Each human body has a unique array of microorganisms, collectively called the “microbiota”. There may be 1000 different species and over 100-fold more genes that are in the human genome.  Studies have demonstrated a symbiotic relationship between the human host and the bacterial microbiota of the gut.  The education and maturation of the intestinal immune system is the result of millions of years of co-evolution with host and their microbiota and dietary intake.

The microbiota serves as a metabolic “organ’ that actively participates in host metabolism.  These bacteria are involved in regulating inflammation, energy, and immunity, playing a role in the development of metabolic and immunological diseases. In addition, the microbiota can improve nutritional status by aiding in digestion, extracting nutrients, and synthesizing vitamins and certain amino acids.

Nutrition plays a prominent role in promoting a healthy gut microbiome. Plant-based eating patterns – one that is high in unrefined carbohydrates and low in fat while providing adequate amounts of protein – support a microbiota that is robust in health-promoting species while preventing overgrowth of pathogenic bacteria.


You may have heard that omega-3 fatty acids are good for your health, but did you know that they can actually help you lower your risk of death? According to a study that was recently featured in the Journal of Clinical Lipidology, women between the ages of 65 and 80 who have the highest omega-3 blood levels are 20% less likely to die—from any cause—than those whose blood levels are in the lowest quartile.


While this is not the only time that scientists have studied the correlation—and confirmed the link—between longer life expectancies and higher omega-3 blood levels, it is the largest. The data analyzed was taken from a sample of over 6,500 women beginning in 1996 with outcomes being tracked until 2014.


Throughout the study, scientists estimated that an intake of 1g of EPA (eicosapentaenoic acid) and DHA (docosahexaenoic acid) per day could increase omega-3 status from the lowest quartile to the highest. 1g a day of omega-3 fatty acids, which is well below the level deemed to be safe by the FDA, could equal:

  • Two and a half to three salmon fillets in a week
  • 1-3 soft gel supplements daily
  • 1 teaspoon of liquid omega-3 supplements daily

There are many other foods rich with omega-3 fatty acids that you could introduce to your diet as well.


How does adding that 1g to your diet lower your risk of death? Omega-3 fatty acids help your body to:

  • Boost immunities
  • Maintain cardiovascular health
  • Stabilize blood sugar levels
  • Lower inflammation
  • Treat digestive disorders
  • Reduce cancer risks and reoccurrence

In addition to the above, DHA and EPA fatty acids can also improve mental health by preventing depression and helping with focus and learning.


As a Registered Dietician, Certified Nutritional Specialist, and Certified Dietitian Nutritionist in the state of New York, Nancy Mazarin loves helping people get healthy on their terms. Offering medical nutrition therapy and weight management, she provides specialized programs that focus on your individual needs and health goals. These programs focus on a number of things, including education, behavior modification, and meal planning.

Are you ready to make some adjustments to your diet that could help you to improve your overall health? Contact Nancy today via email (nmeatrite@mazarinrd.com) to learn more about what individualized plan can help you to get the long-term health results you’re looking for.


We have the answers to these questions, kept in the shadows impressively well by the peddlers of pepperoni and bacon.

  • The range of saturated fat intake examined is pretty narrow. In the first meta-analysis, the top and bottom of the range often differed by only a few percentage points, and even the bottom of the range was above current recommendations. The later meta-analysis compared the top third of the population to the bottom third and, again, the difference was small.
  • To the extent saturated fat intake has gone down over time in the U.S. – and it hasn’t gone down much – it has mostly been replaced by sugar and refined carbohydrates.

A generally neglected consideration is that overall diet quality was comparably bad at the “extremes” of the rather narrow saturated fat range observed. That’s about what we would expect if the main alternatives to saturated fat from burgers, pizza and ice cream were refined carbohydrate and sugar from soda cookies, fries and donuts.

The available evidence suggests that is exactly what happens. Data from both the U.S. Department of Agriculture and the Centers for Disease Control and Prevention shows that animal fat intake in the U.S. has stayed fairly constant over recent decades, while sugar intake, refined carbohydrate intake and total calories have gone up.

The crucial question that neither meta-analysis answered is this: How does variation in saturated fat intake affect rates of heart disease when the alternatives to saturated fat calories are assessed? A 2015 paper provides the answer. In roughly 125,000 people over nearly 30 years, heart disease rates went from bad to even worse if trans-fat replaced saturated fat, stayed the same when sugar and refined carbohydrates replaced saturated fat and declined significantly when saturated fat calories were replaced with either calories from whole grains or calories from unsaturated fats coming from nuts, seeds, olive oil, avocado, fish and seafood. A more recent study of comparable size and methods appended this: Rates of heart disease go up when more of total dietary fat is saturated, and go down as more of total dietary fat is unsaturated.

Shockingly at odds with those making a case for saturated fat, what all of these data seem to indicate is just what both science and sense suggested all along: A diet made poor by an excess of saturated fat from the usual sources –  beef, processed meats, fast food and processed dairy – is almost exactly as bad for health outcomes as a diet made poor by an excess of sugar and refined carbohydrate from the usual sources. There is more than one way to eat badly – and we seem dedicated to exploring them all.

It is certainly true that saturated fat is not, and never was, the one and only thing wrong with our diets. It’s also true that not all saturated fats are created equal. But those are not the propositions that are being peddled. The misguided premise is that we must choose the one, true dietary scapegoat from either saturated fat or sugar.

The fundamentals of a genuinely healthful diet are clear, supported by vast and diverse evidence and a matter of global consensus. They translate into dietary patterns of wholesome foods in any of various sensible combinations that are inevitably low in added sugar, refined carbohydrate and saturated fat alike. Applied routinely, they could add years to lives, and life to years – and benefit the planet too.


For decades the American public has been warned that eating saturated fat, the type found in meat and processed foods, can lead to heart disease.  Now there is a booming cottage industry peddling the argument that saturated fat is good for us. Unfortunately, for those who wish to believe this, the argument is invalid.

The relevant literature has already been summarized for us in some rather famous, if not infamous, systematic reviews. The very purpose of systematic reviews, and their quantitative counterpart, meta-analysis, is to help establish conclusions based not just on any one study, but the overall weight of evidence. Systematic reviews and meta-analyses about saturated fat and health outcomes are readily available.

There are only two reviews that suggest we consume more saturated fat. The first dates from 2010; the second from 2014. They differ in many details, but they effectively address the same basic issue. What did they find? Rates of heart disease were high, and almost exactly the same, at the high and low ends of the saturated fat intake range. The currently popular argument is that rates of heart disease did not go down when saturated fat intake went down; and therefore, saturated fat must be good for us.

These studies represent poor science. We could use exactly the same data, and just the same “logic,” to argue that rates of heart disease did not go down when saturated fat intake went up; and therefore, saturated fat must be bad for us (still).

The simple fact is that neither of these assertions is valid. If heart disease rates don’t change across the range of saturated fat being examined, all it does is raise additional questions. How much variation is there in saturated fat intake in the first place? If there isn’t much, it’s no surprise that outcomes affected by saturated fat don’t vary much either.  When saturated fat intake goes down, what is replacing it – and what is happening to the overall diet quality?


“Calcium supplements could increase risk of heart disease, new study finds” said a Washington Post headline in October. “Calcium supplements could give you a heart attack,” wrote the New York Daily News.

Researchers at Johns Hopkins and other universities analyzed data from the Multi-Ethnic Study of Atherosclerosis Study, which was conducted from 2000 to 2012. The 5,458 study participants came from Baltimore, Chicago, New York City, Los Angeles, Minnesota and North Carolina. At the start of the study, the calcium content of their diets and of their dietary supplements and the amount of calcification in their coronary arteries was recorded. Ten years later, the coronary calcification of the 2,742 remaining participants was again measured.

The results: for those who had some calcification to start with, how much calcium they consumed, whether from food or supplements, didn’t matter. For them, calcium supplements clearly did not increase their risk of heart disease.

Among the participants who had no calcification at the beginning of the study, those who consumed the most calcium from food and supplements – an average of about 2,150 mg – significantly lowered their risk of developing calcification by 27 percent. That means the risk of heart disease was lower, not higher.

Among the participants who began the study with no calcification, those who consumed the least amount of calcium from supplements – an average of 90 mg a day – had the highest risk of developing calcifications. And those who consumed more calcium from supplements than that – an average of 165 mg to 1,125 mg – had no greater risk of developing calcification. Somehow this got translated by the media into “calcium supplements could give you a heart attack”. Bizarre to say the least!

Two weeks after this study appeared, reason prevailed. The American Society for Preventive Cardiology and the National Osteoporosis Foundation assured the public that calcium supplements have no impact on heart attacks, stroke, or other cardiovascular disease. These two organizations based this advice on a new review of 31 studies – four clinical trials and 27 observational studies – by an expert panel which found no increased risk of cardiovascular disease in people who consumed up 2,500 mg of calcium in supplements a day.

As a medical nutrition consultant, I continue to tell my patients is if they don’t get 1,000 to 1200mg of calcium a day from food they should take a supplement, so between their diet and supplements calcium intake is adequate.

Learn more about me, Nancy Mazarin, medical nutritional therapy and weight management at www.mazarinrd.com.

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Great Neck, New York 11021

BIGGEST LOSER – a misleading report
The grim message from the recent New York Times article is that dieting is futile and re-gain is all but pre-ordained. The authors of the original research didn’t interpret their results that we are doomed to battle our biology or remain fat, which is certainly what the New York Times article implies. The researchers stated that in this subgroup we need to explore other approaches

The artificial environment of “The Biggest Loser” – being followed with cameras 24/7, exercising 9 hours daily and watched by millions for seven months – resulted in extreme weight loss: 8 pounds/week for 34 weeks. By comparison, weight loss after bariatric surgery averages 3 pounds/week which is still considered a rapid rate of loss. The goal rate for a healthy and sustainable loss is an average of ¾ pound /week.
When comparisons were made between contestants and gastric by-pass (RYBP) patient’s, they found considerably more muscle mass was sustained by the contestants, yet their RMR was slower. An anomaly occurred that is not customarily seen in the normal dieting population. The findings, in fact, are consistent with current data that show the response to starvation. This is in contrast to data about the RYGB that shows no slowing of the metabolic rate. Also with the RYBP hunger goes away whereas the lower leptin levels in the Biggest Loser Contestants (BLC) probably leads to more hunger or at least less satiation. What must be considered is that extreme, massive weight loss in so short a time may have created an aberrant metabolism. Changes that occurred in these individuals (e.g. hormonal, metabolic), cannot be extrapolated to individuals losing weight at a slower rate.

The article implied that the decrease in the metabolic rate is the primary cause of contestants weight gain. The drop in metabolic rate (using the numbers they gave us) is not enough to account for the regain, nor is it the only issue, nor does it seem to happen in everyone to the same extent or even at all. In reference to the contestants’ calorie intake, food consumption was not measured. Hunger, cravings, and disordered eating can quickly return. These effects were unquantified.
The study in Obesity that prompted the article in the Times measured contestants RMR 6 years after the end of the competition. They concluded that calorie restriction along with vigorous exercise in the BLC participants resulted in the preservation of fat-free mass (FFM) and greater metabolic adaption compared to RYGB subjects despite comparable weight loss. Metabolic adaptation was related to the degree of energy imbalance and the changes in circulating leptin
Dr. Hall used a mathematical computer model of human metabolism – currently intended for research conducted by scientists and health professionals – to calculate the diet and exercise changes underlying the observed body weight loss. The computer model simulated the results of diet alone and exercise alone to estimate their relative contributions. These simulations suggest that the participants could sustain their weight loss and avoid weight regain by adopting more moderate lifestyle changes – like 20 minutes of daily vigorous exercise and a 20% calorie restriction – than those demonstrated on the television program.
“Dieters are not at the mercy of their bodies, and this is not a subset of the most successful dieters”, stated Dr. David Ludwig, director of the New Balance Foundation Obesity Prevention Center at Boston’s Children’s Hospital. They are abnormal dieters who abused their bodies and minds with restrictive programs that are consistent with deprivation. Food problems remained unresolved and accurate education elusive.
In all my years of practice, I have never worked with an individual who could not lose weight and sustain their optimal weight if they were willing to invest the time and effort needed. The National Weight Control Registry reaffirms that obese individuals can lose weight and sustain the weight loss for many years (average loss of 73 lbs. maintained for more than 5 years). Furthermore, individuals who have undergone bariatric surgery often maintain an optimal weight. Is the regain that is often seen a result of a metabolic abnormality that follows a diet or a significant increase in calories that is a backlash to restriction or a return to customary intake and behaviors? If people continued to eat healthy and exercise, they wouldn’t regain 100 to 200 lbs.
There is no situation where an optimal weight is maintained without effort. With weight loss, reduced caloric need, often coupled with a reduced metabolic rate (previously elevated) is to be expected. The body is smaller so requirements are reduced for feeding and moving. We need to understand that as all of us age, in this obesogenic environment, selectivity with respect to what to eat, when to eat and how much to eat is needed. We all live in a very toxic food environment, and maintaining weight loss is not easy.
As stated by Dr. Griffin Rodgers, the NIDDK Director, “This study reinforces the need for a healthy diet and exercise in our daily lives”. The take home message should have been that you cannot abuse your body with extreme dieting without severe repercussions. It’s time to Stop Dieting. Overweight individuals need to learn how to eat in a healthy, enjoyable and sustainable manner with the goal of attaining and maintaining an optimal weight.

The U.S. Department of Health and Human Services just released the dietary guidelines for 2015–2016.  The nation’s “best and brightest nutrition experts”, who pored over the scientific evidence, made the following recommendations:

Healthy eating selections include:

  • A variety of vegetables
  • Whole fruits
  • Grains, at least, half of which are unrefined
  • Fat-free or low-fat dairy
  • A variety of proteins, including seafood, poultry,
    lean meat, eggs, legumes, nuts, seeds and soy products
  • Oils

Healthy eating patterns limit:

  • Saturated fat
  • Trans fats
  • Added Sugars
  • Sodium

Samples of Health eating plans

The Healthy U.S. –Style Eating Pattern, based on lean proteins, whole grains, fruits, and vegetables

The Healthy Mediterranean-Style Eating Pattern focused on seafood, legumes, whole grains, fruits, and vegetables

The Healthy Vegetarian-Style Eating Pattern, which highlights low-fat dairy products, eggs, legumes, whole grains, fruits and vegetables

For more information visit http://health.gov/dietaryguidlines/









THE SOY HYPE IS RIGHT. In the last few years, we are constantly reading about the seemingly endless benefits of soy products. When a food is touted in every health and nutrition column, in newspapers, magazines, and the internet, the extravagant claims are usually of questionable authenticity. But not so with soy. Epidemiological studies have shown a correlation between the consumption of soy foods and low rates of certain diseases, including coronary heart disease, hormone-dependent cancers such as breast, prostate and colon cancer, osteoporosis, and problems associated with menopause and menstrual irregularities.

Soybeans are legumes that are rich in phytoestrogens, plant-derived non-steroidal compounds that possess estrogen-like biological activity. It is the isoflavone component which is believed to provide many of the health protective effects. Isoflavones are a class of phytoestrogens that influence estrogen receptor binding, function as antioxidants, modulate sex hormone binding globulin, and exert anti-proliferative, anti-angiogenesis, and many other health promoting actions. The three main isoflavones present in soy are genistein, daidzein, and glycitin.

Epidemiological evidence suggests that populations consuming soy in fairly high amounts have lower coronary heart disease mortality. Possible mechanisms that may affect the cardiovascular system and atherosclerosis include inhibiting platelet activating factor and thrombin formation, lowering triglycerides and total cholesterol, improving arterial elasticity and inhibiting LDL oxidation.

Soy isoflavones may help prevent the development of osteoporosis at different stages. A bone-conserving action is considered to result from the direct estrogen receptor-mediated action of genistein on osteoblasts and their precursor cells. Independent of the estrogenic effects may be the enhancement of calcium absorption and retention.

A significant body of research, including epidemiological, in vitro, and animal studies, suggests that soy isoflavones may help to reduce cancer risk, specifically breast, prostate, and colon cancer. Several mechanisms have been proposed and researched include inhibition of enzymes whose actions promote cell differentiation through their effects on growth factor stimulation, inhibition of angiogenesis, and stimulation of sex hormone binding globulin.

Isoflavones are reported to exert a balancing effect on reproductive hormones in both pre- and postmenopausal women. It appears that they exert mild agonistic (estrogenic) and antagonistic (anti-estrogenic) effects, depending on the level of endogenous estrogen present. Isoflavones possess weak estrogenic activity and compete with the most potent endogenous estrogens at the receptor site, thereby reducing the total estrogen burden on the body. In this respect, the isoflavones are regarded as exerting anti-estrogenic effects.

Conversely, as natural estrogen production declines with the onset of menopause, isoflavones may help to offset this decline through their estrogenic effects. This hormonal duality is part of the reason these compounds seem to exert such a range of health effects. Theoretically, problems associated with estrogen imbalance, such as endometriosis, cervical dysplasia, breast cancer, menstrual irregularities, and symptoms commonly seen with both premenstrual syndrome and menopause, may improve with soy isoflavone intake.

Due to recent industry developments, however, one no longer must eat soy foods to get isoflavones. Several companies are now marketing soy/isoflavone pills. Given America’s proclivity for pills, it is not surprising that the supplement industry has capitalized on the excitement over the hypothesized health benefits of isoflavones. There are numerous reasons for promoting soy foods, rather than soy pills.

One is that there are other phytochemicals in soy foods, such as phenolic acids and saponins that may exert beneficial effects and that are not present in significant amounts in the pills. Two, for most people, incorporating soy foods into the diet will lead to a diet lower in saturated fat and cholesterol and higher in fiber. Three, there are potentially critical differences in isoflavone composition between the soy pills and soy foods. Four, limited dose-response data are available. Five, though results of human intervention studies remain inconclusive, there is concern that isoflavones in pill form may exert a stimulating effect on breast cancer.

Though several lines of evidence, including in vitro, animal, and human research indicate that phytoestrogens have direct beneficial effects on the arteries and bones, may reduce the risk of certain forms of cancer, and might help alleviate menopausal symptoms, the exact amount of isoflavones needed for these benefits is unknown. Finally, it must be recognized that researchers are only beginning to understand the effects of phytoestrogens. Studies have not yet clarified whether it is isoflavones in the soy foods or other components of soybeans acting alone or in conjunctions with isoflavones that are responsible for the health benefits. The health implications of these differences need to be researched and addressed.

For assistance with your dietary needs, look to medical nutrition consultant, Nancy Mazarin.

The relationship between cancer and nutrition is complex and multifactorial. Nutrition may play a major role in the development and progression of tumors, and conversely, not only may the neoplastic process have a detrimental effect on the nutritional status of the patient with breast cancer, but so too can the treatment modalities used to control the disease.

The nutrition management of the patient with breast cancer depends on the presence or absence of active disease, recent medical treatment, weight status, and nutrition status. The management of nutrition problems in the malnourished breast cancer patient is similar to that in other cancer patients. Obesity and weight gain, however, are more commonly seen and are a significant health risk among patients with localized breast cancer as well as those with advanced disease.

Since obesity and the risk for breast cancer increase with age, interventions that encourage weight control may influence cancer survival rates. Furthermore, obesity (25% or more over optimal weight for height) is a significant prognostic factor for those with the disease. Obesity is associated with increased estrogen production secondary to increased peripheral aromatization (i.e., the production of estrogen in fat cells). Consequently, the estrogen-sensitive tissues of obese women are exposed to more stimulation than those tissues in leaner women. The effect is significant because ovaries no longer contribute to the production of estrogen. The prognosis for these women is adversely affected by obesity. Weight gain may also be one of the most distressing side effects since it may significantly affect their self-esteem when it is superimposed on a change in body image due to the loss of a breast and/or other toxicities associated with breast cancer therapy. Because of the high frequency of weight gain, its psychological impact, and its associated health risk, efforts to control obesity and weight gain are strongly recommended.

The exciting news is that what you eat may interfere with the many stages of the cancer process. Evidence continues to mount indicating that there are hundreds, perhaps thousands, of phytochemicals (chemicals synthesized by plants) that may slow down, stop, or even reverse cancer development. More specifically, foods that can interfere with the metabolism and absorption of estrogen may present a unique mechanism to discourage breast cancer. Other mechanisms include inactivation of mutagens and carcinogens, increased excretion of carcinogens and toxic chemicals, scavenging active oxygen radicals, reducing damage to DNA and cellular membranes, and impeding or retarding the proliferation and promotion process of cancer. Though the influence of food upon cancer is complicated, not fully understood, and entwined with many other factors, your diet may make a significant difference.

If you are in the Long Island, New York area and would like to receive more information, please contact Nancy Mazarin at 516-466-9087 or visit her website.

The holiday season, along with holiday weight gain, sneaks upon us every year. With all the yummy food, it is hard to say no to the delectable treats found in stores, at the office, and at home. You may be thinking that eating a cookie and gaining a few pounds during the holiday season is not a big deal but studies have shown that people do not lose the weight they gained during this time. Here are a few ways you can prevent seasonal weight gain.

Holiday parties are one of the main reasons for weight gain since there is food galore. Mingling plus eating can lead to overeating quite quickly. Avoid this by not arriving hungry to a party. If it is a potluck or hors d’oeuvre format, you can eat a light meal beforehand so you can sample some food but not eat too much and you will not appear rude. If it is a holiday dinner, eat a healthy snack beforehand to manage your hunger.

Focus on other things than food when you are at a holiday event. Use the time to catch up with friends and family members you have not seen in a while. You might even play with the children for a bit, running around with them is a good way to burn calories. Limit your alcohol consumption as well. It is not just because of the calories drinks contain but also to maintain control. Drinking can cause you to lose your resolve and lead to more eating. If you feel out of place without a drink in your hand, sip on water (flat or sparkling) from an attractive glass.

Take your own delicious but healthy dish or treats with you when you go. That way you can be sure the food you eat is what you want and is good for you. Your host and other guests will certainly appreciate it. For additional tips and tricks to maintaining your healthy lifestyle during the holiday season, seek the help of a professional dietitian nutritionist.