rezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_DiscoveryPanel.Pubmed_RVAbs\

tractPlus>,

*Holtmann G*

</sites/entrez?Db=pubmed & Cmd=Search & Term=%22Holtmann%20G%22%5BAuthor%5D & itool=En\

trezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_DiscoveryPanel.Pubmed_RVAb\

stractPlus>.

Department of Gastroenterology and Hepatology, University of

Adelaide, Royal Adelaide Hospital, South Australia, Australia.

BACKGROUND AND AIMS: We set out to test the hypothesis that

irritable bowel syndrome (IBS) is characterized by an augmented

cellular immune response with enhanced production of proinflammatory

cytokines. We further aimed to explore whether symptoms and

psychiatric comorbidity in IBS are linked to the release of

proinflammatory cytokines. METHODS: We characterized basal and

Escherichia coli lipopolysaccharide (LPS)-induced cytokine

production in peripheral blood mononuclear cells (PBMCs) from 55 IBS

patients (18 mixed-, 17 constipation- , 20 diarrhea-predominan t)

and 36 healthy controls (HCs). PBMCs were isolated by density

gradient centrifugation and cultured for 24 hours with or without (1

ng/mL) LPS. Cytokine production (tumor necrosis factor [TNF]-alpha,

interleukin [iL]-1beta, and IL-6) was measured by enzyme-linked

immunosorbent assay. Abdominal symptoms and psychiatric

comorbidities were assessed by using the validated Bowel Disease

Questionnaire and the Hospital Anxiety and Depression Scale.

RESULTS: IBS patients showed significantly (P < .017) higher

baseline TNF-alpha, IL-1beta, IL-6, and LPS-induced IL-6 levels

compared with HCs. Analyzing IBS subgroups, all cytokine levels were

significantly (P < .05) higher in diarrhea-predominan t IBS (D-IBS)

patients, whereas constipation- predominant IBS patients showed

increased LPS-induced IL-1beta levels compared with HCs. Baseline

TNF-alpha and LPS-induced TNF-alpha and IL-6 levels were

significantly higher in patients reporting more than 3 bowel

movements per day, urgency, watery stools, and pain associated with

diarrhea compared with patients without these symptoms (all P <

.05). LPS-induced TNF-alpha production was associated significantly

(r = 0.59, P < .001) with anxiety in patients with IBS. CONCLUSIONS:

Patients with D-IBS display enhanced proinflammatory cytokine

release, and this may be associated with symptoms and anxiety.

* *Am J Gastroenterol. 2009 Feb;104(2):392- 400. Epub 2009 Jan 13.

*Mucosal immune activation in irritable bowel syndrome:

gender-dependence and association with digestive symptoms.*

*Cremon C*

</sites/entrez?Db=pubmed & Cmd=Search & Term=%22Cremon%20C%22%5BAuthor%5D & itool=Entr\

ezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_DiscoveryPanel.Pubmed_RVAbst\

ractPlus>,

*Gargano L*

</sites/entrez?Db=pubmed & Cmd=Search & Term=%22Gargano%20L%22%5BAuthor%5D & itool=Ent\

rezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_DiscoveryPanel.Pubmed_RVAbs\

tractPlus>,

*Morselli-Labate AM*

</sites/entrez?Db=pubmed & Cmd=Search & Term=%22Morselli-Labate%20AM%22%5BAuthor%5D & \

itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_DiscoveryPanel.Pub\

med_RVAbstractPlus>,

*Santini D*

</sites/entrez?Db=pubmed & Cmd=Search & Term=%22Santini%20D%22%5BAuthor%5D & itool=Ent\

rezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_DiscoveryPanel.Pubmed_RVAbs\

tractPlus>,

*Cogliandro RF*

</sites/entrez?Db=pubmed & Cmd=Search & Term=%22Cogliandro%20RF%22%5BAuthor%5D & itool\

=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_DiscoveryPanel.Pubmed_R\

VAbstractPlus>,

*De Giorgio R*

</sites/entrez?Db=pubmed & Cmd=Search & Term=%22De%20Giorgio%20R%22%5BAuthor%5D & itoo\

l=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_DiscoveryPanel.Pubmed_\

RVAbstractPlus>,

*Stanghellini V*

</sites/entrez?Db=pubmed & Cmd=Search & Term=%22Stanghellini%20V%22%5BAuthor%5D & itoo\

l=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_DiscoveryPanel.Pubmed_\

RVAbstractPlus>,

*Corinaldesi R*

</sites/entrez?Db=pubmed & Cmd=Search & Term=%22Corinaldesi%20R%22%5BAuthor%5D & itool\

=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_DiscoveryPanel.Pubmed_R\

VAbstractPlus>,

*Barbara G*

</sites/entrez?Db=pubmed & Cmd=Search & Term=%22Barbara%20G%22%5BAuthor%5D & itool=Ent\

rezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_DiscoveryPanel.Pubmed_RVAbs\

tractPlus>.

Department of Internal Medicine and Gastroenterology, St. Orsola

Hospital, Center for Applied Biomedical Research, Bologna, Italy.

OBJECTIVES: Immune activation may be involved in the pathogenesis of

irritable bowel syndrome (IBS). However, the relative magnitude of

this immune component and its correlation with gender and

gastrointestinal complaints in IBS patients remains poorly

elucidated. METHODS: We enrolled 48 IBS patients, with either

diarrhea or constipation, 12 patients with microscopic colitis, 20

patients with ulcerative colitis, and 24 healthy controls. Colonic

immunocytes were identified with quantitative immunohistochemistr y

on mucosal biopsies. Gastrointestinal symptoms were assessed using a

validated questionnaire. RESULTS: IBS patients showed a significant

72% increase in mucosal immune cells compared to controls (P<0.001).

Further analyses showed that increased immune cells were present in

50% of the IBS patients. The magnitude of the immune infiltrate in

IBS was significantly lower than that of microscopic colitis or

ulcerative colitis (42% and 124% increases vs. IBS, respectively;

P<0.001). Compared with controls, IBS patients had increased numbers

of CD3+, CD4+, and CD8+ T cells and mast cells (P<0.001). Compared

to male IBS patients, female IBS patients had greater numbers of

mast cells (P=0.066), but lower numbers of CD3+ and CD8+ T cells

(P=0.002 and <0.001, respectively) . Mucosal mast cell infiltration

of IBS patients was significantly associated with abdominal bloating

frequency (P=0.022) and with symptoms of dysmotility- like dyspepsia

(P=0.001), but not ulcer-like dyspepsia. CONCLUSIONS: A large subset

of IBS patients shows gender-dependent mucosal infiltration of

immunocytes that correlates with abdominal bloating and dysmotility-

like dyspepsia. These results provide the rationale for considering

immune mechanisms as a pathophysiological component in a subset of

IBS patients.

PMID: 19174797 [PubMed - indexed for MEDLINE]

Excerpt: Is functional bowel disease really functional?

http://www.springer link.com/ content/d034728l 2811nv79/

<http://www.springerlink.com/content/d034728l2811nv79/>

colleen0632 wrote:

>

>

> Hi all!

>

> We have heard all the advice on what works for IBS but does anyone

> know first hand what really works?

>

[Guest guest]

Colleen,

Here is some information on what DOES work for most IBS.

Most cases of IBS (diarrhea predominant or cyclic) involve delayed type

hypersensitivities to foods and food chemicals, therefore having a

strong immune component. An elimination diet would work; blood

testing to identify both type III and type IV delayed hypersensitivities

works faster to identify those foods that are activating the immune

response. I use Mediator Release Testing (MRT) aka LEAP testing. I

have used LEAP personally, though am new at working with clients and

not yet certified. Many RD LEAP therapists who have had hundreds of

patients see 50-80% improvement in sx within 7-10 days with continuing

improvement in the ensuing days/weeks. I can send you information on

MRT testing if you'd like. Below are some research articles on the

role of the immune system in IBS below.

Pat Bollinger, MS RD

Helena, MT

Gastroenterology. 2007 Mar;132(3):913- 20. Epub 2007 Jan 26.

Immune activation in patients with irritable bowel syndrome.

*Liebregts T*

</sites/entrez?Db=pubmed & Cmd=Search & Term=%22Liebregts%20T%22%5BAuthor%5D & itool=E\

ntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_DiscoveryPanel.Pubmed_RVA\

bstractPlus>,

*Adam B*

</sites/entrez?Db=pubmed & Cmd=Search & Term=%22Adam%20B%22%5BAuthor%5D & itool=Entrez\

System2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_DiscoveryPanel.Pubmed_RVAbstra\

ctPlus>,

*Bredack C*

</sites/entrez?Db=pubmed & Cmd=Search & Term=%22Bredack%20C%22%5BAuthor%5D & itool=Ent\

rezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_DiscoveryPanel.Pubmed_RVAbs\

tractPlus>,

*Röth A*

</sites/entrez?Db=pubmed & Cmd=Search & Term=%22R%C3%B6th%20A%22%5BAuthor%5D & itool=E\

ntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_DiscoveryPanel.Pubmed_RVA\

bstractPlus>,

*Heinzel S*

</sites/entrez?Db=pubmed & Cmd=Search & Term=%22Heinzel%20S%22%5BAuthor%5D & itool=Ent\

rezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_DiscoveryPanel.Pubmed_RVAbs\

tractPlus>,

*Lester S*

</sites/entrez?Db=pubmed & Cmd=Search & Term=%22Lester%20S%22%5BAuthor%5D & itool=Entr\

ezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_DiscoveryPanel.Pubmed_RVAbst\

ractPlus>,

*Downie-Doyle S*

</sites/entrez?Db=pubmed & Cmd=Search & Term=%22Downie-Doyle%20S%22%5BAuthor%5D & itoo\

l=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_DiscoveryPanel.Pubmed_\

RVAbstractPlus>,

* E*

</sites/entrez?Db=pubmed & Cmd=Search & Term=%22%20E%22%5BAuthor%5D & itool=Entre\

zSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_DiscoveryPanel.Pubmed_RVAbstr\

actPlus>,

*Drew P*

</sites/entrez?Db=pubmed & Cmd=Search & Term=%22Drew%20P%22%5BAuthor%5D & itool=Entrez\

System2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_DiscoveryPanel.Pubmed_RVAbstra\

ctPlus>,

*Talley NJ*

</sites/entrez?Db=pubmed & Cmd=Search & Term=%22Talley%20NJ%22%5BAuthor%5D & itool=Ent\

rezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_DiscoveryPanel.Pubmed_RVAbs\

tractPlus>,

*Holtmann G*

</sites/entrez?Db=pubmed & Cmd=Search & Term=%22Holtmann%20G%22%5BAuthor%5D & itool=En\

trezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_DiscoveryPanel.Pubmed_RVAb\

stractPlus>.

Department of Gastroenterology and Hepatology, University of

Adelaide, Royal Adelaide Hospital, South Australia, Australia.

BACKGROUND AND AIMS: We set out to test the hypothesis that

irritable bowel syndrome (IBS) is characterized by an augmented

cellular immune response with enhanced production of proinflammatory

cytokines. We further aimed to explore whether symptoms and

psychiatric comorbidity in IBS are linked to the release of

proinflammatory cytokines. METHODS: We characterized basal and

Escherichia coli lipopolysaccharide (LPS)-induced cytokine

production in peripheral blood mononuclear cells (PBMCs) from 55 IBS

patients (18 mixed-, 17 constipation- , 20 diarrhea-predominan t)

and 36 healthy controls (HCs). PBMCs were isolated by density

gradient centrifugation and cultured for 24 hours with or without (1

ng/mL) LPS. Cytokine production (tumor necrosis factor [TNF]-alpha,

interleukin [iL]-1beta, and IL-6) was measured by enzyme-linked

immunosorbent assay. Abdominal symptoms and psychiatric

comorbidities were assessed by using the validated Bowel Disease

Questionnaire and the Hospital Anxiety and Depression Scale.

RESULTS: IBS patients showed significantly (P < .017) higher

baseline TNF-alpha, IL-1beta, IL-6, and LPS-induced IL-6 levels

compared with HCs. Analyzing IBS subgroups, all cytokine levels were

significantly (P < .05) higher in diarrhea-predominan t IBS (D-IBS)

patients, whereas constipation- predominant IBS patients showed

increased LPS-induced IL-1beta levels compared with HCs. Baseline

TNF-alpha and LPS-induced TNF-alpha and IL-6 levels were

significantly higher in patients reporting more than 3 bowel

movements per day, urgency, watery stools, and pain associated with

diarrhea compared with patients without these symptoms (all P <

.05). LPS-induced TNF-alpha production was associated significantly

(r = 0.59, P < .001) with anxiety in patients with IBS. CONCLUSIONS:

Patients with D-IBS display enhanced proinflammatory cytokine

release, and this may be associated with symptoms and anxiety.

* *Am J Gastroenterol. 2009 Feb;104(2):392- 400. Epub 2009 Jan 13.

*Mucosal immune activation in irritable bowel syndrome:

gender-dependence and association with digestive symptoms.*

*Cremon C*

</sites/entrez?Db=pubmed & Cmd=Search & Term=%22Cremon%20C%22%5BAuthor%5D & itool=Entr\

ezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_DiscoveryPanel.Pubmed_RVAbst\

ractPlus>,

*Gargano L*

</sites/entrez?Db=pubmed & Cmd=Search & Term=%22Gargano%20L%22%5BAuthor%5D & itool=Ent\

rezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_DiscoveryPanel.Pubmed_RVAbs\

tractPlus>,

*Morselli-Labate AM*

</sites/entrez?Db=pubmed & Cmd=Search & Term=%22Morselli-Labate%20AM%22%5BAuthor%5D & \

itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_DiscoveryPanel.Pub\

med_RVAbstractPlus>,

*Santini D*

</sites/entrez?Db=pubmed & Cmd=Search & Term=%22Santini%20D%22%5BAuthor%5D & itool=Ent\

rezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_DiscoveryPanel.Pubmed_RVAbs\

tractPlus>,

*Cogliandro RF*

</sites/entrez?Db=pubmed & Cmd=Search & Term=%22Cogliandro%20RF%22%5BAuthor%5D & itool\

=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_DiscoveryPanel.Pubmed_R\

VAbstractPlus>,

*De Giorgio R*

</sites/entrez?Db=pubmed & Cmd=Search & Term=%22De%20Giorgio%20R%22%5BAuthor%5D & itoo\

l=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_DiscoveryPanel.Pubmed_\

RVAbstractPlus>,

*Stanghellini V*

</sites/entrez?Db=pubmed & Cmd=Search & Term=%22Stanghellini%20V%22%5BAuthor%5D & itoo\

l=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_DiscoveryPanel.Pubmed_\

RVAbstractPlus>,

*Corinaldesi R*

</sites/entrez?Db=pubmed & Cmd=Search & Term=%22Corinaldesi%20R%22%5BAuthor%5D & itool\

=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_DiscoveryPanel.Pubmed_R\

VAbstractPlus>,

*Barbara G*

</sites/entrez?Db=pubmed & Cmd=Search & Term=%22Barbara%20G%22%5BAuthor%5D & itool=Ent\

rezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_DiscoveryPanel.Pubmed_RVAbs\

tractPlus>.

Department of Internal Medicine and Gastroenterology, St. Orsola

Hospital, Center for Applied Biomedical Research, Bologna, Italy.

OBJECTIVES: Immune activation may be involved in the pathogenesis of

irritable bowel syndrome (IBS). However, the relative magnitude of

this immune component and its correlation with gender and

gastrointestinal complaints in IBS patients remains poorly

elucidated. METHODS: We enrolled 48 IBS patients, with either

diarrhea or constipation, 12 patients with microscopic colitis, 20

patients with ulcerative colitis, and 24 healthy controls. Colonic

immunocytes were identified with quantitative immunohistochemistr y

on mucosal biopsies. Gastrointestinal symptoms were assessed using a

validated questionnaire. RESULTS: IBS patients showed a significant

72% increase in mucosal immune cells compared to controls (P<0.001).

Further analyses showed that increased immune cells were present in

50% of the IBS patients. The magnitude of the immune infiltrate in

IBS was significantly lower than that of microscopic colitis or

ulcerative colitis (42% and 124% increases vs. IBS, respectively;

P<0.001). Compared with controls, IBS patients had increased numbers

of CD3+, CD4+, and CD8+ T cells and mast cells (P<0.001). Compared

to male IBS patients, female IBS patients had greater numbers of

mast cells (P=0.066), but lower numbers of CD3+ and CD8+ T cells

(P=0.002 and <0.001, respectively) . Mucosal mast cell infiltration

of IBS patients was significantly associated with abdominal bloating

frequency (P=0.022) and with symptoms of dysmotility- like dyspepsia

(P=0.001), but not ulcer-like dyspepsia. CONCLUSIONS: A large subset

of IBS patients shows gender-dependent mucosal infiltration of

immunocytes that correlates with abdominal bloating and dysmotility-

like dyspepsia. These results provide the rationale for considering

immune mechanisms as a pathophysiological component in a subset of

IBS patients.

PMID: 19174797 [PubMed - indexed for MEDLINE]

Excerpt: Is functional bowel disease really functional?

http://www.springer link.com/ content/d034728l 2811nv79/

<http://www.springerlink.com/content/d034728l2811nv79/>

colleen0632 wrote:

>

>

> Hi all!

>

> We have heard all the advice on what works for IBS but does anyone

> know first hand what really works?

>

[Guest guest]

Colleen,

Here is some information on what DOES work for most IBS.

Most cases of IBS (diarrhea predominant or cyclic) involve delayed type

hypersensitivities to foods and food chemicals, therefore having a

strong immune component. An elimination diet would work; blood

testing to identify both type III and type IV delayed hypersensitivities

works faster to identify those foods that are activating the immune

response. I use Mediator Release Testing (MRT) aka LEAP testing. I

have used LEAP personally, though am new at working with clients and

not yet certified. Many RD LEAP therapists who have had hundreds of

patients see 50-80% improvement in sx within 7-10 days with continuing

improvement in the ensuing days/weeks. I can send you information on

MRT testing if you'd like. Below are some research articles on the

role of the immune system in IBS below.

Pat Bollinger, MS RD

Helena, MT

Gastroenterology. 2007 Mar;132(3):913- 20. Epub 2007 Jan 26.

Immune activation in patients with irritable bowel syndrome.

*Liebregts T*

</sites/entrez?Db=pubmed & Cmd=Search & Term=%22Liebregts%20T%22%5BAuthor%5D & itool=E\

ntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_DiscoveryPanel.Pubmed_RVA\

bstractPlus>,

*Adam B*

</sites/entrez?Db=pubmed & Cmd=Search & Term=%22Adam%20B%22%5BAuthor%5D & itool=Entrez\

System2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_DiscoveryPanel.Pubmed_RVAbstra\

ctPlus>,

*Bredack C*

</sites/entrez?Db=pubmed & Cmd=Search & Term=%22Bredack%20C%22%5BAuthor%5D & itool=Ent\

rezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_DiscoveryPanel.Pubmed_RVAbs\

tractPlus>,

*Röth A*

</sites/entrez?Db=pubmed & Cmd=Search & Term=%22R%C3%B6th%20A%22%5BAuthor%5D & itool=E\

ntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_DiscoveryPanel.Pubmed_RVA\

bstractPlus>,

*Heinzel S*

</sites/entrez?Db=pubmed & Cmd=Search & Term=%22Heinzel%20S%22%5BAuthor%5D & itool=Ent\

rezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_DiscoveryPanel.Pubmed_RVAbs\

tractPlus>,

*Lester S*

</sites/entrez?Db=pubmed & Cmd=Search & Term=%22Lester%20S%22%5BAuthor%5D & itool=Entr\

ezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_DiscoveryPanel.Pubmed_RVAbst\

ractPlus>,

*Downie-Doyle S*

</sites/entrez?Db=pubmed & Cmd=Search & Term=%22Downie-Doyle%20S%22%5BAuthor%5D & itoo\

l=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_DiscoveryPanel.Pubmed_\

RVAbstractPlus>,

* E*

</sites/entrez?Db=pubmed & Cmd=Search & Term=%22%20E%22%5BAuthor%5D & itool=Entre\

zSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_DiscoveryPanel.Pubmed_RVAbstr\

actPlus>,

*Drew P*

</sites/entrez?Db=pubmed & Cmd=Search & Term=%22Drew%20P%22%5BAuthor%5D & itool=Entrez\

System2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_DiscoveryPanel.Pubmed_RVAbstra\

ctPlus>,

*Talley NJ*

</sites/entrez?Db=pubmed & Cmd=Search & Term=%22Talley%20NJ%22%5BAuthor%5D & itool=Ent\

rezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_DiscoveryPanel.Pubmed_RVAbs\

tractPlus>,

*Holtmann G*

</sites/entrez?Db=pubmed & Cmd=Search & Term=%22Holtmann%20G%22%5BAuthor%5D & itool=En\

trezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_DiscoveryPanel.Pubmed_RVAb\

stractPlus>.

Department of Gastroenterology and Hepatology, University of

Adelaide, Royal Adelaide Hospital, South Australia, Australia.

BACKGROUND AND AIMS: We set out to test the hypothesis that

irritable bowel syndrome (IBS) is characterized by an augmented

cellular immune response with enhanced production of proinflammatory

cytokines. We further aimed to explore whether symptoms and

psychiatric comorbidity in IBS are linked to the release of

proinflammatory cytokines. METHODS: We characterized basal and

Escherichia coli lipopolysaccharide (LPS)-induced cytokine

production in peripheral blood mononuclear cells (PBMCs) from 55 IBS

patients (18 mixed-, 17 constipation- , 20 diarrhea-predominan t)

and 36 healthy controls (HCs). PBMCs were isolated by density

gradient centrifugation and cultured for 24 hours with or without (1

ng/mL) LPS. Cytokine production (tumor necrosis factor [TNF]-alpha,

interleukin [iL]-1beta, and IL-6) was measured by enzyme-linked

immunosorbent assay. Abdominal symptoms and psychiatric

comorbidities were assessed by using the validated Bowel Disease

Questionnaire and the Hospital Anxiety and Depression Scale.

RESULTS: IBS patients showed significantly (P < .017) higher

baseline TNF-alpha, IL-1beta, IL-6, and LPS-induced IL-6 levels

compared with HCs. Analyzing IBS subgroups, all cytokine levels were

significantly (P < .05) higher in diarrhea-predominan t IBS (D-IBS)

patients, whereas constipation- predominant IBS patients showed

increased LPS-induced IL-1beta levels compared with HCs. Baseline

TNF-alpha and LPS-induced TNF-alpha and IL-6 levels were

significantly higher in patients reporting more than 3 bowel

movements per day, urgency, watery stools, and pain associated with

diarrhea compared with patients without these symptoms (all P <

.05). LPS-induced TNF-alpha production was associated significantly

(r = 0.59, P < .001) with anxiety in patients with IBS. CONCLUSIONS:

Patients with D-IBS display enhanced proinflammatory cytokine

release, and this may be associated with symptoms and anxiety.

* *Am J Gastroenterol. 2009 Feb;104(2):392- 400. Epub 2009 Jan 13.

*Mucosal immune activation in irritable bowel syndrome:

gender-dependence and association with digestive symptoms.*

*Cremon C*

</sites/entrez?Db=pubmed & Cmd=Search & Term=%22Cremon%20C%22%5BAuthor%5D & itool=Entr\

ezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_DiscoveryPanel.Pubmed_RVAbst\

ractPlus>,

*Gargano L*

</sites/entrez?Db=pubmed & Cmd=Search & Term=%22Gargano%20L%22%5BAuthor%5D & itool=Ent\

rezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_DiscoveryPanel.Pubmed_RVAbs\

tractPlus>,

*Morselli-Labate AM*

</sites/entrez?Db=pubmed & Cmd=Search & Term=%22Morselli-Labate%20AM%22%5BAuthor%5D & \

itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_DiscoveryPanel.Pub\

med_RVAbstractPlus>,

*Santini D*

</sites/entrez?Db=pubmed & Cmd=Search & Term=%22Santini%20D%22%5BAuthor%5D & itool=Ent\

rezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_DiscoveryPanel.Pubmed_RVAbs\

tractPlus>,

*Cogliandro RF*

</sites/entrez?Db=pubmed & Cmd=Search & Term=%22Cogliandro%20RF%22%5BAuthor%5D & itool\

=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_DiscoveryPanel.Pubmed_R\

VAbstractPlus>,

*De Giorgio R*

</sites/entrez?Db=pubmed & Cmd=Search & Term=%22De%20Giorgio%20R%22%5BAuthor%5D & itoo\

l=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_DiscoveryPanel.Pubmed_\

RVAbstractPlus>,

*Stanghellini V*

</sites/entrez?Db=pubmed & Cmd=Search & Term=%22Stanghellini%20V%22%5BAuthor%5D & itoo\

l=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_DiscoveryPanel.Pubmed_\

RVAbstractPlus>,

*Corinaldesi R*

</sites/entrez?Db=pubmed & Cmd=Search & Term=%22Corinaldesi%20R%22%5BAuthor%5D & itool\

=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_DiscoveryPanel.Pubmed_R\

VAbstractPlus>,

*Barbara G*

</sites/entrez?Db=pubmed & Cmd=Search & Term=%22Barbara%20G%22%5BAuthor%5D & itool=Ent\

rezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_DiscoveryPanel.Pubmed_RVAbs\

tractPlus>.

Department of Internal Medicine and Gastroenterology, St. Orsola

Hospital, Center for Applied Biomedical Research, Bologna, Italy.

OBJECTIVES: Immune activation may be involved in the pathogenesis of

irritable bowel syndrome (IBS). However, the relative magnitude of

this immune component and its correlation with gender and

gastrointestinal complaints in IBS patients remains poorly

elucidated. METHODS: We enrolled 48 IBS patients, with either

diarrhea or constipation, 12 patients with microscopic colitis, 20

patients with ulcerative colitis, and 24 healthy controls. Colonic

immunocytes were identified with quantitative immunohistochemistr y

on mucosal biopsies. Gastrointestinal symptoms were assessed using a

validated questionnaire. RESULTS: IBS patients showed a significant

72% increase in mucosal immune cells compared to controls (P<0.001).

Further analyses showed that increased immune cells were present in

50% of the IBS patients. The magnitude of the immune infiltrate in

IBS was significantly lower than that of microscopic colitis or

ulcerative colitis (42% and 124% increases vs. IBS, respectively;

P<0.001). Compared with controls, IBS patients had increased numbers

of CD3+, CD4+, and CD8+ T cells and mast cells (P<0.001). Compared

to male IBS patients, female IBS patients had greater numbers of

mast cells (P=0.066), but lower numbers of CD3+ and CD8+ T cells

(P=0.002 and <0.001, respectively) . Mucosal mast cell infiltration

of IBS patients was significantly associated with abdominal bloating

frequency (P=0.022) and with symptoms of dysmotility- like dyspepsia

(P=0.001), but not ulcer-like dyspepsia. CONCLUSIONS: A large subset

of IBS patients shows gender-dependent mucosal infiltration of

immunocytes that correlates with abdominal bloating and dysmotility-

like dyspepsia. These results provide the rationale for considering

immune mechanisms as a pathophysiological component in a subset of

IBS patients.

PMID: 19174797 [PubMed - indexed for MEDLINE]

Excerpt: Is functional bowel disease really functional?

http://www.springer link.com/ content/d034728l 2811nv79/

<http://www.springerlink.com/content/d034728l2811nv79/>

colleen0632 wrote:

>

>

> Hi all!

>

> We have heard all the advice on what works for IBS but does anyone

> know first hand what really works?

>

[Guest guest]

I have found probiotics to help the majority of my patients with IBS.

Judy D. Simon MS, RD, CD, CHES

Clinic Dietitian/Nutritionist

University of Washington Medical Center-Roosevelt Campus

Campus mail: box 354700

4245 Roosevelt Way NE

Seattle, WA 98105-6902

Phone:

E-mail: jdsimon@...

" The above email may contain patient identifiable or confidential information.

Because email is not secure, please be aware of associated risks of email

transmission. If you are a patient, communicating to a UW Medicine Provider via

email implies your agreement to email communication; see

http://www.uwmedicine.org/Global/Compliance/EmailRisk.htm.

The information is intended for the individual named above. If you are not the

intended recipient, any disclosure, copying, distribution or use of the contents

of this information is prohibited. Please notify the sender by reply email, and

then destroy all copies of the message and any attachments. See our Notice of

Privacy Practices at www.uwmedicine.org. "

what really works for IBS?

Hi all!

We have heard all the advice on what works for IBS but does anyone know first

hand what really works?

[Guest guest]

I have found probiotics to help the majority of my patients with IBS.

Judy D. Simon MS, RD, CD, CHES

Clinic Dietitian/Nutritionist

University of Washington Medical Center-Roosevelt Campus

Campus mail: box 354700

4245 Roosevelt Way NE

Seattle, WA 98105-6902

Phone:

E-mail: jdsimon@...

" The above email may contain patient identifiable or confidential information.

Because email is not secure, please be aware of associated risks of email

transmission. If you are a patient, communicating to a UW Medicine Provider via

email implies your agreement to email communication; see

http://www.uwmedicine.org/Global/Compliance/EmailRisk.htm.

The information is intended for the individual named above. If you are not the

intended recipient, any disclosure, copying, distribution or use of the contents

of this information is prohibited. Please notify the sender by reply email, and

then destroy all copies of the message and any attachments. See our Notice of

Privacy Practices at www.uwmedicine.org. "

what really works for IBS?

Hi all!

We have heard all the advice on what works for IBS but does anyone know first

hand what really works?

[Guest guest]

I strongly second Pat's comments.  I have had over 500 LEAP patients - a mix of

mostly IBS and/or migraine and a few others too - gastroparesis, Crohns, eczema,

RA, fibromyalgia and others, and can honestly say that I have only had a handful

of patients that have not responded.   Most cases of IBS are triggered by

cell-mediated delayed-type hypersensitivities.   LEAP testing is an end-point

test that unmasks all non-IgE responses to foods and food chemicals (i.e. MSG,

aspartame, food dyes, caffeine, solanine, tyramine, etc).   The approach is to

place the patient on a 4 week oligoantigenic diet, or eating protocol, where

they are focused on eating their non-reactive foods exclusively.   By doing so,

they avoid all untested reactive foods by default, which gives their immune

system time to calm down.   If we aren't introducing ANY reactive foods, their

immune system begins calming down immediately, and their symptoms begin to

subside

immediately as well.   Our approach also unmasks food intolerances or hidden

allergies.   We start off with 20-25 safe foods the first week, then add one new

tested safe food per day for the next 3 weeks.   The reason for this is

two-fold.   First of all, the patient can react to a food 3 days after

consumption and adding in multiple foods at once can make it difficult to detect

a problem food.   Second, LEAP doesn't test for allergies, and cannot detect

food intolerances (not an immune response), so adding in one new food per day

and testing for oral tolerance gives the patient's immune system time to " calm

down " and uncover any untested problem foods. 

As Pat mentioned, we usually see a 50-80% improvement within the first 7-10

days, which further helps establish patient compliance.   Many of my patients

have been from doctor to doctor to doctor, and finally have relief after a few

days.   It is the most exciting work I've ever done, and it never gets old.   Of

course, as someone else mentioned, as dietitians we also work with the whole

patient.   The goal is long-term gut health, not just symptom remission.   Food

sensitivities are usually a symptom, not the initial trigger.   Because 70-80%

of the immune system is in the gut,  many factors could have played a role

" insulting " the immune system.   Probiotics and other supplements are things we

frequently recommend to maintain long-term gut health.  

 

Another nice thing about LEAP is the support and training that is available.  

Most of us did not study immunology in depth in our degree programs, but the

training to become a CLT involves CPE eligible coursework that gives a nice

foundation in immunology, especially as it relates to IBS and migraine.   We

also have a very helpful list-serve and a mentorship program to help new CLTs

get their feet wet.  

 

 

I'm speaking on food sensitivities at FNCE,  please come if this is a topic that

interests you.   Personally, I believe that many of our patients, no matter what

their primary diagnosis is, also have comorbid food sensitivities.   Because the

mediators triggered by the immune system can travel anywhere that blood flows,

and even cross the blood-brain barrier, we frequently see patients with

depression, anxiety, insomnia, joint pain, canker sores, itchy ears, urinary

frequency, water retention, etc etc.... conditions that many patients would not

correlate to their food, but they are symptoms that we see improve along with

IBS and migraine.  

 

 

 

Linke, MS RD LD CLT

Certified LEAP Therapist

CLT Mentor

1400 Preston Road, Suite 400

Plano, TX 75093

Tel:

Fax:

www.susanlinke.com (under construction)

Subject: what really works for IBS?

To: rd-usa

Date: Wednesday, August 19, 2009, 8:46 PM

 

Hi all!

We have heard all the advice on what works for IBS but does anyone know first

hand what really works?

[Guest guest]

I strongly second Pat's comments.  I have had over 500 LEAP patients - a mix of

mostly IBS and/or migraine and a few others too - gastroparesis, Crohns, eczema,

RA, fibromyalgia and others, and can honestly say that I have only had a handful

of patients that have not responded.   Most cases of IBS are triggered by

cell-mediated delayed-type hypersensitivities.   LEAP testing is an end-point

test that unmasks all non-IgE responses to foods and food chemicals (i.e. MSG,

aspartame, food dyes, caffeine, solanine, tyramine, etc).   The approach is to

place the patient on a 4 week oligoantigenic diet, or eating protocol, where

they are focused on eating their non-reactive foods exclusively.   By doing so,

they avoid all untested reactive foods by default, which gives their immune

system time to calm down.   If we aren't introducing ANY reactive foods, their

immune system begins calming down immediately, and their symptoms begin to

subside

immediately as well.   Our approach also unmasks food intolerances or hidden

allergies.   We start off with 20-25 safe foods the first week, then add one new

tested safe food per day for the next 3 weeks.   The reason for this is

two-fold.   First of all, the patient can react to a food 3 days after

consumption and adding in multiple foods at once can make it difficult to detect

a problem food.   Second, LEAP doesn't test for allergies, and cannot detect

food intolerances (not an immune response), so adding in one new food per day

and testing for oral tolerance gives the patient's immune system time to " calm

down " and uncover any untested problem foods. 

As Pat mentioned, we usually see a 50-80% improvement within the first 7-10

days, which further helps establish patient compliance.   Many of my patients

have been from doctor to doctor to doctor, and finally have relief after a few

days.   It is the most exciting work I've ever done, and it never gets old.   Of

course, as someone else mentioned, as dietitians we also work with the whole

patient.   The goal is long-term gut health, not just symptom remission.   Food

sensitivities are usually a symptom, not the initial trigger.   Because 70-80%

of the immune system is in the gut,  many factors could have played a role

" insulting " the immune system.   Probiotics and other supplements are things we

frequently recommend to maintain long-term gut health.  

 

Another nice thing about LEAP is the support and training that is available.  

Most of us did not study immunology in depth in our degree programs, but the

training to become a CLT involves CPE eligible coursework that gives a nice

foundation in immunology, especially as it relates to IBS and migraine.   We

also have a very helpful list-serve and a mentorship program to help new CLTs

get their feet wet.  

 

 

I'm speaking on food sensitivities at FNCE,  please come if this is a topic that

interests you.   Personally, I believe that many of our patients, no matter what

their primary diagnosis is, also have comorbid food sensitivities.   Because the

mediators triggered by the immune system can travel anywhere that blood flows,

and even cross the blood-brain barrier, we frequently see patients with

depression, anxiety, insomnia, joint pain, canker sores, itchy ears, urinary

frequency, water retention, etc etc.... conditions that many patients would not

correlate to their food, but they are symptoms that we see improve along with

IBS and migraine.  

 

 

 

Linke, MS RD LD CLT

Certified LEAP Therapist

CLT Mentor

1400 Preston Road, Suite 400

Plano, TX 75093

Tel:

Fax:

www.susanlinke.com (under construction)

Subject: what really works for IBS?

To: rd-usa

Date: Wednesday, August 19, 2009, 8:46 PM

 

Hi all!

We have heard all the advice on what works for IBS but does anyone know first

hand what really works?

[Guest guest]

I strongly second Pat's comments.  I have had over 500 LEAP patients - a mix of

mostly IBS and/or migraine and a few others too - gastroparesis, Crohns, eczema,

RA, fibromyalgia and others, and can honestly say that I have only had a handful

of patients that have not responded.   Most cases of IBS are triggered by

cell-mediated delayed-type hypersensitivities.   LEAP testing is an end-point

test that unmasks all non-IgE responses to foods and food chemicals (i.e. MSG,

aspartame, food dyes, caffeine, solanine, tyramine, etc).   The approach is to

place the patient on a 4 week oligoantigenic diet, or eating protocol, where

they are focused on eating their non-reactive foods exclusively.   By doing so,

they avoid all untested reactive foods by default, which gives their immune

system time to calm down.   If we aren't introducing ANY reactive foods, their

immune system begins calming down immediately, and their symptoms begin to

subside

immediately as well.   Our approach also unmasks food intolerances or hidden

allergies.   We start off with 20-25 safe foods the first week, then add one new

tested safe food per day for the next 3 weeks.   The reason for this is

two-fold.   First of all, the patient can react to a food 3 days after

consumption and adding in multiple foods at once can make it difficult to detect

a problem food.   Second, LEAP doesn't test for allergies, and cannot detect

food intolerances (not an immune response), so adding in one new food per day

and testing for oral tolerance gives the patient's immune system time to " calm

down " and uncover any untested problem foods. 

As Pat mentioned, we usually see a 50-80% improvement within the first 7-10

days, which further helps establish patient compliance.   Many of my patients

have been from doctor to doctor to doctor, and finally have relief after a few

days.   It is the most exciting work I've ever done, and it never gets old.   Of

course, as someone else mentioned, as dietitians we also work with the whole

patient.   The goal is long-term gut health, not just symptom remission.   Food

sensitivities are usually a symptom, not the initial trigger.   Because 70-80%

of the immune system is in the gut,  many factors could have played a role

" insulting " the immune system.   Probiotics and other supplements are things we

frequently recommend to maintain long-term gut health.  

 

Another nice thing about LEAP is the support and training that is available.  

Most of us did not study immunology in depth in our degree programs, but the

training to become a CLT involves CPE eligible coursework that gives a nice

foundation in immunology, especially as it relates to IBS and migraine.   We

also have a very helpful list-serve and a mentorship program to help new CLTs

get their feet wet.  

 

 

I'm speaking on food sensitivities at FNCE,  please come if this is a topic that

interests you.   Personally, I believe that many of our patients, no matter what

their primary diagnosis is, also have comorbid food sensitivities.   Because the

mediators triggered by the immune system can travel anywhere that blood flows,

and even cross the blood-brain barrier, we frequently see patients with

depression, anxiety, insomnia, joint pain, canker sores, itchy ears, urinary

frequency, water retention, etc etc.... conditions that many patients would not

correlate to their food, but they are symptoms that we see improve along with

IBS and migraine.  

 

 

 

Linke, MS RD LD CLT

Certified LEAP Therapist

CLT Mentor

1400 Preston Road, Suite 400

Plano, TX 75093

Tel:

Fax:

www.susanlinke.com (under construction)

Subject: what really works for IBS?

To: rd-usa

Date: Wednesday, August 19, 2009, 8:46 PM

 

Hi all!

We have heard all the advice on what works for IBS but does anyone know first

hand what really works?

[Guest guest]

I make the following recommendations:

1. Go to the LEAP website!

2. Probiotics to help restore the gut environment

3. Good omega-6 to omega-3 balance to help reduce the pro-inflammatory

potential of the internal environment. One of my clients was doing #1 and #2

perfectly and it wasn't until we shifted her fat balance that things finally

resolved. My finding is often that these people don't just have one

inflammatory process going on...so you need to think globally, not just

bowelly/locally!

Also, I learned with eating disorder work do a lot of work with journaling. It

can become a habit to blame how you feel on what you last ate, when it's

actually stress. You can end up narrowing your food choices down unnecessarily,

and that ends up increasing your exposure to foods that trigger problems.

That's what's helpful with LEAP, it is a concrete list of " dont's " . But with

people who have some fears around foods, it's important to check to be sure

they're gradually erasing an unnecessary list and getting a wide variety of

choices.

I frame it this way: If your intestines were a wall you were repainting, LEAP

is the list of corrosive ingredients you want to keep away from your repainted

masterpiece, probiotics are the special ingredients you want in your paint to

help restore good color and texture, and omega-6/omega-3 balance act like

rust-proofing so there is hopefully more tolerance of more variety and not as

much need to be so restrictive.

I'm posting some recent abstracts mentioning bowels and omega-3's.

Monika M. Woolsey, MS, RD

http://www.incyst.blogspot.com

http://www.afterthediet.com

Am J Health Syst Pharm. 2009 Jul 1;66(13):1169-79. LinksTherapeutic potential of

n-3 polyunsaturated fatty acids in disease.

Fetterman JW Jr, Zdanowicz MM.

Department of Pharmaceutical Sciences, School of Pharmacy, South University,

Savannah, GA 31406, USA. jfetterman@...

PURPOSE: The potential therapeutic benefits of supplementation with n-3

polyunsaturated fatty acids (PUFAs) in various diseases are reviewed, and the

antiinflammatory actions, activity, and potential drug interactions and adverse

effects of n-3 PUFAs are discussed. SUMMARY: Fish oils are an excellent source

of long-chain n-3 PUFAs, such as eicosapentaenoic acid and docosahexaenoic acid.

After consumption, n-3 PUFAs can be incorporated into cell membranes and reduce

the amount of arachidonic acid available for the synthesis of proinflammatory

eicosanoids (e.g., prostaglandins, leukotrienes). Likewise, n-3 PUFAs can also

reduce the production of inflammatory cytokines, such as tumor necrosis factor

alpha, interleukin-1, and interleukin-6. Considerable research has been

conducted to evaluate the potential therapeutic effects of fish oils in numerous

conditions, including arthritis, coronary artery disease, inflammatory bowel

disease, asthma, and sepsis, all of which have inflammation as a key component

of their pathology. Additional investigations into the use of supplementation

with fish oils in patients with neural injury, cancer, ocular diseases, and

critical illness have recently been conducted. The most commonly reported

adverse effects of fish oil supplements are a fishy aftertaste and

gastrointestinal upset. When recommending an n-3 PUFA, clinicians should be

aware of any possible adverse effect or drug interaction that, although not

necessarily clinically significant, may occur, especially for patients who may

be susceptible to increased bleeding (e.g., patients taking warfarin).

CONCLUSION: The n-3 PUFAs have been shown to be efficacious in treating and

preventing various diseases. The wide variation in dosages and formulations used

in studies makes it difficult to recommend dosages for specific treatment goals.

Mol Nutr Food Res. 2008 Aug;52(8):885-97. LinksPolyunsaturated fatty acids,

inflammatory processes and inflammatory bowel diseases.

Calder PC.

Institute of Human Nutrition, School of Medicine, University of Southampton,

Southampton, UK. pcc@...

With regard to inflammatory processes, the main fatty acids of interest are the

n-6 PUFA arachidonic acid (AA), which is the precursor of inflammatory

eicosanoids like prostaglandin E(2) and leukotriene B(4), and the n-3 PUFAs

eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA). EPA and DHA are

found in oily fish and fish oils. EPA and DHA inhibit AA metabolism to

inflammatory eicosanoids. They also give rise to mediators that are less

inflammatory than those produced from AA or that are anti-inflammatory. In

addition to modifying the lipid mediator profile, n-3 PUFAs exert effects on

other aspects of inflammation like leukocyte chemotaxis and inflammatory

cytokine production. Some of these effects are likely due to changes in gene

expression, as a result of altered transcription factor activity. Fish oil has

been shown to decrease colonic damage and inflammation, weight loss and

mortality in animal models of colitis. Fish oil supplementation in patients with

inflammatory bowel diseases results in n-3 PUFA incorporation into gut mucosal

tissue and modification of inflammatory mediator profiles. Clinical outcomes

have been variably affected by fish oil, although some trials report improved

gut histology, decreased disease activity, use of corticosteroids and relapse.

[Guest guest]

I make the following recommendations:

1. Go to the LEAP website!

2. Probiotics to help restore the gut environment

3. Good omega-6 to omega-3 balance to help reduce the pro-inflammatory

potential of the internal environment. One of my clients was doing #1 and #2

perfectly and it wasn't until we shifted her fat balance that things finally

resolved. My finding is often that these people don't just have one

inflammatory process going on...so you need to think globally, not just

bowelly/locally!

Also, I learned with eating disorder work do a lot of work with journaling. It

can become a habit to blame how you feel on what you last ate, when it's

actually stress. You can end up narrowing your food choices down unnecessarily,

and that ends up increasing your exposure to foods that trigger problems.

That's what's helpful with LEAP, it is a concrete list of " dont's " . But with

people who have some fears around foods, it's important to check to be sure

they're gradually erasing an unnecessary list and getting a wide variety of

choices.

I frame it this way: If your intestines were a wall you were repainting, LEAP

is the list of corrosive ingredients you want to keep away from your repainted

masterpiece, probiotics are the special ingredients you want in your paint to

help restore good color and texture, and omega-6/omega-3 balance act like

rust-proofing so there is hopefully more tolerance of more variety and not as

much need to be so restrictive.

I'm posting some recent abstracts mentioning bowels and omega-3's.

Monika M. Woolsey, MS, RD

http://www.incyst.blogspot.com

http://www.afterthediet.com

Am J Health Syst Pharm. 2009 Jul 1;66(13):1169-79. LinksTherapeutic potential of

n-3 polyunsaturated fatty acids in disease.

Fetterman JW Jr, Zdanowicz MM.

Department of Pharmaceutical Sciences, School of Pharmacy, South University,

Savannah, GA 31406, USA. jfetterman@...

PURPOSE: The potential therapeutic benefits of supplementation with n-3

polyunsaturated fatty acids (PUFAs) in various diseases are reviewed, and the

antiinflammatory actions, activity, and potential drug interactions and adverse

effects of n-3 PUFAs are discussed. SUMMARY: Fish oils are an excellent source

of long-chain n-3 PUFAs, such as eicosapentaenoic acid and docosahexaenoic acid.

After consumption, n-3 PUFAs can be incorporated into cell membranes and reduce

the amount of arachidonic acid available for the synthesis of proinflammatory

eicosanoids (e.g., prostaglandins, leukotrienes). Likewise, n-3 PUFAs can also

reduce the production of inflammatory cytokines, such as tumor necrosis factor

alpha, interleukin-1, and interleukin-6. Considerable research has been

conducted to evaluate the potential therapeutic effects of fish oils in numerous

conditions, including arthritis, coronary artery disease, inflammatory bowel

disease, asthma, and sepsis, all of which have inflammation as a key component

of their pathology. Additional investigations into the use of supplementation

with fish oils in patients with neural injury, cancer, ocular diseases, and

critical illness have recently been conducted. The most commonly reported

adverse effects of fish oil supplements are a fishy aftertaste and

gastrointestinal upset. When recommending an n-3 PUFA, clinicians should be

aware of any possible adverse effect or drug interaction that, although not

necessarily clinically significant, may occur, especially for patients who may

be susceptible to increased bleeding (e.g., patients taking warfarin).

CONCLUSION: The n-3 PUFAs have been shown to be efficacious in treating and

preventing various diseases. The wide variation in dosages and formulations used

in studies makes it difficult to recommend dosages for specific treatment goals.

Mol Nutr Food Res. 2008 Aug;52(8):885-97. LinksPolyunsaturated fatty acids,

inflammatory processes and inflammatory bowel diseases.

Calder PC.

Institute of Human Nutrition, School of Medicine, University of Southampton,

Southampton, UK. pcc@...

With regard to inflammatory processes, the main fatty acids of interest are the

n-6 PUFA arachidonic acid (AA), which is the precursor of inflammatory

eicosanoids like prostaglandin E(2) and leukotriene B(4), and the n-3 PUFAs

eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA). EPA and DHA are

found in oily fish and fish oils. EPA and DHA inhibit AA metabolism to

inflammatory eicosanoids. They also give rise to mediators that are less

inflammatory than those produced from AA or that are anti-inflammatory. In

addition to modifying the lipid mediator profile, n-3 PUFAs exert effects on

other aspects of inflammation like leukocyte chemotaxis and inflammatory

cytokine production. Some of these effects are likely due to changes in gene

expression, as a result of altered transcription factor activity. Fish oil has

been shown to decrease colonic damage and inflammation, weight loss and

mortality in animal models of colitis. Fish oil supplementation in patients with

inflammatory bowel diseases results in n-3 PUFA incorporation into gut mucosal

tissue and modification of inflammatory mediator profiles. Clinical outcomes

have been variably affected by fish oil, although some trials report improved

gut histology, decreased disease activity, use of corticosteroids and relapse.

[Guest guest]

I make the following recommendations:

1. Go to the LEAP website!

2. Probiotics to help restore the gut environment

3. Good omega-6 to omega-3 balance to help reduce the pro-inflammatory

potential of the internal environment. One of my clients was doing #1 and #2

perfectly and it wasn't until we shifted her fat balance that things finally

resolved. My finding is often that these people don't just have one

inflammatory process going on...so you need to think globally, not just

bowelly/locally!

Also, I learned with eating disorder work do a lot of work with journaling. It

can become a habit to blame how you feel on what you last ate, when it's

actually stress. You can end up narrowing your food choices down unnecessarily,

and that ends up increasing your exposure to foods that trigger problems.

That's what's helpful with LEAP, it is a concrete list of " dont's " . But with

people who have some fears around foods, it's important to check to be sure

they're gradually erasing an unnecessary list and getting a wide variety of

choices.

I frame it this way: If your intestines were a wall you were repainting, LEAP

is the list of corrosive ingredients you want to keep away from your repainted

masterpiece, probiotics are the special ingredients you want in your paint to

help restore good color and texture, and omega-6/omega-3 balance act like

rust-proofing so there is hopefully more tolerance of more variety and not as

much need to be so restrictive.

I'm posting some recent abstracts mentioning bowels and omega-3's.

Monika M. Woolsey, MS, RD

http://www.incyst.blogspot.com

http://www.afterthediet.com

Am J Health Syst Pharm. 2009 Jul 1;66(13):1169-79. LinksTherapeutic potential of

n-3 polyunsaturated fatty acids in disease.

Fetterman JW Jr, Zdanowicz MM.

Department of Pharmaceutical Sciences, School of Pharmacy, South University,

Savannah, GA 31406, USA. jfetterman@...

PURPOSE: The potential therapeutic benefits of supplementation with n-3

polyunsaturated fatty acids (PUFAs) in various diseases are reviewed, and the

antiinflammatory actions, activity, and potential drug interactions and adverse

effects of n-3 PUFAs are discussed. SUMMARY: Fish oils are an excellent source

of long-chain n-3 PUFAs, such as eicosapentaenoic acid and docosahexaenoic acid.

After consumption, n-3 PUFAs can be incorporated into cell membranes and reduce

the amount of arachidonic acid available for the synthesis of proinflammatory

eicosanoids (e.g., prostaglandins, leukotrienes). Likewise, n-3 PUFAs can also

reduce the production of inflammatory cytokines, such as tumor necrosis factor

alpha, interleukin-1, and interleukin-6. Considerable research has been

conducted to evaluate the potential therapeutic effects of fish oils in numerous

conditions, including arthritis, coronary artery disease, inflammatory bowel

disease, asthma, and sepsis, all of which have inflammation as a key component

of their pathology. Additional investigations into the use of supplementation

with fish oils in patients with neural injury, cancer, ocular diseases, and

critical illness have recently been conducted. The most commonly reported

adverse effects of fish oil supplements are a fishy aftertaste and

gastrointestinal upset. When recommending an n-3 PUFA, clinicians should be

aware of any possible adverse effect or drug interaction that, although not

necessarily clinically significant, may occur, especially for patients who may

be susceptible to increased bleeding (e.g., patients taking warfarin).

CONCLUSION: The n-3 PUFAs have been shown to be efficacious in treating and

preventing various diseases. The wide variation in dosages and formulations used

in studies makes it difficult to recommend dosages for specific treatment goals.

Mol Nutr Food Res. 2008 Aug;52(8):885-97. LinksPolyunsaturated fatty acids,

inflammatory processes and inflammatory bowel diseases.

Calder PC.

Institute of Human Nutrition, School of Medicine, University of Southampton,

Southampton, UK. pcc@...

With regard to inflammatory processes, the main fatty acids of interest are the

n-6 PUFA arachidonic acid (AA), which is the precursor of inflammatory

eicosanoids like prostaglandin E(2) and leukotriene B(4), and the n-3 PUFAs

eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA). EPA and DHA are

found in oily fish and fish oils. EPA and DHA inhibit AA metabolism to

inflammatory eicosanoids. They also give rise to mediators that are less

inflammatory than those produced from AA or that are anti-inflammatory. In

addition to modifying the lipid mediator profile, n-3 PUFAs exert effects on

other aspects of inflammation like leukocyte chemotaxis and inflammatory

cytokine production. Some of these effects are likely due to changes in gene

expression, as a result of altered transcription factor activity. Fish oil has

been shown to decrease colonic damage and inflammation, weight loss and

mortality in animal models of colitis. Fish oil supplementation in patients with

inflammatory bowel diseases results in n-3 PUFA incorporation into gut mucosal

tissue and modification of inflammatory mediator profiles. Clinical outcomes

have been variably affected by fish oil, although some trials report improved

gut histology, decreased disease activity, use of corticosteroids and relapse.