|
Other articles of interest
Fighting E. coli the old-fashioned way,
Op-ed,
San Francisco Chronicle
Are
daily dietary fibre recommendations too low? an evolutionary
perspective.
Network
Health Dietitians Magazine
May, 2008 (go to page 12).
E.
coli and the future health of America, The
Packer Op-ed, (produce industry newspaper) (July 2007).
|
A
version of this article
appeared as an Op-ed in the
Gut
Check
By
Jeff
D Leach
The ongoing
outbreak of Salmonella Saintpaul has drawn outcry from media,
predictable knee-jerk proposals from lawmakers, and understandable fear
and confusion among consumers. As with outbreaks in the past, the Food
and Drug Administration (FDA), Centers for Disease Control and
Prevention (CDC), and processing plants and farmers continue to take the
blame for tainted food making us ill. But is our All-American sick gut
deserving of some blame as well?
While our
attention is focused on farm-to-table food safety and disease
surveillance once we have gotten sick, the biological question of
why we got sick is all but ignored.
Most experts
working within what might be called the U.S. Food Safety System, that
includes the efforts of some 15,000 people from 15 federal agencies,
would readily acknowledge the complexity of detecting the admittedly
small numbers of pathogenic bacteria and viruses in the 350 billion
pounds of food in a farm-to-table chain that often spans multiple time
zones and countries, as an insensitive prevention strategy at best.
Likewise, once
an outbreak has been detected, sourcing the offending pathogen can prove
difficult, as the ongoing Salmonella Saintpaul outbreak demonstrates
even when a genetic match is made. While good farming practices,
sampling and testing for detection, and the secondary prevention of
tracking down the bad bug once an outbreak has been recognized are
critical to a safe food supply, understanding why a person succumbs to
what is often a very small number of initial organisms may be a relevant
question and an additional strategy in reducing human suffering from
foodborne pathogens.
By adding the
biological question of why an individuals natural defenses failed
to the intellectual concepts of testing, detection, and
surveillance, we correctly insert personal responsibility into our
national strategy and more importantly, draw attention to the much
larger public health crisis, of which illness from foodborne pathogens
is only a symptom: our sick, leaky guts.
The CDC
warns “The elderly, infants, and those with
impaired immune systems are more likely to have a severe illness”
associated with tainted food (and water). By “impaired” the CDC is
saying that within the complex network of specialized cells and organs
that work together to defend against attacks from foreign invaders like
Salmonella, something has gone wrong, increasing risk of getting sick –
or worse.
A critical component to a properly
functioning immune system is a healthy, and balanced population of
bacteria. With names like bifidobacterium and lactobacillus, these and
other natural inhabitants of the human gut make it their evolutionary
job to fight invaders by competing for nutrients (which the invader
needs to survive), compete for attachment sites on our intestinal walls
(which the invader must do to cause harm), production of organic acids
(that the invader does not like), and changing of pH of intestinal
ecosystem (which the pathogen does not like either, but fast learning
how to adapt). The things that are
This germ-on-germ warfare is literally
fought daily in the American gut. When the good guys lose, we know this
as diarrhea, fever, and abdominal cramps – or worse. We have all
experienced or witnessed these lost battles at varying levels from being
restricted to the house, visits to the emergency room, or in some
extreme cases, the morgue. While this germ warfare has raged in the
human gut as long as humans have been around, the rules of the battle
are changing as humanity has started a large-scale experiment by
shifting to a highly processed diet that has changed the nutrient supply
that our friendly microbes evolved to depend upon.
The irony of the public running from
vegetables and fruits that have been suspected in an outbreak, is that
these foods contain essential nutrients (dietary fiber) that our gut
bugs need to fight the good fight. Our change in diet, coupled with
uncontrolled use of antibiotics, may be adversely altering our organic
relationship with our most important weapon against foodborne pathogens.
The disruption and increased gut
infections caused by pathogens is possibly having an irreversible impact
on our entire gastrointestinal system. Like a siege of cannon fire on
the walls of a fortress, the walls (barrier) begin to crumble (impaired)
and become prone to invasion. Mounting evidence suggests acute and
chronic infection by pathogens damage the delicate mucosal barrier that
separates trillions of bacteria in our intestinal system from the
sterile environment of our blood. As the steady flow of lost battles
accumulate, the barrier and our immune system as whole become impaired,
resulting in inflammation and movement of pathogens (and endotoxins)
into our sterile blood. An impaired and leaky gut barrier plays an
important role in a range of maladies such as irritable bowel disease,
some cancers, sepsis, organ failure, heart disease and a cascade of
other metabolic disorders.
By inserting personal responsibility and
some basics of host-pathogen germ warfare into the multi stakeholder
strategy for addressing foodborne threats, we may start to realize that
we may not simply be experiencing a mathematical rise in foodborne
illness as a result of sloppy farming and poor government oversight, but
rather a tectonic-like shift in our nutritional landscape that has
opened the pathogens door just enough for us to glimpse the future of
human suffering. Just the thought makes my gut ache.
Comments
welcome jeff@paleobioticslab.com
Further
Reading
Bouhnik,
Y., L. Raskine, et al. (2004). "The capacity of nondigestible
carbohydrates to stimulate fecal bifidobacteria in healthy humans: a
double-blind, randomized, placebo-controlled, parallel-group,
dose-response relation study." Am J Clin Nutr 80(6):
1658-1664.
Cani,
PD, A. M. Neyrinck, F. Fava, C. Knauf, R. G. Burcelin, K. M. Tuohy,
G. R. Gibson and N. M. Delzenne
(2007) Selective increases of bifidobacteria in gut microflora
improve high-fat-diet-induced diabetes in mice through a mechanism
associated with endotoxaemia. Diabetologia, Volume 50,
Number 11 / November
Garcia-Lafuente,
A., M. Antolin, et al. (2001). "Modulation of colonic barrier
function by the composition of the commensal flora in the rat." Gut
48(4): 503-507.
Guarner,
Francisco (2005). Inulin and oligofructose: impact on intestinal diseases
and disorders. British Journal of Nutrition, 93,
pp S61-S65
Huerta,
M. G. and J. L. Nadler (2002). "Role of inflammatory pathways in the
development and cardiovascular complications of type 2 diabetes." Curr
Diab Rep 2: 396 - 402.
Kennedy,
R. J., S. J. Kirk, et al. (2002). "Mucosal barrier function and the
commensal flora." Gut 50(3): 441-442.
Kleessen,
Brigitta and Michael Blaut (2005). Modulation of gut mucosal
biofilms. British Journal of Nutrition, 93, pp
S35-S40
MacFie,
J., C. O'Boyle, et al. (1999). "Gut origin of sepsis: a prospective
study investigating associations between bacterial translocation, gastric
microflora, and septic morbidity." Gut 45(2): 223-228.
MacFie,
J. (2004). "Current status of bacterial translocation as a cause of
surgical sepsis." Br Med Bull 71(1): 1-11.
Soriani,
M., I. Santi, et al. (2006). "Group B Streptococcus Crosses Human
Epithelial Cells by a Paracellular Route." The Journal of
Infectious Diseases 193(2): 241-250.
Spiller,
R. C., D. Jenkins, et al. (2000). "Increased rectal mucosal
enteroendocrine cells, T lymphocytes, and increased gut permeability
following acute Campylobacter enteritis and in post-dysenteric irritable
bowel syndrome." Gut 47(6): 804-811.
Zareie,
M., K. Johnson-Henry, et al. (2006). "Probiotics prevent bacterial
translocation and improve intestinal barrier function in rats following
chronic psychological stress." Gut 55(11): 1553-1560.
|
