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Stomach acid suppressing meds may cause damage to intestine

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As we all suspected - so many people on PPIs end up with GI issues later.

And, then, the research that shows that GERD may just be a cytokine

response to certain foods, and not acid related at all - so a lot of people on

acid suppressants that should not be.

Let's see, God created stomach acid as part of a healthy body. Why do we

think turning our stomachs into a base environment is healthy for us?

More below.

Jan

Public release date: 1-Sep-2011

Contact: McGuire

_vmcguir@..._

(http://us.mc840.mail.yahoo.com/mc/compose?to=vmcguirmcmaster (DOT) ca)

90-552-

McMaster University

McMaster study finds more gut reaction to arthritis drugs

Stomach acid supressing drugs appear to cause damage to the small intestine

Hamilton, ON (Sept. 1, 2011) – Patients often take drugs to lower

stomach acid and reduce the chances they will develop ulcers from taking

their anti-inflammatory drugs for conditions such as arthritis, but the

combination may be causing major problems for their small intestines,

McMaster researchers have found.

A team from the Farncombe Family Digestive Health Research Institute has

found those stomach acid-reducing drugs, known as proton pump

inhibitors, may actually be aggravating damage in the small intestine

caused by the nonsteroidal anti-inflammatory drugs, also known as NSAIDs.

In a study published in the medical journal Gastroenterology, principal

investigator Wallace says the extent of the hard-to-detect damage

caused to the small intestine has only recently been discovered through

use of small video cameras swallowed like pills.

" Suppressing acid secretion is effective for protecting the stomach from

damage caused by NSAIDs, but these drugs appear to be shifting the

damage from the stomach to the small intestine, where the ulcers may be

more dangerous and more difficult to treat, " said Wallace. He is

director of the Farncombe institute and professor of medicine of the

G. DeGroote School of Medicine at McMaster.

He added that the use of probiotics is being investigated as a potential

cure for the small intestine damage.

###

The study was funded by the Canadian Institutes of Health Research

(CIHR) and a CIHR/Canadian Association of Gastroenterology Fellowship.

For more information, please contact:

McGuire

Media Relations Coordinator

Faculty of Health Sciences

McMaster University

, ext. 22169

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(http://us.mc840.mail.yahoo.com/mc/compose?to=vmcguirmcmaster (DOT) ca)

McGuire

Media Relations, Faculty of Health Sciences,

McMaster University

, ext. 22169

_vmcguir@..._

(http://us.mc840.mail.yahoo.com/mc/compose?to=vmcguirmcmaster (DOT) ca)

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_http://www.eurekalert.org/pub_releases/2011-09/mu-msf090111.php_

(http://www.eurekalert.org/pub_releases/2011-09/mu-msf090111.php)

Reflux esophagitis due to immune reaction, not acute acid burn,

UT Southwestern researchers report

Dr Rhonda Souza

Dr Stuart

_SJSpechler@..._ (mailto:SJSpechler@...)

EMAIL HIM!!!

Media Contact: LaKisha Ladson

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DALLAS - Nov. 19, 2009 - Contrary to current thinking, a condition

called gastroesophageal reflux disease (GERD) might not develop as a

direct result of acidic digestive juices burning the esophagus, UT

Southwestern Medical Center researchers have found in an animal study.

Rather, gastroesophageal reflux spurs the esophageal cells

to release chemicals called cytokines, which attract inflammatory cells

to the esophagus. It is those inflammatory cells, drawn to the esophagus

by cytokines, that cause the esophageal damage that is characteristic of

GERD. The condition is manifested by symptoms such as heartburn and

chest pain.

" Currently, we treat GERD by giving medications to prevent

the stomach from making acid, " said Dr. Rhonda Souza, associate

professor of internal medicine at UT Southwestern and lead author of the

study appearing the November issue of Gastroenterology. " But if GERD is

really an immune-mediated injury, maybe we should create medications

that would prevent these cytokines from attracting inflammatory cells to

the esophagus and starting the injury in the first place. "

In the study, researchers created GERD in rats by

connecting the duodenum to the esophagus. This operation allows stomach

acid and bile to enter the esophagus. Researchers were surprised to

learn that esophagitis didn't develop for a number of weeks after the

operation.

" That doesn't make sense if GERD is really the result of an

acid burn, as we all were taught in medical school, " said Dr. Stuart

Spechler, professor of internal medicine at UT Southwestern and senior

author of the study. " Chemical injuries develop immediately. If you

spill battery acid on your hand, you don't have to wait a month to see

the damage. "

About 40 percent of Americans suffer symptoms of GERD at

some point, and 20 percent on a weekly basis, Dr. Souza said. Over the

long term, GERD could eventually lead to esophageal cancer.

Previous studies had shown that if an animal esophagus is

perfused with highly concentrated acid, esophageal damage develops

quickly. In humans, however, the large majority of reflux episodes do

not contain such highly concentrated acid, Dr. Souza said.

" In animal models of reflux esophagitis designed to mimic

the human disease, researchers hadn't looked at the early events in the

development of esophageal injury, " Dr. Souza noted. " Most of those

investigators have been interested in the long-term consequences of

GERD, and we found virtually no published data about what happens later

that induces gastroesophageal reflux. "

Dr. Souza, who is also a staff physician at the Dallas

Veterans Affairs Medical Center and part of the Harold C.

Comprehensive Cancer Center at UT Southwestern, and Dr. Spechler, chief

of gastroenterology at the Dallas VA, said the method they used to

produce GERD in rats is a reasonable representation of how GERD develops

in humans - acidic digestive juices from the stomach surge into the

esophagus.

Soon after the operation, they expected to see the death of

surface cells of the esophagus, and they expected to see the injury

progress later to the deeper layers. Instead, they found the opposite.

Three days after the surgery, there was no damage to surface cells, but

the researchers did find inflammatory cells in the deeper layers of the

esophagus. Those inflammatory cells didn't rise to the surface layer

until three weeks after the initial acid exposure.

The next step for researchers is to conduct additional

studies in humans.

Other UT Southwestern researchers involved in the study

included Dr. Xiaofang Huo, postdoctoral researcher in internal medicine;

Dr. Vivek Mittal, postgraduate trainee in internal medicine; Dr. ne

Carmack, postgraduate trainee in pathology: Dr. Huiying Zhang,

instructor of internal medicine; Dr. Genta, clinical professor of

pathology and internal medicine; Dr. Kathy Hormi-Carver, assistant

professor of internal medicine; and Dr. Xi Zhang and Dr. Chunhua Yu,

both research associates in internal medicine.

The study was supported by the Dallas VA Medical Center and

the National Institutes of Health.

Visit _http://www.utsouthwestern.org/digestive_

(http://www.utsouthwestern.org/digestive) to learn

about UT Southwestern's clinical services for digestive disorders.

###

This news release is available on our World Wide Web home page at

_http://www.utsouthwestern.edu/home/news/index.html_

(http://www.utsouthwestern.edu/home/news/index.html)

Jan Patenaude, RD, CLT

Director of Medical Nutrition

Signet Diagnostic Corp.

Telecommuting Nationwide

(Mountain Time)

Fax:

DineRight4@...

Certified LEAP Therapist and specialist in food sensitivity for IBS,

migraine, fibromyalgia and multiple inflammatory conditions. Co-author of the

Certified LEAP Therapist (CLT) Training Course.

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