<http://www.theherald.co.za/herald/news/n13_26022008.htm>

Vaccinations urged as killer ‘sheep Aids‘ hits Southern Cape

Janine Oelofse GARDEN ROUTE BUREAU CHIEF

SOUTHERN Cape farmers have been urged to be on the lookout for symptoms of
a deadly sheep disease which authorities say has slowly spread to
“hundreds” of farms in the Western Cape.

The agriculture department appealed to Western Cape sheep farmers this
week to remain calm in the face of the spread of Ovine Johne‘s Disease
(OJD), commonly referred to as “sheep Aids” because of the emaciation it
causes.

The disease was first detected on 47 farms in Caledon, Ceres and Mossel
Bay a decade ago, but has slowly spread to hundreds of farms, especially
in the Caledon area and the Southern Cape.

But the provincial agriculture department has moved to reassure farmers
that their interests would be protected by the department.

“The situation is under control,” said the MEC‘s spokesman, Alie van
Jaarsveld. “We have vets working on it full-time.”

OJD, or paratuberculosis, is a chronic and contagious disease found
worldwide, characterised by persistent and progressive diarrhoea, weight
loss, debilitation, the thickening of the mucous membranes, and eventual
death.

It is considered a “problem” in South Africa because it is hard to detect
and can kill up to 20 per cent of sheep in highly infected flocks.

Van Jaarsveld said an official count of sheep currently affected was not
available yet, but the supply of mutton to the market could drop if it
spread further and it was decided to slaughter the sheep in the infected
areas.

The Small Stock Health Advisory Body, which was formed to deal with the
problem, has advised that heavily infected areas be declared “OJD Control
Areas”. This will allow free movement of live animals within these
confines, but prevent their transportation to the outside world except for
slaughter.

This would prevent the legal requirement of placing infected flocks under
quarantine, he said.

The body also advised farmers to vaccinate their sheep and announced the
requirement of written vendor declarations on the OJD status of their
flocks.

“The veterinary services of the national government and the provinces
launched an intensive round of workshops and meetings ... to formulate a
policy to address this situation,” Van Jaarsveld said.

This led to the formation of the advisory body, which will present its
final policy proposals to Agriculture Minister Lulu Xingwana and her nine
provincial MECs.

State veterinary surgeon Dr Dempsey de Lange said yesterday the only cases
confirmed so far in the Southern Cape were in Mossel Bay. He urged farmers
to be on the lookout for unexplained diarrhoea with chronic progressive
wasting in their adult sheep.

“Farmers who notice (this) should consult their vet and those who lose
their animals due to these symptoms should have them sent for an autopsy,”
De Lange added.

<http://www.iol.co.za/index.php?set_id=1&click_id=594&art_id=vn20080225041030310\
C554637>
Sheep Aids hits hundreds of farmers

February 25 2008 at 07:22AM


By Karen Breytenbach

The Department of Agriculture has appealed to Western Cape sheep farmers
to remain calm in the face of the spread to hundreds of farms of Ovine
Johne's Disease, better known as "sheep Aids" because of the emaciation it
causes.

The disease was first detected on 47 farms in Caledon, Ceres and Mossel
Bay a decade ago, but has slowly spread to hundreds of farms, especially
in the Caledon area and Southern Cape. Some cases were also reported in
Cradock in Eastern Cape.

But the Western Cape Agriculture Department has moved to reassure farmers
that their interests would be protected. "The situation is under control,
we have vets working on it full-time," said spokesperson Alie van
Jaarsveld.
--
Dale
<http://DaleRoose.com/>
"There are two fundamental errors we could make in post-war Iraq. We could
stay too long, denying Iraqi sovereignty to a proud and talented people
who have the human and material resources to build a progressive and
modern Arab state..."
--Senator John McCain, February 12, 2004
100 years in Iraq "would be fine with me."
--Senator John McCain, January 3, 2008

How are you doing?  Sorry I haven't gotten back to you, but I have
hardly been at home.  Thank you so much for all your information, I am
going to post some of the links on my website, www.crohnscanada.org

As soon as I have a little time I will post, I promise, I hope you are
doing a little better.  hugs Diane

[The article only mentions having followed the patients for one year,
which is hardly long enough to determine the long term effect of increased
suppression of the immune system to deal with a slow-growing Mycobacterium
infection. "Financial support for the trial was provided by Centocor BV
and Schering-Plough, which make the two immunosuppressive drugs used."]

<http://www.forbes.com/forbeslife/health/feeds/hscout/2008/02/22/hscout612876.ht\
ml>

Aggressive Therapy for Crohn's Disease Produces Better Outcomes

02.22.08, 12:00 AM ET


FRIDAY, Feb. 22 (HealthDay News) -- Treating Crohn's disease more
aggressively resulted in better outcomes for patients, an international
team of researchers reports.

Using more than one immunosuppressive drug shortly after a person was
diagnosed with the disease was more effective in inducing remission than
starting patients on corticosteroids, according to the study in the Feb.
23 issue of The Lancet.

"One swallow doesn't make a spring," said study co-author Dr. Brian
Feagan, referring to the fact that clinical practice is rarely modified
based on just one study. "[But] this is provocative in the sense that it's
saying, if you treat patients earlier with more aggressive therapy that
may be better than the conventional approach. There will need to be other
studies."

"It is an exciting development," added one expert, Dr. Roshini Rajapaksa,
an assistant professor of medicine at NYU School of Medicine in New York
City. "We're always looking for ways to avoid steroids."

Crohn's disease involves an inflammation of the gastrointestinal tract
that most often affects the lower part of the small intestine. Swelling
leads to pain and diarrhea.

"We don't really know the cause, but the current wisdom is [that] you've
lost tolerance to normal bacteria in the gut. Normally, you have to get
along with bacterial cells, because there are so many of them," explained
Feagan, director of Robarts Clinical Trials at Robarts Research Institute
at The University of Western Ontario in London, Ontario, Canada. "The
immune system is in a controlled inflammatory state. In Crohn's disease,
it's thought that the immune system is becoming unhappy with normal flora.
White blood cells migrate into the tissue and release nasty things and
cause damage."

Currently, standard treatment for Crohn's patients starts with
corticosteroids. Then, if side effects or steroid resistance develop, it
moves on to broad-spectrum immunosuppressive drugs such as Rheumatrex
(methotrexate). If all else fails, doctors try tumor necrosis factor
(TNF)-blockers, a targeted therapy.

"There is no evidence that that approach is superior to any other
approach," Feagan said. "We just eased into that over time, because that's
the way the drugs were developed."

For this study, Feagan and his colleagues randomly assigned 133 patients
at 18 centers in Belgium, Holland and Germany to receive either combined
immunosuppression or the conventional approach.

Financial support for the trial was provided by Centocor BV and
Schering-Plough, which make the two immunosuppressive drugs used.

Sixty-seven patients assigned to combined immunosuppression received three
infusions of Remicade (infliximab) with Imuran (azathioprine) at the
start, two weeks later and four weeks after that.

The remaining 66 patients received steroids followed by Imuran and
Remicade.

At six months, 60 percent of 65 patients in the combined immunosuppression
group were in remission without steroids or surgery, compared with 35.9
percent of 64 people in the other group.

At one year, 61.5 percent of those in the combined group were in remission
versus 42.2 percent in the control group.

"There was clinically meaningful and statistically significant improvement
at six months in favor of the combined immunosuppression," Feagan said.

According to an accompanying commentary, the results of another, similar
trial are due in late 2008. If those researchers reach the same
conclusion, conventional treatment for Crohn's could well change, the
commentary noted.

Rajapaksa had one reservation, however.

" Remicade has its own issues. For instance, it's given intravenously so
the individual has to go to the doctor's office," she said.

"And because it works for severe cases and difficult-to-treat cases, you
might want to reserve it" for such cases, she added.

<http://newsstore.smh.com.au/apps/previewDocument.ac?docID=GCA00812776GIA&f=pdf>
[pdf]

CLINICAL PHASE PILOT STUDY RESULTS

SINGLE CAPSULE MYOCONDA® DEMONSTRATES A GOOD SAFETY PROFILE Sydney,
Australia, 18 February 2008. Giaconda Ltd (ASX: GIA) today announces the
results of a study investigating the predicted effectiveness and safety of
Myoconda® for the treatment of Mycobacterium avium paratuberculosis (MAP)
infection in Crohn’s Disease. The components, Rifabutin, Clarithromycin
and Clofazimine, are all approved for use in humans as separate agents.
This pilot pharmacokinetic study was designed to optimize the formulation
of Myoconda® by combining the three components into a single capsule
following discussions with the US Food and Drug Administration (FDA). The
study was included as part of the IND (Investigational New Drug
Application) that was approved by the FDA last year.

The study design used 24 normal, healthy, non-smoking male and female
subjects under a randomized, open-label, single-dose, 1-way 2-arm,
parallel design. There were no significant or serious adverse events
reported in either arm.

The significant finding was that in the ‘all-in-one’ formulation the blood
concentrations of Rifabutin and Clarithromycin achieved were more optimal,
for both components causing no significant adverse effects with
potentially increased efficacy. Previous studies indicated that
concomitant use of these two agents can elevate the levels of Rifabutin in
the blood, increasing the potential for side effects and reduce the levels
of Clarithromycin, thus potentially reducing the efficacy of this
important active ingredient. The new formulation has improved both the
pharmacokinetic availability of both ingredients and reduced the side
effect potential, providing a novel and significant improvement on
previous formulations. A patent application has been filed by Giaconda Ltd
to protect the novel formulation technique.

“This study is an important step in the development of a solid safety and
efficacy profile for Myoconda in the treatment of MAP infection in Crohn’s
Disease, and reflects the resourceful and innovative support we have
received from our formulation consultants,” said Patrick McLean, CEO of
Giaconda.

“The metabolic benefits of the new formulation add value to an already
promising product. This result bolsters Myoconda®’s already impressive
record in the clinic, which, with the new formulation patent, will help
support our ongoing negotiations with potential distribution and marketing
partners and in our fundraising efforts,” Mr McLean added.

--ENDS—

About Giaconda Limited

Giaconda Limited is a life sciences company involved in developing and
commercialising innovative and cost effective medical therapies in the
field of gastroenterology. Giaconda’s products are targeted towards the
treatment of serious conditions that are not adequately addressed by any
existing therapy. In this way, Giaconda’s products are intended to satisfy
these significant unmet medical needs of the gastrointestinal market. The
Giaconda portfolio consists of five products, all of which are novel
combinations of known compounds. Giaconda has two lead products, Myoconda®
for the treatment of Crohn’s Disease and Heliconda® for the treatment of
resistant Helicobacter pylori infection.

For more information please visit www.giacondalimited.com

About Myoconda® – A Combination Antibiotic Therapy for the Treatment of
Crohn’s Disease

Myoconda®, the Company’s Anti-MAP therapy for the treatment of Crohn’s
Disease is a combination of three registered anti-mycobacterial drugs -
rifabutin, clarithromycin and clofazimine. These three drugs are widely
marketed world-wide for the treatment of mycobacterial and other
infections. Myoconda® presents these three compounds in a specific
patented combination in a unique format. The combination has undergone a
Phase III trial in Australia across 22 centres and has demonstrated the
highest remission rates of any major trial published to date with fully
66% of all patients in remission at 16 weeks. Giaconda has completed
formulation development, manufactured clinical trial product material
under cGMP conditions and has just completed a pharmacokinetic study in
healthy humans. The FDA has approved a Phase II/III clinical study as part
of the regulatory path toward registration in the US.

Myoconda® is based on the proposition that MAP infection is a significant
factor in Crohn’s Disease. Prof. Borody has long been at the forefront of
this approach, which is gaining increasing acceptance among
gastrointestinal specialists worldwide. Prof. Borody has published
significant data demonstrating that patients treated with anti-MAP
combination therapy such as that found in Myoconda® experience long-term
remission of clinical symptoms and inflammation, some for up to nine years.

About Crohn’s Disease

Crohn’s Disease is a chronic inflammatory disease of the gastrointestinal
tract. The disease most commonly affects the lower small intestine and the
large intestine. Symptoms of Crohn’s Disease include abdominal pain,
diarrhoea, fever and weight loss. In severe cases, the intestine can
become blocked or obstructed, requiring surgery. Young patients with
Crohn’s Disease may also suffer growth retardation. Patients suffering
Crohn’s Disease are conventionally treated with drugs aimed at reducing
inflammation and other associated symptoms. The cause of Crohn’s Disease
is unknown, thus the standard treatments aim to treat symptoms rather than
the cause of the disease. The bacterium Mycobacterium avium ss.
paratuberculosis (MAP) is the lead candidate as an infectious cause of
Crohn’s Disease. By targeting the MAP infection, Myoconda® is designed to
address a possible source of the disease, rather than attempting to merely
alleviate its symptoms.

Except for historical information, this news release may contain
forward-looking statements that reflect the Company’s current expectation
regarding future events. These forward looking statements involve risk and
uncertainties, which may cause but are not limited to, changing market
conditions, the successful and timely completion of clinical studies, the
establishment of corporate alliances, the impact of competitive products
and pricing, new product development, uncertainties related to the
regulatory approval process, and other risks detailed from time to time in
the Company’s ongoing quarterly and annual reporting. CONTACTS:

Company
Prof. Tom Borody – Chief Medical Officer
T: +61 (2) 9713-4011

Media & Investor Relations
Fay Weston – Talk Biotech
T: +61 422 206036

Giaconda Limited
Ground Floor
44 East Street
Five Dock NSW 2046
Phone: [612] 9370-0069
Fax: [612] 9712-1469
email: info@...
ABN 68 108 088 517
www.giacondalimited.com

USDA has ordered the recall of 143,000,000 lbs. of beef produced as far
back as February 1, 2006 (more than two years). How much of this beef,
some of it from uninspected downer animals, was contaminated with
paratuberculosis bacteria? How many Arizonans became infected? How many
  from welfare programs? How many from school lunch programs? Piss on Mad
Cow Disease; how many people will die from Crohn's Disease?

I asked you in person to do something about paratuberculosis infections in
dairy and beef herds. What have you done?

<http://news.bbc.co.uk/1/hi/world/americas/7249911.stm>

US orders massive recall of beef

The US Department of Agriculture (USDA) has ordered the recall of 143m lb
(64.9m kg) of beef - the largest meat recall in the country's history.

The recalled products come from a California meat plant, which officials
say broke rules on cattle inspections.

However the department says the health hazard is minimal. Much of the meat
was purchased for school lunch and other federal nutrition programmes.

The plant is also being investigated over alleged animal cruelty.

Caution

The USDA recalled beef products from the Westland/Hallmark Meat Co, dating
back to 1 February 2006.

The move surpasses a 1999 recall of 35m lbs of ready-to-eat meats,
officials said.

Some of the beef was destined for federal welfare assistance programmes,
as well as some major fast-food chains.

But officials said most of the recalled meat has probably already been
eaten.

The USDA described the recall as Class 2 - meaning there is a remote
probability that the product could harm health if consumed.

"We don't know how much product is out there right now. We don't think
there is a health hazard, but we do have to take this action," Dick
Raymond, USDA undersecretary for food safety, told AP news agency.

Downer

The recall was ordered after department officials said the plant did not
consistently order inspections of cattle which became non-ambulatory prior
to slaughter.

Such "downer" cattle are at greater risk of contamination by E. coli,
salmonella or contracting mad cow disease, as they have weaker immune
systems and greater contact with faeces than walking cattle.

They should either be removed from the food supply, or receive a more
thorough inspection following slaughter, officials say.

Operations at the plant had already been suspended after an undercover
video shot by the Humane Society of America came to light.

The video appeared to show crippled and ill animals being prodded with the
blades of a forklift truck, kicked, given electric shocks and sprayed with
high-pressure water hoses by staff.

Two former employees were charged with animal cruelty on Friday, and the
investigation continues.

The company says it has now taken action to ensure all employees handle
animals humanely.

<http://www.canada.com/theprovince/news/unwind/story.html?id=1ddb3a72-30d9-4f0e-\
a702-1af142dc87ca>

Winning an uphill battle

With six summits down, Rob Hill embarks on the ultimate expedition to
Mount Everest this spring
Neville Judd, The Province
Published: Sunday, February 17, 2008

A little more than a decade ago, 23-year-old Rob Hill embarked on one of
the toughest climbs of his life.

Holed up in his parents' North Van basement suite and weighing 105 pounds,
Hill's unsteady ascent of the stairs to the kitchen that day in 1994
represented his own personal Everest. His message from the top was simple
and Rob's mom, Cheryl, will never forget it.

"He said, 'I think I'm dying,'" recalls Cheryl.

Next month, Rob Hill sets off for another tough climb. This time he's
heading for Nepal to climb Mount Everest in May.

Reaching the 29,035-foot (8,850 metres) peak will likely demand as much
willpower as it took Hill to get up those stairs 14 years ago. How he got
there is the story of No Guts, Know Glory.

- - -

In 1993 Rob Hill was in the best shape of his life. He loved the mountains
and climbed whenever he could. He had a good job with Motorola in
Richmond, worked out regularly in a nearby gym and competed in marathons
and triathlons. (He ran his first marathon in Grade 2.)

Then he ate some bad cream cheese.

"That triggered it. Vomiting, diarrhea, pain, nausea and weight loss."

Hill was diagnosed with Crohn's disease, an inflammatory bowel disease
that causes painful swelling of the digestive tract.

Hill had never heard of it.

"'What is it?', was my first reaction," says Hill. "The symptoms are
pretty scary and for me they were really bad. I just never seemed to get
healthy.

"Crohn's can be triggered by food that's gone off. In my case it was bad
cream cheese."

For the next 18 months, Hill's condition worsened. His muscular five foot
eleven frame dwindled alarmingly from 185 pounds to 105 pounds. Then he
stopped weighing himself.

"It was very difficult," recalls Cheryl, who watched her son's "unique,
wicked sense of humour" disappear to be replaced by brooding silence
punctuated only by bouts of anger.

"He was very angry. He blew up from time to time, he had a short temper
and his answers were short ... shorter than they needed to be."

Hill says he thought he was being punished for something. "I asked, 'Why
me?'"

"I considered taking my own life."

Life appeared to be slipping away anyway.

In 1995, Hill underwent surgery to remove his large intestine. When
colorectal surgeon Dr. Michael Pezim opened up the patient it first
appeared he had cancer.

"The intestine wall had attached itself to Rob's liver," says Cheryl.
"Robert was quite correct. He was dying."

Minus his large intestine, Hill was equipped with an ostomy -- an external
pouch attached to his ileum through the abdominal wall to collect stools.
With his body stabilized and the pain regulated, Hill was able to regain
physical strength and prepare for a life with Crohn's.

"When it came down to losing my colon or losing my life, it wasn't a hard
decision to make," says Hill.

But a nagging question persisted.

"Turned out an auntie of mine had Crohn's, but no one talked about it and
that puzzled me," says Hill. "You don't talk to people about it, it's just
frightening, it's about going to the bathroom. It took eight years to the
point where I was willing to speak about it."

Downsized from his high-tech job at Motorola, Hill enrolled in a
wilderness leadership program at North Vancouver's Capilano College in
2001. There, he rediscovered his love of the mountains and an idea was
hatched.

Bothered by what he saw as the social stigma of Crohn's and other
digestive disorders, such as ulcerative colitis and irritable bowel
syndrome, he decided to do something about it.

...

A WORD ABOUT CROHN'S

Crohn's and a related disease, ulcerative colitis, are the two main
disease categories that belong to a larger group of illnesses called
inflammatory bowel disease (IBD).

Edmonton Oilers forward Fernando Pisani was diagnosed with the latter last
year.

They are marked by an exaggerated response by the body's immune system.
Researchers believe that the immune system mistakes bacteria that is
normally found in the intestines for foreign or invading substances, and
launches an attack. The body then sends white blood cells into the lining
of the intestines, where they produce chronic inflammation. These cells
then generate harmful products that ultimately lead to ulcerations and
bowel injury.

<http://seattletimes.nwsource.com/html/health/2004179538_vitamind13m.html>

Wednesday, February 13, 2008 - Page updated at 07:59 AM

Does our lack of sun put your health in danger?

By Sandi Doughton

Seattle Times science reporter

The Northwest's dreary winters are infamous for inducing depression. But
being starved for sunlight can do more than kick you into a psychic hole.

A growing body of evidence suggests it can raise your risk of cancer,
increase susceptibility to heart attack, diabetes and other disorders, and
at least partly account for the region's sky-high rates of multiple
sclerosis.

The reason is vitamin D, an essential nutrient produced in abundance by
skin exposed to the sun's rays. Long dismissed as being important mainly
for strong bones, the so-called sunshine vitamin is now recognized as a
key player throughout the body, including the immune system.

Experts say vitamin D deficiency is much more common than previously
believed — especially in northern climes like Washington, where solar
radiation from October to March is too puny to maintain healthy levels.

"You're in a dark, gloomy place," said Bruce Hollis, a leading vitamin D
researcher at the Medical University of South Carolina. "In the winter,
you could stand outside naked for five hours and nothing is going to
happen."

Increased use of sunscreen has turned a seasonal shortfall into a
year-round condition for many people. A recent survey in Britain found 87
percent of adults tested during winter, and more than 60 percent in
summer, had subpar vitamin D levels. Doctors in many parts of the world —
including California — report a resurgence of childhood rickets, soft
bones caused by lack of vitamin D.

While supplements offer a cheap and easy solution, Hollis and other
researchers argue the recommended intake is too low to provide many health
benefits. A Canadian medical organization advises that pregnant and
nursing women take 10 times the amount suggested in the U.S.

"You're more likely to live longer and you're less likely to die of
serious chronic disease if you have adequate vitamin D on board," said Dr.
Michael Holick of Boston University School of Medicine, one of the world's
top experts. "It may well be the most important nutrient of the decade."

Risks of low levels

When Lisa Hill went to her doctor complaining of joint pain, she was
surprised to get a diagnosis of vitamin D deficiency. "I had never heard
of it," said the 54-year-old Gig Harbor woman.

Since leaving her native Southern California, her sun exposure has dropped
dramatically.

"You're like a little mole in a hole," she said. "You just don't get much
sun here."




Many doctors once scoffed at the notion of vitamin D deficiency, but
testing has become more routine and is covered by most insurance.

University of Washington heart surgeon Dr. Donald Miller Jr. tested 78 of
his patients and found three-quarters had "insufficient" levels of vitamin
D.

"It was really pretty shocking," said Miller.

In a study of 1,739 Boston-area residents reported last month, rates of
heart attack, stroke and heart failure were about 50 percent higher in
those with low levels of vitamin D.

In addition to strengthening bones, muscles and joints, high vitamin D
levels have been linked with lower rates of colon, prostate, breast,
esophageal and pancreatic cancer.

Harvard scientists found that high levels of vitamin D reduced children's
odds of developing asthma, while researchers in Pittsburgh reported that
pregnant women with low vitamin D had greater risk of preeclampsia, a
dangerous form of high blood pressure.

Vitamin D also appears to be one of the reasons multiple sclerosis and
other autoimmune diseases are twice as common in northern vs. southern
states. Washington's rate of MS, which causes progressive nerve damage, is
one of the highest in the nation.

Blood samples from more than 7 million military personnel showed people
with the highest levels of vitamin D were 62 percent less likely to
develop MS than those with the lowest concentrations. A study in Finland
found similar results.

What D can do

Formed in skin cells exposed to UVB, the invisible form of light that
causes sunburn, vitamin D and its breakdown products act throughout the
body.

The compounds are believed to regulate as many as 1,000 genes, including
genes that weed out precancerous cells and genes that slow the runaway
reproduction typical of cancer.

Molecular geneticist John White and his colleagues at McGill University in
Montreal discovered vitamin D also switches on an arm of the immune system
that kills bacteria — including the bug responsible for tuberculosis.

"It's a kind of front-line response to infection," he said.

That may explain why TB patients in the early 1900s who basked in the sun
at sanitariums were often cured, added White, author of a recent
Scientific American article on vitamin D.

The compound has an anti-inflammatory effect, too, which probably plays a
role in preventing heart disease and autoimmune disorders.

The evolutionary angle is also being explored, with the suggestion that
early people who migrated north from the equator lost skin pigmentation to
maximize vitamin D production. Today, dark-skinned people in northern
latitudes are among the most vulnerable to vitamin D deficiency.

Inconclusive studies

While the evidence is piling up, most of it is still based only on
association. Scientists count cancer cases, infer or measure vitamin
intake, then look for correlations. Some researchers advise caution until
there's more data from controlled trials, where one group gets vitamin D,
while another gets a placebo.

One such trial last year found 1,000 international units (IU) a day
slashed cancer risk for women. But a much bigger study found women who
took vitamin D supplements had the same risk of colon cancer as those who
didn't.

"I would say the jury is out," said Ulrike Peters, who studies nutrition
and cancer at the Fred Hutchinson Cancer Research Center.

Women in the large experiment took 400 IU a day of vitamin D — the amount
in a typical multivitamin.

Hollis, the South Carolina researcher, says the results simply show that
standard doses aren't enough.

The U.S. Institute of Medicine (IOM) recommends 200 IU a day up to age 50,
and 400 to 600 IU for older people. The Canadian Paediatric Society
recently urged pregnant and nursing women to take 2,000 IU a day — which
the IOM designates as the maximum safe dose.

Vitamin D experts say much higher doses are safe. Exposing just your arms
and legs to the summer sun for less than 15 minutes can generate 5,000 IU,
Holick pointed out.

It is possible to go overboard with supplements and trigger dangerous
calcium deposits in kidneys and blood vessels, but Holick says it takes a
lot: more than 10,000 IU a day for a year.

Milk and some cereals are fortified with small amounts of vitamin D to
prevent rickets, but few foods are significant natural sources.

Tanning beds that produce UVB will generate vitamin D, though
dermatologists go ballistic when Holick points that out. About 5 percent
of his research funding has come from the indoor tanning industry, and he
was fired from a joint appointment in Boston University's dermatology
department after authoring a book on the benefits of UV radiation.

Still, he continues to advocate "sensible" sun exposure that shields the
face and stops far short of sunburn. He also recommends most people take
1,000 to 1,500 IU a day of vitamin D. Cholecalciferol, or D3, is the
preferred form. Hollis takes 4,000 IU a day and recommends 2,000 IU daily
for everyone.

Both continue to agitate for a change in official guidelines. But that
would require a costly research review and isn't likely to happen soon.

"Vitamin D is so cheap, nobody makes any money on it," Hollis said. "So
there's nobody to push it."

Sandi Doughton: 206-464-2491 or sdoughton@...

Copyright © 2008 The Seattle Times Company

Multiple Sclerosis Drug May Be Linked to Melanoma

Doctors report 2 cases of the deadly skin cancer developing in patients
taking Tysabri
By Amanda Gardner
Posted 2/6/08

WEDNESDAY, Feb. 6 (HealthDay News) -- Almost immediately after a
46-year-old woman with multiple sclerosis received her first dose of the
drug Tysabri, a mole that had been on her shoulder for years suddenly took
on a dangerous new character.

It turned out to be a melanoma that spread like wildfire. The woman now
has just a few months to live.

At almost the same time, a 45-year-old woman who also has multiple
sclerosis developed melanoma in her retina after receiving several doses
of Tysabri. She had a family history of melanoma and also had atypical
moles on her body; the mole on her retina went back at least nine years.

Although these are just two -- albeit dramatic -- examples, the authors of
a letter in the Feb. 7 issue of the New England Journal of Medicine are
cautioning doctors who care for MS patients to keep this potential risk in
mind.

"Neurologists who have patients who report a family history of melanoma or
have funny moles should send them to a dermatologist first. Don't just
start them on drugs [Tysabri]," said Dr. John Thomas Mullen, co-author of
the letter and a surgical oncologist with Beth Israel Deaconess Medical
Center, in Boston.

"I can't say it's cause-and-effect definitively because it's just an
observation, but the first patient had had that mole forever. She took the
drug and almost instantaneously the lesion changed," added Mullen, who saw
both patients.

"We don't know if the two are related right now," said Patricia O'Looney,
vice president of biomedical research at the National Multiple Sclerosis
Society. "There are so many people taking Tysabri, we should go forward
with caution... One should always consult with their doctor and go over
their personal family history and decide what is best."

Tysabri (natalizumab), a monoclonal antibody that helps treat autoimmune
disorders such as MS and Crohn's disease, has had a clouded history. It
first received U.S. Food and Drug Administration approval in November
2004, only to be pulled from the market three months later after several
patients in clinical trials developed a rare but deadly viral infection of
the brain called progressive multifocal leukoencephalopathy.

In June 2006, the FDA allowed the drug back on the market but with strict
conditions governing its use.

Just last month, the FDA approved Tysabri to treat people with a moderate
to severe form of Crohn's disease.

But there is basic science to support Mullen's observations.

One of the participants in an earlier study of Tysabri had developed (and
subsequently died of) a metastatic melanoma that appeared as soon as he
got his first dose of the drug, Mullen said.

And in a study done before Tysabri received FDA approval, melanomas in
mice that were given the drug had an increased tendency to detach from the
primary tumor and spread.

Tysabari may have a dampening effect on the immune system that encourages
the formation of the potentially deadly skin cancer, the letter stated.

And now that Tysabri has been approved for people with Crohn's disease,
more people may be at risk, although those with no family history of
melanoma and no moles probably don't need to worry, Mullen said.

"Doctors should ask for a family history of melanoma and do a quick skin
check," he said. "Tysabri isn't the only drug in our arsenal. You could
give the patient something else if you were concerned about that."

More information

The National Multiple Sclerosis Society has more on treatments for MS.

Copyright � 2008 ScoutNews, LLC. All rights reserved.

Hi Dale

Sorry I haven't been able to get back to you, but I have had a really busy
week, taking care of my brothers grandchildren.  Very hectic, I promise I
will be in touch this week end.  I hope you are doing better.  God Bless
Diane,
----- Original Message -----
From: "Dale" <dale@...>
To: <paratuberculosis@yahoogroups.com>
Sent: Thursday, February 07, 2008 12:23 AM
Subject: [paratuberculosis] Two-year combination antibiotic therapy...


> They concluded that the antibiotics didn't have a sustained benefit in
> treating Crohn's then went on to say: "Short-term improvement was seen
> when this combination was added to corticosteroids, most likely because of
> nonspecific antibacterial effects."
>
> Corticosteroids suppress the imune system and reduce inflammation? So I
> take it while they were trying to see if antibiotics would kill the
> bacteria, they were simultaneously suppressing the immune system
> inhibiting it from killing the bacteria.
>
> Maybe they were using some kind of corticosteroids that don't ... oh,
> nevermind.
>
> -- Dale
> <http://DaleRoose.com/>
>
> Gastroenterology. 2007 Jun;132(7):2313-9. Epub 2007 Mar 21.
>
> Comment in:
> Gastroenterology. 2007 Jun;132(7):2594-8.
> Gastroenterology. 2007 Nov;133(5):1742-3; author reply 1745-6.
> Gastroenterology. 2007 Nov;133(5):1742; author reply 1745-6.
> Gastroenterology. 2007 Nov;133(5):1743-4; author reply 1745-6.
> Gastroenterology. 2007 Nov;133(5):1744-5; author reply 1745-6.
>
> Two-year combination antibiotic therapy with clarithromycin, rifabutin,
> and clofazimine for Crohn's disease.
>
> Selby W, Pavli P, Crotty B, Florin T, Radford-Smith G, Gibson P, Mitchell
> B, Connell W, Read R, Merrett M, Ee H, Hetzel D; Antibiotics in Crohn's
> Disease Study Group.
>
> Royal Prince Alfred Hospital, Sydney, Australia.
> warwicks@...
>
> BACKGROUND & AIMS: Mycobacterium avium subspecies paratuberculosis has
> been proposed as a cause of Crohn's disease. We report a prospective,
> parallel, placebo-controlled, double-blind, randomized trial of 2 years of
> clarithromycin, rifabutin, and clofazimine in active Crohn's disease, with
> a further year of follow-up. METHODS: Two hundred thirteen patients were
> randomized to clarithromycin 750 mg/day, rifabutin 450 mg/day, clofazimine
> 50 mg/day or placebo, in addition to a 16-week tapering course of
> prednisolone. Those in remission (Crohn's Disease Activity Index <or=150)
> at week 16 continued their study medications in the maintenance phase of
> the trial. Primary end points were the proportion of patients experiencing
> at least 1 relapse at 12, 24, and 36 months. RESULTS: At week 16, there
> were significantly more subjects in remission in the antibiotic arm (66%)
> than the placebo arm (50%; P=.02). Of 122 subjects entering the
> maintenance phase, 39% taking antibiotics experienced at least 1 relapse
> between weeks 16 and 52, compared with 56% taking placebo (P=.054). At
> week 104, the figures were 26% and 43%, respectively (P=.14). During the
> following year, 59% of the antibiotic group and 50% of the placebo group
> relapsed (P=.54). CONCLUSIONS: Using combination antibiotic therapy with
> clarithromycin, rifabutin, and clofazimine for up to 2 years, we did not
> find evidence of a sustained benefit. This finding does not support a
> significant role for Mycobacterium avium subspecies paratuberculosis in
> the pathogenesis of Crohn's disease in the majority of patients.
> Short-term improvement was seen when this combination was added to
> corticosteroids, most likely because of nonspecific antibacterial effects.
>
>
>
> Yahoo! Groups Links
>
>
>

Gastroenterology. 2006 Jul;131(1):85-96.

Does cross-reactivity between mycobacterium avium paratuberculosis and
human intestinal antigens characterize Crohn's disease?

Polymeros D, Bogdanos DP, Day R, Arioli D, Vergani D, Forbes A.

University College London, London, United Kindgom.

BACKGROUND & AIMS: Most Crohn's disease (CD) patients show seroreactivity
against Mycobacterium avium paratuberculosis (MAP), suggesting a
pathogenic role for this organism. Our aim was to seek amino acid
similarities between MAP and intestinal proteins that, through molecular
mimicry, could serve as targets for cross-reactive immunity in CD.
METHODS: Fifty-three peptides comprising 23 sets of MAP/human intestinal
peptidyl mimics chosen for maximal homology were constructed and tested
for immunologic cross-reactivity by enzyme-linked immunosorbent assay in
50 patients with CD, 50 with ulcerative colitis, and 38 healthy controls.
RESULTS: Antibody reactivity was present in only 7 of 23 peptide sets.
MAP/self-reactivity in at least 1 of the 7 reactive sets was present in 21
(42%) CD patients but was virtually absent in the controls. Significant
double-reactivity was found against MAP glycosyl transferase d
(gsd)(230-244)/human gastrointestinal glutathione peroxidase
(GPg)(111-125) homologues in 15 of 50 (30%) CD patients; MAP
alkylohydroperoxidase C (ahpC)(20-34)/human tumor overexpressed protein
(TOG)(637-651) double-reactivity was present in 10 (20%) CD patients, but
in none of the controls. Inhibition studies confirmed that simultaneous
reactivity to mimics was caused by cross-reactivity. Three-dimensional
modeling predicts GPg(111-125) will be exposed in a solvent-accessible
surface region of the protein compatible with antibody recognition.
Antibody affinity was greater for the MAP mimics than for the
self-sequences, suggesting that reactivity to the mycobacterial sequences
precedes that against self-sequences. CONCLUSIONS: We describe
MAP/self-mimics as targets of cross-reactive antibody responses
characterizing patients with CD. Our findings indicate gastrointestinal
glutathione peroxidase as a novel autoantigen in CD.

They concluded that the antibiotics didn't have a sustained benefit in
treating Crohn's then went on to say: "Short-term improvement was seen
when this combination was added to corticosteroids, most likely because of
nonspecific antibacterial effects."

Corticosteroids suppress the imune system and reduce inflammation? So I
take it while they were trying to see if antibiotics would kill the
bacteria, they were simultaneously suppressing the immune system
inhibiting it from killing the bacteria.

Maybe they were using some kind of corticosteroids that don't ... oh,
nevermind.

-- Dale
<http://DaleRoose.com/>

Gastroenterology. 2007 Jun;132(7):2313-9. Epub 2007 Mar 21.

Comment in:
Gastroenterology. 2007 Jun;132(7):2594-8.
Gastroenterology. 2007 Nov;133(5):1742-3; author reply 1745-6.
Gastroenterology. 2007 Nov;133(5):1742; author reply 1745-6.
Gastroenterology. 2007 Nov;133(5):1743-4; author reply 1745-6.
Gastroenterology. 2007 Nov;133(5):1744-5; author reply 1745-6.

Two-year combination antibiotic therapy with clarithromycin, rifabutin,
and clofazimine for Crohn's disease.

Selby W, Pavli P, Crotty B, Florin T, Radford-Smith G, Gibson P, Mitchell
B, Connell W, Read R, Merrett M, Ee H, Hetzel D; Antibiotics in Crohn's
Disease Study Group.

Royal Prince Alfred Hospital, Sydney, Australia.
warwicks@...

BACKGROUND & AIMS: Mycobacterium avium subspecies paratuberculosis has
been proposed as a cause of Crohn's disease. We report a prospective,
parallel, placebo-controlled, double-blind, randomized trial of 2 years of
clarithromycin, rifabutin, and clofazimine in active Crohn's disease, with
a further year of follow-up. METHODS: Two hundred thirteen patients were
randomized to clarithromycin 750 mg/day, rifabutin 450 mg/day, clofazimine
50 mg/day or placebo, in addition to a 16-week tapering course of
prednisolone. Those in remission (Crohn's Disease Activity Index <or=150)
at week 16 continued their study medications in the maintenance phase of
the trial. Primary end points were the proportion of patients experiencing
at least 1 relapse at 12, 24, and 36 months. RESULTS: At week 16, there
were significantly more subjects in remission in the antibiotic arm (66%)
than the placebo arm (50%; P=.02). Of 122 subjects entering the
maintenance phase, 39% taking antibiotics experienced at least 1 relapse
between weeks 16 and 52, compared with 56% taking placebo (P=.054). At
week 104, the figures were 26% and 43%, respectively (P=.14). During the
following year, 59% of the antibiotic group and 50% of the placebo group
relapsed (P=.54). CONCLUSIONS: Using combination antibiotic therapy with
clarithromycin, rifabutin, and clofazimine for up to 2 years, we did not
find evidence of a sustained benefit. This finding does not support a
significant role for Mycobacterium avium subspecies paratuberculosis in
the pathogenesis of Crohn's disease in the majority of patients.
Short-term improvement was seen when this combination was added to
corticosteroids, most likely because of nonspecific antibacterial effects.

Gastroenterology. 2007 Nov;133(5):1487-98. Epub 2007 Aug 3.

Microbial mannan inhibits bacterial killing by macrophages: a possible
pathogenic mechanism for Crohn's disease.

Mpofu CM, Campbell BJ, Subramanian S, Marshall-Clarke S, Hart CA, Cross A,
Roberts CL, McGoldrick A, Edwards SW, Rhodes JM.

Division of Gastroenterology, School of Clinical Science, University of
Liverpool, Liverpool, United Kingdom.

BACKGROUND & AIMS: Crohn's disease (CD) is mimicked by inherited phagocyte
disorders and is associated with circulating antibodies against yeast
mannan (anti-Saccharomyces cerevisiae antibody; ASCA). We speculated that
mannans might impair phagocyte function. METHODS: S cerevisiae mannan was
assessed for its effects on human peripheral blood neutrophils, adherent
monocytes, and monocyte-derived macrophages (MDM). RESULTS: Mannan caused
dose-related increased survival of CD Escherichia coli HM605 within
adherent monocytes from 24% +/- 10.5% (control) to 114% +/- 22.7% with
mannan 1 mg/mL at 2 hours (mean +/- SEM, n = 9; P = .0002). Electron
microscopy showed E coli HM605 surviving and probably replicating within
macrophage vesicles. Mannan (1 mg/mL) inhibited the respiratory burst in
neutrophils and monocytes (both P = .002) and bacterial killing within MDM
(P < .001). E coli survival was increased within macrophages from
TLR4(-/-) (126% +/- 3.5% survival at 2 hours) and MyD88(-/-) (134.8% +/-
6.5%) mice compared with wild-type mice (both P < .0001). Mannan had no
additional effect, showing that TLR4 and MyD88 are involved in bacterial
killing by macrophages and its inhibition by mannan. Putative
CD-associated micro-organisms were screened for the ASCA mannan epitope by
Galanthus nivalis lectin (GNA) blotting. ASCA epitope was expressed by
Candida albicans and Mycobacterium paratuberculosis but not by
Mycobacterium tuberculosis or E coli. Supernatants from M paratuberculosis
culture inhibited killing of E coli HM605 by adherent human monocytes and
murine macrophages. The inhibitory activity was removed by GNA-affinity
chromatography. CONCLUSIONS: Suppression of mucosal phagocyte function by
microbial mannans, possibly of Mycobacterial origin, may contribute to CD
pathogenesis.

Gastroenterology. 2007 Dec;133(6):1779-86. Epub 2007 Sep 26.

Mortality by medication use among patients with inflammatory bowel
disease, 1996-2003.

Hutfless SM, Weng X, Liu L, Allison J, Herrinton LJ.

Epidemiology Department, Harvard School of Public Health, Boston,
Massachusetts, USA.

BACKGROUND & AIMS: Most previous population-based studies of mortality in
inflammatory bowel disease (IBD) did not account for medication use. We
evaluated mortality by IBD medication use among members of the Kaiser
Permanente Northern California IBD Registry. METHODS: The retrospective,
population-based cohort study included 9032 persons who received at least
one inpatient or 2 outpatient diagnoses of IBD during 1996-2002. Age and
sex standardized mortality ratios measured the associations between IBD
and all-cause and cause-specific mortality. Age, sex, and smoking adjusted
odds ratios measured the association of mortality by IBD medication use.
RESULTS: Compared with health plan members without IBD, mortality was
increased in patients with Crohn's disease (CD) (1.4; 95% confidence
interval, 1.2-1.6) but not ulcerative colitis (UC) (1.0; 95% CI, 0.9-1.2).
CD was associated with increased mortality from infectious and parasitic
diseases (4.1; 95% CI, 1.7-8.5), septicemia (6.8; 95% CI, 2.2-15.8), small
intestinal cancer (48.1; 95% CI, 5.8-17.4), respiratory diseases (1.9; 95%
CI, 1.3-2.7), digestive diseases other than IBD (2.4; 95% CI, 1.0-4.8),
and liver diseases (2.6; 95% CI, 1.0-5.3). UC was associated with
increased mortality from digestive diseases other than IBD (3.9; 95% CI,
2.4-6.0). The relationship with CD mortality was 0.7 for aminosalicylates
(95% CI, 0.5-1.1), 1.3 (95% CI, 0.9-1.9) for immunomodulators, and 1.0
(95% CI, 0.7-1.4) for corticosteroids. Among patients with UC, these odds
ratios were 0.8 (95% CI, 0.5-1.1) for aminosalicylates, 0.5 (95% CI,
0.3-0.9) for immunomodulators, and 0.8 (95% CI, 0.6-1.1) for
corticosteroids. CONCLUSIONS: Mortality is increased in CD. Infections,
respiratory diseases, and digestive diseases are important specific causes
of death. IBD medication use has varying associations with mortality.

Curious, it took nearly a week for this post to get from Comcast to Yahoo:

X-Received: from unknown (HELO QMTA04.westchester.pa.mail.comcast.net)
(76.96.62.40)
    by mta18.grp.scd.yahoo.com with SMTP; 5 Feb 2008 04:40:28 -0000
X-Received: from OMTA05.westchester.pa.mail.comcast.net ([76.96.62.43])
	 by QMTA04.westchester.pa.mail.comcast.net with comcast
	 id iowB1Y0040vyq2s0503K00; Tue, 29 Jan 2008 02:08:54 +0000

This drug keeps leukocytes from migrating into the body's organs, at a
cost of about US$28,400 per year. I gather this will be yet another
expensive medication for Crohn's that reduces inflammation at the expense
of capacity of the immune system to fight infections.


On Mon, 28 Jan 2008 19:08:39 -0700, Dale <dale@...> wrote:

> BACKGROUND (article follows), According to Wikipedia (wfiw):
>
> "...Natalizumab [aka Tysabri] is the first alpha-4 antagonist in a new
> class of agents called selective adhesion-molecule (SAM) inhibitors.
> Alpha-4 integrin is required for leukocytes to migrate into the body's
> organs such as the brain and gut; natalizumab prevents leukocytes from
> doing that."
>
> "...In these trials[1][2], natalizumab was shown to reduce relapses in MS
> patients by 68% vs. a placebo, a margin far greater than had been seen
> for
> other approved MS therapies."
>
> "...Also in these trials natalizumab slowed the progression of disability
> (as measured by EDSS) by approximately 50% [3] (the US and EU medical
> authorities use slightly different measures of disability progression,
> and
> use values of between 42% and 54%)."
>
> "...In Crohn's, a randomized controlled trial found that natalizumab
> increased the rate of remission."
>
> "...Two further randomized controlled trials have confirmed natalizumab's
> effectiveness in increasing the rate of remission and in maintaning
> remission in Crohn's."
>
> "...the annual costs for Tysabri is approximately US$28,400 (not
> including
> costs associated with infusion services)..."
>
> Tysabri had been withdrawn from the market after the occurance of a rare
> brain disease in two patients taking the drug.
>
> <http://en.wikipedia.org/wiki/Natalizumab>
>
> -- Dale
> <http://DaleRoose.com>
> If a small improvement in the DNA of cattle could give them the power of
> speech, would that genetic modification be allowed?
>   - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - -
> - -
> - - -
>
<http://www.boston.com/business/globe/articles/2008/01/15/biogen_idecs_ms_drug_o\
kd_for_crohns_disease/>
>
> Biogen Idec's MS drug OK'd for Crohn's disease
>
> But approval includes warnings on safety
>
> By Todd Wallack
> Globe Staff / January 15, 2008
>
> Federal regulators yesterday gave Biogen Idec Inc. good news about one of
> the Cambridge biotech company's key drugs.
>
> Tysabri, a treatment for multiple sclerosis, won approval from the Food
> and Drug Administration to be used against another debilitating illness,
> Crohn's disease.
>
> The move comes six months after an FDA advisory panel voted 12 to 3 to
> recommend the drug's approval to treat some forms of Crohn's, a chronic
> inflammatory disease of the intestinal tract. FDA officials said the
> final
> decision was delayed because Biogen Idec and Elan Corp., the Irish
> company
> that comarkets the drug, made changes to their application for a Crohn's
> approval.
>
> European regulators recently rejected a similar request to use the drug
> as
> a Crohn's treatment, arguing the risk of infection outweighed the
> relatively modest benefit of Tysabri.
>
> Biogen Idec temporarily shelved the drug three years ago after it was
> linked to a rare brain disease. The company says there have not been any
> additional cases of the disease since sales resumed in 2006, with new
> guidance on how it should be used. But some doctors remain wary of the
> treatment, even though it has been shown to be highly effective in some
> patients.
>
> Despite the safety concerns, Biogen Idec has predicted Tysabri will
> eventually become a major source of revenue. This month, the company
> reaffirmed predictions it will be used by 100,000 patients by the end of
> 2010, up from more than 21,000 at the end of 2007.
>
> Biogen Idec shares rose late in the day after the FDA news was released.
> The shares finished up 96 cents to $59.98, a gain of 1.6 percent.
>
> Doctors already had permission to use the drug to treat Crohn's disease
> on
> their own, but Biogen Idec needed formal approval to start marketing the
> drug for that purpose.
>
> The FDA decision does carry some caveats. Specifically, the agency
> approved the drug to treat patients with moderate to serious cases of the
> disease who can't be treated effectively with other drugs, such as
> steroids. The label will also carry safety warnings to reduce the risk
> that patients will contract the brain disease or other infections.
>
> About 500,000 people in the United States suffer from Crohn's, but it is
> unclear how many of them will qualify to use Tysabri. The disease
> frequently causes diarrhea and abdominal cramps; symptoms can also
> include
> fever, bleeding, and weight loss. There is no cure.
>
> Biogen Idec and Elan said they expect the drug to be available for
> Crohn's
> patients by the end of February.
>

BACKGROUND (article follows), According to Wikipedia (wfiw):

"...Natalizumab [aka Tysabri] is the first alpha-4 antagonist in a new
class of agents called selective adhesion-molecule (SAM) inhibitors.
Alpha-4 integrin is required for leukocytes to migrate into the body's
organs such as the brain and gut; natalizumab prevents leukocytes from
doing that."

"...In these trials[1][2], natalizumab was shown to reduce relapses in MS
patients by 68% vs. a placebo, a margin far greater than had been seen for
other approved MS therapies."

"...Also in these trials natalizumab slowed the progression of disability
(as measured by EDSS) by approximately 50% [3] (the US and EU medical
authorities use slightly different measures of disability progression, and
use values of between 42% and 54%)."

"...In Crohn's, a randomized controlled trial found that natalizumab
increased the rate of remission."

"...Two further randomized controlled trials have confirmed natalizumab's
effectiveness in increasing the rate of remission and in maintaning
remission in Crohn's."

"...the annual costs for Tysabri is approximately US$28,400 (not including
costs associated with infusion services)..."

Tysabri had been withdrawn from the market after the occurance of a rare
brain disease in two patients taking the drug.

<http://en.wikipedia.org/wiki/Natalizumab>

-- Dale
<http://DaleRoose.com>
If a small improvement in the DNA of cattle could give them the power of
speech, would that genetic modification be allowed?
   - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - -
- - -
<http://www.boston.com/business/globe/articles/2008/01/15/biogen_idecs_ms_drug_o\
kd_for_crohns_disease/>

Biogen Idec's MS drug OK'd for Crohn's disease

But approval includes warnings on safety

By Todd Wallack
Globe Staff / January 15, 2008

Federal regulators yesterday gave Biogen Idec Inc. good news about one of
the Cambridge biotech company's key drugs.

Tysabri, a treatment for multiple sclerosis, won approval from the Food
and Drug Administration to be used against another debilitating illness,
Crohn's disease.

The move comes six months after an FDA advisory panel voted 12 to 3 to
recommend the drug's approval to treat some forms of Crohn's, a chronic
inflammatory disease of the intestinal tract. FDA officials said the final
decision was delayed because Biogen Idec and Elan Corp., the Irish company
that comarkets the drug, made changes to their application for a Crohn's
approval.

European regulators recently rejected a similar request to use the drug as
a Crohn's treatment, arguing the risk of infection outweighed the
relatively modest benefit of Tysabri.

Biogen Idec temporarily shelved the drug three years ago after it was
linked to a rare brain disease. The company says there have not been any
additional cases of the disease since sales resumed in 2006, with new
guidance on how it should be used. But some doctors remain wary of the
treatment, even though it has been shown to be highly effective in some
patients.

Despite the safety concerns, Biogen Idec has predicted Tysabri will
eventually become a major source of revenue. This month, the company
reaffirmed predictions it will be used by 100,000 patients by the end of
2010, up from more than 21,000 at the end of 2007.

Biogen Idec shares rose late in the day after the FDA news was released.
The shares finished up 96 cents to $59.98, a gain of 1.6 percent.

Doctors already had permission to use the drug to treat Crohn's disease on
their own, but Biogen Idec needed formal approval to start marketing the
drug for that purpose.

The FDA decision does carry some caveats. Specifically, the agency
approved the drug to treat patients with moderate to serious cases of the
disease who can't be treated effectively with other drugs, such as
steroids. The label will also carry safety warnings to reduce the risk
that patients will contract the brain disease or other infections.

About 500,000 people in the United States suffer from Crohn's, but it is
unclear how many of them will qualify to use Tysabri. The disease
frequently causes diarrhea and abdominal cramps; symptoms can also include
fever, bleeding, and weight loss. There is no cure.

Biogen Idec and Elan said they expect the drug to be available for Crohn's
patients by the end of February.

As the US government gradually moves closer to a Euthanasia program for
the nonproductive, the State of Mississippi is considering legislation to
deny food service to the obese, disregarding the cause of the disease,
other health factors, or the effects of starvation. See below.

-- Dale
<http://DaleRoose.com>
Moral relativism is saying that waterboarding may or may not be torture
relative to the circumstances.

   - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - -
- -

<http://rawstory.com/news/2007/State_Big_Dietitian_watching_you_0202.html>

State: Big Dietitian is watching youNick Langewis
Published: Saturday February 2, 2008

   del.icio.us |

Print This  Email This


A bill recently introduced in Mississippi's state legislature would bar
restaurants from serving people determined to be obese.

House Bill 282 aims to require dining establishments with seating capacity
of five or more to follow guidelines set by the state's health department
to determine a prospective customer's obesity, turning away those
considered too fat to serve.

A copy of the bill follows in two images below [converted to text]

    -  -  -  -  -  -  -  -  -  -  -  -  -  -  -  -  -  -  -  -  -  -  -  -

MISSISSIPPI LEGISLATURE

By: Representatives Mayhall, Read, Shows

REGULAR SESSION 2008

To:  Public Health and Human Services; Judiciary B


HOUSE BILL NO.  282

1      AN ACT TO PROHIBIT CERTAIN FOOD ESTABLISHMENTS FROM SERVIING
1  FOOD TO ANY PERSON WHO IS OBESE, BASED ON CRITERIA PRESCRIBED BY
3  THE STATE DEPARTMENT OF HEALTH; TO DIRECT THE DEPARTMENT TO
4  PREPARE WRITTEN MATERIALS THAT DESCRIBE AND EXPLAIN THE CRITERIA
5  FOR DETERMINING WHETHER A PERSON IS OBESE AND TO PROVIDE THOSE
6  MATERIALS TO THE FOOD ESTABLISHMENTS; TO DIRECT THE DEPARTMENT TO
7  MONITOR THE FOOD ESTABLISHMENTS FOR COMPLIANCE WITH THE PROVISIONS
8  OF THIS ACT; AND FOR RELATED PURPOSES.

9        BE IT ENACTED BY THE LEGISLATUR OF THE STATE OF MISSISSIPPI:

10      SECTION 1.  (1)  The provisions of this section shall apply
11  to any food establishment that is required to obtain a permit from
12 the State Department of Health under Section 41-3-15(4) (f), that
13 operates primarily in an enclosed facility and that has five (5)
14  or more seats for customers.
15      (2)  Any food establishment to which this section applies
16  shall not be allowed to serve food to any person who is obese,
17  based on criteria prescribed by the State Department of Health
18  after consultation with the Mississippi Council on Obesity
19  Prevention and Management established under Section 41-101-1 or
20 its successor. The State Department of Health shall prepare
21  written materials that describe and explain the criteria for
22  determining whether a person is obese, and shall provide those
23  materials to all food establishments to which this section
24  applies. A food establishment shall be entitled to rely on the
25  criteria for obesity in those written materials when determining
26  whether or not it is allowed to serve food to any person.
27        (3)  The State Department of Health shall monitor the food
28  establishments to which this section applies for compliance with
29  the provisions of this section, and may revoke the permit of any

H. B. No.   282
08/HR03/R51
Page 1 (RF/LN)    G1/2

30  food establishment that repeatedly violates the provisions of this
31  section.
32         SECTION 2.  This act shall take effect and be in force from
33  and after July 1, 2008.

Hi Diane:

On Sun, 03 Feb 2008 09:59:26 -0700, Diane Fagen <dianef84@...>
wrote:

> Hi Dale
>
> How are you?

Not so hot. I've had the winter inflammation set for a few months: lungs,
thyroid, heart, gut, and whatever else.

> Thank you for emailing me the information.  As far as your
> hypothesis, I agree with the link between MS and Crohn's.  I also think
> that
> Autism is linked also, as well as Fibromyalgia.
> My theory is that MAP attacks everyone in one way or another.  You know
> what
> I mean, every family has a predisposition to a particular illness.  I
> feel
> that Map is doing damage to the immune system and affecting people in
> different ways.  What do you think about my theory?

Assuming that the core problem is MAP and that MAP isn't secondary to
immune deficiency, I think it makes sense that the effect would be
dependent upon where the infection is located. There's clearly a genetic
component to MAP infection as can be seen when comparing the
susceptibility of cattle compared with the susceptibility of primates.
Cattle seem to be more susceptible because they swallow their food, pass
it down into the system where it picks up MAP that's already there, then
they regurgitate it to infect upper portions of the intestines. With
primates, the path is basically one-way tending to make them less
susceptible but they may live longer which could increase the risk. Even
between humans, we're not all as similar as doctors would like to believe.

Besides genetics, there are other factors which could affect both
susceptibility and the location of the infection. Our diets affect the
intestinal environment and the natural balance of intestinal flora which
competes with MAP. The more of a bacteria that we're exposed to, the more
likely we are to become infected.

About 65-90% of fibromyalgia cases are in women, so gender is clearly an
important factor as it is with many diseases. One study found that
fibromyalgia patients were significantly more likely to have: depression,
anxiety, headache, irritable bowel syndrome, Chronic Fatigue Syndrome,
systemic lupus erythematosus, and rheumatoid arthritis. Chronic Fatigue
Syndrome researchers have been unable to find a clear distinction between
CFS and fibromyalgia with the two conditions forming a continuum of
symptoms. When the healthcare profession can't identify an infectious
agent causing inflammation, they tend to assume that it must be autoimmune
even if the epidemiology is more suggestive of an infectious agent.

I haven't seen data on where fibromyalgia occurs. It would be interesting
to find out if it's more common in some locations than others.

Many years ago, a doctor at the University of Arizona gave me a skin prick
test using common antigens and the results suggested that I'm almost
completely immune deficient, but he said that I couldn't be that immune
deficient or I'd be having a lot of opportunistic infections. Since then,
other doctors have insisted that my chronic infections can't be
opportunistic because I'm not immune deficient. They order a CBC and look
at the white cell count. It's normal even when I have a serious infection,
which is abnormal, but because it's normal, they assume that my immune
system is intact. Clueless.

My immune system is down but I can't get tested for MAP because I'm not a
cow and no effort has been made to find out what's wrong with my immune
system. In my case, there are too many unknowns to determine what is
causing what else, but the observation that MAP prevents macrophages from
killing E. coli is consistent with the problems I'm having. We desperately
need some serious science for what appears to be an acquired immune
deficiency.

When I had pneumonia last winter, a doctor prescribed an extremely strong
and expensive antibiotic that didn't do a bit of good, I suspect because
it was the wrong antibiotic. This year, I haven't bothered going in
because it's a big waste of money. I have no choice but to see the
cardiologist for him to keep monitoring my blood thinner to prevent a
stroke caused by the heart failure. It's sad that he has no interest in
discovering the cause of the heart failure other than telling me that
atrial fibrillation has suddenly become epidemic which should be a clue.

-- Dale
<http://DaleRoose.com>
Moral relativism is saying that waterboarding may or may not be torture
relative to the circumstances.

Hi Dale

How are you?  Thank you for emailing me the information.  As far as your
hypothesis, I agree with the link between MS and Crohn's.  I also think that
Autism is linked also, as well as Fibromyalgia.
My theory is that MAP attacks everyone in one way or another.  You know what
I mean, every family has a predisposition to a particular illness.  I feel
that Map is doing damage to the immune system and affecting people in
different ways.  What do you think about my theory?  Diane Map-Canada
----- Original Message -----
From: "Dale" <dale@...>
To: <paratuberculosis@yahoogroups.com>
Sent: Tuesday, January 29, 2008 5:28 PM
Subject: [paratuberculosis] FWD: Interactive Teleconference on Inflammatory
Bowel Disease for Patients, Caregivers, and Healthcare Professionals


> -- Dale
> <http://DaleRoose.com>
> There are three kinds of doctors: those who cut; those who represent the
> pharmaceutical industry; and those who've retired. Stimulate the
> phagocytes!
>
>  - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - -
> - - - - - - - -
>
> <http://www.sunherald.com/447/story/332589.html>
>
> Interactive Teleconference on Inflammatory Bowel Disease for Patients,
> Caregivers, and Healthcare Professionals
>
> Educational teleconference on medical therapies to feature Mayo Clinic
> physician
> By Crohn's & Colitis Foundation
>
> NEW YORK, Jan. 29 -- Crohn's disease and ulcerative colitis patients,
> caregivers, and healthcare professionals can now register for
> "Inflammatory Bowel Disease: Why Should I Take My Medications?" This free,
> live, interactive teleconference through the Crohn's & Colitis Foundation
> will take place on Thursday, March 6, from 1:00 pm to 2:15 pm EST and will
> address effective treatment planning for patients with Crohn's and
> colitis. Collectively known as inflammatory bowel disease (IBD), these
> painful and unpredictable digestive diseases debilitate 1.4 million
> Americans. The teleconference will feature Mayo Clinic College of Medicine
> physician, Sunanda V. Kane, MD, MSPH, Associate Professor of Medicine.
>
> To register, call toll-free 1-877-547-5641 or visit www.rmei.com/ccfa.
> Registration is being handled by Robert Michael Educational Institute LLC.
>
> "Patients, caregivers, and professionals will benefit from the Crohn's &
> Colitis Foundation's upcoming teleconference," says Kimberly Frederick,
> Vice President of Patient & Professional Services for the Foundation. "Dr.
> Kane will offer exclusive insight into IBD gained from her experience
> caring for patients as a board-certified physician in internal
> medicine-gastroenterology at the Mayo Clinic College of Medicine, and
> there will be added time for questions and answers from the live telephone
> audience."
>
> In addition to an interactive question-and-answer session, participants
> will learn about various medical therapies used to treat IBD, key goals of
> treatment, the importance of taking medication as prescribed, and tools to
> help patients adhere to medical treatment plans.
>
> Continuing education credit is being offered for nurses through the
> co-sponsorship of Robert Michael Educational Institute LLC and
> Postgraduate Institute for Medicine.
>
> About the Crohn's & Colitis Foundation
>
> The Crohn's & Colitis Foundation's mission is to cure Crohn's disease and
> ulcerative colitis, and to improve the quality of life of children and
> adults affected by these diseases. The Foundation ranks third among
> leading health non-profits in the percentage of expense devoted to
> research toward a cure, and more than 83 cents of every dollar the
> Foundation spends goes to mission-critical programs. The Foundation
> consistently meets the standards of organizations that monitor charities,
> including the Better Business Bureau's Wise Giving Alliance (give.org) and
> the American Institute of Philanthropy (charitywatch.org). For more
> information, contact the Foundation at 800-932-2423 or visit www.ccfa.org
> .
>
> SOURCE Crohn's & Colitis Foundation
> Ariella Levine of Crohn's & Colitis Foundation of America,
> +1-646-943-7430, alevine@...; or Erin McCabe of Robert Michael
> Educational Institute LLC, +1-856-547-4141, ext. 226, emccabe@...,
> for Crohn's & Colitis Foundation,
>
>
>
> Yahoo! Groups Links
>
>
>

-- Dale
<http://DaleRoose.com>
There are three kinds of doctors: those who cut; those who represent the
pharmaceutical industry; and those who've retired. Stimulate the
phagocytes!

   - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - -
- - - - - - - -

<http://www.sunherald.com/447/story/332589.html>

Interactive Teleconference on Inflammatory Bowel Disease for Patients,
Caregivers, and Healthcare Professionals

Educational teleconference on medical therapies to feature Mayo Clinic
physician
By Crohn's & Colitis Foundation

NEW YORK, Jan. 29 -- Crohn's disease and ulcerative colitis patients,
caregivers, and healthcare professionals can now register for
"Inflammatory Bowel Disease: Why Should I Take My Medications?" This free,
live, interactive teleconference through the Crohn's & Colitis Foundation
will take place on Thursday, March 6, from 1:00 pm to 2:15 pm EST and will
address effective treatment planning for patients with Crohn's and
colitis. Collectively known as inflammatory bowel disease (IBD), these
painful and unpredictable digestive diseases debilitate 1.4 million
Americans. The teleconference will feature Mayo Clinic College of Medicine
physician, Sunanda V. Kane, MD, MSPH, Associate Professor of Medicine.

To register, call toll-free 1-877-547-5641 or visit www.rmei.com/ccfa.
Registration is being handled by Robert Michael Educational Institute LLC.

"Patients, caregivers, and professionals will benefit from the Crohn's &
Colitis Foundation's upcoming teleconference," says Kimberly Frederick,
Vice President of Patient & Professional Services for the Foundation. "Dr.
Kane will offer exclusive insight into IBD gained from her experience
caring for patients as a board-certified physician in internal
medicine-gastroenterology at the Mayo Clinic College of Medicine, and
there will be added time for questions and answers from the live telephone
audience."

In addition to an interactive question-and-answer session, participants
will learn about various medical therapies used to treat IBD, key goals of
treatment, the importance of taking medication as prescribed, and tools to
help patients adhere to medical treatment plans.

Continuing education credit is being offered for nurses through the
co-sponsorship of Robert Michael Educational Institute LLC and
Postgraduate Institute for Medicine.

About the Crohn's & Colitis Foundation

The Crohn's & Colitis Foundation's mission is to cure Crohn's disease and
ulcerative colitis, and to improve the quality of life of children and
adults affected by these diseases. The Foundation ranks third among
leading health non-profits in the percentage of expense devoted to
research toward a cure, and more than 83 cents of every dollar the
Foundation spends goes to mission-critical programs. The Foundation
consistently meets the standards of organizations that monitor charities,
including the Better Business Bureau's Wise Giving Alliance (give.org) and
the American Institute of Philanthropy (charitywatch.org). For more
information, contact the Foundation at 800-932-2423 or visit www.ccfa.org .

SOURCE Crohn's & Colitis Foundation
Ariella Levine of Crohn's & Colitis Foundation of America,
+1-646-943-7430, alevine@...; or Erin McCabe of Robert Michael
Educational Institute LLC, +1-856-547-4141, ext. 226, emccabe@...,
for Crohn's & Colitis Foundation,

Hypothesis: MAP and MS

Just a guess but suppose it's more than a coincidence that Tysabri helps
both MS (multiple sclerosis) and Crohn's.

With MS, the myelin sheathing around the nerves becomes damaged in an
inflammatory response generally assumed to be autoimmune. That sheathing
relies on the glial cells in the CNS. MAP has an affinity for glial cells.
See where I'm going with this?

A large study conducted by the U.S. military found that persons with
subclinical deficiencies of Vitamin D are significantly more likely to
develop MS. Vitamin D is absorbed in the ileum which is the primary site
of MAP infection and Crohn's damage. Crohn's disease can reduce absorption
in the ileum. See where I'm going with this?

Here's the hypothesis: MAP infection begins in the ileum and spreads to
other parts of the body. It inflames the ileum resulting in Vitamin D
deficiency. It infects glial cells in the CNS cutting off the supply lines
to the myelin sheathing resulting in deterioration to the myelin
sheathing. Depending on the site of predominant effect of the infection,
the patient gets Crohn's, MS, or a combination of both.

Although much has been discovered about MS, the cause remains unknown.
Both MS and Crohn's go through periods of remission and relapse. Both have
genetic predisposing factors.

The prevalence of both MS and Crohn's vary geographically. Both MS and
Crohn's are more common in northern latitudes. It might be interesting to
take a closer look at this and compare MS to milk consumption.

-- Dale
<http://DaleRoose.com>
If a small improvement in the DNA of cattle could give them the power of
speech, would that genetic modification be allowed?
--
Dale
<http://DaleRoose.com>
If a small improvement in the DNA of cattle could give them the power of
speech, would that genetic modification be allowed?

BACKGROUND (article follows), According to Wikipedia (wfiw):

"...Natalizumab [aka Tysabri] is the first alpha-4 antagonist in a new
class of agents called selective adhesion-molecule (SAM) inhibitors.
Alpha-4 integrin is required for leukocytes to migrate into the body's
organs such as the brain and gut; natalizumab prevents leukocytes from
doing that."

"...In these trials[1][2], natalizumab was shown to reduce relapses in MS
patients by 68% vs. a placebo, a margin far greater than had been seen for
other approved MS therapies."

"...Also in these trials natalizumab slowed the progression of disability
(as measured by EDSS) by approximately 50% [3] (the US and EU medical
authorities use slightly different measures of disability progression, and
use values of between 42% and 54%)."

"...In Crohn's, a randomized controlled trial found that natalizumab
increased the rate of remission."

"...Two further randomized controlled trials have confirmed natalizumab's
effectiveness in increasing the rate of remission and in maintaning
remission in Crohn's."

"...the annual costs for Tysabri is approximately US$28,400 (not including
costs associated with infusion services)..."

Tysabri had been withdrawn from the market after the occurance of a rare
brain disease in two patients taking the drug.

<http://en.wikipedia.org/wiki/Natalizumab>

-- Dale
<http://DaleRoose.com>
If a small improvement in the DNA of cattle could give them the power of
speech, would that genetic modification be allowed?
    - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - -
- - -
<http://www.boston.com/business/globe/articles/2008/01/15/biogen_idecs_ms_drug_o\
kd_for_crohns_disease/>

Biogen Idec's MS drug OK'd for Crohn's disease

But approval includes warnings on safety

By Todd Wallack
Globe Staff / January 15, 2008

Federal regulators yesterday gave Biogen Idec Inc. good news about one of
the Cambridge biotech company's key drugs.

Tysabri, a treatment for multiple sclerosis, won approval from the Food
and Drug Administration to be used against another debilitating illness,
Crohn's disease.

The move comes six months after an FDA advisory panel voted 12 to 3 to
recommend the drug's approval to treat some forms of Crohn's, a chronic
inflammatory disease of the intestinal tract. FDA officials said the final
decision was delayed because Biogen Idec and Elan Corp., the Irish company
that comarkets the drug, made changes to their application for a Crohn's
approval.

European regulators recently rejected a similar request to use the drug as
a Crohn's treatment, arguing the risk of infection outweighed the
relatively modest benefit of Tysabri.

Biogen Idec temporarily shelved the drug three years ago after it was
linked to a rare brain disease. The company says there have not been any
additional cases of the disease since sales resumed in 2006, with new
guidance on how it should be used. But some doctors remain wary of the
treatment, even though it has been shown to be highly effective in some
patients.

Despite the safety concerns, Biogen Idec has predicted Tysabri will
eventually become a major source of revenue. This month, the company
reaffirmed predictions it will be used by 100,000 patients by the end of
2010, up from more than 21,000 at the end of 2007.

Biogen Idec shares rose late in the day after the FDA news was released.
The shares finished up 96 cents to $59.98, a gain of 1.6 percent.

Doctors already had permission to use the drug to treat Crohn's disease on
their own, but Biogen Idec needed formal approval to start marketing the
drug for that purpose.

The FDA decision does carry some caveats. Specifically, the agency
approved the drug to treat patients with moderate to serious cases of the
disease who can't be treated effectively with other drugs, such as
steroids. The label will also carry safety warnings to reduce the risk
that patients will contract the brain disease or other infections.

About 500,000 people in the United States suffer from Crohn's, but it is
unclear how many of them will qualify to use Tysabri. The disease
frequently causes diarrhea and abdominal cramps; symptoms can also include
fever, bleeding, and weight loss. There is no cure.

Biogen Idec and Elan said they expect the drug to be available for Crohn's
patients by the end of February.
--
Dale
<http://DaleRoose.com>
If a small improvement in the DNA of cattle could give them the power of
speech, would that genetic modification be allowed?

<http://www.bio.com/newsfeatures/newsfeatures_research.jhtml;jsessionid=HKGZTZ2I\
UKRRXR3FQLMCFEWHUWBNSIV0?cid=32500001>
E. coli Bacteria Linked to Crohn's Disease

08/07/07 -- ITHACA, N.Y. -- A team of Cornell University scientists from
the College of Veterinary Medicine, Weill Cornell Medical College and the
College of Agriculture and Life Sciences have discovered that a novel
group of E. coli bacteria ? containing genes similar to those described in
uropathogenic and avian pathogenic E. coli and enteropathogenic bacteria
such as salmonella, cholera, bubonic plague ? is associated with
intestinal inflammation in patients with Crohn's disease in their research
paper published July 12 by "The ISME Journal: Multidisciplinary Journal of
Microbial Ecology."

Crohn's disease, an incurable inflammatory disorder of the intestine ?
most commonly found in the lower part of the small intestine called the
ileum ? affects 1-in-1,000 people in Europe and North America. Thus far,
gut bacteria have long been suspected in playing a pivotal role in the
development of Crohn's disease, but the specific bacterial characteristics
that drive the inflammatory response have remained elusive.

Researchers at Cornell examined possible causes for the disease in
patients with Crohn's restricted to the ileum and the colon versus healthy
individuals.

"Given that only about 20 percent of fecal bacteria can be cultured, our
group adopted a broad culture-independent approach to target specific
subgroups of bacteria for quantitative in situ analysis and culture based
characterization," said Kenneth Simpson, professor of small animal
medicine at the College of Veterinary Medicine. "Our findings raise the
possibility that a novel group of E. coli contains opportunistic pathogens
that may be causally related to chronic intestinal inflammation in
susceptible individuals. They suggest that an integrated approach that
considers an individual's mucosa-associated flora in addition to disease
phenotype and genotype may improve outcome."

The study found an increased level of E. coli bacteria in more inflamed
areas of the small intestines instead of MAP, a bacterium related to
tubercle bacillus that has been more commonly associated with Crohn's.

On Sat, 26 Jan 2008 20:18:14 -0700, Diane <dianef84@...> wrote:

> The study found an increased level of *E. coli bacteria in more
> inflamed areas of the small intestines instead of MAP, a bacterium
> related to tubercle bacillus that has been more commonly associated
> with Crohn's   Whole article on Bio,  Diane
> http://www.gate2biotech.com/e-coli-bacteria-linked-to-crohns-disease/

Hi Diane:

IMO, this article illustrates an important reason why paratuberculosis
should be considered separately from Crohn's disease. There's a very good
chance that a.) not all persons with Crohn's have paratuberculosis
infection, and b.) not all persons with paratuberculosis infection have
Crohn's. A similar problem exists with HIV and AIDS in which not all
people with HIV have AIDS and not all people with an acquired immune
deficiency have HIV.

MAP in the ileum might be engulfed by macrophages and brought into the
system then spread to the respiratory system or elsewhere. At some point
in the disease process, the most important site of infection might become
the lungs and the heart or the sinus cavities or the skin or other organ.
In this case, a diagnosis of Crohn's disease could be enitrely
innapporopriate.

The observations of these researchers that E. coli is associated with
Crohn's inflammation fits right in with the discovery that MAP releases a
molecule that prevents macrophages from killing E. coli.

The article says that the researchers used a "broad culture-independent
approach to target specific subgroups of bacteria" but that approach is
not explained clearly. Considering that MAP is extremely difficult to grow
in culture and far more difficult to isolate from the many other bacteria,
it's not surprising that a broad approach might be unable to find MAP. In
fact, MAP often doesn't culture even in ruminants like cattle where the
population is probably of the bacterium in any given sample may be much
higher. As far as I know, MAP's relative, Mycobacterium leprae which
causes Hanson's disease, still has not been grown in culture.

In comparing MAP and E. coli, I believe that while the primary site of
infection for MAP is the ileum and the primary location for Crohn's is the
ileum, the most common site for E. coli infetion is by far the urinary
tract. If E. coli where primary, one might expect that most of the
infection would be in the urinary tract rather than the ileum where Peyser
cells normally kill K. coli.

The authors raise the "possibility that a novel group of E. coli contains
opportunistic pathogens..." which would parallel the proposed theory that
E. coli is an opportunistic pathogen due to immune deficiency caused by
MAP.

Of course the fitting together of all these pieces of the puzzle could
just be a very unlikely coincidence.

-- Dale
<http://DaleRoose.com>
"Government should help the most those who need help least."
--U.S. Biparty Rules of Acquisition #1

E. coli Bacteria Linked to Crohn's Disease
A team of Cornell University scientists from the College of
Veterinary Medicine, Weill Cornell Medical College and the College
of Agriculture and Life Sciences have discovered that a novel group


Hi Dale, have you seen this article, tell me what do you think?

A team of Cornell University scientists from the College of
Veterinary Medicine, Weill Cornell Medical College and the College
of Agriculture and Life Sciences have discovered that a novel
groupof E. coli bacteria containing genes similar to those described
in uropathogenic and avian pathogenic E. coli and enteropathogenic
bacteria such as salmonella, cholera, bubonic plague is associated
with intestinal inflammation in patients with Crohn's disease in
their research paper published July 12 by "The ISME Journal:
Multidisciplinary Journal of Microbial Ecology."


The study found an increased level of *E. coli bacteria in more
inflamed areas of the small intestines instead of MAP, a bacterium
related to tubercle bacillus that has been more commonly associated
with Crohn's   Whole article on Bio,  Diane
http://www.gate2biotech.com/e-coli-bacteria-linked-to-crohns-disease/
















http://www.gate2biotech.com/e-coli-bacteria-linked-to-crohns-disease/



Did you enjoy this article? Link it!

A recent investigation found that paratuberculosis bacteria has a high
affinity for glial cells. Glial cells are necessary for building and
maintaining the blood brain barrier. The blood brain barrier is necessary
to prevent toxins and infectious organisms from attacking the central
nervous system.

It's reasonable to propose that:
Once paratuberculosis gets past the blood brain barrier, it infects and
damages the glial cells eventually resulting in a breakdown of the blood
brain barrier. With the blood brain barrier compromised, toxins can get
into the central nervous system resulting in chemical hypersensitivities
and chemical hyperreactivities. The breakdown of the blood brain barrier
will increase susceptibility to infections including more paratuberculosis
bacteria. Even though the infection may begin in a small spot, the
breakdown of the blood brain barrier combined with immune deficiency of
macrophages could allow the permeability to spread albeit slowly.

-- Dale
<http://DaleRoose.com>
"Government should help the most those who need help least."
--U.S. Biparty Rules of Acquisition #1

Some (most?) M.D.'s will say that a person can't have Crohn's if they
aren't underweight because Crohn's and paratuberculosis are usually
associated with weight loss. Here's my hypothesis and answer to this
objection:

Crohn's and Johne's are often referred to as "wasting diseases" because
they usually cause food to pass through the intestines so rapidly that it
doesn't get absorbed. However, the inflammation caused by paratuberculosis
can also cause intestinal blockage in the terminal ileum. The result can
be that food backs up into the upper intestines enhancing absorption of
most but not all substances. Vitamins B-12 and D are absorbed primarily in
the terminal ileum where food still passes quickly causing deficiencies of
these vitamins.

Since these vitamins are necessary in the mitochondria to phosphorylate
ADP into ATP which is the source of energy for cells, deficiencies can
drastically lower metabolism even though absorption of fats and simple
carbohydrates is enhanced. The result would logically be weight gain. It's
well established that some cattle even in the later stages of Johne's
disease have chronic diarrhea without weight loss and Crohn's disease can
cause morbid obesity.

-- Dale
<http://DaleRoose.com>

I have just started advertising this group on Crohn's Messageboards.
Should bring some traffic.  Thanks again. Sleep Well Diane

From cattlenetwork
<http://www.cattlenetwork.com/content.asp?contentid=192272>

Questions & Answers About Johne's Disease In Cattle

Q. What is Johne's disease and what animals get Johne's disease?
A. Johne's (pronounced "Yo-nees") disease is an infectious bacterial
disease primarily affecting the intestinal tract. Johne’s disease should
be considered a herd problem as well as an individual animal problem.

Animals most commonly affected are cattle, sheep, and goats. Johne’s
disease has been reported in several species of wild ruminants, both
captive and free–ranging. In addition, a few reports of isolated cases in
nonruminants, including nonhuman primates, have occurred, but none of
these species are believed to be sources for Johne’s disease in cattle.
Some recent reports claimed to have cultured the microbe from, or detected
its genetic components in, humans. However, the significance of these
findings in humans as they relate to any human disease has yet to be
determined.

Q. What causes Johne’s disease?
A. Johne’s disease is caused by a bacterium named Mycobacterium
paratuberculosis. It is a distant relative of the bacterium Mycobacterium
bovis that causes tuberculosis (TB) in humans and animals, but does not
cause TB.

The bacteria grow and multiply inside the immune cells of an animal. When
the microbe is excreted in the feces, it can contaminate the soil or
water. Outside the animal, the organism does not multiply well, if at all,
but it can survive over a year in the environment because of its
resistance to heat, cold, and drying. Therefore, the primary source of
infection is directly from infected animals.

Q. What are the signs of disease?
A. Because of the slow, progressive nature of the infection, signs of
Johne’s disease may not be seen until years after initial infection.
Cattle may be infected for years before they show any signs of disease.
When they finally do occur, the signs of Johne’s disease are long-lasting
diarrhea and weight loss despite a good appetite. Affected cattle do not
generally have a fever. Some infected animals appear malnourished and
often weak while others just have chronic diarrhea. The signs of this
disease can easily be confused with several other diseases. In the
infected cow or heifer, noticeable signs commonly start within a few weeks
after a stressful event like calving.

Q. What causes the signs of disease?
A. The bacteria are taken up by specialized cells in the small intestine
called the ileum where nutrients are absorbed from the feed. As the body
tries to rid itself of these bacteria, the immune response causes a
thickening of the intestinal lining, preventing it from functioning
normally. This leads to poor absorption of nutrients and eventual
diarrhea. As a result, although animals may be feeling and eating well,
they begin to lose weight gradually.

Q. How can I tell if my herd is infected?
A. Some animals may be infected, appear normal, and be culled before they
show any clinical signs. Some owners may never realize their herd is
infected. One hint in these herds could be that herd production is going
down or is not as high as it should be, especially in 3- to- 6-year-old
cows. In attempting to find the cause of low herd production, owners
should test several ill-appearing animals for Johne’s disease. In other
herds, owners who may see one or more cows with diarrhea or weight loss
should consider Johne’s disease as a possible cause.

Q. How can some cattle be infected with Johne’s disease, yet not show
signs?
A. Infectious diseases, including Johne’s disease, typically pass through
four stages. Stage I is the initial infection. The animal is infected, not
showing signs of disease and may be shedding small numbers of microbes
into the environment that are not detectable by diagnostic tests. In Stage
II, the infection is progressing and the animal still does not show any
clinical signs. Nevertheless, the organism is being excreted in very high
numbers, probably enough to infect others nearby. Infection is detectable
by fecal culture techniques but not often by blood tests. In Stage III,
the animal is showing the early signs of disease and many types of
diagnostic tests can detect the infection. Stage IV is the obvious
clinical disease and readily recognized by the trained observer and
detected by diagnostic tests. It may take 2-6 or more years for Johne’s
disease to progress through all of these stages.

In some herds with Johne’s disease, animals in all four stages of disease
exist. For each animal showing obvious signs of Johne’s disease (Stage
IV), 5 to 15 other animals at various stages of infection are not showing
signs.

Q. What are common sources of Johne’s disease?
A. The most common source of infection is feces or manure. While protected
in fresh manure, the organism can remain alive in the environment for over
a year, depending on conditions. Ingestion of manure containing the
microbe is the most common way animals become infected.

Johne’s disease typically enters a herd as an infected, but
healthy-looking, animal in Stage I. As the disease progresses in that
animal, the frequency and number of bacteria being excreted increase.
Every day, billions of Johne’s microbes may be excreted from an animal in
Stage III or IV of the disease.

Another source of infection is milk from infected dams. The likelihood of
Johne’s bacteria being excreted in milk of infected females increases as
the disease progresses. Studies suggest that 36 percent of Stage III and
IV cows could have Johne’s microbes in their colostrum. In beef herds,
where calves remain with their mothers and nurse daily, the chance for
transmission of the infection through colostrum and milk is high. These
bacteria may be excreted directly through the mother's milk or it might be
present on the outside the teats in contaminated feces.

Prenatal exposure may be a source of infection for calves. Becoming
infected before birth is possible for a fetus, if its mother is in the
late stages of disease. Studies have shown that, in disease Stages III and
IV in the dam, 8 to 40 percent of fetuses were infected from their mothers
while still in the womb. Risk for infection of the fetus is low from
mothers in disease Stages I and II.

Pond water contaminated with infected feces is another potential source of
infection. Other possible, but less likely infection sources, are pastures
contaminated with infected feces.

Q. Can humans get Johne’s disease?
A. So far, no epidemiological studies have been published that examine any
connection between contact with animals with Johne’s disease and humans
who develop Crohn's Disease, a human illness that in some ways, resembles
Johne’s disease.

Q. Where can I obtain more information on Johne’s disease?
A. For more information on Johne’s disease, contact:

Dr. Michael Carter
USDA-APHIS-VS
Center for Animal Health Programs4700 River Road
Riverdale, MD 20737
Phone: (301) 734-4194
or visit the APHIS Web site at www.aphis.usda.gov.

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Source: http://www.johnesdisease.org/about/AboutJohnes.htm