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Diet studio 2 0 1 59 develop your own diet based on your physiology and way of li

Diet studio 2 0 1 59 develop your own diet based on your physiology and way of li

Diet studio 2 0 1 59 develop your own diet based on your physiology and way of li

Diet studio 2 0 1 59 develop your own diet based on your physiology and way of li

Diet studio 2 0 1 59 develop your own diet based on your physiology and way of li

16.02.2018 – This is a great meal any time of day. Clearly, a strong body of evidence is required before deriving more stringent recommendations on the basis of the results.

Diet studio 2 0 1 59 develop your own diet based on your physiology and way of li miles hour

Diet studio 2 0 1 59 develop your own diet based on your physiology and way of li

What’s New?

1. 8Which of the following qualities can help to identify produce that is rich in antioxidants? The major cause of undernutrition in the United States is?
2. 7 It can be made into a stir fry that is delicious with some grilled chicken or fish.http://softik.org/ccleaner-for-windows-10-free/Tomatoes also have dietary fiber and protein, as well as a number of organic compounds like lycopene that also contribute to the overall health benefits. Keep portion sizes small of any desserts or sweets and never consume alcohol on an empty stomach.

3. 6 Which of the following is a good source of provitamin A? Targeted short-term fluconazole prophylaxis among very low birth weight and extremely low birth weight infants. http://softik.org/call-of-duty-black-ops-all-updates79/ http://softik.org/call-of-duty-black-ops-crack-only13/Atkins New Diet Revolutionand other doctors began to publish books based on the same principles. Analyses which neglect these factors are misleading and will not result in a working diet, or at least one which works as intended.

INTRODUCTION

Diet studio 2 0 1 59 develop your own diet based on your physiology and way of li

4. 3 Cutting out sources of refined sugar sweets, biscuits and cake etc but forgetting about refined carbs such as white rice, white pasta and white bread which also break down into glucose.Diet studio 2 0 1 59 develop your own diet based on your physiology and way of liWe hypothesized that coconut oil might inhibit C. She should do which of the following?

5. 9 Add half of the peppercorns and stir frequently, until aromatic, about 1 minute. I teach them basic carbohydrate counting, and provide them with a sample meal plan to review portion sizes, food pairing, and timing of eating.

6. 5 Find a great coach and you’ll wonder why you didn’t start sooner. Objectives The aim of this study was to examine the benefit of combined low-risk diet and healthy lifestyle practices on the incidence of MI in men.

7. 5 Another mistake is going out to buy specialist expensive foods that are not required or recommended.

Diet studio 2 0 1 59 develop your own diet based on your physiology and way of li download

Go to top of page. Objectives The aim of this study was to examine the benefit of combined low-risk diet and healthy lifestyle practices on the incidence of MI in men. Methods The population-based, prospective cohort of Diet men comprised to year-old men who completed a detailed questionnaire on diet and lifestyle at baseline in In total, 20, men with no history of cancer, cardiovascular disease, diabetes, hypertension, or high cholesterol physiology were followed through Low-risk behavior included 5 factors: Results During 11 years of follow-up, we ascertained 1, incident cases of MI.

The low-risk dietary choice together with moderate alcohol consumption was associated with a relative risk of 0. Conclusions Almost 4 of 5 MIs in men may be preventable with a combined low-risk behavior.

In contrast to drug therapies, medication-free strategies to help prevent CHD are mostly without the risk of side effects. Because population-wide strategies to shift the entire distribution of risk cannot rely on prescription medication, effective lifestyle-based prevention is essential.

Yet, there is limited information available on community-based populations, especially in men. We estimated the burden of CHD that could potentially have been avoided had all men adhered to the low-risk practice of a healthy diet, moderate alcohol consumption, no smoking, being physically active, and avoiding abdominal adiposity.

A separate analysis was performed among men with hypertension and high cholesterol. Finally, we excluded those with implausible values for total energy intake i. After these exclusions, 20, men remained for the main analyses.

A separate your was performed of 7, men with hypertension and high cholesterol at baseline and with complete information on all exposure variables. The Regional Ethical Review Board at Karolinska Institutet approved the study, and return of the completed questionnaire was considered to imply informed consent.

Diet was assessed using a self-administered semiquantitative food frequency questionnaire FFQ including questions on 96 commonly eaten foods. The validity of the FFQ compared with 14 h dietary recall interviews with Swedish men 40 to 74 years of age were mean Spearman correlation coefficient 0.

The Recommended Food Score is highly predictive of mortality 4,19 and includes foods with a beneficial based on cardiovascular health 1,20,21such as, fruits, vegetables, legumes, nuts, own dairy products, whole grains, and fish.

The information on smoking included details on the number of years since smoking was stopped. Physical activity was assessed with a validated questionnaire Participants reported their level of activity at work and home and during leisure time in the year before study enrollment, including questions on time spent walking or bicycling 6 predefined duration categories and leisure time exercise 5 develop duration categories.

We obtained self-reported information on level of education, marital status, family history of MI in parents or siblings before the age of 60 years, and use of aspirin.

Dates of death were ascertained through the Swedish Death Registry. Follow-up was censored at the date of first event of MI, death, or end of follow-up, whichever occurred first.

All associations between low-risk diet and lifestyle factors and MI were adjusted for the following established or proposed risk factors: Additional models were mutually adjusted for the low-risk behaviors.

Way a mean of 11 years withperson-years of follow-up, we ascertained 1, incident cases of primary MI. Overall, men with a low-risk diet were more likely to have attained a higher level of education and to not smoke and were less likely to live alone compared with men with lower scores of recommended foods.

Each lifestyle factor was inversely and, after mutual adjustment for the other elements of the low-risk profile, independently associated with the risk of coronary events. In the final analysis, we further investigated the combined effect of the entire low-risk practice by combining the low-risk diet and moderate alcohol consumption with the 3 independent low-risk nondietary modifiable lifestyle factors: The absolute rate difference between men having no low-risk factors and men having 5 low-risk factors was cases perperson-years.

Excluding alcohol from the low-risk profile i. On additional analyses, we assessed the association between the low-risk practices and MI risk among 7, men with hypertension and high cholesterol at baseline with ascertained incident cases of MI.

A decrease in risks with increasing adherence to the low-risk behaviors was also observed in men with hypertension and high cholesterol. We used the Recommended Food Score 19 to identify a healthy diet, a joint measure of the consumption of different healthy foods fruits, vegetables, legumes, nuts, reduced-fat dairy products, whole grains, and fish known to have a beneficial effect on cardiovascular health 1,20, In this cohort of men without a history of cardiovascular disease CVDhypertension, high cholesterol, or diabetes at baseline, the observed reduction in primary MI incidence associated with a healthy diet together with moderate alcohol consumption was similar to that recently your in a primary prevention trial in Spain examining a Mediterranean diet supplemented with olive oil or nuts The corresponding RR for MI secondary endpoint was 0.

This reduction is in the same range as that observed after primary CHD intervention nonfatal MI with cholesterol-reducing drugs statins in groups at low diet intermediate cardiovascular risk 30— However, even among those and medication for CHD risk factors, a previous study observed that the addition of healthy lifestyle behaviors was associated with substantially reduced CHD risk When consumed in moderate amounts, alcohol is consistently associated with reduced risk of CHD Unlike healthy foods, alcohol consumption cannot be recommended for CHD risk reduction without reservation.

Men who combined the low-risk diet with moderate alcohol consumption and the 3 low-risk behaviors had a very low risk of MI. Very low prevalence 0. This definition included 4 alcohol excluded of 5 low-risk lifestyle choices together with favorable metrics of total serum cholesterol, fasting glucose, and blood pressure.

Clearly, a strong body of evidence is required before deriving more stringent recommendations on the basis of the results. Randomized trials generally represent the most robust study design to establish causality.

Also, testing a combined low-risk behavior in a long-term primary prevention randomized intervention is very complicated and may never be performed. Therefore, well-designed prospective studies have complementary strengths and limitations that are equally robust, and the implementation of prevention strategies should be based on the breadth, depth, and consistency of evidence across multiple research paradigms.

It is, however, also clear that extensive prevention only can be achieved through inhibiting the initiation and establishment of any high-risk behavior 37, Strengths of this study include a prospective population-based design in a contemporary population begun inwhich increases generalizability and relevance to modern guidelines.

The availability of detailed information on diet as well as potential risk factors for CHD is also important. The prospective design prevents recall bias with respect to the outcome and the practically complete follow-up of the study population through linkages to various population-based registries minimizes the concern that our findings could be affected by differential loss to follow-up.

In contrast to most previous studies that focused on cardiovascular mortality and lacked incident morbidity events 4—11we assessed the incidence of primary MI. This allows a more complete picture of the preventive effect of these combined lifestyle practices.

Limitations of our study need to be considered. Inevitable measurement error in self-reports can lead to misclassification of the exposure. Because of the prospective design, the misclassification is most likely nondifferential, which may lead to attenuation of the true association.

Despite a large cohort, studio study is limited by the small number of subjects and cases of MI in the group with all 5 low-risk behaviors, leading to somewhat imprecise estimates; nevertheless, the power was sufficient to observe statistically significant associations.

The gradual decrease in incidence with increasing adherence to low-risk practices was similar to that previously observed in both women 15,16 and men 13 and consistent with findings for cardiovascular mortality 5—10,14, Our study indicates that a healthy diet together with low-risk lifestyle practices and absence of abdominal adiposity may prevent the vast majority of MI events in men.

Combining 5 low-risk behaviors: The incidence of myocardial infarction decreases with the number of positive behaviors in both healthy men and in those with hypertension and high cholesterol.

Funders had no role in the design and conduct of the study; in the collection, analysis, and interpretation of the data; or in the preparation, review, or approval of the manuscript.

The authors have reported that they have no relationships relevant to the contents of this paper to disclose. Thank you for your interest in spreading the word about JACC: We request your email address only as a reference for the recipient.

We do not save email addresses. Skip to main content. Journal of the American College of Cardiology. American College of Cardiology Foundation. Assessment of diet and lifestyle factors Diet was assessed using a self-administered semiquantitative food frequency questionnaire FFQ including questions on 96 commonly eaten foods.

Data analysis Follow-up was censored at the date of first event of MI, death, or end of follow-up, whichever occurred first. Results During a mean of 11 years withperson-years of follow-up, we ascertained 1, incident cases of primary MI.

View inline View popup. Study limitations Limitations of our study need to be considered. Conclusions Our study indicates that a healthy diet together with low-risk lifestyle practices and absence of abdominal adiposity may prevent the vast majority of MI events in men.

Appendix For a supplemental figure, please see the online version of this article. Eur Heart J Int J Cardiol Arch Intern Med Int J Epidemiol Br J Nutr Br J Sports Med Waist Circumference and Waist-Hip Ratio.

BMC Public Health Am J Epidemiol Journal of the American College of Cardiology web site. LarssonAndrea DiscacciatiAlicja Wolk. Sign-in to Email Alerts with your email address. Figures in Article Figures.

Diet studio 2 0 1 59 develop your own diet based on your physiology and way of li bit download free

For children 3 years of age and older, the most useful growth charts are: Oftentimes people are very concerned with sugars without recognizing that the total carbohydrate content of the diet is key. In contrast, the coconut oil diet and the GI contents of coconut oil-fed mice were rich in medium-chain fatty acids MCFAsespecially decanoic In a large bowl, mix the dry ingredients. Alzheimer’s patients are likely to be helped by all of the following except: Upgrade to remove ads. Fill half your plate with them and there is usually some starch and protein to make up the other half of the plate.

Diet studio 2 0 1 59 develop your own diet based on your physiology and way of li free download

Coconut oil and its constituent fatty acids have antifungal activity in vitro ; we hypothesized that dietary coconut oil would reduce GI colonization by C. Colonization was lower in mice fed a coconut oil-rich diet than in mice fed diets rich in beef tallow or soybean oil.

Switching beef tallow-fed mice to a coconut oil diet reduced preexisting colonization. Coconut oil reduced colonization even when the diet also contained beef tallow.

Dietary coconut oil also altered the metabolic program of colonizing C. Long-chain fatty acids were less abundant in the cecal contents of coconut oil-fed mice than in the cecal contents of beef tallow-fed mice; the expression of genes involved in fatty acid utilization was lower in C.

Extrapolating to humans, these findings suggest that coconut oil could become the first dietary intervention to reduce C. By reducing the amount of C. Using a mouse model, we showed that adding coconut oil to the diet could become the first drug-free way to reduce C.

More broadly, this model lets us study the interactions between our diet and the microbes in our body and the reasons why some of those microbes, under certain conditions, cause disease.

A podcast concerning this article is available. Candida albicans , a member of the endogenous human microflora, is the most common human fungal pathogen. While in most healthy individuals C.

Particularly in immunocompromised patients, C. Disseminated candidiasis is difficult to diagnose and treat; although estimates of attributable mortality vary greatly, in a large case-control study, Gudlaugsson et al.

It has thus been proposed that the most effective way to reduce candidemia-associated mortalities is to prevent infections from occurring 2. Current evidence suggests that C.

The incidence of invasive disease can therefore be reduced by decreasing colonization in patients at risk of developing infections by using antifungal prophylaxis; this has been shown to reduce mucosal and invasive candidiasis 4 — 14 and Candida -associated mortalities 4 , 15 — However, the use of antifungal drugs leads to the emergence of antifungal-resistant strains 19 — The goal of this study was to test the effect of a dietary intervention on GI colonization with C.

Coconut oil is a natural product that has been extensively studied; its chemical composition is known see Fig. Coconut oil and its constituent fatty acids, particularly decanoic We hypothesized that dietary coconut oil would reduce GI colonization by C.

We therefore compared the effects of dietary beef tallow, soybean oil, and coconut oil on C. To assess the relative effects of different sources of dietary fat on gastrointestinal GI colonization by C.

Beef tallow and soybean oil are rich in long-chain saturated fatty acids In contrast, coconut oil is rich in medium-chain fatty acids MCFAs; 8: Fatty acid composition of beef tallow, soybean oil, and coconut oil and weight of mice fed diets containing those fats.

Mice fed either a high-fat diet containing either coconut oil, beef tallow, or soybean oil or a standard diet AING were orally inoculated with C. Hence, for the remainder of the experiments we focused on the comparison between dietary coconut oil and beef tallow.

A Colonization was significantly lower in the stomach contents of mice fed the coconut oil diet than in the stomach contents of mice fed the beef tallow diet, soybean oil diet, or AING. B Colonization was significantly lower in the cecal contents of mice fed the coconut oil diet than in the cecal contents of mice fed the beef tallow or soybean oil diet but not AING.

C Colonization was significantly lower in the fecal pellets of mice fed the coconut oil diet than in the fecal pellets of mice fed the beef tallow or soybean oil diet but was not significantly different from colonization in mice fed AING.

Changing to a coconut oil-containing diet reduces preexisting GI colonization by C. To determine whether dietary coconut oil affects colonization by preventing C.

Mice inoculated with C. When mice were switched from the beef tallow diet to the coconut oil diet, C. These data demonstrate that a change in diet can reduce preexisting GI colonization by C. Dietary coconut oil inhibits GI colonization by C.

There are two types of mechanisms by which coconut oil could reduce GI colonization by C. If coconut oil alone is insufficient to support robust colonization, then this colonization defect should be rescued by the addition of beef tallow.

Alternatively, if coconut oil actively inhibits colonization, it may do so in the presence of beef tallow. To distinguish between these possibilities, colonization was measured in mice fed a high-fat diet containing either coconut oil or beef tallow, a high-fat diet containing both coconut oil and beef tallow, or a standard diet AING.

Coconut oil, therefore, reduced colonization even in the presence of beef tallow, suggesting that coconut oil actively inhibits GI colonization by C. A Colonization was significantly lower in the stomach contents of mice fed the coconut oil diet or the diet containing both coconut oil and beef tallow than in the stomach contents of mice fed the beef tallow diet.

B Colonization was significantly lower in the cecal contents of mice fed the coconut oil diet, the diet containing both coconut oil and beef tallow, or AING than in the cecal contents of mice fed the beef tallow diet.

C Colonization was significantly lower in the fecal pellets of mice fed the coconut oil diet, the diet containing both coconut oil and beef tallow, or AING than in the fecal pellets of mice fed the beef tallow diet.

Dietary coconut oil alters the fatty acid composition of the GI contents. We hypothesized that coconut oil might inhibit C. To determine how different dietary fats might impact C. As expected, the fatty acid composition of the GI contents as a molar percentage of total fatty acids reflected the fatty acid composition of the original diets.

Both the beef tallow diet and the GI contents of beef tallow-fed mice contained predominantly long-chain fatty acids LCFAs , particularly hexadecanoic In contrast, the coconut oil diet and the GI contents of coconut oil-fed mice were rich in medium-chain fatty acids MCFAs , especially decanoic Consistent with previous reports describing the absorption of MCFAs in the small intestine, the abundance of MCFAs micrograms of fatty acid per milligram of GI contents decreased between the stomach and the distal small intestine Fig.

Fatty acid profile molar percentage of the GI contents of mice fed diets containing either coconut oil or beef tallow, a diet containing both coconut oil and beef tallow, or a standard diet AING.

Organ contents were harvested from throughout the GI tract, and the fatty acid profiles of these samples, as well as of the original diets, were determined by gas chromatography and expressed as molar percentages.

Data represent the averages for three mice per diet. Fatty acid profile micrograms per milligram, wet weight of the GI contents of mice fed diets containing either coconut oil or beef tallow, a diet containing both coconut oil and beef tallow, or a standard diet AING.

Organ contents were harvested from throughout the GI tract, and the fatty acid profiles of these samples, as well as of the original diets, were determined by gas chromatography and expressed as micrograms of fatty acid per milligram wet weight.

To determine whether the concentration of fatty acids in the GI tract varied significantly between diets, the fatty acids in cecal contents were measured. Significant diet-dependent differences were detected in the concentrations of the long-chain fatty acids octadecanoic acid Medium- and longer-chain fatty acids This suggests that the reduced availability of long-chain fatty acids in the cecal contents of mice fed the coconut oil-containing diets may have contributed to the reduced colonization observed in coconut oil-fed mice.

Long-chain fatty acids are less abundant in the cecal contents of coconut oil-fed mice than in the cecal contents of beef tallow-fed mice. A The concentration of octadecanoic acid B The concentration of hexadecanoic acid Composite results from two experiments are shown, one in which n was 3 mice per diet and one in which samples from three mice per diet were pooled.

Each symbol represents one sample; bars represent averages. Unlike mammals, fungi can grow using lipids as a sole carbon source, as fungi can produce both energy and sugars essential biosynthetic precursors from fatty acids.

Long-chain fatty acids were less abundant in the cecal contents of coconut oil-fed mice than in the cecal contents of mice fed the beef tallow diet. This suggested that there would be less fatty acid catabolism occurring in C.

To test this hypothesis, we measured the expression of C. When used by C. No significant difference in the expression of either gene was observed between C. A Schematic of fatty acid catabolism in C.

B to H The expression of C. Data are expressed as fold change relative to the mean expression in mice fed the coconut oil diet; all gene expression data measured via RT-qPCR have been normalized to reference genes.

In yeasts such as C. The resulting acetyl-CoA must then be transported to the mitochondria; however, acetyl-CoA cannot readily cross plasma membranes. The expression of carnitine acetyltransferase genes was significantly lower in C.

This suggests that there may be less acetyl-carnitine transport occurring in C. This suggests that there is less flux through the glyoxylate cycle in C. Glucose is an essential biosynthetic precursor; among other things, it is required for the production of ribose and thus nucleic acids.

Glucose is thought to be scarce in the GI tract. Thus, the lower expression of glyoxylate cycle genes in C. As predicted, the expression of CDC19 was significantly higher in C. No significant difference in expression was observed between C.

This suggests that glycolysis is increased, and gluconeogenesis decreased, in C. The expression of genes involved in the catabolism of fatty acids was lower in C. Importantly, the expression of these genes was as low in C.

This implies that, while C. These findings are consistent with the hypothesis that colonization is lower in the gastrointestinal tracts of coconut oil-fed mice than in the GI tracts of beef tallow-fed mice at least in part because the long-chain fatty acids that fuel C.

Perhaps most importantly, these data demonstrate that the metabolic program of colonizing cells, which is essential for the adaptation of C. Our results suggest that coconut oil could become the first dietary intervention to reduce GI colonization by C.

Dietary coconut oil both reduced C. These two effects of dietary coconut oil likely occur by two different mechanisms. Colonization was lower in mice fed a coconut oil-rich diet than in mice fed diets rich in beef tallow or soybean oil Fig.

In order to have therapeutic benefit, any dietary intervention must be able to reduce preexisting C. Further, coconut oil actively inhibited murine GI colonization even when the diet also contained beef tallow: Dietary coconut oil may reduce GI colonization by killing or inhibiting the growth of C.

Coconut oil is composed primarily of medium-chain fatty acids MCFAs , which are fungistatic and fungicidal for C. Similar results were found with decanoic acid In the GI tract, lipids are present predominantly as triglycerides, rather than free fatty acids; however, coconut oil has also been shown to have antifungal action against C.

Any direct antimicrobial effects exerted by the MCFAs in coconut oil probably occur in the upper part of the GI tract, because MCFAs are mostly absorbed in the small intestine and are therefore scarce in the contents of the cecum and colon.

Our observation that coconut oil has a greater impact on colonization in the stomach than on colonization in the cecum or fecal pellets is consistent with this hypothesis. Thus, the antimicrobial properties of MCFAs may contribute to the reduced colonization observed in the GI tracts of coconut oil-fed mice.

In addition to directly decreasing GI colonization by C. Long-chain fatty acids were less abundant in the cecal contents of mice fed coconut oil-containing diets than in the cecal contents of mice fed a diet rich in beef tallow Fig.

When carbohydrates are scarce, C. The increased expression of genes involved in these pathways by C. These conditions include exposure to neutrophils 42 , 48 and internalization by macrophages 42 , 44 , 46 ; Lorenz et al.

The ability to use a variety of carbon sources is integral to the commensalism and pathogenicity of C. Local nutrient availability differs widely between the diverse host niches encountered by C.

The metabolic flexibility to assimilate available carbon sources is thus of great importance to C. In addition to providing nutrients for cell growth, metabolic adaptation alters a plethora of other factors that impact C.

Our results therefore suggest that metabolic adaptations by C. Importantly, even when the diet contained beef tallow, these metabolic adaptations were completely ablated by dietary coconut oil.

The effects of coconut oil on GI colonization by C. Because MCFAs are saturated fatty acids, one concern that is often raised about the use of coconut oil as a dietary intervention is the possible health risks associated with saturated fats.

However, it seems unlikely that there would be significant long-term cardiovascular effects from consuming coconut oil as a short-term prophylactic measure. Additionally, it is not clear whether consuming the fatty acids in coconut oil has the same health effects adverse or not as those of eating longer-chain saturated fats.

Once absorbed, MCFAs enter the bloodstream and are transported to the liver via the hepatic portal vein, whereas LCFAs are transported via the lymph system. Once in the liver, MCFAs are also metabolized differently.

These physiological differences suggest that long-term consumption of MCFAs may not have the same effect on cardiovascular health as consumption of LCFAs. Thus, the efficacy of a long-term or intermittent coconut oil-based dietary intervention should be investigated as a possible treatment option for patients with chronic health conditions requiring long-term antifungal prophylaxis.

The next step toward a dietary intervention will be to determine whether the findings reported in this study can be replicated in humans at a reasonable dose. One limitation of this study is the high fat contents of the experimental diets: This suggests that a decrease in C.

This is not the first attempt to identify a dietary intervention to decrease GI colonization by C. Previous studies have examined the effects of dietary carbohydrates on C.

Consumption of a high-glucose diet increased gastrointestinal colonization by C. However, in healthy human subjects, Weig et al. Moreover, they showed that doubling the daily carbohydrate intake of their subjects did not significantly increase gastrointestinal colonization, although they detected an increase in GI colonization in a selected subset of individuals with elevated basal levels of oral C.

Our results are consistent with the conclusion that dietary carbohydrates have a minimal effect on colonization. If a reduction in dietary carbohydrates decreased C. However, we observed the opposite: Of primary importance is the classification of breast cancer by estrogen receptor ER status.

Physicians can use this information in their treatment and disease management decisions. Tumors are scored based on how strongly they express estrogen receptors: Progesterone receptor PR status also is a prognostic indicator.

PR status also may be an important indicator of tumor aggressiveness and, when negative, may indicate that the patient will benefit from using more than one endocrine therapy approach simultaneously.

The least favorable prognosis is associated with tumors that are ER and PR negative and negative for another growth factor called human epidermal growth factor receptor 2. ER Status and Dietary Recommendations Just as the ER status of breast cancer tumors guides treatment decisions, it also should be considered when making dietary recommendations.

WINS, a randomized trial of nearly 2, breast cancer survivors, revealed that a very low-fat diet significantly reduced breast cancer recurrence risk but only among women with ER- breast cancer.

Results from the WHEL study have contributed significantly to our understanding of how diet and physical activity may affect breast cancer recurrence risk. Regardless, this study suggests that increasing vegetable and fruit intake above and beyond the standard five-a-day recommendation for the general public may not reduce breast cancer recurrence.

However, there may be subsets of women who benefit from this dietary intervention. Comorbid Conditions and Breast Cancer Survival One of the most important aspects of breast cancer survival is achieving a healthful body weight.

Obesity is commonly comorbid with breast cancer, and data support that obesity decreases survival. This effect was particularly pronounced within the first two years, when weight gain was associated with a nearly sixfold increase in recurrence risk.

Some future trials will assess biomarkers associated with increased or decreased cancer recurrence risk, such as elevated levels of insulin, insulin-like growth factor, C-reactive protein, and leptin.

Data support that type 2 diabetes, another nutrition-related comorbid condition, is associated with an increased risk of breast cancer and a higher risk of recurrence in women who have been diagnosed with the disease.

These trials address the use of metformin for treating women with early- to late-stage breast cancer and metastatic disease. Cancer-Fighting Foods Unlike the number of metformin studies under way, controlled clinical trials on specific foods to reduce the risk of breast cancer recurrence are few and far between.

Despite this, copious observational data show that certain foods may be worth adding to the diet for the breast cancer survivor. This is particularly true of foods that may have other health benefits and have no known risks.

The sidebar presents a list of foods that may offer anticancer benefits, and that deserve a place in any healthful diet—for cancer survivors and the general public alike.

However, there is confusion about which foods may offer benefits to breast cancer survivors and whether some foods are unsafe and should be avoided. The confusion persists for people affected by cancer and their healthcare providers, and no food exemplifies this issue better than soy.

Many of the anticancer properties attributed to soy are unrelated to so-called estrogenic effects. Three large-scale, well-designed epidemiologic studies report no adverse effects of soy food consumption on breast cancer prognosis.

These three studies concur that not only are soyfoods safe for breast cancer survivors, they also may be protective against breast cancer recurrence. Human feeding studies provide additional reassurance that these foods likely are safe for female breast cancer survivors.

Regardless of the group high vs. A recently published meta-analysis evaluated four studies on breast cancer recurrence and 14 studies on breast cancer incidence.

Evidence for soy-based dietary supplements is lacking, and women should be counseled to avoid soy supplements because of their potential for unnaturally high isoflavone concentrations. However, current human data support that whole soy foods as part of a balanced diet are safe, and possibly beneficial, for women with a history of breast cancer.

This includes women with a history of ER- breast cancer. Despite this, however, the women with ER- breast cancer had profound reductions in their risk of recurrence. This reveals insights that can improve nutrition counseling.

For all breast cancer survivors, the evidence makes clear that achieving a healthy body weight should be a long-term wellness goal. However, tackling weight loss can be fraught with anxiety, guilt, and a host of other negative emotions.

Therefore, it makes sense to work with overweight breast cancer survivors to help them meet their goal of eating more vegetables and fruits—at least five to seven servings per day—and engaging in daily physical activity.

These behavioral changes should take precedence over any weight loss focus unless a client is clear that weight loss is a goal at that time. Finally, dietitians should counsel women in a way that helps remove the fear surrounding nutrition and cancer.

The soy food question presents an excellent example of why this is a valuable approach. Total diet quality matters, and an undue focus on any one food can be counterproductive to dietary improvement.

Along these lines, consider a client who may be experiencing significant stress about reading labels to ensure no soy-based ingredients creep into her diet. Learning Objectives After completing this continuing education activity, nutrition professionals should be better able to:.

Evaluate relevant facts and trends in the epidemiology of breast cancer and its risk factors. Formulate appropriate dietary recommendations for breast cancer survivors based on knowledge of current research.

The risk of dying of breast cancer is similar among different racial and ethnic groups. Which of the following statements regarding a woman with the BRCA1 breast cancer gene is true?

She has a gene that causes cancer that other women do not have. She has a damaged or mutated version of a gene that all women have. When working with breast cancer survivors, why is it important to know the estrogen receptor ER status of their tumor?

It will tell you which patients are more likely to gain weight due to treatment. It will help you determine whether a very low-fat diet is likely beneficial for long-term survival.

Advise her that eating at least 10 servings of vegetables and fruit per day is her most important dietary goal. Make weight loss the No. Help her increase her fruit and vegetable intake to at least five servings per day, and encourage her to engage in daily physical activity, such as brisk walking.

Recommend that she add as many soy foods into her diet as possible. Most women diagnosed with breast cancer will have ER- tumors. Which tumor type will grow in the presence of estrogen?

Estrogen receptor negative ER- b. Your client has a family history of heart disease and is concerned about her own heart disease risk. She enjoys drinking one glass of wine with dinner every night because she read that moderate alcohol consumption is heart healthy.

How would you counsel her regarding alcohol consumption? Given her recent breast cancer diagnosis, tell her she should cut back on the wine and save it only for special occasions.

Suggest she discuss this issue with her physician. All of the above. A woman with a history of breast cancer wants to add apples, nuts, and berries to her diet. This is a good idea.

Hormone replacement therapy b. In utero exposure to diethylstilbestrol c. Risk factors for ductal, lobular, and mixed ductal-lobular breast cancer in a screening population.

Cancer Epidemiol Biomarkers Prev. Updated December 15, SEER stat facts sheet. National Cancer Institute website. Identifying risk factors for disparities in breast cancer mortality among African-American and Hispanic women.

The influence of socioeconomic disparities on breast cancer tumor biology and prognosis: J Womens Health Larchmt. J Natl Cancer Inst. A genome-wide linkage study of mammographic density, a risk factor for breast cancer.

Epidemiology and pathophysiology of alcohol and breast cancer: Moderate alcohol consumption during adult life, drinking patterns, and breast cancer risk. Alcohol and cardiovascular health: J Am Coll Cardiol.

Annual Report to the Nation on the status of cancer, , featuring cancers associated with excess weight and lack of sufficient physical activity. Effect of obesity on survival of women with breast cancer: