The Good Gut

Taking Control of Your Weight, Your Mood, and Your Long-Term Health

I have spent 30+ years in the practice of internal medicine attempting different strategies to change behavior when bad habits happen to good people.  Too often, lifestyle epiphanies occur after major shake-ups such as the diagnoses of diabetes or other serious conditions.  I particularly like the ‘bibliotherapy’ approach, and I’m always on the lookout for good self-help book recommendations to add to my short list of those that truly effect change.

I am pleased to report here that “The Good Gut” is just such a book, well-written in a way that makes it one of those notable non-fiction works that you’ll read cover to cover, not losing interest or comprehension somewhere between a paragraph’s start and finish (no flipping ahead to see how much longer this chapter!).  The Drs. Sonnenburg do not tediously repeat and overstate the standard health caveats to avoid sugar, lose weight, and exercise, but rather expand on their primary point, namely the importance, care, and feeding of our fellow life bacterial travelers. 

As a regular reader of the latest medical literature, much of the content herein was not news to me.  The presentation, however, in everyday layperson language, was personally compelling in ways that the New England Journal of Medicine is not.  A recent search on the NEJM web-site for ‘gut microbiota’ returned 28 articles, not one of which with a title so compelling as to change my diet for life.  Oh right, I’ve already done that, changing out breakfast foods long before the Sonnenburgs’ book and the rest of menu as a result of this read.

I will be recommending this book to my patients, and I also commend it to you.  This book will be released 4/21/15.

Social genomics and loneliness

The term social genomics is a new one to me. The fact that social factors influence health is not.

I wrote some time ago about the effects of self-described loneliness/social isolation has on the health of older adults. UCLA researchers examined the white cells of persons who were highest of the "high-lonely" vs. those "low-lonely" (socially connected) subjects.(1) A total of 209 genes showed different levels of expression between the two groups. Over 4 years of study, the lonely crowd over-expressed genes that resulted in inflammation and under-expressed those involved in antibody production against bacteria and viruses.

These DNA effects of social isolation were very specific to three groups of genes. The first group of affected genes are involved in the early phase of the immune response wherein the body revs up inflammation as a first response to injury or infection. I have written numerous times about the blessing/curse of inflammation insofar as appropriate levels are essential to a successful recovery from infection but too much (think cytokine storm in influenza pneumonia) or wrong place at the wrong time (say in an arterial wall that has cholesterol build-up) can be counter-productive or downright destructive.

The other two groups of immune genes that respond to the lonely soul's transformed internal environment are those that stimulate the production of interferon (a molecule that amplifies immune response against viruses) by lymphocytes and those that stimulate production of antibodies by B lymphocytes. The activity of both these types of genes is diminished in people who are less connected to friends and family.

The psychological literature abounds with studies in which socialization is correlated with susceptibility to viral illness. In another one of those 'who the heck volunteers for these things' type of study, researchers at Carnegie Mellon University assessed 193 subjects for PES (positive emotional style) vs. NES (negative emotional style of course) and then sprayed rhinoviruses/ common cold or influenza viruses up their noses to see who got sick.(2) Those NES-positive individuals, described as anxious, hostile, and depressed were 3 times as likely to succumb to the influx of nasal virus compared to all the PES prone Pollyanna types who were happy, lively, and calm.

Per Steve Cole, co-author of the study on white cells and loneliness: Research in social genomics has now clearly established that our interpersonal world exerts biologically significant effects on the molecular composition of the human body.(3) What remains to be seen is how attitude adjustments of the cognitive or pharmocological variety can affect how our DNA gets activated.
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1) Cole SW, et al. Social Regulation of Gene Expression in Human Leukocytes. Genome Biol. 2007;8(9):R189.
2) Cohen S, et al.Positive emotional style predicts resistance to illness after experimental exposure to rhinovirus or influenza a virus.Psychosom. Med. 2006 Nov-Dec;68(6):809-15. Epub 2006 Nov 13.
3) Cole SW. Social Regulation of Human Gene Expression. Current Dir. In Psych. Sci. 2009 Vol 18 No 3.

Weekly H1N1 flu update

As an internist and primary care provider, I expect to be on the front lines during the upcoming flu season...whatever it may bring. Here's my first weekly flu report; stay tuned for future updates concerning the H1N1 vaccine, the latest in H1N1 research, and ways that you, your family, your friends, and co-workers can stay healthy through the fall and beyond!

A few words about seasonal flu

Influenza viruses are identified by their surface proteins that allow the little buggers to 1) stick to the cells of your throat and 2) thrive and multiply in your airway. H is for hemagluttinin, a protein that hooks the virus up to you, and N is for neuraminidase, a protein that promotes the release of newly made flu virus particles from the infected cell to its uninfected neighbors.

The reason that flu is such an ongoing nightmare is that the virus remakes itself every year with novel H and N proteins so that many people, even those who have previously had flu, aren't immune to the new variety. Every year we try to anticipate what this slippery little devil is going to do with respect to H's and N's and then develop a shot to promote immunity in all vaccinated persons. We particularly target those who are very young, very old, or otherwise affected with a chronic disease which would make them more susceptible to a complicated and dangerous case of the flu.

What's all the fuss about H1N1?

This past spring (late in the flu season) a new strain of flu emerged--first identified in Mexico--with novel H and N proteins. The strain was first traced to pigs--new influenza strains often start in pigs--thus the original name 'swine flu'. This name was dropped after pigs were unfairly targeted as the infectious source of the disease, but now we know of course that you cannot get H1N1 flu from eating pork.

The scary things about this new flu were that 1) it showed up in the Northern Hemisphere at a time when flu should be winding down, and 2) it appeared to be particularly severe or lethal in healthy, young adults, a group generally not at risk for flu complications or death. We are concerned, of course, that this H1N1 flu could cause another worldwide, devastating pandemic like the outbreak of 1918 which was also caused by an H1N1 type of influenza. Bird flu,incidentally, is typed as H5N1.

Lots of research is being done on this new strain, but the findings of flu expert Dr. Peter Palese and his team at Mount Sinai School of Medicine in New York are reassuring. They agree with CDC data that estimate only 10% of household contacts of patients with H1N1 will become infected which suggests that this bad actor is not as tough or transmissible as we originally feared.

What's the scoop on the flu?

Every year, the influenza virus reinvents itself. In the countryside and farms of Southeast Asia, this bad actor mixes up genetic material with its viral cousins, producing brand new strains that then spread throughout the world in the throats and lungs of international travelers. And every year in turn, epidemiologists try to anticipate the new flu variants in order to produce an effective vaccine in time for the next flu season.

But now, as all of you know, the pesky pathogen has performed a new sort of quick change trick. This latest viral transformation apparently occurred in the pig farms of Mexico, and the resultant strain strings together genetic material from human, swine, and avian sources into a novel hybrid to which none of us are immune. This 'swine flu' has produced serious illness in its country of origin, and now the whole world watches in nervous anticipation as it continues its spread.

Let's get the good news out right up front. First of all, flu is seasonal, and the season here is nearly over. While this new strain of flu may resurface next winter, its current run could well be brief. And scientists will have time to develop an effective vaccine before its next world tour. Secondly, the cases thus far identified in the US and abroad have generally been mild and self-limited.

And finally, this swine flu is sensitive to two standard anti-virals--Tamiflu and Relenza. Remember, however, that not only can influenza pull off genetic mixology to produce an entire new strain, it also can acquire the genes for immunity to these drugs. If enough of us twitch and take Tamiflu at the first sign of any viral illness, be it flu, croup, or the common cold, this acquired resistance will be a sure thing. So don't call your doctor for a 'just in case' prescription; Adele and I will say "NO!"

The flu is highly contagious; it's effectively spread by tiny respiratory droplets which remain suspended in air and settled on surfaces for some time after an unrestrained sneeze or cough. Good prevention practices include:

• Cough or sneeze into your sleeve. Using your hands or a tissue to contain your explosion just makes more objects infectious.
• Better yet, stay home with your secretions when ill, and don't expect affected employees or co-workers to crawl on in to work when they are unwell.
• Wash your hands frequently, and don't touch your face or handle food after touching shared surfaces until you've washed up.
• Practice good health habits to enhance your overall immunity and resistance.
• Ask your doctor to check your vitamin D levels, and then discuss supplements with her/him to bring yours up to the ideal range. Influenza is increasingly considered a vitamin D deficiency disease!

For an amusing look at keeping your mucous to yourself, check out this video.

Statins and infection control

I have any number of patients who take statin drugs(1) to lower their cholesterol levels in order to reduce their risk of unwanted cardiovascular outcomes such as stroke or heart attack. I would prefer, in an ideal world, that these patients control their risk factors with healthy habits in diet, exercise, and weight control, but, alas, this is not a perfect world but rather one in which many lack time, will-power, and resources to make these changes in a timely fashion.

In addition to their ability to reduce cholesterol production and increase LDL clearance by the liver, these drugs are known to reduce inflammation in the body. Inflammation is a good thing as a first responder to infection or injury, but inflammation gone amok is part of the pathological process that increases tissue destruction in Alzheimer's disease, athersclerosis (hardening of the arteries), cancer, arthritis, and severe infections.

Danish and American researchers theorized that the anti-inflammatory effects of statins could improve outcomes for patients admitted to the hospital for pneumonia; those persons protected from over-exuberant inflammation by statins might be more likely to walk out of the hospital rather than being rolled out through a basement door on a gurney. They examined the hospital records for nearly 30,000 patients over 7 years looking for pre-admission statin use as correlated with the risk of sepsis and death associated with serious pulmonary infections. Indeed, those patients currently on statins had a 31% better chance of being alive 90 days after their pneumonia diagnosis compared with those in a statin-less state.

Wondering why? Dr. Kasturi Haldar of the Center for Rare and Neglected Diseases (I kid you not) informs us in an editorial in the same Archives issue that it's all about G proteins. Statins block the isoprenylation (whatever that is) of small G proteins. This decreased prenylation business protects against Alzheimer's disease because the beta-amyloid guck that gums of the brainworks in the disease depends on the breakdown of amyloid precursor protein, a process which in turn counts on prenylated G proteins.

In infections, little G proteins increase the inflammatory response which can fill the patient's airway with fluids and white cells instead of the air upon which we depend. G proteins might also promote the bacteria's ability to enter cells and prosper therein. As in Alzheimer's, as statins decrease the prenyl pool upon which G protein function depends, the decreased inflammatory response may reduce the inflammatory response.

So if you are ever called upon to weigh the decision of statins or not in your future health care plan, consider this side benefit of the use of these drugs.
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(1)Lipitor, Crestor, simvastatin, lovastatin, fluvastatin
(2) Thomsen, RW, et al. Preadmission Use of Statins and Outcomes After Hospitalization With Pneumonia. Arch Int Med Vol 168 (No.19), Oct. 27, 2008.

ESBL E. coli

My 60 year old patient needed help from two of us to walk from the waiting room into the exam room. Once there and lying down, her blood pressure was 78/40 and her pulse was 120. I was unable to check her 'postural' blood pressure (comparing values sitting to standing looking for a significant drop indicative of dehydration) as she kept losing her balance and her consciousness in the standing position. Long story short--once admitted to the hospital, her diagnosis was sepsis (invasion of bacteria into the bloodstream) from an overwhelming urinary tract infection caused by ESBL E. coli.

I'll admit, I hadn't heard of this bad boy before Ms. B. nearly died from her infection. Just looking at the culture & sensitivity report, however, was enough to make my heart sink. Cultures of her blood grew an E. coli species resistant to all but 2 antibiotics tested, and those two were 1) only availble by IV, and 2) did not even exist back when I was in training.
Beta-lactam antibiotics are named for a beta-lactam ring in their structure. They include penicillin whose discovery revolutionized the treatment of infectious disease, and cephalexin, the miracle drug discovered after many bacteria developed resistance to penicillins. Extended-spectrum beta-lactamase-producing E. coli (or ESBL E. coli) produce an enzyme (beta-lactamase) that destroys the beta-lactam chemical ring, rendering it useless against the little buggers.

ESBL E. coli has been a problem in Europe for awhile. Its 'extended spectrum' resistance (eats not just one but most beta-lactam antibiotics) is theorized to have developed due to the overuse of antibiotics in animals--particularly chickens--raised for food. More often found in health care institutions such as hospitals, ESBL E. coli is clearly now out in the community where my patient came into contact with it.

Ms. B. survived, barely. When she came in earlier this week with symptoms of weakness and urinary burning and frequency, we both thought...and feared...the same thing. The culture came back yesterday--ESBL E. coli. She cried and I shuddered, feeling like I was glimpsing our future in Ms. B.'s today.

Ms. B. did nothing wrong, nor do we know just what to do right to avoid such a super-infection. I'd suggest hand-washing, scrupulous handling of raw meat especially chicken, vitamin D, and hot, sweaty exercise as known, immune-enhancing strategies.

Shingles shot

Comment from a 65 year old nurse who came in today with a painful case of shingles on her abdomen:

I could kick myself for not getting the shingles shot.

This after spending 4 and 1/2 hours in the ER two days ago with the pain that preceded the outbreak. She got a CT scan, an ultrasound, many exams, and a raft of bloodwork looking for other causes for the pain.

While people are getting more and more familiar with the patchy, one-sided, blistered skin associated with an outbreak of shingles, many patients don't realize that severe pain is often the first sign of the disease and can predate the rash by several days.

For more information on shingles, see The shingles shot.

Cipro side effects

Chances are good that if you go to an urgent care center for treatment of a urinary tract infection, you will end up with a prescription for Cipro. This fluoroquinolone antibiotic is also commonly used for intestinal infections, and its cousin Levaquin is a favorite choice for the treatment of pneumonia. Some of my patients request these antibiotics by name as their use was particularly effective for some previous bacterial infection.

Powerful medications are a good thing when battling serious infections, but you should know that the fluoroquinolones now have a 'black box warning' per the FDA. This cautionary material is rimmed by a bold black square in the PDR and on the product insert. This particular alert was issued 7/8/08 and reads in part:

Fluoroquinolones are associated with an increased risk of tendinitis and tendon rupture. This risk is further increased in those over age 60, in kidney, heart, and lung transplant recipients, and with use of concomitant steroid therapy. Physicians should advise patients, at the first sign of tendon pain, swelling, or inflammation, to stop taking the fluoroquinolone, to avoid exercise and use of the affected area, and to promptly contact their doctor about changing to a non-fluoroquinolone antimicrobial drug.

The achilles tendon is particularly susceptible to this inflammatory weakening, and, per a physical therapist I know, the loss of tendon strength and substance associated with drug-induced tendinitis is particularly devastating and hard to reverse.

So while fluoroquinolones, when indicated, are effective drugs and potentially life-saving, their routine use in uncomplicated urinary infections is unwise. Ask your doctor about using other choices in cystitis or bladder infections, and ask him/her to consider ordering a culture of your urine sample to confirm that your infection is susceptible to the antibiotic prescribed.

Vitamin D and immunity

Sometimes I read a research report so compelling I just have to get up and do something about it. Just now, that instant reaction included heading downstairs to pop my second vitamin D supplement of the day. Did you get the memo? If not, here's the scoop.

Simply put, influenza viruses hate sunshine. The seasonality --here in winter, gone in summer-- of flu epidemics has long been noted but only more recently understood. The reason, it turns out, that flu bugs hate sunshine is that sunshine on un-sunblocked skin during summer months causes production of vitamin D. D in turn acts on portions of human DNA to produce antimicrobial peptides which are worthy little proteins deadly to the influenza virus.

If the prevention of influenza infections were just a matter of producing 'herd immunity,' than populations in which a large number of individuals had been immunized should have fewer members die of flu. In fact, a study of Italian old folks showed that the death rate dropped not a whit over a 15 year time period during which immunization rates rose from 10% to 60%.

Once the vitamin D/influenza connection was made, other investigators herded together some postmenopausal women and hooked half the old gals up with extra vitamin D. Those in the group without supplements were three times more likely to fall ill with influenza compared to D other group. By the third year of their trial, a higher dose of supplemental D (2000 IU/day) "virtually eradicated all reports of colds or flu."

Virtually and eradicated are strong words. So strong, I went down and took my second 1000 IU D pill for the day. I need all the D I can get to get through the rest of this nasty flu season.

Wind, wound, water, and walk*

This is the little mnemonic that medical students use when searching for the source of a post-operative fever. It's coming in handy this day, years past med school, as I think through why a certain old lady might be running a temp near 102. I'll add colitis to the list as she's been on antibiotics for her arm wound (which is much improved, so that's not where the fever is coming from).

Antibiotics can cause a dangerous shift in the body's resident bacteria. While a little diarrhea might be a small price to pay for the treatment of a serious infection, one antibiotic-related bowel infection--Clostridium difficile-- is a bad actor that you do not want in your intestinal tract. The last time Mom did battle with that little hummer, she became septic (the bacteria was released into her bloodstream, causing a systemic infection) and nearly died.

You don't have to be a frail little old lady to get a c. diff infection. I've had two otherwise healthy adults get c. diff colitis after a course of oral antibiotics for no-big-deal infections. While neither one was seriously ill, they had some serious diarrhea for a long time and required yet another antibiotic to clear this microbe out of their colons. All the more reason to skip antibiotics if possible through the flu season.
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*Wind = Respiratory infection or pulmonary embolus
Wound = Surgical site or any opening in the skin from injury or ulceration
Water = Urinary tract infection
Walk = Deep venous thrombosis or clot

Who needs a shingles shot?

Leftover chickenpox can cause a world of trouble.

My 59 year old patient was miserable. I saw her two days after the onset of painful blisters on her ear and in her ear canal. Besides the discomfort, she had terrible bouts of vertigo, and her mouth drooped on the same side as the blisters. "What is it?" I asked neurologist Adam Wolff, MD by phone. "Ramsay Hunt Syndrome," he answered, kindly not adding the word 'obviously.'

Nearly all of us of a certain age have done battle as children with the herpes zoster virus. Way back when, we broke out in the characteristic bite-like rash of chickenpox. Since then, we have carried the residual zoster virus-particles in our nerve cell bodies along the spine and the base of our brain. Our immune system has kept a lid on the little buggers who now wait for an immune lapse so they can break free of surveillance and multiply along the axons of the nerves. When they do, we will develop a painful blistering rash in the area of skin supplied by the affected nerves, and, occasionally, paralysis in the facial muscles or other neurological syndromes such as Bell's Palsy or this Ramsay Hunt business.

While immune problems from cancer, chemotherapy, AIDS, or steroid therapy increase our risk of shingles, just ourselves growing older are at elevated risk. And the older we get, the more likely we are to develop complications with shingles, in particular a prolonged pain syndrome known as post-herpetic neuralgia (PHN) that can last for months to years past the breakout.

Researchers from the Mayo Clinic sorted through scores of medical records from adult Minnesotans to determine the incidence of recurrent herpes zoster (HZ) illness in both the healthy and immunocompromised residents of the area prior to the availability of the shingles shot (Zostavax). Most Minnesotans with HZ troubles were free of immune troubles, succumbing to shingles at a rate of 4 per 1,000 each year. The older the subjects, the more likely they were to let loose their resident HZ and suffer from painful complications. Specifically, 68% of the affected group were 50 and over, and 1 in 4 of them developed HZ-related complications.

So who needs a shingles shot? It is specifically indicated for persons over 60 who wish not to suffer from PHN in their golden years. Trust me, my patients with PHN find those years of pain not so very golden. While it is not yet tagged for persons between 50-59, this younger group of oldsters could benefit as well. The problem for them, for now, is that insurance may not pay for this pricey shot until the FDA approves the vaccine for that age group.