The first study that looked at whether antibiotic use increased the risk of HUS in children was published in 2000. [1] The study found that antibiotic use was a strong and independent risk for the development of HUS regardless of the severity of the inciting infection.  Two years later, a meta-analysis of nine pooled studies found no effect in the risk for HUS with antibiotic use. [2] But the analysis noted that limitations in the studies examined limited interpretation of the data.

More recent studies indicate that the risk of HUS is increased by the use of some antibiotics.  The differing mechanisms of action in different antibiotics impact the production of Shiga toxin (Stx) differentially. [3]

In a study that used piglets as a model for human infection, ciprofloxacin (Cipro) increased the production of Shiga toxin 2 (Stx2) but not the production of Stx1. Azithromycin [4] caused no significant increase in Shiga toxin production. After treatment with ciprofloxacin, infected piglets had diarrhea and the severe fatal neurological symptoms associated with Stx2 intoxication. “Characteristic petechial hemorrhages in the cerebellum were more severe in ciprofloxacin-treated animals than in control animals. In contrast, azithromycin-treated piglets survived the infection and had little or no brain hemorrhaging.” [5]

The study concludes that: “The increased in vitro toxin production caused by ciprofloxacin was strongly correlated with death and an increased rate of cerebellar hemorrhage, in contrast to the effect of azithromycin. The piglet is a suitable model for determining the effectiveness and safety of antibiotics available to treat patients.” [6]

A just published study [7] assessed Stx production in the presence of different types of antibiotics.  The authors report that: “Sub-inhibitory levels of antibiotics that target DNA synthesis [8], including ciprofloxacin (CIP) increased Stx production, while antibiotics that target the cell wall, transcription, or translation did not….Remarkably, very high levels of Stx were detected even when growth of O157:H7 was completely suppressed by CIP. In contrast, azithromycin (AZM) significantly reduced Stx levels even when O157:H7 viability remained high.” [9]

So the evidence mounts that the class of antibiotic that includes Cipro (a fluoroquinolone) may drive the risk of HUS through increased Stx production. However, it is important to note that antibiotics are clearly indicated for some gram negative bacterial infections of the gut including infections such as Campylobacter jejuni and Shigella, which clinically resemble E. coli O157:H7 enteritis.  Further, antibiotic use in the elderly, immune compromised, and those with co-morbidities may be indicated even if the face of a Shiga toxin-producing infection. Thus, wholesale avoidance of antimicrobials for infectious diarrhea is not prudent, but identification of the infectious agent before antibiotic administration is very helpful.

Antibiotics are often prescribed to patients who have presumed bacterial gastroenteritis without consideration of the effects beyond the acute illness.  Because antibiotics can dramatically affect the native bacteria in the intestines, they have the potential to increase a patient’s risk of infection.  Persons who are already receiving antimicrobial treatment are more susceptible to infection with drug-resistant pathogens. [10]

Few of us consider the effects of bacteria on the natural flora of our intestinal tracts–unless one develops post-infection GI problems.  But the use of antibiotics has effects well past the time of consumption and may leave the user vulnerable to opportunistic bacterial pathogens.

Experiments done with mice show that antibiotic treatment alters the gut flora but does not eliminate it. [11] The effects of antimicrobials on microflora vary with the type of antibiotic and the location–the small intestine versus the beginning and end of the large intestine.  The graph below shows the recovery of aerobic bacteria after withdrawal of antibiotics in the mice.  There was a rapid overgrowth of aerobic bacteria which steadily fell over the next three weeks.
The same study shows the relative numbers of Salmonella in the GI tract after antibiotic treatment of the mice for one week.  Three days after Salmonella bacteria were inoculated in the gut of the mice they were sacrificed in order to assess the extent of introduction of Salmonella colonization. While results varied by antibiotic, all antibiotics used increased the presence of Salmonella versus controls. [12]

The disruption of intestinal mucosa, among other things, appears to increase host susceptibility to Salmonella infection.  As the Discussion section of the study emphasizes, even careful use of antibiotics poses potential risks:

“Even routine and appropriate use of antibiotics may have a detrimental impact on the host microbial ecosystem, which is important for host mucosal protection….Oral Salmonella challenge of antibiotic-treated mice resulted in comparable increases in intestinal Salmonella colonization, enteritis, and invasion irrespective of the antibiotic combinations used…. Despite the rapid recovery of several measurable parameters of the biome, residual subtle alterations in bacterial composition can persist and result in profoundly enhanced susceptibility to bacterial enteritis.” [13]

Cirpo is a widely prescribed antibiotic for bacterial infections of the GI tract.  It is often prescribed as empirical treatment–treatment before a diagnosis is confirmed–which can be problematic if the diagnosis is infection with Shiga toxin-producing E. coli.  Presented with a patient suffering bloody diarrhea, the clinician is probably advised to avoid Cipro and choose an antimicrobial with a different mechanism of action if antibiotic treatment is deemed necessary.  A person suffering gastroenteritis who is offered antibiotic treatment is well-served to ask questions about potential deleterious effects.

And for those Cipro users who don’t worry about the microbiotic flora of their intestines, you may want to watch your joints.  In July 2008, the FDA directed the maker of Cipro to add a black bo
x warning to the drug’s label about increased risk of developing tendinitis and tendon rupture in patients taking fluoroquinolones.

References

1.  Wong CS et al. The risk of the hemolytic-uremic syndrome after antibiotic treatment of Escherichia coli O157:H7 infections. N Engl J Med 2000 Jun 29 342 1930 -1936.  This cohort study found a 14 fold increase in the risk of HUS when antibiotics were used.

2.  Safdar N, et al. Risk of hemolytic uremic syndrome after antibiotic treatment of Escherichia coli O157:H7 enteritis. JAMA 2002;288(8):996-1001.

3.  McGannon CM et al, Different classes of antibiotics differentially influence Shiga toxin production Antimicrob. Agents Chemother. doi:10.1128/AAC.01783-09. Published online ahead of print: http://aac.asm.org/cgi/content/abstract/AAC.01783-09v1.

4.  Azithromycin prevents bacteria from growing by interfering with their protein synthesis. It is a macrolide antibiotic chemically related to erythromycin and clarithromycin.  It is among the more widely prescribed antibiotics in the US.

5.  Zhang Q et al, Gnotobiotic piglet infection model for evaluating the safe use of antibiotics against Escherichia coli O157:H7 infection.  J Infect Dis. 2009 Feb 15;199(4):486-93.

6.  Id.

7.  Supra, note 3.

8.  Cipro kills bacteria by interfering with an enzyme (DNA gyrase) that causes DNA to unwind and duplicate and thus stops cell division.

9.  Supra, note 3.

10.  Mølbak K. Human health consequences of antimicrobial drug-resistant Salmonella and other foodborne pathogens. Clin Infect Dis. Dec 1 2005;41(11):1613-20.

11.  Croswell A, et al, Prolonged Impact of Antibiotics on Intestinal Microbial Ecology and Susceptibility to Enteric Salmonella Infection.  Infect Immun. 2009 July; 77(7): 2741-2753.

12.  DSI = distal small intestine and LI = large intestine.

13.  Id.

Unlike diets that are high in natural foods, diets based on processed foods have lots of sodium and little potassium.  How big is the effect of a high sodium diet?  Hypertension affects less than 1 percent of people in isolated societies, but about one-third of adults in industrialized societies.   It is not just a high sodium problem; it is a low potassium problem. “One of the most prevalent and modifiable risk factors for hypertension is an inadequate consumption of potassium. Only about 2 percent of U.S. adults meet the current guideline for dietary potassium intake (at least 4.7 grams per day).”[1] In combination, low potassium and high sodium consumption effects on blood pressure and resulting morbidity are enormous.  Population studies have consistently shown that as potassium intake goes up, blood pressure goes down along with the prevalence of hypertension and the risk of stroke.

We are not made for a high sodium diet and our changing Western diet has far outstripped our bodies’ ability to accommodate too much sodium.  Our kidneys are designed to preserve sodium and excrete potassium.  In the tubules of the kidneys, sodium is reabsorbed and as sodium concentrations go up so does potassium excretion.  This worked very well for our forbearers who had no processed foods to eat.   It is a disaster for many of us today.  As the CDC puts it:

“Current dietary guidelines for Americans recommend that adults in general should consume no more than 2,300 mg of sodium per day. At the same time, consume potassium-rich foods, such as fruits and vegetables. However, if you are in the following population groups, you should consume no more than 1,500 mg of sodium per day (approximately 2/3 teaspoon), and meet the potassium recommendation (4,700 mg/day) with food.

•    You are 40 years of age or older.
•    You are African American.
•    You have high blood pressure.

“A CDC report shows that 2 out of 3 (69 percent) adults in the United States fall into these three groups who are at especially high risk for health problems from consuming too much sodium. Eating less sodium can help prevent, or control, high blood pressure.”[2]

Our bodies spend considerable energy regulating the concentration of sodium and potassium in and out of our cells.  You may recall the sodium/potassium pump (Na⁺/K⁺–ATPase) from high school biology that shuttles sodium ions into the cell and potassium ions out.  When excess sodium is retained, sodium concentration goes up in cells of arterial smooth muscle cells and ultimately drives calcium into cells. The net effect is contraction of the smooth muscle and arteriolar vasodilatation.  The resulting vascular resistance helps drive up pressure in tiny vessels.[3]

Despite its well-demonstrated risks, dietary salt has resisted regulation.  The double whammy of claims of Big Brother government in the kitchen and the salt-dependent food industry has so far saved salt from the fate of trans-fats and the current cut-back in added fructose.  Yet it is easier to draw a straight line from too much salt to measurable deleterious health effects that with either trans-fats or fructose.  When New York Mayor Michael Bloomberg recently called for food companies to reduce their salt in processed foods by 25 percent, he was hit with a withering barrage of criticism.  Food industry giant Cargill meanwhile, can’t say enough about the wonders of salt and urges consumers to add it to everything from fresh fruit to ice cream.[4]

It’s an interesting notion that compared to the world of foodborne pathogens, salt may indirectly account for far more excess deaths than any microbe.  The CDC counted 23,855 deaths due to hypertension in 2006.[5] If there were a foodborne bacterial agent killing 20,000 Americans a year one likes to think there would be a significant effort to limit that agent’s presence in food.  With salt, the fight may just be beginning, though a significant reduction in the sodium content of processed foods is still not in sight.

As Food Safety News has reported, Mayor Bloomberg’s efforts to reduce sodium in the American diet resulted in The National Salt Reduction Initiative (NSRI), a public-private partnership which has enlisted a wide array of food manufacturers and restaurants.[6] Still, the goals of the NSRI are modest: a 20 percent reduction in sodium in prepared foods over five years.  Given the ubiquity of salt in processed foods, a top-down regulatory approach seems ill suited to address this public health issue.  A combination of consumer awareness (including the need for increasing potassium consumption)[7] and voluntary industry action may reduce our over-consumption, but is unlikely to solve the problem.  With salt, the fight may just be beginning, and a reduction in the sodium content of processed foods sufficient to benefit the health of Americans is not yet in sight.

References

1.  Consensus Report: “A Population-Based Policy and Systems Change Approach to Prevent and Control Hypertension” report brief,  Board on Population Health and Public health Practice, Institute of Medicine of the National Academies:  http://www.iom.edu/Reports/2010/A-Population-Based-Policy-and-Systems-Change-Approach-to-Prevent-and-Control-Hypertension.aspx.

2.  See, http://www.cdc.gov/salt/.

3.  Yes, the processes involved in hypertension are vastly more complicated and well beyond the scope of this article.

4.  See, http://www.salt101.com/#/kitchen/finishing.  Diamond Crystal salt is part of the Cargill “family of products.”

5.  See, http://www.cdc.gov/nchs/fastats/hyprtens.htm.

6.  See, Flynn D, “Kraft, Subway, Starbucks to Cut Salt,” Food Safety News, April 29, 2010: https://www.foodsafetynews.com/2010/04/food-industry-taking-challenge-to-cut-salt/.

7.  I wonder how long before the fresh fruit and produce industries tumble to the huge marketing opportunity posed by a hypertensive, potassium poor population.

Consider E. coli O157:H7 which was identified as a human pathogen in 1982, some 17 years after the serious complication it can cause, the hemolytic uremic syndrome (HUS) was first described by a Swiss physician.  Does this mean that HUS causing E. coli had been around for a long time waiting to be recognized? Almost certainly. Remember, we are barely a century removed from the first direct lines drawn between various bacterial pathogens and the diseases they cause.  We still have a lot to learn about the effect of bacterial and viral organisms on human health.

The entire E. coli O157:H7 genome has been sequenced and geneticists have identified numerous apparently intermediate forms that point to a common ancestor. It is now believed that E. coli O157:H7 evolved from enteropathogenic E. coli serotype O55:H7, a cause of nonbloody diarrhea, through the sequential acquisition of phage-encoded Stx2, a large virulence plasmid, Stx1, and additional chromosomal mutations.[1] The phages that contribute to genetic change are viruses that can infect bacteria and plant their genetic material which is then incorporated into future generations of that bacterium.  

So while bacteria are “descended” from common ancestors they are also changing constantly due to “horizontal transfer” of genetic material from other contemporaneous microbes.  Geneticists can calculate the rate of change and thus the age of common ancestral forms by tracking genes that are basic to the function of the bacteria.  The rate of genetic mutation of E. coli O157:H7 indicates that the common ancestor of current E. coli O157:H7 clades[2] likely existed some 20,000 years ago.[3] E. coli O157:H7 is a relentlessly evolving organism[4], constantly mutating and acquiring new characteristics, including virulence factors that make the emergence of more dangerous variants a constant threat.[5]

And while we refer to E. coli O157:H7 and its brethren as Shiga toxin-producing E. coli, there are numerous other virulence factors within these bacteria that allow them to inflict damage.  These factors include the ability of the bacteria to attach to human cells, transmit toxin into the cells, and secrete powerful inflammatory factors that incite host response that is itself injurious.  These virulence factors are acquired over time and are constantly shifting among bacteria as they adopt to their host organisms.  In this way horizontal gene transfer and genome plasticity likely contribute to the evolution of pathogenic variants from non-pathogenic colonizers.  E. coli O157:H7 is adopted to live in the gut of cattle and other ruminants.   It may be that some of the virulence factors enhance the survival of these bacteria by providing protection against predation by bactivorous protozoa, nematodes or other predators in the soil, water, or the gastrointestinal tract of their bovine hosts.[6]

Therefore, pathogenic Shiga toxin producing E. coli (STEC) may arise when a given set of virulence genes come together in an E. coli host. What drives the selection of particular genes to create a STEC pathogen is unknown. However, because the existence of a primarily bovine animal reservoir of infection is a major difference between STEC and other pathotypes of E. coli, some genes, such as ehxA and espP[7] may be acquired by STEC to facilitate survival and persistence in the bovine gut.[8]

But haven’t we already discovered all the bugs that make us sick?  Consider the curious history of one of the more common human ailments: peptic ulcer disease.  Ulcers of the stomach and the duodenum, the first part of the small intestine, are exceedingly common.  For almost all of the last century, modern medicine recommended diet and lifestyle changes to treat peptic ulcer disease. Avoid spicy foods, reduce your stress, and your ulcer problem should get better, physicians counseled patients.  Unfortunately, that advice was largely useless because the true cause of the problem was not identified until 1982, yes, the same year that E. coli O157:H7 was first identified.

Two Australian researchers, Barry Marshall and Robin Warren identified a bacteria, Helicobacter pylori, that was consistently present in cases of peptic ulcer disease.  Their investigations, including self-infection with H. pylori, demonstrated that antibiotic treatment could rid the gut of the bacteria and cure ulcers.  The medical establishment initially responded with skepticism, but over the next twenty years the role of H. pylori in peptic ulcer disease and the treatment of it with antibiotics became an accepted part of basic medicine.  Marshall and Warren were awarded the Nobel Prize for their work in 2005.

Most humans carry H. pylori in  their stomachs, though only a modest percentage of us develop peptic ulcer disease.  While H. pylori is today one of the more heavily researched bacteria, it was completely off the radar until very recently.  How does a common bacterium responsible for a significant disease burden escape notice and why are so many of us carrying around this pathogen in our stomachs?   

It is accepted that this organism has colonized humans for many thousands of years, and the successful persistence of H. pylori in human stomachs for such a long period suggests that this bacteria may be advantageous to its host.[9] There is evidence that H. pylori provide protection against gastroesophageal disease (GERD) and some esophageal cancers.[10] However, since H. pylori is also implicated in serious human disease, including carcinoma of the stomach, it is hard to consider this bacteria as co-evolving with its human hosts in a mutually beneficial relationship.  Here again the geneticists offer insights.  Research suggests that H. pylori’s acquisition of certain virulence factors is quite recent, perhaps as a result of human interaction with various animal populations.[11] One of the many lessons about pathogenic bacteria is that what is tolerated or welcomed by one animal host made be disastrous to another.  And today’s benign bacteria may become a serious pathogen in the hugely mutable world of microbes.

When the CDC talks about the risks of “emerging pathogens” it is fair to think of those pathogens as finally coming into our view rather than into existence.  What we don’t know in a microbiological sense, can and will hurt us.  It is fair to assume that the years ahead will lead to the “discovery” of new pathogens implicated in human disease that have been doing their damage for centuries just waiting for us to notice.

[1] Kaper JB and Karmali MA.  The Continuing Evolution of a Bacterial Pathogen.  PNAS vol. 105 no. 12 4535-4536 (March 2008); Wick LM, et al.  Evolution of genomic content in the stepwise emergence of Escherichia coli O157:H7.  J Bacteriol 187:1783-1791(2005).

[2] A group of biological taxa (as species) that includes all descendants of one common ancestor.

[3] Zhang W, et al.  Probing genomic diversity and evolution of Escherichia coli O157 by single nucleotide polymorphisms.  Genome Res 16:757-767 (2006).

[4] Robins-Browne RM.  The relentless evolution of pathogenic Escherichia coli.  Clin Infec Dis. 41:793-794 (2005).

[5] Manning SD, et al.  Variation in virulence among clades of Escherichia coli O157:H7 associated with disease outbreaks.  PNAS vol. 105 no. 12 4868-4873 (2008).  (“These results support the hypothesis that the clade 8 lineage has recently acqui
red novel factors that contribute to enhanced virulence.  Evolutionary changes in the clade 8 subpopulation could explain its emergence in several recent foodborne outbreaks; however, it is not clear why this virulent subpopulation is increasing in prevalence.”)

[6] Steinberg KM and Levin BRGrazing protozoa and the evolution of the Escherichia coli O157:H7 Shiga toxin-encoding prophage Proc. R. Soc. B (2007) 274, 1921-1929

[7] Encoding for hemolysin, an exotoxin which can lyse–cut apart–red blood cells and  extracellular serine protease which can cleave coagulation factors.

[8]Shiga Toxin-producing Escherichia coli Strains Negative for Locus of Enterocyte Effacement
Hayley J. Newton,1 Joan SloanEmerging Infectious Diseases • www.cdc.gov/eid • Vol. 15, No. 3, March 2009

[9]Ahmed N, 23 years of the discovery of Helicobacter pylori: Is the debate over? Ann Clin Microbiol Antimicrob. 2005; 4: 17.

[10] Shahabi S, et al, Protective effects of Helicobacter pylori against gastroesophageal reflux disease may be due to a neuroimmunological anti-inflammatory mechanism.  Immunology and Cell Biology 86, 175-178 (February 2008).

[11]Ahmed N, et al, Helicobacter pylori – a seasoned pathogen by any other name.  Gut Pathogens 2009, 1:24.

Glyphosate (Roundup® and other products) is a valuable herbicide for corn and soybean growers. When applied post emergence to Roundup Ready® soybean varieties and corn hybrids, glyphosate provides broad-spectrum, low-cost weed control with excellent crop safety. It is better than many other herbicides at controlling larger weeds, has no soil activity (allowing for flexible crop rotations), and has low environmental and human health risks. In several respects, glyphosate and Roundup Ready® crops have simplified weed management. Even before Roundup Ready® crops were introduced, glyphosate was (and continues to be) a valuable herbicide in no-till cropping systems, and saves soil, fuel, and labor. No other single herbicide has provided these benefits to U.S. corn and soybean growers.

Glysophate-based herbicides all work by inhibiting a critical plant enzyme–EPSP synthase[3]–needed to make proteins essential to plant growth.  Since most plants share this enzyme, glysophate is effective across a broad spectrum of plants. The chart below depicts the rapid rise of herbicide-tolerant (HT, i.e. Roundup Ready®) crops in the US.  Bt is Bacillus thuringiensis, the naturally occurring soil-borne bacterium that is fatal to some insect larvae and now also a standard part of many genetically modified crops. The enormous success of Roundup Ready® crops has, of course, meant a concomitant increase in the use of Roundup as a frontline agricultural herbicide.  As seen below, the use of Roundup (glysophate) took off in the 1990s and is still climbing.  This has proven to be a brilliant business model for Monstanto, which supplies the GMO seed and the companion herbicide while taking market share from other competing herbicides.  The widespread use of Roundup® is due to the acknowledged benefits of glyphosate: it is less toxic and persists in the environment for a shorter time than most of its older competitors. But as the National Research Council report notes, one of the risks of the continued widespread use of glyphosate is the seemingly inevitable rise of glyphosate-tolerant weeds.  This is already happening.  Since the late 1990s various glyphosate-resistant broadleaf weeds have been reported across the U.S. and in other parts of the world.[4] Additionally, an increasing number of week species have become resistant to ALS-inhibitors (acetolactate synthase), a group of herbicides that kill weeds by preventing the plants from producing essential amino acids that are needed for proper growth and development.  As weeds become resistant, their progeny also carry genes resistant to herbicides.  Unless control measures are targeted and immediate, the spread of herbicide-resistant weeds grows. What this means for the genetically modified crops that form the backbone of U.S. agriculture remains to be seen.  But it is certainly true that part of the answer will include divergence from the routine and homogeneous use of Roundup® and a change in basic weed management practices.  For those opposed to GMOs, the triumph of “weed resistance” will provide fodder for commentaries on the dangers of tinkering with plant genes even as the benefits are documented. If Nature has its way, it may just be the weeds that alter the course of genetically modified crops and agribusiness in the U.S.  Or as the noted writer and lepidopterist Robert M. Pyle has aptly put it: “But make no mistake: the weeds will win; nature bats last.” References 1.  Impact of Genetically Engineered Crops on Farm Sustainibility in the United States.  Committee on the Impact of Biotechnology on Farm-Level Economics and Sustainability; National Research Council 2010, 318 pages.  To purchase: http://www.nap.edu/catalog.php?record_id=12804. 2.  See Facts about Glysophate Resistant Weeds on the web at:  www.ces.purdue.edu/extmedia/GWC/GWC-1.pdf.  The authors are part of a group of university based scientists from primary agricultural states. The group’s website is www.glysophateweedscrops.org. 3.  5-enolpyruvylshikimate-3-phosphate.  If you are really up on your biochemistry, see http://gpries.myweb.uga.edu/bcmb8010/. 4.  The first glyphosate resistant weed was rigid ryegrass (Lolium rigidum) in Australia in 1996.  The distinction in the US appears to go to Horseweed or Marestail (Conyza Canadensis) an annual weed, formerly of little import that is now becoming a significant problem.

Dietary and lifestyle factors in the US are responsible for death rates that exceed most other Westernized countries.  Primary preventable causes of death include: smoking (465,000 per year), hypertension (395,000), obesity (216,000), physical inactivity (191,000), high blood glucose levels (190,000), high levels of low-density lipoprotein cholesterol (113,000), and other dietary risk factors also mean that major changes in diet combined with changes in health care could make huge differences in our population’s health.[1]

Indeed, four of the ten leading causes of death in the U.S., including the top 3, can be influenced by diet: coronary heart disease, cancer, stroke, and diabetes.  Critical dietary factors associated with these conditions include those that are too high in calories, fat, saturated fat, cholesterol, and sodium or too low in fiber-containing foods.[2]

Diabetes treatment now costs over $100 billion annually, a figure that is projected to triple by 2034 to an annualized figure of $334 billion.[3] About 90% of those with diabetes have type 2 in which the pancreas produces insulin but the body becomes increasingly resistant to insulin’s ability to break down glucose.  A leading risk factor for type 2 diabetes is being overweight.

There is, of course, an ongoing torrent of specialty diets which often feature fundamentally opposing approaches to what constitutes healthy eating.  For instance, the Atkins Diet focuses on consumption of high levels of protein and fat with few carbohydrates; the book The China Study insists that all animal protein is bad and that fruits and vegetables hold the key to a healthy life; while Gary Taubes’s Good Calories, Bad Calories takes issue with the notion that fat is bad and places the blame for America’s diet-related health maladies on the amount of refined carbohydrates we eat.  This idea that refined carbohydrates (sugar, high fructose corn syrup, white flour, French fries) are particularly bad rests on research showing that they play havoc with the body’s blood sugar (glucose) levels and provoke storage of excess fat.  Another potential side effect of refined carbohydrate consumption is that it may actually increase feelings of hunger leading to a cycle of over consumption.

And if it sounds like a lot of your favorites are on the “eat less” list, consider that alcohol is another problematic consumable. The potential virtues of red wine aside, alcohol itself is devoid of nutrients.  And while pure alcohol contains no carbohydrates (the sugars present in grain are consumed during distillation) it is highly caloric (7 calories per gram versus 4 calories per gram of carbohydrate).  Alcohol is also preferentially metabolized and may slow normal fat metabolism.  The intermediate byproduct of alcohol metabolism in the liver–acetaldehyde–is toxic and is associated with several types of cancer.

There are legions of Americans who assume they are avoiding the dangers of a diet featuring carbohydrates in the form of high fructose corn syrup by consuming vast quantities of diet drinks.  Not so fast.  An intriguing commentary in the Journal of the American Medical Association makes the case that while artificial sweeteners have the potential for at least short term weight loss when substituted for sugared foods, the long-term effects may be just the opposite.[4] This can occur due to the ability of intense sweeteners to:

…cause taste preferences to remain in, or revert to, an infantile state (ie, with limited tolerance for more complex tastes). Individuals who habitually consume artificial sweeteners may find more satiating but less intensely sweet foods (eg, fruit) less appealing and unsweet foods (eg, vegetables, legumes) less palatable, reducing overall diet quality in ways that might contribute to excessive weight gain.[5]

Of particular concern is the ability of diet drinks, consumed in the absence of other foods, to produce “a dissociation between sweet taste and calorie intake.”[6] Limited research on rats suggests that this may disrupt hormonal and neurobiological pathways leading to long-term increased calorie consumption and weight gain.  Long-term studies on humans are needed to “flesh out” this hypothesis.

Few of us probably sufficiently ascribe the quality of our diet to our basic state of health.  And while it is very easy to become overwhelmed with the endless claims of various diets, there are a few truths that ought to inform how we eat: eating too much is bad and eating too much of certain things like highly refined carbohydrates is particularly bad.  A diet high in saturated fat and cholesterol is not good; a diet high in non-starchy vegetables is good, as is one that features whole grains and lean proteins.  Moderation in all things is very good.

And so as 2010 unfolds, take time to consider the fundamentals of your diet and the critical food safety issue it represents.  Contaminated foods can certainly result in very serious illness, but a good diet can help ensure long-term health.

1.  Danaei G, Ding EL, Mozaffarian D, et al. The preventable causes of death in the United States: comparative risk assessment of dietary, lifestyle, and metabolic risk factors. PLoS Med 2009;6:e1000058-e1000058.
2.  Frazão, E., The American Diet: A Costly Health Problem FoodReview (202) 219-0911(1996).
3.  Huang, ES et al. Projecting the Future Diabetes Population Size and Related Costs for the U.S. DIABETES CARE December 2009 vol. 32 no. 12: 2225-2229.
4.  Ludwig DS, Artificially Sweetened Beverages Cause for Concern.  JAMA. 2009;302(22):2477-2478.
5.  Id.
6.  Id.

Norovirus is such a common problem precisely because it is a virus.  Viruses are small, really small.  Viruses range from 20 to 250 nanometers (one nanometer is a billionth of a meter).  By comparison, bacteria are more on the order of 1,000 nanometers.  If a bacterium were the size of a human, a virus particle would be a mouse.  Mind you, bacteria are plenty small themselves.  We have about 10 times as many bacteria in our bodies and we have cells.  You could fit hundreds of thousands of bacteria on the head of a pin.  

And here is the bad news: it takes only 10 to 100 norovirus particles to cause an infection.  But because those particles are so infinitesimal, a single vomiting episode can expel over 30 million particles.  But the bad news does not end there. Two other factors help make norovirus the most common cause of foodborne illness: unlike bacterial gastroenteritis in which the infectious bacteria is contained only in the feces, norovirus is present in both the vomitus and feces of an infected person; further, because it is so tiny, norovirus can aerosolize.  If an infected person vomits, norovirus is in the air.  Flush the toilet and you cause aerosol generation.  Those aerosolized viral particles can then settle on any surface ready to be picked up by the next pair of hands.

And that is another important point about norovirus as compared to bacterial food pathogens.  As the CDC reports, foodborne outbreaks of norovirus occur most often when infected food handlers fail to wash their hands properly after using the toilet.  With bacterial pathogens, the contamination typically occurs independently from food handlers.   

Symptoms of a norovirus infection can occur as early as 12 hours after exposure, but typically within 24 to 48 hours after the virus is ingested. Noroviruses cause the classic “stomach flu.”  Real influenza, such as H1N1, is an upper respiratory illness.  Symptoms of a norovirus infection typically begin abruptly and include nausea, vomiting, diarrhea and stomach cramps.  A low-grade fever, chills, headache, and muscle aches may also occur.  Vomiting is often relentless during the first 24 hours.  But if there is any good news about norovirus infections, they are usually relatively short-lived and a full recovery generally occurs after a couple of days.  

As with most viral illnesses, there is not much to do about a norovirus infection except suffer through it.  A visit to the doctor during the acute illness is only apt to risk infection of others.  Occasionally, a norovirus infection can cause a very serious illness, typically in the elderly or those with underlying health problems.  The most likely complication is volume depletion–dehydration–particularly since rehydration is most difficult while vomiting continues.  In cases of serious volume depletion a trip to the ER and an IV may provide the only relief.  

If you suspect you have suffered a norovirus infection–stay home!  Make sure you use a disinfectant in your bathroom, wash your hands ruthlessly, and try to limit contact with other people until at least three days after recovery.