Eating Local

Yesterday, the hottest day of the year (94.1°F) we canned peaches. We were out doing grocery shopping yesterday and stopped by Smith Orchard’s stand on the top of nearby Cooper Mountain and we picked up a bushel of canning peaches. We put a serious dent in this half-bushel:

We went sugarless this year, just 1/2 teaspoon white vinegar (to help retain color) plus 3-4 whole cloves (for a bit of pep — plus we have a large jar of them!) per quart. After 3 hours of dunking in hot water, peeling, quartering, and tight-packing to squeeze up a bit of juice), we had these seven quarts:

We pressured-canned them for the recommended 10 minutes at 6 pounds (much quicker than the 25 minutes at 11 pounds needed for tomatoes). They took all night to cool off; here they are in this morning’s early light:

We’ll do another 7 quarts in a couple of days; the second half-bushel is not quite ripe.

And today’s main meal this afternoon was steak salad: local greens (endive), a local tomato (marinated with home-grown garlic and commercial basalmic viegar) commercial blue cheese, and — the star — leftover local, pasture-raised, dry-aged steak (grilled rare earlier this week):


And, I’ll close with an image from a favorite tee shirt:

Pool Noodles for Head Safety! (However…)

One consequence of our having poured a concrete floor in our old basement is that the old, rusty I-beam (that was added at some point to help stabilize the bounciness of the upstairs floor) is now 5′ 9″ off the floor. I am taller than that. So I had this idea to buy pool noodles, cut a slit lengthwise, and, voilà! Head safety.


When I first bought the noodles at the local Family Dollar, I only bought enough for the main basement. When I went back to get some for the smaller cellar, they were sold out. Not to worry, I went to the Dollar General a minute away on the edge of town. They had them. And now, a PSA for those of you in the market for dollar store pool noodles: Family Dollar pool noodles are superior to Dollar General pool noodles in every possible way: they are thicker, denser, longer, and made in the USA (DG’s are from Canada). Same price, of course: $1.

On a less lighthearted note, it turns out that head safety was the least of my worries. (In the journalism business they call this burying the lede.) Yesterday, while using my table saw to cut pieces for our addition ramp guardrail, my hand slipped and the tip of my thumb grazed the blade. In over 35 years of woodworking this was my first trip to the ER. I will spare you the gruesome details, suffice it to say that my left thumb is now a wee bit shorter and sans thumbnail. It took two hours and nine stitches. The pharmaceuticals are doing their job so it does not feel too bad at the moment. The official diagnosis, on the other hand, sounds rather dire:
2017 ICD-10-CM Diagnosis Code S68.022A
Mr. Google tells me that this is diagnosis code S68.022A in the current, and quite comprehensive, ICD-10.

H5N1 Flu Pandemic Watch

Note: if you are new to H5N1 flu info you may want to start at the Background section below.

July 14th 2008 Update

A new article in Nature, The Long War Against Flu, is a very worthwhile read.

“That the H5N1 strain of bird flu has not yet caused a pandemic is no cause for complacency. Preparations for the inevitable must be redoubled to mitigate the potential devastation.”

We suggest that you give the whole thing a read (it’s not very long).

May 25th 2006 Update

Over the past year, there have been sporadic cases of human H5H1 influenza in many places throughout Europe, Africa, and Asia. One country that has had many flu-watchers perpetually on edge is Indonesia — it is often described as a simmering pot that might boil over at any time. Over the past month, there has been the largest cluster of human H5N1 infection to date: 8 people, only 1 of whom has survived. There is evidence that this time the virus has been transmitted human-to-human-to-human. Unfortunately, the WHO seems to be putting politics above science and is continuing to keep the virus sequences private, while making vague public statements about how the virus does not show “significant” mutations. Many of us would like to have the sequences available for other scientists to examine before we can take any comfort in the WHO’s comments.

H5N1 may never become a human pandemic. But there is every chance that it will. We continue to urge you to review our Resources section below and formulate your own personal, family, and community preparedness plans.

January 13th 2006 Update

In the past several weeks human H5N1 flu infections have been popping up all over Turkey. The symptoms include bleeding in the throat. The is much discussion as to whether this flu is being transmitted bird-to-human (B2H) or human-to-human (H2H). Part of that answer lies in the genetic sequences in the H5N1 strain. The Effect Measure blog had a nice summary today; here are the good bits:

The news dribbling out about the sequencing of the Turkish isolates is not encouraging but also not surprising. As I noted several days ago, the proposition that the hemagglutinin protein of the isolates is “very close” to the avian sequences is not very informative because extremely small changes can cause important changes in host range, as studies by Stevens et al. on the 1918 HA show. That paper described studies with glycan arrays (see previous post) that looked at the binding of various viral HAs to various linkages of sialic acid, the cellular receptor. Sialic acid is linked in two forms, one characteristic of bird intestinal cells, one characteristic of human lower respiratory tract cells, although we now know that humans have avian-type linkages in sialic acid in their upper respiratory tract. Most avian viruses bind well to the avian receptor, human viruses to the human linked receptor, but the HA protein from a case from New York’s second wave in the 1918 pandemic showed some affinity for both humans and birds.

I haven’t seen the sequences for the Turkish cases, but news reports suggest this kind of adaptation to humans is what is being seen in some of the Turkish isolates.


The sequencing also shows that there are many genetic variants out there, sometimes infecting the same individual. Again, this is to be expected. This virus replicates into billions of copies in an infected person and it is lack of fidelity in this replication which is one source of the genetic variation upon which selective pressures act.

This mutation has been seen before in isolates from Hong Kong in 2003 and Vietnam in 2005 (Branswell, CTV). The Turkish sequences also bear similarity to the Chinese Qinghai viruses responsible for a mass kill of migratory birds there. For some technical details, see post by Henry Niman of Recombinomics which he has kindly reprinted in the comments of a recent post here. Many experts believe Turkey’s location along north-south bird flyways has made it especially prone to infection of its poultry stock. Opponents of this notion point to the lack of documented outbreaks at intermediate points along the flyways. However we neither know the pattern of viral shedding along flyways nor can we be sure that outbreaks have not occurred undetected in many of the remote areas concerned.

There is some good news in the sequencing. Apparently the virus is sensitive to both classes of antivirals (amantadine/rimantadine and oseltamivir (Tamiflu)/zanamivir (Relenza). (Branswell, CTV). But all in all, the Turkish picture is one of continued progression geographically and genetically. It is not time to panic, because it is never time to panic. But making appropriate preparations in your area might be prudent.

October 9th 2005 Update

The Effect Measure blog had a nice summary today, so we reproduce it here:

Pandemic Flu Awareness Week officially ends today. We’d like to say we planned the timing of all this, but in fact it was conceived over a month ago by the three blogger partners-in-crime who started the Flu Wiki (DemFromCT of The Next Hurrah, Melanie Mattson of Just a Bump in the Beltway and The Reveres of Effect Measure. Then there was still little MSM attention to bird flu. Obviously this has all changed (late, but better late than never). The new attention has had the added effect of bringing many people to The Flu Wiki, which now averages almost 3000 visits a day.

So where are we? DemFromCT has an excellent wrap up of This Week in Bird Flu at DailyKos. Here’s my overall take on it from the perspective of a practicing epidemiologist with 40 years in medicine and public health. I’ll try to make it as succinct as I can (no easy task for me, as you know).

* The threat of a serious influenza pandemic with a large global and national death toll globally is real, but of uncertain magnitude and timing.

* Even in the worst plausible case, we’re not all going to die if it happens. Not even most of us will die. Probably the majority of people (but possibly a bare majority) will be unaffected or affected little by the virus. But very many people will get quite sick and many of them will experience a protracted period of recovery lasting weeks or longer. A significant number will die in a relatively short period of time. This happens in any influenza outbreak but will be much worse if a pandemic strain emerges.

* Because of an anticipated high rate of absenteeism (perhaps 30% or more), many things we take on faith as “just working” won’t work as well or at all. For example, if there is a major snow storm and power is lost to a wide area, it may make take considerably longer to restore if the trucks haven’t been maintained, the number of linemen is much reduced, the roads aren’t cleared and the inventory of repair supplies is interrupted by transportation failures. The reductions in each sector can add to each other and cause a much larger effect than would be anticipated from any one separately.

Or not. As difficult as many of these issues are, they can be substantially ameliorated by advance planning.

For example, pharmacies and supermarkets typically use “just in time inventory” systems, meaning they have in stock only a quantity sufficient for short term demandThey depend on frequent deliveries to keep supplies current. If deliveries are interrupted, as they were in Katrina, many people who depend on life sustaining medicines like insulin or blood pressure medication will be in trouble. The just-in-time system is now a deeply ingrained practice and can’t be reversed. But interrupted supplies are not very important for most of what pharmacies carry. Who cares if the deodorant or the viagra doesn’t come in? What we need is a short list of half a dozen or a dozen high-use critical medications (insulin, blood pressure meds, some antibiotics, etc.) and an emergency source that pharmacies, hospitals and patients can access. This is a task for state and local health authorities. The National Guard can be used for transportation and logistics and community centers or other facilities used as access points. The same can be done with food staples. You won’t still have your Cheezits. But you will have milk. I’m not going to spell it all out here, because you get the idea. All it takes is some forethought and planning.

Which hasn’t been done, for the most part. This is a problem of community mobilization. Leadership is needed, so if your “leaders” are missing in action, step up and lead yourself. If we sit down rationally and calmly BEFORE [it] hits the fan we will be able to get through it rationally and calmly. It will still be painful, but less painful and more easily endured. Share what you know and what you learn with others. The Flu Wiki is designed for that.

Background (August 2005)

An extraordinary event is happening right now in Southeast Asia
that has the potential to affect humanity in ways thought banished
years ago. Scientists are closely monitoring what looks like the
birth of a super strain of one of man’s oldest and most persistent
nemesis, the influenza virus. This new strain has the potential to
kill hundreds of millions given the right conditions. According to
the World Health Organization and the US Centers for Disease Control
and Prevention, the required conditions are now in place. We stand on
the verge of a once in a 100-year influenza pandemic that is an event
quite different from our routine seasonal flu. Pandemic flu spreads
like wildfire through the human race leaving death, chaos, and civil
disorder in its wake.

It is certain that we will have
another influenza pandemic, and probably soon. What is not known is
whether the pandemic will be of the major variety resembling the 1918
flu, or a minor one more like the 1958 flu pandemic. My advice is to
prepare for the worst and hope for the best.

The above quote is from a monograph written recently by
Grattan Woodson, MD, FACP, a doctor in Decatur, Georgia, USA. His
motivation? “I wrote it both to inform [my patients] about this
health threat and to provide them with some practical guidance on how
they can survive the pandemic.” This paper is the single best
resource we have found on this subject. If you only read one
thing about the coming flu pandemic make it this
. (Download
available below in the Resources section

We have been
following the news of H5N1 avian flu in Asia since January, and have come to the conclusion that there
is a good chance that H5N1 will blow up into a full-fledged
world-wide pandemic. Soon. As in winter 2005/6, perhaps. We are not alone
in this thought. I won’t go into all the details here since you can
delve into the sites listed in the Resources
section below if you care to, but I do breifly outline why we are concerned below.

It may be that this pandemic will be a
minor one such as 1958’s Asian Flu Pandemic, just a worse-than-usual
flu season.
It may be that it won’t happen this season and that
governments around the world will realize what they should be doing
to prepare and spend the next year doing it. But it may well be that
this will be major pandemic event like the 1918 Spanish Flu.

The 1918 Spanish Flu came on very fast and was quite deadly. Fast,
as in weeks from first case to everywhere. Many, many people were
very sick, many people died. The next flu pandemic could easily be as
bad, or even worse. A much greater percentage of the world’s
population now live in urban areas where a virus can spread quickly, and
there are lots more people everywhere now than in 1918.

Our much-improved medical
technology really can’t help us with a pandemic flu virus. There are
not nearly enough hospital beds for so many ill patients; flu often kills
with respiratory symptoms, including secondary infections
such as pneumonia, that would require being on a ventilator in a
hospital. There are only a handful of antiviral medications available
and they appear to have limited effectiveness
on H5N1. Our flu vaccine is still produced using 1940’s technology:
virus is killed (and perhaps genetically modified to make is less
virulent) and the virus is inoculated into
fertile chicken eggs; the whole process
takes at least 6 months; H5N1 is evolving very rapidly and there are
several fairly different strains on loose in Asia. In the last few
months there have been some attempts by governments to provide
incentives for drug companies to increase their manufacturing
capacity and to develop new vaccine technologies, but the fruition of
these efforts is years away. We likely do not have years.

Our best hope, therefore, is for each of us to inform and
prepare ourselves as best we can. Fortunately, the internet
is allowing many scientists and knowledgeable
laypersons (and, yes, some wacko nut jobs,
too!) to share and pool their knowledge of what is happening with
H5N1 right now in the world. We urge you to take the time now
to peruse the resources below and perhaps begin to form your own
family preparedness plan. We all will be taking our
chances with H5N1 flu, but, as Louis Pasteur pointed out: Chance
Favors the Prepared Mind.

Reasons For Our Concern

  • Statistically, we are due for a flu pandemic
  • The last three pandemic human flu virii had avian flu components
  • Avain flu type H5N1 is presently endemic in much of Asia
  • Over 150 million chickens and ducks have died or been culled (killed) worldwide due to H5N1
  • Humans have no natural immunity to H5N1
  • H5N1 since late 2004 has definitely infected and killed humans in Vietnam, Cambodia, Thailand, Indonesia, and more
  • H5N1 in 2005 has most likely infected and killed humans in China (unconfirmed reports imply China may even have “culled” several villages)
  • A few months ago over 6,000 migratory birds of 5 species were killed by H5N1 at Quinghai Lake in China
  • Quinghai lake is at the crossroads of several major migratory bird flyways
  • All 12 of the sequenced Quinghai Lake H5N1 virii had a mutation (PB2 E627K) rarely found in bird flu but always found in mamallian flu
  • The genetic sequencing that has been done on H5N1 shows that it is rapidly changing
  • There were two distinct strains of human H5N1 in Vietnam, one much more deadly that the other
  • The migrating birds have been spreading H5N1 bird deaths all over asia, europe, and the middle east

Should H5N1 hit a magic combination of genetic material the renders it easily transmitted human to human, there will be no stopping it.


the link above and Save As to download this 635K PDF file. It is a
27-page monograph written by a doctor in Georgia USA for his
patients. This new version replaces the first one Dr. Woodson wrote in the summer — “The content is virtually the same except I have removed some of the older tables and written a new portion addressing the containment of the spread of infection within the household.” The first few sections deal with topics related to the
influenza virus, with special attention on the 1918 Spanish Flu,
which was the last major pandemic. What happened then is the best
source of information on what could happen now. Given the predictable
effect a major pandemic will have on society and essential services,
several prudent suggestions are provided for you to consider taking
before the pandemic sets in. Sections include: “Practical
Pre-Pandemic Preparations for Individuals”, “Symptoms of
Influenza”, “Supportive Treatment of Influenza”, and
“Advanced Home Treatment Considerations for Health
Professionals”. If you only read one thing about the
coming flu pandemic please make it this

Henry Niman is virologist with a particular interest in how virus
evolve via recombination, which is the swapping of genetic
information within specific genes. (Viruses also evolve using a
method known as reassortment, which is the
swapping of genetic information between genes from different viruses.
This occurs when an animal is “dual infected” with two or
more viruses at the same time.) Niman posts his views on the news at
in his “What’s New” section. He generally posts several
times a day and is not shy in expressing his opinion (which is, BTW,
that H5N1 entered the final Pandemic Phase 6, increased and sustained
transmission in general population, back in June — the problem
remains the lack of confirmation of human cases in China and
inadequate information about cases in Vietnam.)

The are several good blogs that cover
the flu news: Avian
Flu – What we need to know
, Crofsblogs’
, and The
Coming Influenza Pandemic?
are ones we visit often.

In addition to the blogs, there are also discussion forums in
which folks share their views, fears, and questions about the coming
pandemic. CurEvents
is a good one with an active Flu Clinic. There are several “sticky”
threads at the top where you can find some folks’ preparation lists as
well as the infamous and utterly amazing, long, detailed, thought-provoking, and downright
frightening H5N1:
My Town – A Projected Epidemic
by CanadaSue.

Another good forum is the SARS, Bird Flu and Other Contagious Diseases board at Dr. Niman posts here frequently.

A good evolving resource is the Flu Wiki
The purpose of the Flu Wiki is to help local communities prepare for
and perhaps cope with a possible influenza pandemic. This is a task
previously ceded to local, state and national governmental public
health agencies. No one, in any health department or government
agency, knows all the things needed to cope with an influenza
pandemic. But it is likely someone knows something about some aspect
of each of them and if we can pool and share our knowledge we can
advance preparation for and the ability to cope with events. For
those unfamiliar with this topic, or just getting started, the amount
of material presented (and the site itself) may seem daunting. Click
on “Where To Start” and heed to advice therein.

is a forum for progressive public health discussion and
argument as well as a source of public health information from around
the web that interests the Editor(s), which includes H5N1. The
Editors of Effect Measure are senior public health scientists and
practitioners. Their names would be immediately recognizable to many
in the public health community. They prefer to keep their online
and public lives separate to allow maximum freedom of expression.
Paul Revere was a member of the first local Board of Health in the
United States (Boston, 1799). The Editors sign their posts “Revere”
to recognize the public service of a professional forerunner better
known for other things. Don’t miss the comments, they are
consistently good. Fair warning, Revere’s political posture is very
left-of-center and his religious views are, well, anti-religion. If
these postures would bother you and hinder you from gleaning the flu
info he has to offer, then by all means give this site a miss.

E. Coli in Your Salad? Just Nuke It!

For three years now my family has been enjoying fresh produce from theCommunity Supported Agriculture (CSA) program at Arnold’s HighlanderFarm in Augusta, WV. This has taken a bit of adjustment in my cookinghabits, because every Friday, May through October, I receive a bushelof fresh vegetables. I usually have some idea of what will be coming,but the crop is weather-dependent, and there is usually a greatabundance of it. I have honed my freezing and canning skills over theyears, and although I work full-time, it’s not as time-consuming asit sounds. Having lots of quart jars of tomato sauce flavored witheither basil or hot peppers all winter long is a great incentive.

There is also the seasonal nature of things. I enjoy the first greens andasparagus in May, the summer vegetables for ratatouille and tomatosandwiches from July through September, and greens again with wintersquash in October. Then there are the strawberries in June: small,but so much sweeter than the ones in the grocery store.

As of late, this country has been having some serious problems withfresh produce in fast-food restaurants and grocery stores. Salmonellaand E. coli have sickened hundreds of people this fall. Despite this,I was disturbed to read an article in the New England Journal ofMedicine supporting irradiation of fresh produce as a remedy to theoutbreaks ( author grew up in a rural area and knows something of the healthyproducts that a strong local agricultural base can yield, yet insteadof advocating for more local food production, he embraces theoverlaying of even more technology. Irradiation would not necessarilykill the hepatitis A virus that sickened people eating green onionsat Chi-Chi’s in 2003. Bacteria may also become resistant toirradiation just as they have become resistant to antibiotics.

Right now we have a centralized food production system which greatlyincreases the probability of multi-state and even multi-countrycontamination of food. This occurred first with beef and poultry.Irradiation seems to have only partially solved that problem, but nowit is happening with produce. Where will it end? Worse, what ifsomeday it is illegal to sell produce that hasn’t been irradiated?This happened with the pasteurization of milk. For both good and badreasons, raw milk is no longer legal or readily available for sale inmost states – even right off the farm.

The adverse human health aspects of our food production model are justnow coming to light. The environmental and social downsides have beenevident for some time. Think of migrant workers, manure lagoons andthe recent Swift meatpacking plant debacle. My suggestion for whatit’s worth is to look around, find local food, and embrace it. Or,just grow some of your own.

Start small, stay local, eat seasonally. To find a CSA program or farmers’market near you, go to

Clostridium Difficile Colitis Update

Clostridium difficile is aslow-growing, gram positive, anaerobic bacillus. Clostridia species formspores which are resistant to ultra-violet radiation, temperature extremes andcommon hospital disinfectants. These spores are highly persistent andubiquitous in the environment. C. difficile produces two types of toxins; toxinA, an enterotoxin, and toxin B, a cytotoxin. Both toxins bind to specializedreceptors on intestinal mucosal cells and play a role in the organism’spathogenicity. These toxins can act synergistically. In addition, a thirdbinary CDT toxin exists in some strains. The pathenogenicity of this toxin iscurrently less clear.

Since its identification as thecausative organism in pseudomembranous colitis in 1978, infectious outbreakshave sporadically occurred in several hospitals throughout the US. This hasbrought about various institutional responses, including restricting certainantibiotics, changing housekeeping procedures, and establishing activemultidisciplinary antibiotic management programs. These measures in combinationhave met with some level of success.[i]Restricting the use of clindamycin has reduced Clostridium difficile-relateddiarrhea (CDAD) in some hospitals in the short term[ii],but increasingly other broad-spectrum antibiotics such as cephalosporins andquinolones cause the disease, so restricting clindamycin as a sole containmentpolicy is of very limited use.

New insight into thepathenogenesis of C. difficile infections has recently been gained. A highlytoxinogenic strain was identified in six US states, and in Alberta and Quebec,Canada between 2001 and 2004.[iii]The Society for Healthcare Epidemiology of America said at its 15thannual meeting in April 2005 that this strain, designated as ribotype 027,toxinotype III, has caused outbreaks in 7 hospitals in 6 US states. Thetoxinotype III strain produces 16 times more toxin A and 20 times more toxin Bin vitro than the more commonly isolated toxinotype 0 strain. This may be dueto the deletion of the tcdC gene, a negative regulator of toxin production.This gene limits toxin production in the log (exponential) phase of bacterialgrowth, delaying its production until the stationary phase of growth.[iv]This strain of C. difficile is responsible for the recent epidemic at StokeMandeville Hospital in the UK, announced on June 5th, 2005. Thisepidemic affected 300 persons at the small specialty hospital and killed 12patients, precipitating possible government action regarding hospital hygieneand the interaction between infected patients, staff, and visitors. Subsequentto the reports at Stoke-Mandeville, fourteen other UK hospitals were found tohave patients infected with the 027 strain.[v]Clostridium difficile has recently become a reportable disease in the UK. It’soccurrence is not yet a mandatory reporting issue in the US or Canada.

On July 6th,, 2005the 027 strain was identified at two hospitals in the Netherlands.[vi]Of particular concern was a lack of apparent clinical response to metronidazole.This phenomenon had been empirically observed previously in Canada. Curiously,the strain was susceptible to metronidazole in vitro by E-test.

A disturbance in the usualcontingent of human gut flora brings about C. difficile super infection andresultant diarrhea and colitis. This disruption of microbial flora is mostcommonly associated with orally administered antibiotics and/or broad- spectrumantibiotics. Canadian interventionists have reported a possible relationshipbetween the use of proton pump inhibitors and the disease, but in view of thevery rapid formation of large amounts of toxin, it is unclear how large a rolethe use of these medications play in the pathenogenesis of the toxinotype IIIstrain. The odds ratio of the instance of proton inhibitor use in a smaller(n=94) case-control study portion of their research was nearly equivalent tothat of other risk factors, such as hospital admission in the last 3 months(2.7 and 2.6, respectively). In addition, patients placed on proton pumpinhibitors are often more ill than other patients.[vii]

Since the year 2000, mortalityper case of C. difficile has been rising. Data presented at the 2004 InfectiousDiseases Society of America meeting has indicated that the C. difficile isresistant to fluoroquinolones, especially levofloxacin.[viii][ix] Previously, quinolones were thought to pose a low risk of C. difficileinfection.[x]Other evidence suggests that resistance to metronidazole may be occurring, aswell as documented resistance to macrolides and clindamycin. The risk ofinfection is now highest with cephalosporins and ampicillin/amoxicillin,presumably because they are the most widely used antibiotics. Indeed, almostall classes of antibiotics have been implicated, and even brief exposure to anysingle antibiotic can cause C. difficile colitis.

The C. difficile speciesinvolved in major hospital outbreaks appear to have both a dominant clonalstrain and resistance to a commonly used antibiotic. C. difficile selects forspecific antibiotic resistance and then can proliferate largely because it isresistant to that antibiotic. The antibiotic itself is responsible forobliterating much of the host’s protection by suppressing the bowel flora. C.difficile then produces copious amount of toxins. Hence, reduction of overallantibiotic use is necessary to reduce endemic CDAD rates in hospitals.

A recently reported randomizedcontrol study demonstrates the value of changing overall antibiotic usagepatterns. It involved 807 uncomplicated acute bronchitis patients treated inprimary care facilities that were assigned to one of three treatment arms,including: no antibiotics offered (n = 273), delayed antibiotics via a writtenprescription (n = 272), and immediate antibiotics ( n = 262). According toresponses from 78% of the patients, there was little difference in resolutionof symptoms. Prescribing practices that involved the delayed use or the non-useof antibiotics were effective in 70% to 90% of patients, resulted in adequatesymptom control, and were acceptable to patients.[xi]This study is important because evidence suggests that community-acquired C.difficile may be a problem. Since January 2005, this hospital has seen manycases of community-acquired C. difficile-associated diarrhea. Nearly all the patientswere previously treated with amoxicillin, Augmentin or a cephalosporin. Thistrend indicates that outpatient prescribing practices will play a role in thefuture of the disease.

Clostridium difficile colitisis no longer confined to elderly and very infirm nursing home or hospitalizedpatients. As with MRSA and VRE, utilizing strict enteric contact isolation isan essential means of controlling CDAD spread. Mandating hand-washing withchlorhexidine (not alcohol) before and after patient contact for all staff andvisitors, full personnel protective gowning and gloving, exclusive use ofdiagnostic equipment such as stethoscopes and blood-pressure cuffs on one andonly one patient, and cleaning rooms and equipment with a chlorine-baseddisinfectant must be initiated. Other approaches to combating the diseaseinclude improved surveillance and disease data collection, rapid same-day toxintesting and reporting, and developing new molecular typing systems using wholegenome sequences of C. difficile. Further understanding of the mode of actionof the pathogen, development and application of new treatment strategies,stressing the need for using non-antibiotic treatment modalities such as theuse of antitoxin, probiotic treatment and fecal donation, will also benecessary.

C. difficile is present in thegut of 50% of all neonates and in 7% of adults. It has only recently beenconsidered a pathogen instead of a commensurate organism. Its emergence isrelated to the widespread use of broad-spectrum antibiotics. Policies must beput in place that include the strict practice of enteric contact isolation andan active antibiotic management program, in order to reduce CDAD incidence andprotect patients and staff.

UPDATE: October 2006

A study from 6 North Carolina hospitals has indicated thatcommunity-acquired C. difficile-associated diarrhea (CA-CDAD) is indeed anincreasing problem. Moreover, the spread of the disease may not involve theprior use of antibiotics. C. difficile has been known to spread from patient topatient in hospitals. Now there is some basis to believe that it can spreadamong healthy individuals in the community as well. Of a total of 1137 cases of CDAD reviewed at 6 NorthCarolina hospitals between Jan and Dec 2005, nearly one in 5 (209, 18 percent)were acquired in the community, with 50 percent of those cases not originatingfrom prescription of an antimicrobial, stressed Dr. McDonald.” Cit. ProMedarchive number 20061018. Costridiumdifficle, community acquired – USA (NC).

[i]JohnsonStuart, Samore Matthew, et al. Epidemics of diarrhea caused by a clindamycinresitant strain of Clostridium difficile in four hospitals. NEJM Vol. 341, No.22: 1645-1651. Nov. 25th, 1999.

[ii]EggertsonLaura, Sibbald Barbara. Hospitals battling outbreaks of C. difficile. CMAJ171(1). July 6th, 2004.

[iii]ProMEDDigest. V2005, #155.

[iv]ProMEDDigest. V2005, #235.

[v]ProMEDDigest. V2005, #275.

[vi]ProMEDDigest. V2005, #286.

[vii]DialSandra, Alrasadi Khalid, et al. Risk of Clostridium difficile among hospitalinpatients prescribed proton pump inhibitors: cohort and case-control studies.Can. Med. Assoc. J. 2004 171: 33 – 38.

[viii]StephensonMichelle, correspondent. New epidemic strain of Clostridium difficilehas emerged. Infectious Disease News, February 2005.

[ix]MutoCarlene, Pokrywka Marian, Shutt Kathleen, et al. A large outbreak ofClostridium difficile-associated disease with an unexpected proportion ofdeaths and colectomies at a teaching hospital following increasedfluoroquinolone use. Infection Control and Hospital Epidemiology. Vol 26, No 3,273 – 279. March 2005.

[x]GorbachSherwood. Antibiotics and Clostridium difficile. NEJM Vol 341, No 22. Nov.25th,1999.

[xi]LittlePaul, Rumsby K, et al. Information Leaflet and Antibiotic PrescribingStrategies for Acute Lower Respiratory Tract Infection. JAMA June 22/29, 2005.Vol.293, No. 24, 3029-3035.

The Real Culture Of Life

“Nothing is one” says Murray Bail, author of the book Eucalyptus. To me, this means that life is by definition a cooperative venture. The presence of other living creatures is imperative for our own survival. Competition does occur, but it is far less taxing and potentially more rewarding to cooperate. Medical science often uses the analogy of “waging war” when dealing with microbes. The arsenal for this war includes antibiotics, literally meaning against life. This is an example of competition. However, from time immemorial, humans have been using probiotic (literally for life) cultures of microorganisms in a cooperative alliance for good health. Since humans are so clearly outnumbered, it would be in our best interest to forge a cooperative relationship with the microbial world.

A specific example of cooperation exists in our digestive system. Many different bacteria and fungi live in this environmental niche. We provide these organisms with food and safety. They provide us with better immune function, better availability of vitamins and minerals, and the elimination of the toxic by-products of digestion. A whole constellation of these “probiotic” organisms have been identified by Western science. Most well-known are members of the genus Lactobacillus, which was first identified by Elie Metchnikoff in nineteenth-century Bulgaria. He wrote a book about these bacteria entitled “The Prolongation of Life” which promoted eating live bacteria for good health. This genus of bacteria converts lactose, the sugar in milk, to lactic acid and is also known as acidophilus. Other organisms include the yeast Saccharomyces, and bacteria such as Streptococcus, Klebsiella, Bifidobacteria, and Staphylococcus. There are doubtless many more comprising the unique terroir1 of our colon. These organisms must also co-exist with each other in order to survive. When this cooperation is compromised, the result is that the lining of the colon wall becomes weakened due to inflammation of the GI tract. This “leakiness” of the gut lining allows the inflammatory substances to gain access to other areas of the body. Aside from obvious effects like diarrhea, poor absorption of necessary vitamins and minerals, and stomach-ache, this can also lead to other inflammatory conditions such as arthritis and allergies. Infection with a disease organism, such as C. difficile, can also occur.

Since a healthy group of gut flora is essential to our health, some means of encouraging them seems like a good idea. Despite this, lactobacilli are scarce in the GI tracts of people living in industrialized nations. In one study, L. plantarum was present in only 25% of the US population, but in 100% of both Asian and African populations. The low population of lactobacilli is probably because of the lack of living foodstuffs available in the Western diet due to pasteurization and processing. Otherwise, lactobacilli are ubiquitous in the environment. They are responsible for the fermentation of foods such as sauerkraut, salami, and kimchee. Lactobacilli occur naturally with other microorganisms in raw dairy products like yogurt and kefir. Many commercially-prepared fermented products in industrialized countries undergo pasteurization before sale, which kills the probiotic organisms except when a commercially prepared culture is added back afterward. In developing countries, the acidification that results from lactobacillus fermentation serves to preserve food and enhance its nutrient content and digestibility.

These organisms don’t stay in our GI tract, but instead must be constantly replenished from a dietary source. This is why live-culture foods should be a part of our daily intake. In order for these organisms to perform their vital function they must first be alive, be able to adhere to the GI tract, be metabolically active, be acid and bile resistant, have antimicrobial activity against pathogens, and reduce colonic pH. There are many commercially available probiotic formulations of variable microbe content and efficacy, but they are much more expensive than cultured foods prepared at home. In addition, there isn’t any conclusive evidence that the best mix of organisms is the same from person to person or from place to place. Many studies have shown commercial probiotics to provide health benefits, but to my knowledge there is no study comparing commercial products and probiotic foodstuffs, such as sauerkraut, kimchee, and yogurt, which can easily, safely and inexpensively be made at home.

We cannot live healthy lives without these organisms. Although antibiotics and pasteurization can save lives, their over-use has consequences, such as increasing the rates of asthma in children as well as the incidence of C. difficile colitis and the emergence of other resistant disease organisms. Unlike our microflora, antibiotics are not essential to health, and with the ever-growing problem of microbial resistance to antibiotics, we should change our medical prescribing habits and dramatically increase our consumption of probiotics. In 1994, the WHO deemed probiotics to be the most important immune defense when microbial resistance to antibiotics is a factor. Since in study after study probiotics have been shown to help the immune function of patients with a wide variety of diseases, probiotics would seem to be the best defense – period. Probiotics do not cause any serious adverse reactions the way antibiotics can. Lactobacilli and Saccharomyces boulardii will not cause disease even in immunocompromised patients such as those with HIV/AIDS. In fact, these particular microorganisms have been shown to restore immune function to those who had lost it altogether.

So why are we killing our allies? The antibiotic culture at the USDA and FDA needs to be re-appraised. The current policy of food pasteurization is useful in mass-production facilities, but in artisanal and local markets it is a ruinous practice. To blindly pasteurize a properly crafted raw food is to completely spoil a health-giving and vital product that poses no real threat to human health. A sea change in the bureaucratic culture must happen so that these unique products will continue to be available. Rather than forcing producers to adhere to regimented processing procedures and to purchase expensive equipment, government officials should instead be testing the producer’s final product. This would not only reduce the costs imposed on would-be artisans, it would prevent some of the food poisoning that already occurs in the supposedly “safe” food chain. “The proof of the pudding is in the eating”- ergo, it is not in the kitchen. Food poisoning continues to be a problem despite, or in some cases because of the use of pasteurization and chemical sterilizers. Making the world unwelcome for one type of microorganism only creates an opportunity for another, perhaps less friendly one. As the ancient Roman poet Horace said, Naturam expellas furca tamen usque recurret — Nature can be expelled with a pitchfork, but she always returns.

1 Terroir is a French term originally used by wine and coffee aficionados to denote the special characteristics of geography that bestowed individuality upon the food product. It can be very loosely translated as “a sense of place” which is embodied in certain qualities, and the sum of the effects that the local environment has had on the manufacture of the product. Some assert that terroir is distinct from the characteristics imparted by the plant variety, the vintage and production methods (vinification, etc.), and is the product of a range of local influences that are transmitted into the character of the product. [from Wikipedia] This concept can be extended to include any microclimate.



In the Fall of 2000 two studies were published in JAMA and NEJM which purported to prove that COX-2 inhibitors had a significant GI safety advantage over their predecessors, the NSAIDs. The CLASS1 and VIGOR2 trials, for Celebrex and Vioxx respectively, were large studies carried out by the manufacturers of the drugs and reviewed by gastroenterologists.

The CLASS study, conducted by Pharmacia, consisted of two separate 12- and 15-month trials with Celebrex (celecoxib) 800 mg daily and either ibuprofen 2400mg daily or diclofenac 150mg daily. The data the reviewers saw, however, was a combined analysis of the first 6 months of the two trials.3 Other data was omitted, and the JAMA editor was not informed of the omission. When the entire data set was subsequently reviewed, the GI advantage attributed to celecoxib was found to be non-existent, and in June 2002 the FDA mandated that the claim of greater GI safety be removed from the Celebrex label. The consumer information section of the FDA website compares Celebrex to other NSAIDs in its ability to cause stomach ulcers.4 In a July 2001 letter to JAMA, Dr. James Wright, a clinical pharmacologist at the University of British Columbia, suggested that the complete data from the CLASS study indicated that celecoxib may actually cause worse side effects than either diclofenac or ibuprofen.5

In the 15-month VIGOR study, conducted by Merck and reviewed by the NEJM, Vioxx (rofecoxib) produced fewer perforations, ulcerations and bleeds (PUBs) than did naproxen. However, the FDA maintained that fewer PUBs was not necessarily indicative of fewer GI complications. Merck also failed to reveal that the rofecoxib subjects in the study had a much greater incidence of cardiovascular side effects, which were possibly due to COX-2 inhibitors having pro-thrombotic properties. The patients in the VIGOR study were not permitted to take low-dose aspirin as subjects in the CLASS trials were. As early as 1999 the FDA was concerned about “excess deaths and cardiovascular events experienced in Group A (Vioxx) as compared to Group B (naproxen).”6 In March 2002, five cases of aseptic meningitis in patients on Vioxx were reported.7 In April 2002 the FDA required that a warning of cardiovascular risks be placed on the label.8

As a result of these disturbing revelations involving selective reporting of pharmaceutical data, the 11 editors of the International Committee of Medical Journal Editors have issued new requirements for publication acceptance of research funded by interested parties.


Neither of these large studies included patients who were taking warfarin (Coumadin), or patients who had a history of GI disease. There is no supporting evidence for improved GI safety of either Vioxx or Celebrex when used with warfarin. However, there are many post-marketing surveillance reports of significantly elevated INRs and bleeding episodes when either of these agents are administered with warfarin. A memorandum from the FDA written shortly after these medications were approved cited 73 US deaths attributed to celecoxib and rofecoxib. These patients were generally considered to be high-risk patients “because of past medical history, a recent major systemic medical event, or concomitant therapy with aspirin or another antiplatelet drug, corticosteroids, warfarin, or another NSAID.”9

1 Silverstein FE, Faich G, Goldstein JL, et al. Gastronintestinal toxicity with celecoxib vs nonsteroidal antiinflammatory drugs for osteoarthritis and rheumatoid arthritis. The CLASS study: a randomized controlled trial. JAMA 2000; 284:1247-1255.

2 Bombardier C, Laine L, Reicin A, et al, for the VIGOR study group. Comparison of upper gastrointestinal toxicity of rofecoxib and naproxen in patients with rheumatoid arthritis. N Engl J Med. 2000; 343:1520-1528.

3 Wright, JM, Perry TL, Basset KL, Chambers GK. Reporting of 6-month vs 12-month data in a clinical trial of celecoxib. JAMA 2001; 286:2398-2400.

4 FDA Celebrex Consumer Information Sheet. Revised November 11th, 2002. Accessibility verified May 17th, 2004.

5 Okie S. Missing data on Celebrex: Full Study Altered Picture of Drug. Washington Post, August 5th 2001; p. A11.

6 Targum, S.L. Consultation NDA 21-042, S-007: Review of cardiovascular safety database. FDA CDER Memorandum, February 1st, 2001. Accessibility verified May 17th, 2004.
7 Bonnel, R.A., et. al. Aseptic Meningitis Associated With Rocfecoxib. Archives of Internal Medicine 2002;162:713-715. Accessibility verified May 17th, 2004.
8 FDA Talk Paper T02-18. April 11th , 2002. Accessibility verified May 17th, 2004.
9 Weaver, J. OPDRA Postmarketing Safety Review. FDA CDER Memorandum, December 29th, 2000; p. 1. Accessibility verified May 17th, 2004.

Crohn’s Disease and Johne’s Disease
– Is There a Connection?

Johne’s disease, caused by Mycobacterium avium subspecies paratuberculosis (MAP), manifests itself as a chronic diarrheal disease marked by wasting and eventual death . It occurs in wild and domesticated animals essentially worldwide, with the possible exception of Sweden and parts of Australia.

USDA officials view Johne’s disease with some concern, as it is costly to manage and results in the early cull of infected animals and loss of production in dairy herds. Endemically infected herds worsen over time as the disease spreads. Johne’s disease affects all ruminants, and cross-species infection has occurred. Johne’s can be transmitted through feces, though milk, and via the womb. Young animals are especially susceptible. Although the cause of the disease was discovered in the early 20th century, many US beef and dairy producers are not familiar with it’s full implications. There are increasing concerns that the disease may pose a threat to public, as well as ruminant health.1

In contrast, Australia has a very proactive stance on Johne’s disease, including testing programs, zone reporting, and abbatoir monitoring.2 Crohn’s disease (CD) occurs in humans, and has symptoms very similar to Johne’s disease. It affects mainly people between the ages of 20 to 40 years. Many of them endure multiple surgical bowel resections and other serious sequelae. The suffering endured by the patient, family and friends of these patients is enormous, as is the cost. Current CDC estimates for the USA are that approximately 500,000 people have Crohn’s disease. Formerly, CD was thought to be an autoimmune disease influenced by diet and stress. An infectious cause of this disease is now under investigation.

Evidence is growing that the same microorganism, MAP, plays a role in both diseases. In 1999, the CDC acknowledged a probable link between Crohn’s and Johne’s diseases. In its “Infectious Causes of Chronic Diseases” monograph, it cited the theory that MAP may cause both diseases and set goals for further action.3

Mycobacteria are notoriously difficult to culture as they are very slow growing and fastidious, drawing attention to our ignorance concerning microbial growth requirements. Staining methods used to characterize different types of bacteria, for example the “Gram” stain, are ineffective if the bacteria in question don’t have cell walls. Hence the Ziehl-Neelsen (“acid-fast”) method of staining, which helps to identify most mycobacteria, can’t be used to identify the prevalent strain of MAP involved in CD, as it is cell-wall deficient, or a spheroplast, form. This makes applying Koch’s Postulates rather difficult. Briefly, these postulates maintain that to prove an organism causes a disease, you must remove it from a diseased organism, grow it in pure culture, inject it into a healthy organism, and produce the same disease. Until recently, this was the gold standard proof of pathology. Mycobacteria in general make this difficult because the disease may take years to manifest itself or the animal may be a carrier of the disease without ever showing any symptoms. It should be noted that Koch’s postulates have never been met in the case of Mycobacterium leprae and leprosy, although this organism is widely held to be the cause. Thus the inability of researchers to consistently produce Johne’s disease in animals from people infected with Crohn’s disease is not surprising but has nevertheless led to a lot of controversy. However, there are documented cases in which Mycobacterium from Crohn’s patients inoculated into an animal host have produced Johne’s disease.4

Enter biotechnology, genome sequencing and polymerase chain reaction techniques (PCR). It turns out that there are fragments of the genetic code in organisms, specifically in the small subunit ribosomal RNA and DNA, that reliably provide the ancestral “fingerprint” of a microbe, even when its in the soup of infected host tissue. Over the past 20 years, quite a library of specific “fingerprints “has been identified, thus increasing the usefulness of this technique. Many previously uncharacterized microbes have been identified in this way.

Another method of identifying the etiology of CD involves the use of known antigens. Antibodies are part of a host’s immune system and form in response to the presence of a specific invading organism or “antigen”. A recent study tested two antigens from the MAP genomic library, identified as p35 and p36, and found the following results: 75% of 53 CD patients and 14% of 35 normal patients reacted to the p35 antigen, and 89% of 89 CD patients and 14% of 50 normal patients reacted to the p36 antigen, only the Crohn’s disease patients reacted to both antigens. For anyone fond of statistics, this resulted in a 98% positive predictive value with 98% specificity. Thus the reactivity of CD patients to these two antigens suggests a causal role for MAP in the disease.5

Mycobacteria produce what is called “protean” disease. This means the disease is not specific to one organ, but may occur any place in the body. For example, people usually associate tuberculosis, caused by M. tuberculosis, as a disease of the lungs, but it can appear in other forms, notably an intestinal one, as well. It is very difficult for diagnosticians to distinguish intestinal tuberculosis from CD. This may be because the causative organisms are very similar. To extend this analogy, tuberculosis and CD both show a mild and a severe forms. This too is typical of diseases caused by Mycobacteria. At the beginning of the 20th century, another species of Mycobacterium, M. bovis, caused tuberculosis in humans. This organism was mainly spread by drinking cow’s milk instead of droplet infection, as with M. tuberculosis. All of these bacteria can remain alive in cool, moist conditions for protracted periods of time. M. bovis survives in cow dung for about 5 months. MAP can survive in pond water for up to a year. Since they are intracellular organisms which reside inside the macrophages of their host’s cells (the very organelle that is responsible for digesting and eliminating bacteria), they resist normal immune intervention and evade destruction. They are indeed very robust and versatile organisms!

For those who ascribe to the theory that CD is indeed caused by MAP, the source of the infection would appear to be drinking milk or eating meat from herds with endemic Johne’s disease. This is certainly a plausible assumption, since as of 1996, the USDA estimated its prevalence in dairy herds at 22%.6 With very little testing or control in place, the percentage could by now be higher. This begs the question: how safe is the milk supply?Studies have been undertaken to address this concern. In 1996,samples of pasteurized milk were collected from shops in various locations in England and Wales throughout the year. The prevalence of MAP organisms found averaged 7%. Curiously, the prevalence was seasonal. It rose to 25% in the autumn and winter months, and was non-existent in the late spring and summer.7 A 2002 study in Canada on the effects of pasteurization on the viability of MAP found that out of 7 batches at regular pasteurization temperatures, (63 degrees C. for 30 minutes), no surviving organisms were found after 15 minutes. Yet out of 11 high-temperature short-term (HTST) batches at 72 degrees C. for 15 seconds, MAP was detected in 2 batches. This indicates that MAP may survive HTST pasteurization when present in sufficient quantity.8 Other studies indicate that MAP is less susceptible to heat-killing than other food-borne bacterial pathogens.9 A “smoking gun” was found in 1988 when MAP cervical lymphadenitis (swollen neck glands) occurred in a 7-year old boy inEngland. These nodes were removed and found to contain an abundant quantity of MAP organisms. Five years later, the patient developed achronic inflammation of the intestine indistinguishable from Crohn’s disease. After being treated with antibiotics for MAP, he went into complete remission.10 His initial presentation was similar to the pre-pasteurization era presentations of M. bovis infection, i.e. Swollen lymph glands nearest the avenue of infection – in this case, the mouth. Since then, many Crohn’s patients have responded to antibiotic treatment regimens tailored to Mycobacteria. The advent of macrolide antibiotics such as clarithromycin have provided much hope for those suffering from CD.

There seems little room for doubt that MAP can cause CD in humans, but many questions remain. Why doesn’t it present as its cousin, M. bovisdoes, with swollen cervical lymph glands? Why is it we see thes pheroplast (un-walled) form in CD rather than the bacillary (walled) form as we do in animal infection? This may have to do with the level of host resistance, the quantity of organisms present upon initial infection, or something completely different. In any case, the subject is an interesting one, and warrants concerted and earnest attention from livestock farmers, medical professionals, and the informed consumer if we are to protect both human and animal health.

Some things have to be believed in to be seen.

-Ralph Hodgson

1 USDAAPHIS Info Sheet. What do I Need to Know about Johne’s Disease in Beef Cattle? August 1999.

2 JDNews, Animal Health Australia. Winter 2002.

3 Centersfor Disease Control and Prevention report, as viewed January 2004 atthe PARA website

4 Greenstein,RJ. 2003. Is Crohn’s disease caused by a mycobacterium? Comparisonswith leprosy, tuberculosis, and Johne’s disease. Lancet Infect. Dis.2003 Aug; 3(8): 507-14.

5 Naser SA, Hulten, K et al. 2000. Specific seroreactivity of Crohn’sdisease patients against p35 and p36 antigens of M. avium subsp.paratuberculosis. Vet. Microbiol. 2000 Dec 20: 77(3-4): 497-504.

6 Stabel JR. 2000. Johne’s disease and milk: do consumers need to worry? JDairy Sci. 2000 Jul; 83(7): 1659-63.

7 MillarD, Ford J, Sanderson J, et al. 1996. IS900 PCR to detectMycobacterium paratuberculosis in retail supplies of wholepasteurized cows milk in England and Wales. Applied andEnvironmental Microbiology 62, 3446-52.

8 GaoA, Mutharia L et al. 2002. Effect of pasteurization on survival ofMycobacterium paratuberculosis in milk. J Dairy Sci. 2002 Dec;85(12): 3198-205.

9 Collins,MT. 1997. Mycobacterium paratuberculosis: a potential food-bornepathogen? J Dairy Sci. 1997 Dec; 80(12): 3445-8.

10 Hermon-TaylorJ, Barnes, N., et al. Grand Round: Mycobacterium paratuberculosiscervical lymphadenitis followed five years later by terminal ileitissimilar to Crohn’s Disease. BMJ Feb 7,1998; 316:449-453

Dare to Eat Fat

Now that Dr. Atkins, the American Heart Association, and the Harvard School of Public Health are busy toppling the Food Pyramid end-over-end, it may be time to take a look at the erstwhile tiny tip and realize that not all fats are created equal.

Most people know that fats come in saturated and unsaturated forms, and that the unsaturated ones are generally the better dietary choice. It has recently been shown that trans-fats, aka hydrogenated and partially hydrogenated oils, which are altered to solidify and prolong the shelf-life of margarine and many pre-prepared foods, are unhealthy.

Many people do not realize that some kinds of fat are necessary. These are aptly called the Essential Fatty Acids, or EFAs. Biochemically speaking, there is almost a complete lack of genetic defects in the metabolism of these fats in humans. This is quite rare, since humans exhibit a range of genetic defects in the metabolism of many fats, carbohydrates, and proteins. For example, have you ever noticed the warning on diet soda, “Phenylketonurics, contains phenylalanine”? This indicates a fairly common defect of metabolism that many people have in processing the amino acid phenylalanine. But the EFAs are truly essential to human life — you cannot survive with an inability to process these fats.

The two EFAs have very similar names: linoleic (LA) acid and linolenic (LNA) acid. LA is found in plant oils such as corn, sunflower and soybean oil. LNA is mainly found in cold water fishes like salmon, although there are a few good terre strial sources like purslane, perilla and borage. The parent compound of the omega-3 fatty acids is LNA, and although it is metabolized preferentially over the omega-6 parent, LA, there is still a deficit of omega-3 in the US population. This is because the current American/Western diet is composed of a much higher ratio of LA:LNA, in some cases as high as 20:1. Since these two essential fatty acids compete for the same desaturase and elongase enzymes, the products from LNA are suppressed. That is, there is ample substrate for producing arachidonic acid and very little substrate for producing eicosapentaenoic acid. Many countries have proposed reduced dietary ratios of omega-6 to omega-3, including Japan (between 2:1 and 4:1), Sweden (5:1), as well as the WHO (between 5:1 and 10:1). Currently, the US has no formal recommendations for dietary omega-3 intake.

The ratio is important because these fatty acids are the precursors of the eicosanoids. Eicosanoids are potent, locally acting hormones present in virtually all cell membranes. Like many hormones, they can act in opposition to each other. Since the omega-6 pathway makes many more pro-inflammatory hormones than the omega-3 pathway, the imbalance of the two can lead to many serious chronic inflammatory conditions. Some diseases influenced by this balance include cancer, obesity, hyperlipidemia and hypertri glyceridemia, arthritis, arteriosclerosis, eclampsia, cystic fibrosis, Crohn’s disease, and depression. Therapies currently used to treat some of these conditions, including NSAIDS, steroids, and sulfasalazine may further shift the balance because they inhibit both types of eicosanoids.

The ratio of EFAs in the so-called Paleolithic diet was probably 1:1. What has happened since then to so radically alter this ratio? Vegetable oil-containing processed foods have increasingly been consumed instead of fish, lean meats, vegetables and fruits. The omega-3 content of these vegetable oils has also been altered by plant-breeding programs to reduce LNA and thus improve stability during storage. In addition, the fatty-acid content of the fish and livestock we raise for food has changed as a resu lt of feeding practices. Ruminant animals, such as cows, sheep and goats, are uniquely designed to ingest grass as their primary foodstuff. Grass-fed and wild animals have a significant amount of omega-3 in their tissue fatty acids and a LA:LNA ratio of 1:1. In contrast, feed-lot animals and farm-raised fish, which are fed mainly corn, have a ratio typically greater than 50:1.

To further confound the issue of good fats vs. bad fats, a new form of LA was discovered in the late 1970’s by Dr. Michael Pariza. Dubbed “conjugated linoleic acid” or CLA because of its unusual conjugated diene structure, it differs from linoleic acid only by having two double bonds, which LA lacks. Many isomers exist, but the biologically active one is formed only as a digestive by-product of ruminant fermentation by the bacterium Butyvibrio fibrisolvens. Plant-based CLA is inactive, so the only way to obtain it is from animal products, particularly dairy. Whole milk, whole-fat cheeses, lamb and beef are good sources of CLA. Again, grass-fed animal products have much higher levels of CLA than their grain-fed counterparts.

CLA is a potent antioxidant and mimics many of the anti-inflammatory properties of LNA, while LA is the only fatty acid proven to enhance carcinogenisis in experimental animals.

Physiologic concentrations of CLA can inhibit cultured cells of human malignant melanoma, colorectal cancer, and breast cancer. While this may be attributable in part to its antioxidant activity, CLA also modulates cytochrome P450 activity and suppresses the activity of ornithine decarboxylase and protein kinase C, enzymes involved in carcinogenesis. It inhibits angiogenesis in cancerous growths as well.

CLA also has a role in body fat reduction. It exerts direct dose-dependent reduction in lipoprotein lipase activity and an increase in carnitine palmitoyltransferase activity in adipocytes and skeletal muscle cells. Inhibition of fat storage in adipocytes as well as an increase of skeletal muscle mass has been demonstrated in a number of animal species, including mice, rats, pigs and humans.

So, if you choose carefully and consume in moderation, you can enjoy having a nice glass of whole milk, an extra pat of butter, or a juicy steak this holiday season!

Farmer + Pharmacist = Farmercist

A talk for Capon Bridge Middle School
Career Day 2002

RxPharmacists are allied health professionals. It now takes six years to become a Doctor of Pharmacy or PharmD. You need to go at least two years to a regular college or university, and then four years to a school of pharmacy. You must pass a test called the PCAT in order to get into a pharmacy school. In order to graduate, you must perform several different externships. An externship is a real-life situation where you do real work at a pharmacy under the supervision of an experienced registered pharmacist. After you graduate from pharmacy school, you must pass a State Board examination before you can practice pharmacy. Once you are a pharmacist you must complete 15 credit hours of continuing education every year to keep your license. It sounds like a lot of work, and it is, but most pharmacists in the U.S. make $80,000 a year or more!

There are many specialties in pharmacy. These include community and chain store pharmacists. Some are employed in matters of pharmacy law and pharmacy administration. Others are researchers and educators. Some work in hospitals, and some administer IV medications to patients in their homes.

A lot of pharmacists work part-time. I am one of those.

I worked full time for a number of years in a very busy food and drug store near Washington DC. I’ve also worked in hospitals and I still work part-time for one nearby. I’ve noticed over the years that a lot of people take medication they might not need (or at least not as much of) if they would just watch their diet more closely. There are a lot of serious medical conditions that can be greatly influenced by the food we eat. They include, but are not limited to, type II diabetes, arthritis, heart disease, high cholesterol, high blood pressure, cancer, and depression. I started paying attention to where my family’s food came from and what was in it. I saw lots of processed ingredients like partially hydrogenated oils (or trans-fat) and corn syrup in simple foods like bread and crackers. I also learned that a synthetic growth hormone was used in cows to make them produce more milk, but the milk isn’t labeled as such. I even found out that we routinely use some of the same antibiotics on chickens that we use to treat human disease. This is helping to cause these antibiotics to become less effective against the germs. All this made me want to learn how to grow healthier food, so I began a new profession – I became a farmercist!

Career DayFarmers raise food. On our farm we have goats, sheep, chickens, ducks, and rabbits. We have a vegetable and flower garden, and we’ve planted some fruit trees. We produce our own meat, milk, cheese, eggs, and vegetables. We can also sell extras to our neighbors. Some things we must have money for, like building a barn and fencing in the animals. Expensive things like these would be almost impossible to do without some sort of income outside the farm itself. That’s why working part-time is a great help – I earn money but still have time to manage the farm. We still buy some of our food, but we try to get it locally so we can see where it comes from and how it is cared for. That helps other people stay on their farms, too.

There are as many different kinds of farmers as there are pharmacists. Some raise cows, or grow corn, wheat or soybeans. Others grow mushrooms, vegetables, flowers, or herbs. Some have thousand-acre ranches in the West, and some have just 100 acres in the Northeast. There are even farms on 3-acre plots in the suburbs! You can farm part-time or full-time, but just like any profession, it is the interest and care that you put into your product that determines if you do good work.

Cheap Food

An acquaintance of mine was bragging the other day about how he had filled his freezer with cheap chicken, chicken priced so low it surely cost more to produce it. I’ve often listened to stories such as this through gritted teeth – don’t get me wrong, I too love a bargain. I just happen to think that cheap food is no bargain.

Cheap food invariably means that the food was raised according to an industrial model. In this case of this cheap chicken, the birds had no doubt been debeaked to prevent cannibalism in their overcrowded conditions. They were raised in tiny wire cages, never seeing actual sunshine. They were given doses of antibiotics from the egg on up to prevent disease stemming from the layer of fecal dust coating the entire chicken warehouse and the increased susceptibility of the birds to disease due to constant stress, and also in the belief that it promotes faster growth of the bird. As dismal as this sounds, the slaughter and processing was worse. Reams have been written in every politically-flavored, educationally-adjusted material, from Eric Schlosser’s Fast Food Nation to JAMA to Joel Salatin’s Pastured Poultry Profits to the journal Nature. Chicken raised in any other manner (by definition more humane!) costs more, and given a choice Americans almost always buy the cheaper product.

Cheap food is not just bad for the animals. Air, soil, and water quality also suffer. Cheap food means lots of herbicides and chemical fertilizers, and these literally kill the life in the soil. Manure lagoons are created that threaten air and water quality. One reason food thus produced is so cheap is because the inevitable costs of reclaiming the soil or cleaning up the water are never included in the equation — the corporation simply moves on to another location, leaving scorched earth in its wake.

The high concentration and long-distance shipping of animals necessitated by large-scale corporate “farming” guarantees the spread of disease. The CDC estimates that foodborne diseases cause approximately 76 million illnesses, 325,000 hospitalizations, and 5,000 deaths in the United States each year. The cost to our economy in lost wages and medical treatment is staggering — in excess of $35 billion 1999. As consumers we are “instructed” on the “proper” way to handle food – as if the increasing toxicity in our food were the result of our improper handling rather than their improper production and processing! Do you suppose that folks at our parents’ and grandparents’ church suppers were that much more adept at “proper food handling” than we are? Isn’t it more likely that the food they were starting with was less toxic than our generation’s cheap food?

The true legacy of our agribusiness-model cheap food is antibiotic-resistant strains of Salmonella, Campylobacter, and E. coli . It is the emerging pandemic of “mad cow” disease (vCJD or nvCJD in humans), the current US epidemic of Type II Diabetes in our young people, and the UK’s current Foot and Mouth Disease epidemic (the worst in recorded history).

Not to mention outlandish government subsidies: in FY 2000 the USDA paid farmers over $32 billion — an average of $16,000 per farmer, but big-business “farmers” got the lion’s share. This is our money folks, yours and mine. That’s how they can stay in business even with the price of food below the cost of production.

Beginning to see what “cheap” food is really costing you?

Foot and Mouth

Did you keep up with the Foot and Mouth Disease (FMD) crisis in Britain in 2001? Did you know that 4,206,000 animals (583,000 cattle, 3,474,000 sheep, 145,000 pigs, 3,000 goats, 1,000 deer, and 1,000 other animals) were slaughtered? Did you know that the vast majority of these slaughtered animals did not have FMD and were perfectly healthy? Did you know that FMD is rarely fatal and that animals usually fully recover within 2 – 3 weeks? Did you know that there is a vaccination against FMD? If this weren’t so tragic it’d be funny.

Two good sites that collect news and information on FMD — not to mention “Mad Cow” disease, vCJD, genetically-modified (GM) foods, etc. — are and — the second one is run by a molecular biologist in the Pacific Northwest and we like his occasional pithy comments that he interjects in some of his articles, though, unfortunately it is not being kept up to date. As you peruse these sites you most likely experience a powerful cocktail of emotions: scepticism, sorrow, disbelief, rage, and disgust, to name just a few. A few interesting articles from these and other sites:

And, from the “It couldn’t happen here, could it?” files: