Whether or not we want to live to be a centenarian, most of us want to live the healthiest life possible with the fewest chronic diseases, medications, and impediments to daily life.

While exercise is one component of lifestyle modification, diet is an essential part, as well. The most surprising result, at least to me, is that it is unclear how much sodium we should consume. But before you start putting salt on your food, know that the research agrees about too much sodium being dangerous. What that number is, however, varies. What we do know is that the average sodium intake in the U.S. is 3.4 grams (1). This is greater than recommendations from the American Heart Association, which has the strictest guideline of <1,500 mg daily for most Americans; however, the Dietary Guidelines Advisory Committee (DGAC) 2015 recommends <2,400 mg per day (2). The consensus is that we consume too much sodium, period!

Did you get question 3 on the quiz correct? Well, microwaving, contrary to prevailing thought, is not necessarily the enemy. It depends on which compounds in the foods we are testing.

It is most important to realize that healthy eating is not about individual nutrients, but rather about diet as a whole. DGAC emphasizes the importance of a nutrient-rich diet with a focus on fruits, vegetables, nuts, seeds, whole grains, fish and low or nonfat dairy. In addition, it recommends minimal red meat, especially processed meats, and minimal processed sugars and refined grains (3).

Let’s look at the evidence.

IS SODIUM THE VILLIAN?
Of course not! We all need sodium. However, some in the medical community would argue that “moderate” amounts of between 3 and 6 grams a day are okay. I am specifically referencing an article written by Dr. Aaron Carroll in the New York Times, “Simple Rules for Healthy Eating.” It was one of the most popular articles recently. While he does have good suggestions, with a disclaimer that these are only his opinions, I disagree with his third point regarding salts and fats. He believes that salt can be used in “moderation”; seasoning your food with it is fine.
In the article, he references a large observational study, the PURE study. Its results suggest that a high urinary excretion of sodium, >7 grams per day, correlated with an increased risk of all-cause mortality compared to 4 to 5.99 grams per day (4). But surprisingly, those who had a urinary excretion of <3 grams per day of sodium also had an increased risk of all-cause mortality. This study had over 100,000 participants, but there were significant weaknesses. For one, the researchers estimated the 24-hour sodium urine excretion because they only had one snapshot sample. Also, there was only one urine sample taken during the study, so it is not clear whether the participants increased or decreased their sodium excretion during the study.
Finally, urinary excretion of sodium does not necessarily correlate with sodium intake (5). It is considered a standard measurement, but it is still an indirect marker.
In another article, “Behind the Dietary Guidelines, Better Science,” Dr. Carroll argues that low sodium could potentially be dangerous. Here, he uses a study with heart failure patients (6). The results show that those heart failure patients who were in the lowest sodium intake group had more hospitalizations than those in the modest sodium intake group. However, those in the lowest group also had hyponatremia (reduction in blood levels of sodium) due to significantly reduced sodium intake. This most likely is the major contributor to the hospitalizations. On the surface, it looks like a good study, but once you analyze the data, it is not.
In fact, there are studies showing that lowering sodium has significantly positive effects. In one, lowering the sodium in pre-hypertension patients reduced the risk of cardiovascular events, including heart attacks, strokes and cardiovascular death, by 30 percent (7).

FATS
In “Simple Rules for Healthy Eating,” Dr. Carroll also writes about fats, claiming that butter should be used as needed. However, the study he uses to substantiate this concerns replacing butter with high amounts of carbohydrates or other potentially unhealthy fats, such as omega-6 fatty acids only, not foods that contain good fats such as omega-3s (8). This is a flawed comparison since the substitutes are no better than saturated fats.

EXERCISE
Though some of us would like it to be true that exercise allows us to eat with impunity, it is a myth. In a recent editorial, the author mentions that obesity and disease are caused more by poor diet and that exercise, while substantial to overall health, cannot overcome this effect (9). The author goes on to say that the type of calorie is important; 150 calories of sugar increase the risk of type 2 diabetes by 11 times more than 150 calories of fats or protein. Even more horrifying is that 4 in 10 normal-weight individuals will be afflicted by high cholesterol, high blood pressure, cardiovascular disease and nonalcoholic fatty liver disease. Just because you are thin does not mean you’re healthy or “fit.” Poor diet has more negative effects than smoking, sedentary behavior and drinking combined. Thus, exercise alone may not be able to compensate for unhealthy diet.

MICROWAVE
The theory has been that microwaves destroy valuable nutrients. However, is that always the case for vegetable-rich, plant-based foods? According to the Harvard Health Letter of Jan. 2, 2015, cooking vegetables for a shorter amount of time with less water helps them retain their phytochemical nutrients better. Microwaving fits this parameter. In a study testing this theory with cruciferous vegetables, results showed that microwaved foods retain a significant amount of glucosinolates (nutrients), holding their own when compared to boiling and steaming (10). However, each method lost a substantial amount of vitamin C. There are a number of critics of microwaves though. Who is right? We cannot be sure, but food content is more critical than the type of cooking preparation, with some exceptions.
The bottom line is that we should focus on a vegetable-rich, plant-based diet with proportions that vary based on an individual’s goals and health status. The extremes should be avoided. We don’t want extreme exercise or extremes in different nutrients such as fats, protein and carbohydrates. In fact, low sugar is not good either; fruits contain plenty of sugars. We should not aim to eliminate a nutrient from our diet. Preparation of these foods in terms of cooking techniques is less important, except, of course, for charring animal protein and deep frying.

REFERENCES
(1) CDC.gov. (2) Heart.org; health.gov. (3) health.gov. (4) N Engl J Med 2014;371:612-623. (5) Hypertension 1980;2:695-699. (6) Clin Sci 2008;114:221-230. (7) BMJ 2007;334(7599):885. (8) Open Heart 2014;1(1):e000032. (9) Br J Sports Med online April 22, 2015. (10) J Agric Food Chem 2010;58(7),4310-4321.

Dr. Dunaief is a speaker, author and local lifestyle medicine physician focusing on the integration of medicine, nutrition, fitness and stress management. For further information, go to the website www.medicalcompassmd.com and/or consult your personal physician.

Eczema is such a common problem in both children and adults that you would think there would be a plethora of research, right? Well, that’s only partly true. While there is a significant amount of research in primarily neonates and some on pediatric patients, there is not a lot of research on adults with eczema. But in my practice, I see a good number of patients who present with, among other disorders, eczema.
The prevalence of this disease rivals the prevalence of diabetes. In the United States, more than 10 percent of the adult population is afflicted (1). Twice as many females as males are affected, according to one study (2). Thus, we need more research.
Eczema is also more broadly referred to as atopic dermatitis. The cause is unknown, but it is thought that nature and nurture are both at play (3). Eczema is a chronic inflammatory process that involves symptoms of pruritus (itching) pain, rashes and erythema (redness) (4). There are three different severities: mild, moderate and severe. Adults tend to have eczema closer to the moderate-to-severe range.
Factors that can trigger eczema flare-ups include emotional stress, excessive bathing, dry skin, dry environment and detergent exposure (5). Treatments for eczema run the gamut from over-the-counter creams and lotions to prescription steroid creams to systemic (oral) steroids. Some use phototherapy for severe cases, but the research on phototherapy is scant. Antihistamines are sometimes used to treat the itchiness. Also, lifestyle modifications may play an important role, specifically diet. Two separate studies have shown an association between eczema and fracture, which we will investigate further.
Let’s look at the evidence.
ECZEMA DOESN’T JUST SCRATCH THE SURFACE
Eczema causes cracked and irritated skin, but it may also be related to broken bones. In a newly published observational study, results showed that those with eczema had a 44 percent increased risk of injury causing limitation and an even more impressive 67 percent risk of bone fracture and bone or joint injury for those 30 years and older (6). And if you have both fatigue or insomnia and eczema, you are at higher risk for bone or joint injury than having one or the other alone. Antihistamines may cause more fatigue. One reason for increased fracture risk, the researchers postulate, is the use of corticosteroids in treatment.
A side effect of steroids is that they may weaken bone, ligaments and tendons and may cause osteoporosis by decreasing bone mineral density. Chronic inflammation may also contribute to the risk of bone loss. There were 34,500 patients involved in the study ranging in age from 18 to 85.
Another study corroborates these results that eczema increases the risk for sustained injury (7). There was a 48 percent increased risk of fracture at any location in the body and an even greater 87 percent increased risk of fracture in the hip and spine when compared to those who did not have eczema. Interestingly, researchers’ hypotheses for the causes of increased fracture risk were similar to those of the above study: systemic steroid use and chronic inflammation of the disease. The researchers analyzed the database from NHANES 2005-2006, with almost 5,000 patients involved in this study. When oral steroid was given for at least a month, there was a 44 percent increased risk of osteoporosis. For those who have eczema and have been treated with steroids, it may be wise to have a DEXA scan.
ARE SUPPLEMENTS THE ANSWER?
The thought of supplements somehow seems more appealing for some than medicine. There are two well-known supplements for helping to reduce inflammation, evening primrose oil and borage oil. Are these supplements a good replacement for medications or at least a beneficial addition? The research is really mixed, leaning toward ineffective. In a recent meta-analysis (involving seven randomized controlled trials, the gold standard of studies), evening primrose oil was no better than placebo in treating eczema (8). The researchers also looked at eight studies of borage oil and found there was no difference from placebo in terms of symptom relief. One positive is that these supplements only had minor side effects. But don’t look to supplements for help.

WHERE ARE WE ON THE
DRUG FRONT?
The FDA has given fast track processing to a biologic monoclonal antibody known as dupilumab (9). In trials, the drug has shown promise for treating moderate to severe eczema when topical steroids are not effective. We will have to wait to see what the verdict is on this drug in development.

DO PROBIOTICS HAVE A PLACE?
When we think of probiotics, we think of taking a pill. However, there are also potentially topical probiotics with atopic dermatitis. In preliminary in-vitro (in a test tube) studies, the results look intriguing and show that topical probiotics from the human microbiome (gut) could potentially work as well as steroids (10). This may be part of the road to treatments of the future. However, this is in very early stage of development.

WHAT ABOUT LIFESTYLE
MODIFICATIONS?
Wouldn’t it be nice if what we ate could make a difference in eczema? Well, in a study involving pregnant women and their offspring, results showed that when these women ate either a diet high in green and yellow vegetables, beta carotene or citrus fruit there was a significant reduction in the risk of the child having eczema of 59 percent, 48 percent and 47 percent, respectively, when comparing highest to lowest consumption quartiles (11). This was a Japanese study involving over 700 mother-child pairings.
Elimination diets may also play a role. One study’s results showed when eggs were removed from the diet in those who were allergic, according to IgE testing, eczema improved significantly (12).
From an anecdotal perspective, I have seen very good results when treating patients who have eczema with dietary changes. My patient population includes about 15-20 percent of patients who suffer some level of eczema. Recently, a young adult had eczema mostly on the extremities. When I first met the patient, these were angry, excoriated, erythematous and scratched lesions. However, after several months of a vegetable-rich diet, the patient’s skin had all but cleared.
I also have a personal interest in eczema. I suffered from hand eczema, where my hands would become painful and blotchy and then crack and bleed. This all stopped for me when I altered my diet over eight years ago.
Eczema exists on a spectrum from annoying to significantly affecting a patient’s quality of life (13). Supplements may not be the solution, at least not borage oil or evening primrose oil. However, there may be promising topical probiotics ahead and medications for the hard to treat. It might be best to avoid long-term systemic steroid use; it could not only impact the skin but also may impact the bone. But don’t wait to treat the disease. Lifestyle modifications appear to be very effective, at least at the anecdotal level.
REFERENCES:
(1) J Allergy Clin Immunol. 2013;132(5):1132-8. (2) BMC Dermatol. 2013;13(14). (3) Acta Derm Venereol (Stockh) 1985;117 (Suppl.):1-59. (4) uptodate.com. (5) Br J Dermatol. 2006; 1553:504. (6) JAMA Dermatol. 2015;151(1):33-41. (7) J Allergy Clin Immunol. Online Dec. 13, 2014. (8) Cochrane Database Syst Rev. 2013;4:CD004416. (9) Medscape.com. (10) ACAAI 2014: Abstracts P328 and P329. (11) Allergy. 2010 Jun 1;65(6):758-65. (12) J Am Acad Dermatol. 2004;50(3):391–404. (13) Contact Dermatitis 2008; 59:43–7.

Dr. Dunaief is a speaker, author and local lifestyle medicine physician focusing on the integration of medicine, nutrition, fitness and stress management.  For further information, go to the website www.medicalcompassmd.com and/or consult your personal physician.

To eat fat or to not eat fat is a question that has been dogging the medical community for years. It would seem, at least on the surface, that this should be a simple answer, and it is. Of course, we should eat fat. However, what type of fat is good for us and what type of fat may be detrimental is where it gets downright murky. Is low fat beneficial, or is a normal fat or even a high fat amount okay in our diet? We are constantly discussing fats because they could have an impact on chronic diseases, such as heart disease, stroke, cancer and obesity (1).
The problem is that we are focusing potentially on the wrong issue. It may not be about choosing one macronutrient over another. There are three macronutrients: fats, carbohydrates and protein. You would think with just three macronutrients there can’t be that many permutations to find a diet that works. The upshot is that it may be more important to focus on the diet as a whole rather than on the individual macronutrients. Unfortunately, there is no one specific balance that will fit the population at large.
The reason for writing this article is twofold: There is a recent study touting that fat consumption is not an issue; and there are potential new dietary guidelines on the horizon from the Department of Health and Human Services and the Department of Agriculture as a result of advisory committee recommendations. The government usually follows the recommendations of the advisory committee.
The advisory committee has suggested lifting the current dietary recommendation of 35 percent fat restriction (2). Does this mean we should eat more fat? Not necessarily. However, they have maintained that saturated fat remain less than 10 percent of the diet. This is not as severe as the American Heart Association, which recommends limiting saturated fat to 5 to 6 percent of your diet. Another significant advisory panel recommendation is that the 300-mg cholesterol restriction be removed. The advisory panel emphasized the importance of consuming unsaturated fats including nuts, fish, olive oil and vegetable oils.
It is difficult to cut fat. Do you replace it with protein or with carbohydrates? Food manufacturers have been replacing fat with sugar in processed foods. I know because when fat-free cookies were popular in the 1990s, my wife and I felt guiltless eating them all, although we were overwhelmed by the sugar.
The government is now more interested in reducing sugar than fats. We overconsume sugars by at least twofold. The advisory committee was in line with my comments above about focusing on the whole rather than looking at the parts. We cannot see the forest for the trees.
Let’s cut through the fat and look at the research, metaphorically speaking of course.

SHOULD WE LIMIT FAT AND
SATURATED FAT?
This is a loaded question. In a recent meta-analysis involving a group of six randomized controlled trials, the gold standard of studies, results showed that there were no statistically significant changes in the treatment groups (which one would think would be a “low fat” group) and control groups in regard to overall mortality and heart disease (3). The actual trials were performed from 1977 to 1983. The intent of the meta-analysis was to determine whether or not the original recommendations regarding fat and saturated fat restrictions were based on solid results. The researchers concluded that they were not.
Interestingly, five of six trials did not actually look at limiting overall fat to less than 30 percent or at reducing saturated fat to less than 10 percent. Instead, the trials replaced saturated fat with vegetable oils, which are high in polyunsaturated fats, specifically omega-6s. What is the significance of omega-6s? Keep reading!

ULTIMATELY, WHAT IS THE PROBLEM IF FAT IS NOT THE ISSUE?
There are two questions that stem from either reducing fat overall or replacing saturated fat with polyunsaturated fats. The first is: With what are you replacing the fat? The second is: Are all polyunsaturated fats safe or harmful, compared to saturated fats? Studying saturated fats is complicated because studies that show equivocal  non-harmful results with these types of fats also contained unsaturated omega-3s as well (4). Even if saturated fat has shown no harmful effects, it has not demonstrated beneficial effects either.

REPLACING FATS WITH
CARBOHYDRATES
We had this long-standing belief that fats were the culprit in obesity, metabolic syndrome and diabetes. However, studies have shown that replacing fats with carbohydrates has resulted in an increase in obesity and diabetes, rather than a decrease. In an epidemiologic study, results show that refined carbohydrates, specifically corn syrup, increase the risk of diabetes, while fiber decreased the risk. Fat and protein had no effect (5). In other words, reducing fat may not be the best idea, depending on whether you’re replacing that fat with refined carbohydrates or not.

NOT ALL POLYUNSATURATED FATS ARE EQUAL
Certain types of fat may be more beneficial than others. A study comparing polyunsaturated fats, which include omega-3 fatty acids and omega-6 fatty acids, and their replacement of trans fats and saturated fats showed mixed results (6). Diets that contained both omega-3s and omega-6s had reductions in the risk of heart attack and heart disease death when compared to those containing omega-6s alone, which appeared to increase the risk of heart disease mortality. Certain vegetable oils contain high amounts of omega-6s such as safflower oil.
In the Sydney Diet Heart Study, there was a trend toward increased cardiovascular disease when replacing saturated fats with polyunsaturated omega-6 fatty acids referred to as linoleic acid (7).
Both of these trials were not without their statistical weaknesses. However, caution should be advised when replacing saturated fats with polyunsaturated fats; you should include an increase in omega-3 fatty acids and not necessarily an increase in omega-6s solely.

WHAT TYPE OF DIET IS BENEFICIAL?
Diets rich in heart-healthy foods are better than low-saturated-fat diets at reducing LDL (“bad”) cholesterol levels, a risk factor for heart disease, according to the results of a randomized controlled trial (8). Patients were randomized into three groups: one low-saturated-fat group and two portfolio diet groups, one with intensive counseling and one with moderate counseling. The portfolio diet was a heart-healthy plant-rich diet consisting of viscous fibers (referred to as sticky fibers), nuts, plant sterols, vegetables and soy proteins. Both portfolio diet groups experienced significant reductions in LDL similar to that of an early type statin while the low-saturated-fat diet did not. The study duration was six months, and it involved over 350 participants.
Thus, we need to focus on the diet as a whole, such as the Mediterranean diet, not on a single component, for that is when we get ourselves in trouble. Also, just because the fat is unsaturated does not mean it is necessarily healthy. Omega-3 fatty acids are most likely beneficial. Some vegetable oils are loaded with omega-6 fatty acids that induce inflammation and may be no better than saturated fats. It is important to maintain a reduction in saturated fat as long as it does not mean replacement with refined carbohydrates or potentially harmful omega-6s, though not all omega-6 fatty acids are created equal either.
REFERENCES:
(1) uptodate.com. (2) health.gov. (3) Open Heart 2015;2. (4) Ann Intern Med. 2014; 160(6):398-406. (5) Am J Clin Nutr. 2004;79(5):774-779. (6) Br J Nutr 2010;104:1586–600. (7) BMJ 2013;346:e8707. (8) JAMA 2011; 306:831-839.

Dr. Dunaief is a speaker, author and local lifestyle medicine physician focusing on the integration of medicine, nutrition, fitness and stress management.  For further information, go to the website www.medicalcompassmd.com and/or consult your personal physician.

This article was originally published in the January 23, 2014 issue of Arts and Lifestyles.
Gluten has been gaining in notoriety over the last several years. When we hear someone mention a gluten-free diet, several things tend to come to mind. One may be that this is a healthy diet. Along the same lines, we may think gluten is bad for us. However, gluten-free is not necessarily synonymous with healthy. There are many beneficial products containing gluten.
We might think that gluten-free diets are a fad, like low-fat or low-carb diets. Still, we keep hearing how more people feel better without gluten. Could this be a placebo effect? What is myth and what is reality in terms of gluten? In this article I will try to distill what we know about gluten and gluten-free diets, who may benefit and who may not.
But first, what is gluten? Most people I ask don’t know the answer, which is OK; it is part of the reason I am writing the article. Gluten is a plant protein found mainly in wheat, rye and barley.
Now to answer the question of whether going gluten-free is a fad. The answer is resounding “No,” since we know that patients who suffer from celiac disease, an autoimmune disease, benefit tremendously when gluten is removed.(1) In fact, it is the main treatment.
But what about people who don’t have celiac disease? There seems to be a spectrum of physiological reaction to gluten, from intolerance to gluten (sensitivity) to gluten tolerance (insensitivity). Obviously, celiac disease is the extreme of intolerance, but even these patients may be asymptomatic. Then, there is nonceliac gluten sensitivity, referring to those in the middle portion of the spectrum.(2) The prevalence of NCGS is half that of celiac disease, according to the NHANES data from 2009-2010.(3) However, many disagree with this assessment, indicating that it is much more prevalent and that its incidence is likely to rise.(4) The term was not even coined until 2011.
What is the difference between full-blown celiac disease and gluten sensitivity? They both may have intestinal symptoms, such as bloating, gas, cramping and diarrhea, as well as extraintestinal (outside the gut) symptoms, including gait ataxia (gait disturbance), malaise, fatigue and attention deficit disorder.(5) Surprisingly, they both may have the same results with serological (blood) tests, which may be positive or negative. The first line of testing includes antigliadin antibodies and tissue transglutaminase. These measure a reaction to gluten; however, they don’t have to be positive to have reaction to gluten. HLA–DQ phenotype testing is the second line of testing and tends to be more specific for celiac disease.
What is unique to celiac disease is a histological change in the small intestine, with atrophy of the villi (small fingerlike projections) contributing to gut permeability, what might be called “leaky gut.” Biopsy of the small intestine is the most definitive way to diagnose celiac disease.
Though the research has mainly focused on celiac disease, there is some evidence that shows NCGS has potential validity, especially in irritable bowel syndrome.
Before we look at the studies, what does it mean when a food says it’s “gluten-free”? Well, the FDA has recently weighed in by passing regulation that requires all gluten-free foods to have no more than 20 parts per million of gluten.(6) The agency has given food manufacturers a year to comply with the new standards. Now, let’s look at the evidence.
Irritable bowel syndrome
Irritable bowel syndrome (IBS) is a nebulous disease diagnosed through exclusion, and the treatments are not obvious. That is why the results from a randomized controlled trial, the gold standard of studies, showing that a gluten-free diet significantly improved symptoms in IBS patients, is so important.(7) Patients were given a muffin and bread on a daily basis.
Of course, one group was given gluten-free products and the other given products with gluten, though the texture and taste were identical. In six weeks, many of those who were gluten-free saw the pain associated with bloating and gas mostly resolve; significant improvement in stool composition, such that they were not suffering from diarrhea; and their fatigue diminished. In fact, in one week, those in the gluten group were in substantially more discomfort than those in the gluten-free group. There were 34 patients involved in this study.
As part of a well-written March 4, 2013 editorial in Medscape, by David Johnson, M.D., a professor of gastroenterology at Eastern Virginia Medical School, he questions whether this beneficial effect from the IBS trial was due to gluten withdrawal or to withdrawal of fermentable sugars because of the elimination of some grains, themselves.(8) In other words, gluten may be just one part of the picture. He believes that nonceliac gluten sensitivity is a valid concern.
Autism
Autism is a very difficult disease to quantify, diagnose and treat. Some have suggested gluten may play a role. Unfortunately, in a study with children who had autism spectrum disorder and who were undergoing intensive behavioral therapy, removing both gluten and casein, a protein found in dairy, had no positive impact on activity or sleep patterns.(9) These results were disappointing. However, this was a very small study involving 22 preschool children. Removing gluten may not be a panacea for all ailments.
Antibiotics
The microbiome in the gut may play a pivotal role as to whether a person develops celiac disease. In an observational study using data from the Swedish Prescribed Drug Register, results indicate that those who were given antibiotics within the last year had a 40 percent greater chance of developing celiac disease and a 90 percent greater risk of developing inflammation in the gut.(10) The researchers believe that this has to do with dysbyosis, a misbalance in the microbiota, or flora, of the gastrointestinal tract. It is interesting that celiac disease may be propagated by change in bacteria in the gut from the use of antibiotics.
Not everyone will benefit from a gluten-free diet. In fact, most of us will not. Ultimately, people who may benefit from this type of diet are those patients who have celiac disease and those who have symptomatic gluten sensitivity. Also patients who have positive serological tests, including tissue transglutaminase or antigliadin antibodies are good candidates for gluten-free diets.
There is a downside to a gluten-free diet: potential development of macronutrient and micronutrient deficiencies. Therefore, it would be wise to ask your doctor before starting gluten withdrawal. The research in patients with gluten sensitivity is relatively recent, and most gluten research has to do with celiac disease. Hopefully, we will see intriguing studies in the near future, since gluten-free products have grown to a $4 billion industry that the FDA now has begun to regulate.

References:
(1) Am J Gastroenterol. 2013;108:656-676. (2) Gut 2013;62:43–52. (3) Scand J Gastroenterol. (4) Neurogastroenterol Motil. 2013 Nov;25(11):864-71. (5) medscape.com. (6) fda.gov. (7) Am J Gastroenterol. 2011; 106(3):508-14. (8) medscape.com. (9) 9th annual AIM for Autism Research 2010; abstract 140.007. (10) BMC Gastroenterol. 2013:13(109).

Dr. Dunaief is a speaker, author and local lifestyle medicine physician focusing on the integration of medicine, nutrition, fitness and stress management. For further information, go to the website medicalcompassmd.com or consult your personal physician.

Wouldn’t it be great if cardiovascular disease (CVD) were rare? It’s not like traveling to Mars and back. It is something we have the tools to make happen in the present. However, reality is different from the fantasy. Though fewer people are dying from this compilation of diseases (strokes and heart disease), it still tops the list. In fact, a 30-year-old has a one-in-two chance of developing CVD in his or her lifetime (1). Now that we have shock and awe, where are we with this disease?
We know that greater than 90 percent of the patients that will suffer from CVD have at least one risk factor (2). Most of these risk factors are modifiable. They are the seven pillars: blood pressure, cholesterol, weight, diet, exercise, smoking status and blood sugar. If we control them, the risk of CVD goes down dramatically (3). However, very few of us do it without medication (4).
Factors that might positively influence these pillars include HDL “good cholesterol,” activity, exercise, diet and drugs. We will investigate this further.

DO WE HAVE A GOOD PREDICTOR?
What may be the best potential predictor of cardiovascular disease? Is it BMI, waist circumference, waist-to-hip ratio or sticky bun consumption? To be fair, I don’t think there has been a study done on how many sticky buns it takes to predict CVD, but they certainly contribute. The answer is in the study that follows.
In a recent prospective (forward-looking) study, results showed that waist-to-hip ratio was a better predictor of CVD than either BMI or waist circumference (5). The researchers used a biomarker of atherosclerosis (plaques in the arteries) to measure CVD risk. To measure atherosclerosis and confirm which anthropomorphic (body habitus) measurement was most useful, a Doppler of the carotids and a brachial-ankle pulse wave were used. In postmenopausal women, it appeared that waist-to-hip ratio was directly correlated with carotid Dopplers and brachial-ankle measurements. Those with waist-to-hip ratios above 0.86 were considered at higher risk for atherosclerosis and thus CVD. Waist circumference did correlate to brachial-ankle results, but not to carotid Dopplers. This is best explained by a potential postmenopausal redistribution of fat from the hips and buttock to visceral fat in the belly.

SAY NO TO DRUGS
(FOR PREVENTION)
Would you take a pill once a day with no side effects and no cost for the rest of your life if it meant preventing cardiovascular disease? Of course you would — or would you? In a recent study, patients were asked this very question and the results might be a surprise (6). Approximately one-third of participants would rather lose several months of life, about 12 weeks, than take a single once-a-day drug to prevent CVD. In fact, 20 percent of the participants were even willing to go as far as to pay $1,000 not to take such a medication. Mind you, about half of the participants were already taking three medications. Even more intriguing, it was the participants who were already taking pills that were least likely to want to add the hypothetical CVD prevention pill. Therefore, we need to reduce risk factors in other ways with lifestyle.

COMMON SENSE SAYS THAT
HIGH BLOOD PRESSURE INCREASES RISK BUT …
We all know that high blood pressure is a risk factor for cardiovascular disease, and those who are over the age of 60 will have the highest probability of having CVD. However, in a recent observational study, results show that younger patients with isolated high systolic blood pressure (SBP) have a significantly increased risk of CVD (7). Systolic is the top blood pressure reading number, and isolated high SBP means greater than 140 mmHg with a normal <90 mmHg diastolic (bottom number) pressure. Study participants were between the ages of 18 and 45.
Those who had a higher SBP had a significantly greater risk of dying from cardiovascular disease than those who did not have elevated pressure over a 31-year duration. It turned out that 25 percent of the men and about half as many women had isolated high SBP. However, the women had a greater risk of dying. However, there were several confounding factors that make this not the best type of study.

HDL: IS HIGHER BETTER?
For the longest time, we have thought that high levels of HDL had a protective effect against cardiovascular disease. But this paradigm may not be true. In fact, in a recent study, results show that it may have to do more with functionality of HDL than with the actual number (8). The baseline number for HDL had no impact on reducing cardiovascular risk but functionality did.
Functionality is referred to as the cholesterol-efflux capacity. The cholesterol-efflux occurs when HDL helps remove cholesterol from cells in the arterial walls and shifts it back into the liver. The patients with the highest quartile of cholesterol-efflux capacity had a two-thirds reduction in CVD risk compared to the lowest quartile. The better this process is working, the lower risk of CVD. Thus, it does not relate as much to the level of HDL in the blood but as to its functionality. This suggests that raising HDL by drug therapy may not be the most effective approach. To clarify and make for a more vivid image, as Dean Ornish, M.D., professor of medicine at UCSF has written, if you think of HDL as dump trucks, adding more dump trucks at a stoplight only piles up the trucks; it does not make for more effective transport.

THE DIETARY EFFECT IS NOT WHAT IT SEEMS
Many of us try to live a healthy life by managing our diets. However, not all diets are created equal when it comes to cardiovascular risk. In a recent meta-analysis (a group of 12 randomized controlled trials), the results disappointingly show that four popular diets did not decrease the cardiovascular disease risk, nor did they result in a substantial decrease in weight over the long term, compared to the placebo group (9). These diets included Weight Watchers, Atkins, South Beach and Zone.
Though Weight Watchers did show a significant initial weight loss, some of the weight was regained over time. The duration of the studies was between one and two years. There was no significant effect on markers for cardiovascular risk, such as cholesterol levels, blood pressure and sugar control.
It is disheartening to think that some diets don’t have any effect on cardiovascular disease. So what do we do? It turns out that a diet that has high levels of enterolactone, a biomarker for fiber and vegetables, has shown significant 65 percent reductions in cardiovascular events and mortality in men (10). Thus, a plant-based diet rich in vegetables and fiber has an impressive benefit. Diets such as Mediterranean-type and DASH diets are rich in these components.
Therefore, a productive way to make cardiovascular disease rare is to know your risk factors and to make lifestyle changes that include a plant-rich diet and activity. There are simple ways to determine risk, with waist-to-hip ratio as a useful tool. Reduce your waistline and you reduce your ratio, thus your risk. Eliminating these risk factors will make the probability of suffering from CVD that much less likely.
REFERENCES
(1) Lancet. 2014 May;383(9932):1899-911. (2) uptodate.com. (3) Circulation. 2010;121(4):586-613. (4) JAMA. 2012;307(12):1273-83. (5) Maturitas. online Jan. 12, 2015. (6) Circß Cardiovasc Qual Outcomes. online Feb. 3, 2015. (7) J Am Coll Cardiol. 2015;65(4):327-35. (8) N Engl J Med. 2014;371(25):2383-93. (9) Circ Cardiovasc Qual Outcomes. 2014;7:815-827. (10) Lancet. 1999;354(9196):2112.

Dr. Dunaief is a speaker, author and local lifestyle medicine physician focusing on the integration of medicine, nutrition, fitness and stress management.  For further information, go to the website www.medicalcompassmd.com and/or consult your personal physician.

Let’s begin with a pretest. I want to make it clear that a pretest is not to check whether you know the information, but that you have an open mind and are willing to learn.

1)Which may have the most detrimental impact on your health?
a.    Smoking
b.    Obesity
c.    Inactivity
d.    A and C
e.    All have the same impact

2)People who exercise are considered active.
a.    True
b.    False

3)Inactivity may increase the risk of what? Select all that apply.
a.    Diabetes
b.    Heart disease
c.    Fibromyalgia
d.    Mortality
e.    Disability

A snowy and icy winter is upon us, and our thoughts turn to hibernation and not falling. Who wants to be active when it’s cold and slippery outside? Let me delineate between exercise and inactivity; they are not complete opposites. When we consider exercise, studies tend to focus on moderate to intense activity. However, light activity and being sedentary, or inactive, tend to get clumped together. But there are differences between light activity and inactivity.
Light activity may involve cooking, writing, and strolling. (1). Inactivity involves sitting as in watching TV or in front of a computer screen. Inactivity utilizes between 1-1.5 metabolic equivalent units — better known as METS — a way of measuring energy, while light activity requires greater than 1.5 METS. Thus, in order to avoid inactivity, we don’t have to exercise in dreaded wintery conditions. We need to increase our movement.
What are the potential costs of inactivity? According to the World Health Organization over 3 million people die annually from inactivity. This ranks inactivity in the top five potential underlying causes of mortality (2). The consequences of inactivity are estimated at 1 to 2.6 percent of health-care dollars, which sounds small, but translates into actual dollars spent in the U.S. of between $38 billion and $100 billion (3).
How much time do we spend inactive? Good question. In a recent observational study of over 7,000 women with a mean age of 71 years old, 9.7 waking hours were spent inactive or sedentary. These women wore an accelerometer to measure movements. Interestingly, as BMI and age increased, the amount of time spent sedentary also increased (4).
Inactivity may increase the risk of mortality and plays a role in increasing risk for diseases such as heart disease, diabetes, and fibromyalgia. It can also increase the risk of disability in older adults. Surprisingly, inactivity may be worse than smoking and obesity. Even for those who exercise, inactivity can still occur. There can be a doubling of the risk for diabetes in those who sit for long periods of time, compared to those who sit the least (5).
By the way, the answers to the pretest are 1) e; 2) b; 3) a, b, c, d, e.
Let’s look at the evidence.
DOES EXERCISE TRUMP INACTIVITY?
We tend to think that exercise trumps all; if you exercise, you can eat what you want and, by definition, you’re not sedentary. Right? Not exactly. Diet is important, and you can still be sedentary even if you exercise. In a meta-analysis — a group of 47 studies — results show that there is an increased risk of all-cause mortality with inactivity, even in those who exercised (6). In other words, even if you exercise, you can’t sit for the rest of the day. The risk for all-cause mortality was 24 percent overall.
However, those who exercised saw a blunted effect with all-cause mortality, making it significantly lower than those who were inactive and did very little exercise: 16 percent versus 46 percent increased risk of all-cause mortality. So it isn’t that exercise is not important, it just may not be enough to reduce the risk of all-cause mortality if you are inactive for a significant part of the rest of the day.
In an earlier published study using the Women’s Health Initiative, results showed that those who were inactive most of the time had greater risk of cardiovascular disease (7). Even those who exercised moderately but sat most of the day were at increased risk of cardiovascular disease. Moderate exercise was defined as 150 minutes of exercise per week. Those at highest risk were women who did not exercise and sat at least 10 hours a day. This group had a 63 percent increased risk of cardiovascular disease (heart disease or stroke).
However, those who sat fewer than five hours a day had a significantly lower risk of cardiovascular events. And those who were in the highest group for regular exercise (walking seven hours/week or jogging/running four-to-five hours/week) did see more benefit in cardiovascular health, even if they were inactive the rest of the day. Sitting longer did not have negative impact on the individuals in the high exercise level group.
WORSE THAN OBESITY?
Obesity is a massive problem in this country; it has been declared a disease itself and also contributes to other chronic diseases. But would you believe that inactivity has more of an impact than even obesity? In a newly published observational study, using data from the EPIC trial, inactivity might be responsible for two times as many premature deaths as obesity (8). This was a study involving 330,000 men and women.
Interestingly, the researchers created an index that combined occupational activity with recreational activity. They found that the greatest reduction in premature deaths (in the range of 16 to 30 percent) was between two groups, the normal weight and moderately inactive group versus the normal weight and completely inactive group. The latter was defined as those having a desk job with no additional physical activity. To go from the completely inactive to moderately inactive, all it took, according to the study, was 20 minutes of brisk walking on a daily basis.
ALL IS NOT LOST!
In another recent study evaluating 56 participants, walking during lunch time at work immediately improved mood (9). This small study clearly shows that by being more active at lunch time, there was a change for the better, increasing enthusiasm and reducing stress compared to in the morning before they had walked. Participants had to walk at least 30 minutes three times a week for 10 weeks; pace was not important.
So what have we learned thus far about inactivity? It is all relative. If you are inactive, increasing your activity to be moderately inactive by briskly walking for 20 minutes a day may reduce your risk of premature death significantly. Even if you exercise the recommended 150 minutes a week, but are inactive the rest of the day, you may still be at risk for cardiovascular disease. You can potentially further reduce your risk of cardiovascular disease by increasing your activity with small additions throughout the day.
The underlying message is that we need to consciously move throughout the day, whether at work with a walk during lunch or at home with recreational activity. Those with desk jobs need to be most attuned to opportunities to increase activity. Simply setting a timer and standing or walking every 30-45 minutes may increase your activity levels and possibly reduce your risk. Just because the groundhog saw his shadow, don’t let it influence you to be inactive.
REFERENCES:
(1) Exerc Sport Sci Rev. 2008;36(4):173-178. (2) WHO report: https://bit.ly/1z7TBAF. (3) forbes.com. (4) JAMA. 2013;310(23):2562-2563. (5) Diabetologia 2012; 55:2895-2905. (6) Ann Intern Med. 2015;162:123-132, 146-147. (7) J Am Coll Cardiol. 2013;61(23):2346-54. (8) Am J Clin Nutr. online January 24, 2015. (9) Scand J Med Sci Sports. Online Jan. 6, 2015.

Dr. Dunaief is a speaker, author and local lifestyle medicine physician focusing on the integration of medicine, nutrition, fitness and stress management.  For further information, go to the website www.medicalcompassmd.com and/or consult your personal physician.

Fat in the diet is a highly complicated issue. For decades, we have adopted the notion that fat may be the enemy and, therefore, we should eat a low-fat diet. But is this really true? The answer is that we all need fat, but the sources are important.
The cover of Time magazine’s June 23 edition exclaimed in big yellow letters to “Eat Butter. Scientists labeled fat the enemy. Why they were wrong” (1). It also included a picture of a curl of butter, in case you had forgotten what butter looked like. This cover is provocative and tantalizing. However, it does a disservice to the article itself and to the general population who may have seen it.
The article, itself, is well written. Its focus is not mainly on butter, but rather on different types of fats, saturated and unsaturated. The author Bryan Walsh does make salient points, but my objection is mainly that many of these points are buried deep within a five-page, three-column, single-spaced article among comments that are not necessarily substantiated. You have to wade through paragraph after paragraph to get to some these points. Reading the first page is not good enough.
Let’s look at a few studies presented in the article.
Study: Different types of fat — saturated and unsaturated with heart disease.
There was a recent meta-analysis (a group of 72 studies including both observational and randomized controlled trials) that looked at whether different types of fat had an impact on cardiovascular health (2). The results showed that saturated fats, omega-6 polyunsaturated fats and monounsaturated fats were most likely not harmful and that omega-3 polyunsaturated fats were potentially beneficial. However, trans fatty acids were shown to be potentially harmful, with a 17 percent increased risk of cardiovascular disease outcomes such as heart attacks and heart disease.
While this is an interesting study, there are some significant flaws that need to be highlighted.
1. The conclusions in the study don’t match or only partially match. Let me explain. There is a conclusion in the abstract (a synopsis or summary of the study) and a conclusion in the body of the study. The abstract concludes that polyunsaturated fats, including omega-3 fatty acids, are not necessarily beneficial while saturated fat may not be harmful. In the body of the study, the authors conclude that omega-3 fatty acids significantly reduce cardiovascular events. Why is this important? Many physicians are bombarded by studies and may only have time to read the abstract. Thus, this could wrongly influence the physician.
2. The source of fat is never differentiated in the study. In other words, the saturated fats which are deemed harmless may be from foods or supplements that contain both unsaturated fats and saturated fats or from foods that contain only saturated fats. We see benefit in plant-based foods that have multiple types of fats — saturated and unsaturated — such as olive oil, nuts, seeds and avocado. However, most animal fats, like red meat, pork and chicken, contain only saturated fats. The exception is fish, which contains multiple types of fats.
Also, unlike the Time cover story, the study NEVER mentions butter, cheese or red meat. Therefore, the commentary by the press is based on an extrapolation that cannot and should not be made: that eating butter, cheese and red meat maybe harmless and possibly beneficial.
3. The populations of the studies differed at the starts of the different trials. In other words, some were healthy participants, some were high-risk patients and some already had cardiovascular disease. The main thing these studies had in common was that cardiovascular disease outcomes were an endpoint, but it did not have to be the primary, or main, endpoint. Thus, cardiovascular disease outcomes may not have been the main thrust of all the studies that made up the meta-analysis.
4. A meta-analysis by definition is difficult to perform because researchers combine results from studies that were designed and performed differently from one another. In this meta-analysis, the authors combine the results of observational trials that may have used different types of fat intake from food or from supplements. Usually, supplements, like fish oil, involve both saturated and unsaturated fats, and they may have different effects than food.
5. Finally, the study does not tell us what those who ate lower saturated and unsaturated fats ate instead. For example, it compared those who ate high saturated fats to those who ate low saturated fats. What did the group who ate lower saturated fat eat instead of fat? Was it carbohydrates? If so, were they fries, whole grains or sweet potatoes?
The Time cover article goes on to mention the Mediterranean diet and its beneficial effects with heart disease. There was a recent randomized controlled study, the gold standard of studies, called the
PREDIMED trial, with results that showed that participants who ate a Mediterranean diet with added olive oil or mixed nuts had a 30 percent decreased risk of cardiovascular disease than those in the control arm who were advised to follow a “low-fat” diet (3).
The Mediterranean diet emphasizes vegetables, fruits, whole intact grains, beans, legumes and fish, as well as olive oil and nuts. This was not a low-fat diet. It contained both saturated and unsaturated fats, including polyunsaturated and monounsaturated fatty acids. The caveat to these results is that the “low-fat” group was not actually able to maintain a low-fat diet, but instead ate more like the standard American diet with no restrictions.
Interestingly, researchers using the same Mediterranean diet study, PREDIMED, showed that higher dietary intake of magnesium reduced the risk of cardiovascular mortality risk by 34 percent (4). They compared those in the highest intake of dietary magnesium with those in the lowest. These participants had a high risk of cardiovascular disease. Foods rich in magnesium include dark green leafy vegetables, such as spinach, as well as nuts, seeds, fish, beans, lentils and avocados.
In conclusion, the sources of fats matter. To run out and eat a cheeseburger, without the bun of course, would be to have misunderstood this article and the flaws in the meta-analysis and to have focused only on the cover of the Time magazine article.
The take-home message should be that we need some fats in our diet, but that the sources of these fats are critical. Diet quality is of the utmost importance in reducing disease (5), so put that cheeseburger out of your mind. Many studies have shown that the Mediterranean diet helps reduce the risk of cardiovascular events. For some, this may include the addition of more olive oil and nuts.
References:
(1) Time.com. (2) Ann Intern Med. 2014;160:398-406. (3) N Engl J Med. 2013;368:1279-1290. (4) J Nutr. 2014;144:55-60. (5) Lancet. 2014;383:1999-2007.

Dr. Dunaief is a speaker, author and local lifestyle medicine physician focusing on the integration of medicine, nutrition, fitness and stress management. For further information, go to the website medicalcompassmd.com or consult your personal physician.

Everyone has heard of pancreatic cancer, but pancreatitis is a significantly more common disease in gastroenterology and seems to be on an upward projection. Ironically, this disease gets almost no coverage in the general press. In the United States, it is among the top reasons for patients to be admitted to the hospital (1).

Now that I have your attention, let’s define pancreatitis. A rudimentary definition is an inflammation of the pancreas. There are both acute and chronic forms. We are going to address the acute – abrupt and of short duration – form. There are three acute types: mild, moderate and severe. Those with the mild type don’t have organ failure, whereas those with moderate acute pancreatitis experience short-term or transient (less than 48 hours) organ failure. Those with the severe type have persistent organ failure. One in five patients present with moderate or severe levels (2).

What are the symptoms?
In order to diagnosis this disease, the American College of Gastroenterology guidelines suggests that two of three symptoms be present. The three symptoms include severe abdominal pain; increased enzymes, amylase or lipase, that are at least three times greater than normal; and radiologic imaging (ultrasound, CT, MRI, abdominal and chest X-rays) that shows characteristic findings for this disease (3). Most of the time, the abdominal pain is epigastric, and it may also present with pain in the right upper quadrant of the abdomen (4). Approximately 90 percent of patients may also experience nausea and vomiting (5). In half of patients, there may also be pain that radiates to the back.

What are the risk factors?
There is a multitude of risk factors for acute pancreatitis. These include gallstones, alcohol, obesity and, to much lesser degree, drugs. Gallstones and alcohol may cause up to 75 percent of the cases (2). Many of the other cases of acute pancreatitis are considered idiopathic (of unknown causes). Although medications are potentially responsible for between 1.4 percent and 5.3 percent of cases, making it rare, the number of medications implicated is diverse (6) (7). These include certain classes of diabetes therapies, some antibiotics – Flagyl (metronidazole) and tetracycline – and immunosuppressive drugs used to treat ailments like autoimmune diseases. Even calcium may potentially increase the risk.

Obesity effects
When given a multiple-choice question for risk factors that includes obesity as one of the answers, it’s a safe bet to choose that answer. Pancreatitis is no exception. However, in a recent study, using the Swedish Mammography Cohort and the Cohort of Swedish Men, results showed that central obesity is an important risk factor, not body mass index or obesity overall (8). In other words, it is fat in the belly that is very important, since this may increase risk more than twofold for the occurrence of a first-time acute pancreatitis episode.
Those who had a waist circumference of greater than 105 cm (41 inches) experienced this significantly increased risk compared to those who had a waist circumference of 75 to 85 cm (29.5 to 33.5 inches). The association between central obesity and acute pancreatitis occurred in both gallbladder-induced and nongallbladder-induced disease. There were 68,158 patients involved in the study with a median duration of 12 years. Remember that waistline is measured not from the hips, but rather from the navel. This may be a surprising wake-up call for some.

Mortality risks
What makes acute pancreatitis so noteworthy and potentially dangerous is that the rate of organ failure and mortality is surprisingly high. One study found that the risk of mortality was 5 percent overall. This statistic broke out into a smaller percentage for mild acute pancreatitis and a greater percentage for severe acute pancreatitis, 1.5 percent and 17 percent respectively (9). This was a prospective (forward-looking) observational trial involving 1,005 patients.
However, in another study, when patients were hospitalized for this disease, the mortality rate was even higher at 10 percent overall (10).

Diabetes risks
The pancreas is a critical organ for balancing glucose (sugar) in the body. In a recent meta-analysis (involving 24 observational trials), the results showed that more than one-third of patients diagnosed with acute pancreatitis went on to develop pre-diabetes or diabetes (11). Within the first year, 15 percent of patients were newly diagnosed with diabetes. After five years, it was even worse; the risk of diabetes increased by 2.7-fold. This is scary, considering that diabetes has become a pandemic. If we can reduce the risk of pancreatitis, we may also help to reduce the risk of diabetes.

Surgical treatments
Gallstones and gallbladder sludge are major risk factors, accounting for 35 to 40 percent of acute pancreatitis incidence (12). Gallstones are thought to cause pancreatitis by temporarily blocking the duct shared by the pancreas and gallbladder that leads into the small intestine. When the liver enzyme ALT is elevated threefold (measured through a simple blood test), it has a positive predictive value of 95 percent that it is indeed gallstone-induced pancreatitis (13).
If it is gallstone-induced, surgery plays an important role in helping to resolve pancreatitis and prevent recurrence of acute pancreatitis. In a recent study, results showed that surgery to remove the gallbladder was better than medical treatment when comparing hospitalized patients with this disease (14). Surgery trumped medical treatment in terms of outcomes, complication rates, length of stay in the hospital and overall cost for patients with mild acute pancreatitis. This was a retrospective (backward-looking) study with 102 patients.

Can diet have an impact?
The short answer is: yes. What foods specifically? In a large, prospective observational study, results showed that there was a direct linear relationship between those who consumed vegetables and a decreased risk of nongallstone acute pancreatitis (15). For every two serving of vegetables, there was 17 percent drop in the risk of pancreatitis. Those who consumed the most vegetables – the highest quintile (4.6 servings per day) – had a 44 percent reduction in disease risk, compared to those who were in the lowest quintile (0.8 servings per day). There were 80,000 participants involved in the study with an 11-year follow-up. The authors surmise that the reason for this effect with vegetables may have to do with their antioxidant properties, since acute pancreatitis increases oxidative stress on the pancreas.

References:
(1) Gastroenterology. 2012;143:1179-1187. (2) www.uptodate.com. (3) Am J Gastroenterol. 2013;108:1400-1415. (4) JAMA. 2004;291:2865-2868. (5) Am J Gastroenterol. 2006;101:2379-2400. (6) Gut. 1995;37:565-567. (7) Dig Dis Sci. 2010;55:2977-2981. (8) Am J Gastroenterol. 2013;108:133-139. (9) Dig Liver Dis. 2004;36:205-211. (10) Dig Dis Sci. 1985;30:573-574. (11) Gut. 2014;63:818-831. (12) Gastroenterology. 2007;132:2022-2044. (13) Am J Gastroenterol. 1994;89:1863-1866. (14) Am J Surg online. 2014 Sept. 20. (15) Gut. 2013;62:1187-1192.

Dr. Dunaief is a speaker, author and local lifestyle medicine physician focusing on the integration of medicine, nutrition, fitness and stress management.  For further information, go to the website www.medicalcompassmd.com and/or consult your personal physician.