A recent study, published in the journal Nutrition, demonstrated the effect of broccoli and blueberries on bowel inflammation in an animal model of inflammatory bowel disease (IBD).¹ Researchers fed IBD mice either a control diet, or a diet with 10 percent broccoli or ten percent blueberries. Both the broccoli- and blueberry-fed mice exhibited similar changes in gut microbiota with one exception: the broccoli-fed mice had lower levels of the bacteria Faecalibacterium prausnitzii. Both diets also increased the size of colon crypt cells and number of goblet cells per crypt. (Intestinal crypt cells are located in the “valleys” of the intestinal villi.)

Differences between the broccoli- and blueberry-fed mice were also observed. Higher concentrations of butyric acid and lower concentrations of succinic acid were found in the broccoli-fed mice; the only diet to reduce inflammation in the colon was the broccoli-fed diet; and broccoli-fed mice exhibited less translocation of microbes to mesenteric lymph nodes than the blueberry-fed or control mice. (This means in the broccoli-fed mice gut bacteria stayed in the gut rather than translocating through a leaky gut into gut-associated lymph nodes.)

One reason the blueberry-fed mice may not have had as beneficial an impact as the broccoli-fed mice could be the high fructose content of blueberries. Foods high in fructose can produce fermentation in the gut.² Inflammatory bowel disease involves a gut sensitivity to the microbes residing there. Increased fermentation may further disrupt an already sensitive environment.

Blueberries have been found to benefit microbial metabolism in the colon, likely due to the anti-inflammatory effects of blueberry’s phenolic compounds.³ Broccoli is also well known for its protective effects in the large bowel, mostly attributed to the sulforophane and indole-3-carbinol (I3C) bioactives.⁴

This study is helping to prove that whole foods absolutely affect the microbial population. The moral of the story? Well, more studies need to be done to confirm the effects in humans, and to elucidate the mechanisms at work, but in the meantime, eat more broccoli! In fact, eat more vegetables (and fruits if you aren’t sensitive) in general. The thousands of phytochemicals found in vegetables and fruits have more beneficial effects in our guts—and our entire bodies—than we will ever know.

References

1. G. Paturi, et al., “Influence of dietary blueberry and broccoli on cecal microbiota activity and colon morphology in mdr1a(-/-) mice, a model of inflammatory bowel diseases.” Nutrition. 2011 Nov 22. [Epub ahead of print]
2. P.R. Gibson, et al., “Review article: fructose malabsorption and the bigger picture.” Aliment Pharmacol Ther. 2007 Feb 15;25(4):349-63.
3. W.R. Russell, et al., “Availability of blueberry phenolics for microbial metabolism in the colon and the potential inflammatory implications.” Mol Nutr Food Res. 2007 Jun;51(6):726-31.
4. E.H. Jeffrey and M. Araya, “Physiological effects of broccoli consumption.” Phytochem Rev. 2009;8:283-9.

Leonard Smith, M.D.
Dr. Leonard Smith is a prominent Board-Certified, general, gastrointestinal and vascular surgeon who had a successful private practice for 25 years. In addition to his active surgery practice, he also incorporated lifestyle, diet, supplementation, exercise, detoxification, and stress management into many of the therapies he would prescribe. Many of his patients with cancer, cardiovascular disease, and other serious illnesses did so well under his treatment regimes that he began to devote most of his career to foundational health care and preventive medicine.

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You’ve probably heard about the deadly listeria outbreak linked to cantaloupe grown on a Colorado farm, Jensen Farms. Twenty-one deaths (and counting) have been reported out of 109 people infected with the bacterium Listeria monocytogenes in over 20 states.

The cantaloupes were voluntarily recalled on September 14, but cantaloupes may still be in refrigerators across the country. Jensen Farms or Rocky Ford-branded cantaloupes should be avoided. Worse, listeria infection can take up to two months to develop in a person who has eaten the cantaloupe, so more illnesses are expected to occur, even after the fruits has been recalled. The CDC and FDA say that cantaloupes from other farms are safe to eat, as this outbreak has been linked to only one farm.

Listeriosis, the disease caused by listeria bacteria, is rare, but is deadly to 30 percent of people infected. Among the elderly, 90 percent are hospitalized after infection. In pregnant women listeria usually causes mild illness, but can result in stillbirths or miscarriages. Previously, listeria outbreaks were mostly associated with deli meats and soft cheeses. Pregnant women are usually cautioned to avoid processed meats and soft cheeses for this reason. Cantaloupe may now be added to that list.

Cantaloupes are known to be more susceptible to bacteria contamination due to their rough skin, a veritable hide-out for bacteria. If listeria is present on the rind, when cut open, the bacteria will contaminate the fruit. It is also more difficult to clean cantaloupe because of the rough surface. It’s probably best to clean the skin, and then also rinse the cut fruit before eating.

For the latest updates, visit the CDC’s listeria webpage.

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In some people who take antibiotics, the uncomfortable side effect of diarrhea results. This happens because antibiotics disturb the gut bacterial balance. Antibiotics, aptly named as they are, work by killing bacteria—both good and bad bacteria. This alteration of gut bacteria can result in an imbalance that favors pathogenic bacteria, resulting in diarrhea. This is known as antibiotic-associated diarrhea (AAD). One of the most severe forms of AAD is Clostridium difficile-associated diarrhea.

A recent review of 22 studies, and a recent meta-analysis of randomized controlled trials, both sought to determine the effectiveness of probiotics on the prevention of antibiotic-associated diarrhea. In the review, the lead researcher stated, “Overall in twenty-two studies, probiotic prophylaxis significantly reduced the odds ratio of developing AAD by approximately 60 percent. This analysis clearly demonstrates that probiotics offer protective benefit in the prevention of these diseases.” A researcher presenting the results of the meta-analysis stated, “The preventive effect of probiotic use remained significant regardless of species used, adult versus child populations, study quality score and antibiotic administered.”

These findings were presented at the American College of Gastroenterology’s 76^th Annual Scientific Meeting in Washington, D.C. in late October. The acknowledgement of the beneficial effects of probiotics by such a group is encouraging. Certainly, the evidence is impossible to ignore. Next time you are prescribed antibiotics, ask your doctor about taking probiotics. If your doctor is not familiar with probiotics, educate him/her!

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Small intestinal bacterial overgrowth (SIBO) is gut condition in which there are abnormally large numbers of gut bacteria in the terminal ileum of the small intestine (the end of the small intestine, just before the colon). SIBO is one form of dysbiosis, or gut imbalance. Normally, the colon is where gut bacteria greatly increase in number, with the small intestine housing smaller numbers of bacteria. In SIBO, the high amount of gut bacteria in the small intestine leads to excess gas and discomfort. The condition is common in people with irritable bowel syndrome (IBS).

It has been known for a while that SIBO is more common in alcoholics, but a recent study is the first to look at the relationship of SIBO in people with moderate alcohol consumption. As it turns out, the researchers, from the Mayo Clinic and Dartmouth-Hitchcock Medical Center, found that moderate alcohol consumption—one drink per day in women and two per day in men—could lead to SIBO.

Dr. Gabbard, the lead researcher, stated, “While typical treatment for SIBO has been antibiotics, probiotics or a combination of the two, the question now becomes what is the exact association between moderate alcohol consumption and SIBO and whether alcohol cessation can be used as a treatment for this potentially harmful condition.”

Certainly, the things we consume—food, drink and medication—affect our gut. If you have been considering decreasing your alcohol intake (there are many good reasons to do so), it may just help improve your gut balance.

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The human gut is home to thousands of different bacterial species, totaling 100 trillion bacterial cells—that’s about four pounds of bacteria, or the weight of a brick. The composition of this bacterial population (also known as the gut microbiota), is currently being studied. Dr. Smith recently blogged on it.

A new study by researchers from the University of Pennsylvania, published in Science, takes the findings further. This new study found two major gut types—Bacteroides and Prevotella—based on gut bacterial population groups in 98 healthy volunteers who were asked to fill out questionnaires that assessed dietary habits. Stool samples were collected to determine their gut microbiota composition.

The researchers found a link between dietary habits and gut types. People who ate a diet high in meat and saturated fat were higher in Bacteroides bacteria, and people who had a diet high in carbohydrates had more Prevotella bacteria. Researchers then took ten volunteers and fed half of them a diet high in fat and low in fiber, and fed the other half a low-fat, high-fiber diet. By the end of ten days the bacterial populations had begun to change, but were still predominantly the same Bacteroides and Prevotella groups. This indicates that it’s possible to change the gut microbiota with diet, but it will take more than a short term change to see any major difference.

Next steps will be to replicate these findings to confirm them, and to take the studies further by looking at whether these gut types are associated with health or disease. It’s an exciting area of research, working out the details of what I have said all along—your gut is the foundation of the health of the rest of your body. It all begins in the gut.

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The gut-brain axis involves the connection of the gut to the brain. This connection goes in both directions—from the brain to the gut and from the gut to the brain. In one way, the gut-brain axis is connected by the vagus nerve—a large nerve connecting the brain to the intestines and other organs. The vagus nerve both sends messages to various organs, and also receives messages from these organs—including the gut—to send to the brain. A new study has established the vagus nerve as a main form of communication from the gut bacteria to the brain.

In an animal model, researchers were able to show that mice fed the probiotic Lactobacillus rhamnosus JB-1 showed less stress-, anxiety-, and depression-related behaviors than did mice not fed the bacteria. Further, the probiotic mice had lower levels of the stress hormone corticosterone, and they also experienced changes in the expression of receptors of the neurotransmitter GABA (gamma-aminobutyric acid) in the brain—highlighting the ability of probiotics to directly affect brain chemistry under normal conditions.

This is an early study that will need to be replicated in humans, but studies like these pave the way for our understanding of the complexities of the gut connection. Did you ever think your gut could have such an effect on your health? If you read my blog regularly, I sure hope so!

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Alzheimer disease is the most common form of dementia, accounting for 50 to 80 percent of all dementia cases. Dementia involves memory loss and other impaired intellectual abilities, all of which interfere with everyday life. Though most people with Alzheimer disease are over 65 years, up to five percent have early-onset Alzheimer’s, which usually appears during the mid-40s or 50s.

Beta-amyloid is a peptide found in plaques in the brains of people with Alzheimer disease. For a long time, it has been thought that beta amyloid-played a causative role in the neural degeneration of the disease. This may be a mistaken belief, however, as highlighted by a recent Phase III clinical trial on the anti-amyloid drug semagacestat. Patients in this trial were expected to improve on this drug, which interferes with the production of gamma-secretase, the enzyme that produces beta-amyloid. Instead, the drug “did not slow disease progression and was associated with worsening of clinical measures of cognitions and the ability to perform activities of daily living,” according to a press release put out by the drug manufacturer, pharmaceutical giant Eli Lilly. The trial was stopped before completion.

As it turns out, beta-amyloid is an antimicrobial peptide, and is suggested to be secreted by the brain in self-defense against infectious pathogens, as David Perlmutter, M.D. stated at the Institute for Functional Medicine’s 20^th Symposium this past summer. We know beta-amyloid plaque builds up in the brain in people with Alzheimer disease, but what if its presence was a self-defense mechanism rather than the actual root cause of Alzheimer’s?

In a recent study by researchers at Mass General Institute for Neurodegenerative Disease, we may have our answer. The researchers stated, “Rather than beta-amyloid acting as a sole independent initiator of neuroinflammation, our data raise the possibility that the peptide may be part of a response mounted by the innate immune system. An absence of the peptide may result in increased vulnerability to infection.”¹

Two main pathogens are implicated as possible triggers of Alzheimer disease: Herpes simplex virus 1, the virus known for causing cold sores of the mouth, and found in about 90 percent of all adults; and Chlamydia pneumonia, the respiratory bacteria known to cause pneumonia.

In one study, the presence of anti-HSV IgM antibodies was found to be an even bigger risk factor for the development of Alzheimer disease than even the “Alzheimer’s gene” APOE4 allele.² In describing how Herpes may lead to Alzheimer’s, the researchers state, “Recurrent reactivation of HSV might act as a potent stimulus to the brain microglia, increasing the level of cytokines and initiating a positive feedback cycle that gives rise to an increasing accumulation of pathological changes.”

DNA from HSV1 and from Chlamydia pneumoniae has been found in the brains of people with Alzheimer disease.^3,4 HSV1 was found in specific areas affected by Alzheimer’s, and Chlamydia was actually cultured from brain samples taken from recently-deceased Alzheimer’s patients, indicating the virus was alive in the brain.

Chlamydia pneumonia is also known as the “heart attack” bacteria, found in the intraclavicular space/fluid between gums and teeth. The best prevention for this, incidentally, is the use of Plaquers dental floss; dental floss with a handle. When the bacterium is found, orthodontal work should be performed. People with high levels of hs C-reactive protein (a marker of inflammation in the body) are at particular risk for mouth infection with C. pneumoniae bacteria. C. pneumoniae is associated with heart disease because it is also commonly found in the soft plaques of people who die of acute heart attack.

Dr. Perlmutter recommends L-lysine and vitamin D3 supplementation, in addition to a diet high in lysine, which includes whole grains, fruits, vegetables, cheese, yoghurt and fish, and is low in tofu and other soy foods high in arginine. It is thought that activation of the virus, as with cold sore outbreaks, is a sign the virus might be active in other areas, like the brain. Preventing this may be helpful for people with Alzheimer’s.

So, why do people get infections in the first place, and why do these infections get activated? Well, lack of vitamin D, which is more common than most people realize, and uncontrolled blood sugar levels and insulin resistance, both triggered by a diet high in refined carbohydrates and sugar, are factors which affect both cellular and adaptive immunity, making us more prone to viral and bacterial infections.

It is important to note that there is much more to this story than infections. Alzheimer disease is a multifactorial “perfect storm” of triggers—usually inflammatory triggers—that interact and overlap, creating the final neurodegeneration of Alzheimer’s. Infectious triggers are just one small piece to this puzzle. For general protection against Alzheimer’s, remove sugar from the diet, reduce saturated fat intake, and incorporate vitamin D, omega-3 fish oil, pre- and probiotics, fiber and digestive enzymes. Be sure to sleep well, eliminate regularly, get plenty of exercise and be happy.

References

1. Soscia SJ, et al., “The Alzheimer’s disease-associated amyloid beta-protein is an antimicrobial peptide.” PLoS One. 2010 Mar 3;5(3):e9505.
2. Letenneur L, et al., “Seropositivity to herpes simplex virus antibodies and risk of Alzheimer’s disease: a population-based cohort study.” PLoS One. 2008;3(11):e3637.
3. Itzhaki RF and Wozniak MA, “Herpes simplex virus type 1 in Alzheimer’s disease: the enemy within.” J Alzheimers Dis. 2008 May;13(4):393-405.
4. Gerard HC, et al., “Chlamydophila (Chlamydia) pneumoniae in the Alzheimer’s brain.” FEMS Immunol Med Microbiol. 2006 Dec;48(3):355-66.

Leonard Smith, M.D.
Dr. Leonard Smith is a prominent Board-Certified, general, gastrointestinal and vascular surgeon who had a successful private practice for 25 years. In addition to his active surgery practice, he also incorporated lifestyle, diet, supplementation, exercise, detoxification, and stress management into many of the therapies he would prescribe. Many of his patients with cancer, cardiovascular disease, and other serious illnesses did so well under his treatment regimes that he began to devote most of his career to foundational health care and preventive medicine.

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I have blogged before on superbugs in our bodies—like C. diff, MRSA and Klebsiella pneumoniae. Superbugs is the term for bacteria that have developed antibiotic resistance, making the infections they cause very difficult to treat. The main reason for the development of these superbugs is the overuse of antibiotics—in medicine, food production (livestock) and even in hand soaps.

Now, there’s a new superbug in town, a superbug of a different kind. And who is behind it, but Monsanto, the biotechnology giant. It seems that one of Monsanto’s biggest money-makers—Bt corn, is creating superbugs. The majority of non-organic corn planted in the U.S. is genetically modified to produce a toxic compound against western corn rootworms—a major corn pest. This corn is well-known as Bt corn, because it contains a gene from the soil microorganisms Bacillus thuringiensis (Bt), which produces an insecticide against the corn rootworm.

Genetically modified Bt corn worked so well against the corn rootworm that some farmers began planting it every year, instead of the usual rotation of growing corn one year and soybeans the next—a method that helps reduce pest populations. If there is one thing that farmers should know, it’s that planting the same thing every year is a recipe for disaster (even if it doesn’t seem that way at first).

It turns out the corn rootworms, much like the superbug bacteria infecting humans, are developing a resistance to the Bt toxin that usually destroys the pest. A few farms in Iowa are reporting that the Bt corn no longer kills the corn rootworm, meaning the bugs—now superbugs—have developed resistance to the Bt toxin. First superbugs in our guts, now superbugs on corn, soon superbugs everywhere. (Anyone notice a problem, here?)

Competitors of Monsanto estimate that about one-third of all the corn grown in the U.S. is Monsanto’s Bt corn. These competitors have their own Bt corn, with slightly different genes, that they are offering as a solution for the Bt resistant rootworm. Are you kidding? This seems ridiculous to me. It’s like placing a Band-Aid on a war wound. If they think that the corn rootworm won’t also develop resistance to their Bt toxin, they’re crazy. Unfortunately, it’s all about money. Preserving human health, or even feeding the planet, has nothing to do with it.

Corn and its by-products are in so many foods. Try to buy products using organic corn, or at least non-GM corn, to avoid being part of the human experiment that is the consumption of GM foods in this country. We just don’t know if they’re safe yet, and many studies suggest they’re not.

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Would you be surprised to know that eating a high-fat meal and/or high-sugar meal causes your arteries to not work in a normal manner? Let’s say we start the day with either coffee with cream/sugar and donuts, or same coffee/sugar with eggs and toast with butter/jam. And then for lunch or supper, we eat meals with high-fat meat, bread and butter, a baked potato with sour cream and butter along with an alcoholic drink (or even ice tea with sugar). Then we finish the meal with a nice dessert.

Each of these meals can cause your arteries not to function properly by the end of the meal which could last for several hours!¹ If you tend to eat this way, most of the day your arteries are constricted and not dilating normally in response to routine activities. The result, at the very least, is high blood pressure. This problem can be eliminated simply by cutting out the excess saturated fat and sugar, and adding probiotics or cultured foods high in bifidobacteria, in addition to eating plenty of vegetables throughout the day.

The above illustration of the diet-artery connection illustrates just one of the many ways to create a problem known as endothelial dysfunction, a condition that occurs when the cells lining the arteries, veins, and lymphatics don’t work properly.² There are a multitude of ways to cause the vessels to not dilate or constrict normally, and to cause the lining to leak (let’s call it leaky vessel syndrome). Endothelial dysfunction is a precursor to atherosclerosis.³ Here is a short list of endothelial dysfunction triggers:

1. Smoking, polluted air,⁴ food, and water⁵ – All of these create excess free radicals which are a major cause of endothelial dysfunction.

2. High blood sugar and/or high insulin levels – High blood sugar results in glycosylation (think of it like a sticky sugar coating) of the insulin receptor substrate, which eventually leads to an inability of protein kinase B (Akt) to increase endothelial nitric oxide synthase (eNOS) enzyme activity, resulting in low nitric oxide (NO) and poor blood vessel function.⁶

3. Microbes (bacteria, viruses, fungi and parasites), parts of microbes, and toxins made by microbes migrating from inside the intestinal lumen into the arterial, venous and lymphatic circulation – Microbes and their toxins activate white blood cells and they release bullets (anti-microbial peptides) named alpha-defensins that not only damage the microbes but the endothelial lining as well.

4. Stress – Stress increases cortisol, which can elevate blood sugar and insulin, again sugar coating receptors to result in low NO, and thus, endothelial dysfunction.

5 Aging – Aging decreases stem cells that help with repair processes, increases blood cortisol levels (see number 4), and decreases bifidobacteria levels in the colon. All of this leads to endothelial dysfunction.

6. Increased body fat, especially in abdomen – Even a modest gain of about 8 pounds (which can happen over a vacation) will cause endothelial dysfunction. “In normal-weight healthy young subjects, modest fat gain results in impaired endothelial function, even in the absence of changes in blood pressure. Endothelial function recovers after weight loss. Increased visceral (belly) rather than subcutaneous fat predicts endothelial dysfunction.”⁴

One of the mechanisms by which fat hurts the arteries is by releasing a cytokine known as resistin. Resistin has been shown to cause oxidative stress and decrease endothelial nitric oxide synthetase (eNOS) which is essential for nitric oxide (NO) production, itself essential for arterial health and function.

7. Physical inactivity – Merely by doing nothing, the process of ongoing free radical activity due to diet, stress and environment, will decrease nitric oxide (our natural vasodilator), superoxide dismutase (our own natural anti-oxidant) and citrate synthetase (the enzyme in our mitochondria involved energy production—essential to a healthy heart / blood vessel function). These natural sources of blood vessel protection return merely by walking briskly on a regular basis.⁵

8. Diabetes types 1 and 2 – Again, elevated blood sugar and either high or low insulin levels, as are seen in diabetes, will lead to endothelial dysfunction as described above.

9. Drugs which elevate or lower blood sugar and insulin – Many diabetic drugs can cause endothelial dysfunction by not maintaining steady levels of blood sugar and insulin. Insulin itself is one of the worst offenders.

10. Even children receiving second-hand smoke in a household with smokers, begin developing endothelial dysfunction at an early age.

References

1. Rudolph TK, et al., “Acute effects of various fast-food meals on vascular function and cardiovascular disease risk markers: The Hamburg Burger Trial.” Am J Clin Nutr. 2007 Aug;86(2):334-40.
2. Endemann DH and Schiffrin EL, “Endothelial dysfunction.” J Am Soc Nephrol. 2004 Aug;15(8):1983-92.
3. Davignon J and Ganz P, Role of endothelial dysfunction in atherosclerosis.” Circulation. 2004 Jun 15;109(23 Suppl 1):III27-32.
4. Romero-Corral A, et al., “Modest visceral fat gain causes endothelial dysfunction in healthy humans.” J Am Coll Cardiol. 2010 Aug 17;56(8):662-6.
5. Suvorava T et al., “Physical activity causes endothelial dysfunction in healthy young mice.” J Am Coll Cardiol. 2004 Sep 15;44(6):1320-7.
6. Wautier JL and Schmidt AM, “Protein glycation: a firm link to endothelial dysfunction.” Circ Res. 2004 Aug 6;95(3):233-8.

Leonard Smith, M.D.
Dr. Leonard Smith is a prominent Board-Certified, general, gastrointestinal and vascular surgeon who had a successful private practice for 25 years. In addition to his active surgery practice, he also incorporated lifestyle, diet, supplementation, exercise, detoxification, and stress management into many of the therapies he would prescribe. Many of his patients with cancer, cardiovascular disease, and other serious illnesses did so well under his treatment regimes that he began to devote most of his career to foundational health care and preventive medicine.

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In a recent study published in the journal Clinical Infectious Diseases, meat and poultry samples were tested for the presence of Staphylococcus aureus, a bacteria associated with a wide range of human diseases, including MRSA infection, the most dangerous drug-resistant Staph infection.

In the study, almost half the meat and poultry samples were found to be contaminated with S. aureus, and over half of those bacteria were resistant to at least three classes of antibiotics. Antibiotic-resistant bacteria pose a major health risk, as doctors are running out of antibiotics that will treat these infections. That these bacteria are found on over half the meat at the supermarket is a scary thought.

The bacteria probably come from the food animals themselves, according to the researchers, and proper cooking should kill the bacteria. But cross contamination can occur when preparing the meat, so care needs to be taken during food prep.

A major culprit in bacterial resistance is the overuse of antibiotics in food production. “The fact that drug-resistant S. aureus was so prevalent, and likely came from the food animals themselves, is troubling,” said Dr. Lance B. Price, lead researcher of the study. These animals are exposed to constant low doses of antibiotics, which can trigger the development of antibiotic-resistance in bacteria.

As a matter of fact, consumer groups have recently sued the FDA over the excessive amount of non-therapeutic antibiotics used in animal-food production. The FDA has produced draft guidelines for the phasing out of non-therapeutic antibiotics in food production, but the consumer groups want to put more pressure on the FDA to act with urgency.

In the meantime, I recommend avoiding meats raised with antibiotics. Look for antibiotic-free or organic meat. Those animals are not given antibiotics unnecessarily, and so don’t contribute to the antibiotic-resistant bacteria that are haunting our hospitals.

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