The obvious take home is to shift
your diet away from milk fat in particular to start with and see if it does any
good. This requires a lot of care in terms
of processed food but we knew that anyway.
It is just not obvious which processed food contains milk fat and it has
never been much of an issue.
I suspect that this clue will lead to other strong
suggestions. I would try a vegan diet
without any milk products or fat to see if the condition itself can be allowed
to heal and perhaps to settle down. If
that actually does happen, then I would try out low levels of the problem products
to see if tolerance is possible. It is
not perfect but a protocol of moderate usage does give one ample flexibility.
It is also a warning to all of us that excessive use of
some of our favorites such as ice cream could plausibly bite back more than one
anticipates. The rule has always been
moderation but as we learned in the wheat business, the core product may be
simply too much part of processed foods to easily avoid.
I am becoming progressively less enamored with process
foods in general and have always tried to minimize their availability in my
food solutions anyway. We all need to be
at least as touchy on the subject. My favorite
rule is one portion per month at best to prove I am not a fanatic.
Western Diet
Changes Gut Bacteria and Triggers Colitis in Those at Risk
Newswise
— Certain saturated fats that are common in the modern Western diet can
initiate a chain of events leading to complex immune disorders such as
inflammatory bowel diseases (IBD) in people with a genetic predisposition,
according to a study to be published early online in the journal Nature.
The
finding helps explain why once-rare immune-mediated diseases have become more
common in westernized societies in the last half century. It also provides
insights into why many individuals who are genetically prone to these diseases
are never affected and how certain environmental factors can produce
inflammation in individuals already at risk.
Researchers
at the University
of Chicago found that
concentrated milk fats, which are abundant in processed and confectionary foods,
alter the composition of bacteria in the intestines. These changes can
disrupt the delicate truce between the immune system and the complex but
largely beneficial mix of bacteria in the intestines. The emergence of harmful
bacterial strains in this setting can unleash an unregulated tissue-damaging
immune response that can be difficult to switch off.
“This
is the first plausible mechanism showing step-by-step how Western-style diets
contribute to the rapid and ongoing increase in the incidence of inflammatory
bowel disease,” said study
author Eugene B. Chang, MD, PhD, the Martin Boyer Professor of Medicine at the University of Chicago . “We know how certain genetic
differences can increase the risk for these diseases, but moving from elevated
risk to the development of disease seems to require a second event which may be
encountered because of our changing lifestyle.”
The researchers worked with a mouse model that has many of the characteristics of human IBD. Genetically deleting a molecule, interleukin 10, which acts as a brake on the immune system’s response to intestinal bacteria, caused about 20 percent of mice to develop colitis when fed a low-fat diet or a diet high in polyunsaturated fats. But when exposed to a diet high in saturated milk fats, the rate of disease development within six months tripled, increasing to more than 60 percent. In addition, the onset, severity and extent of colitis were much greater than that observed in mice fed low-fat diets.
Why
would milk fat — a powdered substance that remains when fat has been separated
from butter and dehydrated — trigger inflammation when polyunsaturated fat did
not? The researchers traced the answer to the gut microbiome, the complex mix
of hundreds of bacterial strains that reside in the bowels.
The
researchers found that an uncommon microbe called Bilophila wadsworthia was
preferentially selected in the presence of milk fat. Previous studies had found
high levels of B. wadsworthia in patients with appendicitis and other
intestinal inflammatory disorders, including inflammatory bowel disease.
“That
piqued our interest,” Chang said. “These pathobionts, which are usually
non-abundant, seem to be quite prominent in these diseases.”
Indeed,
while Bilophila wadsworthia levels were almost undetectable in mice on a
low-fat or unsaturated-fat diet, the bacteria made up about 6 percent of all
gut bacteria in mice fed a high milk-fat diet.
“Here
we show how the trend in consumption of Western-type diets by many societies
can potentially tip the mutualistic balance between host and microbe to a state
that favors the onset of disease,” Chang said.
As
its name implies, Bilophila wadsworthia has an affinity for bile, a substance
produced by the liver and released into the intestines to help break down
ingested fats. Milk fats are particularly difficult to digest and require the
liver to secrete a form of bile that is rich in sulfur. B. wadsworthia thrives
in the presence of sulfur. So when the bile created to dissolve milk fats
reaches the colon, it enables wadsworthia to blossom.
“Unfortunately,
these can be harmful bacteria,” Chang said. “Presented with a rich source of
sulfur, they bloom, and when they do, they are capable of activating the immune
system of genetically prone individuals.”
The
byproducts of B. wadsworthia’s interaction with bile also can amplify the
effect. They serve as “gut mucosal barrier breakers,” said Suzanne Devkota,
PhD, a member of Chang’s laboratory and first author of the study. “By
increasing the permeability of the bowel, they enhance immune-cell
infiltration, and that can induce tissue damage.”
Much
of the recent progress in understanding the biology of inflammatory bowel
disease has focused on gene variants that can increase risk, beginning with the
discovery in 2001 of Nod2 by researchers at the University of Chicago .
But the new study puts the focus on changing environmental factors that might
trigger the disease in high-risk patients.
“Right
now we can’t do much about correcting genes that predispose individuals to
increased risk for these diseases,” Chang said, “and while we could encourage
people to change their diets, this is seldom effective and always difficult.”
“However,
the balance between host and microbes can be altered back to a healthy state to
prevent or treat these diseases,” he added. “In essence, the gut microbiome can
be ‘re-shaped’ in sustainable and predictable ways that restore a healthy
relationship between host and microbes, without significantly affecting the
lifestyles of individuals who are genetically prone to these diseases. We are
testing that right now.”
The
National Institutes of Health, the Gastrointestinal Research Foundation, the
Crohn’s & Colitis Foundation of America, the Peter D. and Carol Goldman
Foundation, and the Leona M. and Harry B. Helmsley Charitable Trust supported
this research. Additional authors include Yunwei Wang, Mark Musch, Vanessa
Leone, Hannah Fehlner-Peach, Anuradha Nadimpalli and Bana Jabri from the
University of Chicago, and Dionysios Antonopoulos from the Institute for
Genomics and Systems Biology at Argonne National Laboratory.
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