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Abstract

Objective To investigate whether improving adherence to healthy dietary patterns interacts with the genetic predisposition to obesity in relation to long term changes in body mass index and body weight.

Design Prospective cohort study.

Setting Health professionals in the United States.

Participants 8828 women from the Nurses Health Study and 5218 men from the Health Professionals Follow-up Study.

Exposure Genetic predisposition score was calculated on the basis of 77 variants associated with body mass index. Dietary patterns were assessed by the Alternate Healthy Eating Index 2010 (AHEI-2010), Dietary Approach to Stop Hypertension (DASH), and Alternate Mediterranean Diet (AMED).

Main outcome measures Five repeated measurements of four year changes in body mass index and body weight over follow-up (1986 to 2006).

Results During a 20 year follow-up, genetic association with change in body mass index was significantly attenuated with increasing adherence to the AHEI-2010 in the Nurses Health Study (P=0.001 for interaction) and Health Professionals Follow-up Study (P=0.005 for interaction). In the combined cohorts, four year changes in body mass index per 10 risk allele increment were 0.07 (SE 0.02) among participants with decreased AHEI-2010 score and 0.01 (0.02) among those with increased AHEI-2010 score, corresponding to 0.16 (0.05) kg versus 0.02 (0.05) kg weight change every four years (P<0.001 for interaction). Viewed differently, changes in body mass index per 1 SD increment of AHEI-2010 score were 0.12 (0.01), 0.14 (0.01), and 0.18 (0.01) (weight change: 0.35 (0.03), 0.36 (0.04), and 0.50 (0.04) kg) among participants with low, intermediate, and high genetic risk, respectively. Similar interaction was also found for DASH but not for AMED.

Conclusions These data indicate that improving adherence to healthy dietary patterns could attenuate the genetic association with weight gain. Moreover, the beneficial effect of improved diet quality on weight management was particularly pronounced in people at high genetic risk for obesity.

Obesity is a multifactorial disorder that has a genetic predisposition but requires environmental influences for it to manifest.12 In the US, the past decades witnessed considerable transition of habitual dietary habits from a traditional pattern high in complex carbohydrates and fiber toward one high in sugar, fat, and animal products, which has played a key role in triggering the surge of obesity.34 Compelling evidence has shown that certain dietary factors such as sugar sweetened drinks, fried foods, and coffee might modify the genetic susceptibility to elevated body mass index, supporting potential interactions between genetic predisposition and overall dietary patterns on the risk of obesity.567

On the basis of scientific evidence and dietary recommendations, several diet quality scores have been developed to evaluate the healthfulness of dietary patterns.8910 One such score is the Alternate Healthy Eating Index 2010 (AHEI-2010), which has been consistently associated with lower risk of chronic disease in clinical and epidemiological investigations.8 The other two commonly studied scores are the Dietary Approach to Stop Hypertension (DASH), which represents the DASH-style diet aimed at reducing blood pressure,9 and the Alternate Mediterranean Diet (AMED), which focuses on a Mediterranean dietary pattern.10 Improving adherence to healthy dietary patterns, as assessed by these three diet quality scores, has been associated with less weight gain in previous studies.111213 However, no study has assessed the interactions between changes in adherence to healthy dietary patterns over time and genetic susceptibility to obesity on long term weight gain.

In this study, we prospectively examined the interactions of changes in the AHEI-2010, DASH, and AMED over up to 20 years with genetic predisposition to obesity, as evaluated by a genetic risk score based on 77 genetic variants associated with body mass index, on long term changes in body mass index and body weight in US men and women from two independent, prospective cohorts: the Nurses Health Study and the Health Professionals Follow-up Study.

The Nurses Health Study is a cohort of 121701 female registered nurses aged 30-55 years at enrollment in 1976.14 The Health Professionals Follow-up Study is a cohort of 51529 male health professionals aged 40-75 years at enrollment in 1986.15 Participants were followed with application of biennial validated questionnaires about medical history and lifestyle. For this study, the baseline year in both studies was 1986, when detailed information of diet and lifestyle was available. Between 1989 and 1990, 32826 women in the Nurses Health Study provided blood samples; likewise, between 1993 and 1995, a blood sample was obtained from 18225 men in the Health Professionals Follow-up Study. This analysis included 8828 women and 5218 men of European ancestry who had complete baseline information and available genotype data based on genome-wide association studies1617181920 and were free from diabetes, cancer, or cardiovascular at baseline.

Height was assessed by questionnaires administered at enrollment, and body weight was requested by questionnaires administered at enrollment and at each follow-up. Weights reported in questionnaires and measured by technicians were highly correlated (r=0.97 in both studies) in a validation subsample.21 Body mass index was calculated as weight in kilograms divided by the square of height in meters. Changes in body mass index and weight were evaluated every four years as the differences in body mass index and weight between the beginning and the end of each four year interval, with positive differences representing weight gain and negative differences weight loss.

Dietary intake information was collected by a validated 131 item semiquantitative food frequency questionnaire, administered in 1986 and every four years thereafter.22 Participants were asked how often on average they had consumed each food of a standard portion size over the previous 12 months. The responses had nine frequency categories ranging from never or less than once per month to six or more times per day. The reproducibility and validity of the food frequency questionnaire showed good correlation of food intake with that measured by multiple diet records.2324 Diet quality scores were calculated from the food frequency questionnaires every four years. Criteria for computation of each diet quality score are given in supplementary table A.

The AHEI-2010 score was based on 11 foods and nutrients predictive of chronic disease risk,8 emphasizing higher intake of vegetables (excluding potatoes), fruits, whole grains, nuts and legumes, long chain (n-3) fats, and polyunsaturated fatty acids; moderate intake of alcohol; and lower intake of sugar sweetened drinks and fruit juice, red and processed meats, trans fat, and sodium. Each component was scored from 0 (unhealthiest) to 10 (healthiest) points, with intermediate values scored proportionally. All component scores were summed to obtain a total score ranging from 0 (non-adherence) to 110 (best adherence) points.

The DASH score was based on eight foods and nutrients that were either emphasized or de-emphasized in the DASH-style diet.9 Each component was scored from 1 to 5 points according to fifths of intake, with 5 being the best score for higher intake of vegetables, fruits, nuts and legumes, whole grains, and low fat dairy products and for lower intake of sugar sweetened drinks, red and processed meats, and sodium. The total score ranged from 8 to 40 points.

The AMED score was modified and adapted to a Mediterranean diet in a Greek population.25 This score included nine components and awarded 1 point for an intake equal to or above the cohort specific median for vegetables, fruits, whole grains, nuts, legumes, fish, and ratio of monounsaturated to saturated fat and 1 point for an intake below the cohort specific median for red and processed meat and for alcohol intake 5-15 g/d for women and 10-25 g/d for men.10 The total score ranged from 0 to 9 points, with a higher score representing higher resemblance to the Mediterranean diet.

Changes in the diet quality scores were calculated as their differences between the beginning and the end of each four year interval. Therefore, positive differences represented increased adherence to a high quality diet and negative differences decreased adherence to a high quality diet.

We selected 77 single nucleotide polymorphisms (SNPs) that represent all 77 loci associated with body mass index identified in people of European descent (supplementary table B).26 The detailed information on SNP genotyping and imputation have been described previously.1617181920 Most of the SNPs were genotyped or had a high imputation quality score (r20.8), as assessed with the use of MACH software, version 1.0.16. No proxy SNPs were used.

Consistent with our previous study,27 we used a weighted method to calculate the genetic risk score on the basis of the 77 SNPs. Each SNP was recoded as 0, 1, or 2 according to the number of risk alleles (body mass index increasing alleles), and each SNP was weighted by its relative effect size ( coefficient) on body mass index obtained from the previous genome-wide association study.26 We calculated the genetic risk score by using the equation: GRS=(1SNP1+2SNP2++77SNP77) (77/sum of the coefficients), where SNPi is the risk allele number of each SNP. The genetic risk score ranges from 0 to 154, with each unit corresponding to one risk allele and higher scores indicating a higher genetic predisposition to obesity.

Information on demographics, lifestyle, and medical history came from the biennial questionnaires. We converted leisure time physical activity to metabolic equivalent hours (METs) per week.28 The reproducibility and validity of physical activity have been described previously.29 Alcohol intake was updated on the food frequency questionnaires every four years, and total energy intake was derived from these questionnaires.

In the Nurses Health Study and Health Professionals Follow-up Study, data were analyzed within five intervals of four years during a follow-up of 20 years from 1986 to 2006.27 We used multivariable generalized linear models with repeated measures analyses to assess the main associations of the genetic risk score and changes in the AHEI-2010, DASH, and AMED scores with change in body mass index within each four year interval, the associations between each additional 10 risk allele and change in body mass index according to thirds of changes in the three diet quality scores, and the associations between each 1 SD increase in diet scores and change in body mass index according to genetic risk subgroups. We classified genetic risk as low risk, intermediate risk, and high risk on the basis of thirds of the genetic risk score. We tested interactions of the genetic risk score with changes in the three diet quality scores and each dietary components on change in body mass index by including the respective interaction terms in the models (for example, change in the AHEI-2010genetic risk score), with the main effects included in the models as well. We also examined the genetic associations and interactions on weight change. We used multivariable models to adjust for age, genotyping source, baseline levels of body mass index, respective diet quality scores, physical activity, and other dietary and lifestyle factors at the beginning of each four year interval, as well as concurrent changes in these dietary and lifestyle factors within each four year interval. Missing values for diet, body mass index, and body weight were carried forward only once, and after that the follow-up was censored; for other variables, we coded missing data during any follow-up period as a missing indicator category for categorical variables (for example, smoking status) or used carried forward values for continuous variables.

In sensitivity analyses, considering potential confounding caused by age related or smoking related weight change, we assessed the genetic associations and interactions in participants younger than 65 years by censoring participants who were aged 65 years and in participants who had never smoked throughout the follow-up period. Moreover, we repeated the analyses of genetic association and interactions by using an extensive genetic risk score based on 97 SNPs comprising the 77 SNPs identified in people of European descent and 20 more SNPs identified in a combination of people of European and non-European descent (supplementary table B).26 We pooled the findings across the two cohorts by means of inverse variance weighted fixed effects meta-analysis. All reported P values are nominal and two sided. We used SAS software, version 9.4, for statistical analyses.

No patients were involved in setting the research question or the outcome measures, nor were they involved in recruitment or the design and implementation of the study. No patients were asked to advice on interpretation or writing up of results. There are no plans to disseminate the results of the research to study participants or the relevant patient community.

Table 1 shows characteristics at baseline and the first four year changes in characteristics of women in the Nurses Health Study and men in the Health Professionals Follow-up Study. Compared with participants with relatively stable adherence to diet quality scores, participants with the greatest increases in diet quality scores seemed to have lower diet quality scores at baseline and increased physical activity and less weight gain during the first four year period. The mean genetic risk score was 69.5 (SD 5.5) in the Nurses Health Study and 69.3 (SD 5.6) in the Health Professionals Follow-up Study; the genetic risk score was significantly correlated with body mass index and showed normal distributions across the two cohorts (supplementary figure A).

Characteristics according to first four year changes in three diet quality scores in thirds among 14046 US men and women in Nurses Health Study and Health Professional Follow-up Study

In general, the genetic risk score was associated with increases in body mass index and body weight every four years: in the two cohorts combined, each additional 10 risk allele was associated with 0.02 (SE 0.01) increase in body mass index and 0.05 (SE 0.03) kg increase in body weight (supplementary tables C and D). The difference in body mass index change between people at high genetic risk and those at low genetic risk was more prominent among participants with decreased adherence to the AHEI-2010 (0.12) than those with increased adherence to the AHEI-2010 (0.03); a similar pattern was observed for DASH but not for AMED (fig 1). When viewed jointly, the genetic associations with change in body mass index attenuated in participants who increased adherence to the AHEI-2010 and DASH; from another perspective, the inverse associations of increased adherence to the AHEI-2010 and DASH with change in body mass index were more prominent in participants at high genetic risk. Similar results were observed for weight change (supplementary figure B).

Pooled, multivariable adjusted means of change in body mass index (BMI) every four years, according to categories of genetic risk and changes in diet quality scores in thirds. AHEI-2010=Alternate Healthy Eating Index 2010; AMED=Alternate Mediterranean Diet; DASH=Dietary Approach to Stop Hypertension. Histograms and bars are means and SEs. Decreased, stable, and increased adherence to each diet quality score refers to third 1, 2, and 3 of each score, respectively. Data were derived from repeated measurements analyses for women in Nurses Health Study (five intervals of four years from 1986 to 2006) and men in Health Professionals Follow-up Study (five intervals of four years from 1986 to 2006). Results were adjusted for same set of variables as in table 2. Results for two cohorts were pooled by means of inverse variance weighted fixed effects meta-analysis

The genetic associations with change in body mass index were significantly attenuated with increased AHEI-2010 score in the Nurses Health Study (P=0.001 for interaction) and Health Professionals Follow-up Study (P=0.005 for interaction) (table 2). In the combined cohorts, changes in body mass index per 10 risk allele increment were 0.07 (SE 0.02) among participants in the lowest third with decreased AHEI-2010 score and 0.01 (0.02) among those in the highest third with increased AHEI-2010 score (P<0.001 for interaction), corresponding to a weight change of 0.16 (0.05) kg versus 0.02 (0.05) kg (supplementary table E). Similarly, changes in body mass index per 10 risk allele increment were 0.04 (0.02) among participants with decreased DASH score and 0.01 (0.02) among those with increased DASH score (P=0.01 for interaction); corresponding weight change was 0.07 (0.06) kg versus 0.01 (0.06) kg. No clear interaction pattern was observed for AMED (P=0.33 for interaction).

Body mass index change every four years per 10 risk allele increment, according changes in diet quality scores in thirds*

Increase in each diet quality score was associated with decreases in body mass index and body weight every four years in total participants (supplementary tables C and D), and such association seemed to be more prominent in participants at high genetic risk (fig 2). Changes in body mass index per 1 SD increase in AHEI-2010 score were 0.12 (SE 0.01), 0.14 (0.01), and 0.18 (0.01) among participants at low, intermediate, and high genetic risk, respectively, corresponding to weight changes of 0.35 (0.03), 0.36 (0.04), and 0.50 (0.04) kg, respectively (supplementary figure C). Similarly, changes in body mass index per 1 SD increase in DASH score were 0.14 (0.01), 0.16 (0.01), and 0.19 (0.02) across these genetic risk subgroups. Differences in body mass index changes associated with change in the AMED across these subgroups were not evident. Similar results were observed for weight changes (supplementary figure C).

Pooled, multivariable adjusted body mass index (BMI) change every four years per 1 SD increment of each diet quality score, according to genetic risk. AHEI-2010=Alternate Healthy Eating Index 2010; AMED=Alternate Mediterranean Diet; DASH=Dietary Approach to Stop Hypertension. Histograms and bars are coefficients and SEs. Value of 1 SD: AHEI-2010: 8.38; DASH: 3.71; AMED: 1.72. Data were derived from repeated measurements analyses for women in Nurses Health Study (five intervals of four years from 1986 to 2006) and men in Health Professionals Follow-up Study (five intervals of four years from 1986 to 2006). Results were adjusted for same set of variables as in table 2. Results for two cohorts were pooled by means of inverse variance weighted fixed effects meta-analysis

In the combined cohorts, increases in AHEI-2010 and DASH scores significantly attenuated the genetic association with change in body mass index: each 1 SD increase in the AHEI-2010 and DASH score was associated with 0.05 (95% confidence interval 0.08 to 0.03; P<0.001 for interaction) and 0.04 (0.07 to 0.01; P=0.005 for interaction) change in body mass index attributed to each additional 10 risk allele, respectively (fig 3). Such interaction effect was not statistically significant for AMED. For individual dietary components, each 1 SD increases in fruits ( 0.05, 0.08 to 0.02; P=0.001 for interaction), vegetables (0.04, 0.07 to 0.02; P=0.002 for interaction), long chain (n-3) fats (0.02, 0.04 to 0.001; P=0.037 for interaction), and trans fat (0.04, 0.01 to 0.07; P=0.015 for interaction) showed nominally significant interactions with the genetic risk score per additional 10 risk allele on change in body mass index. Similar interactions for weight change are shown in supplementary figure D.

Interaction of genetic risk score with changes in diet quality scores and dietary components on change in body mass index (BMI) every four years. AHEI-2010=Alternate Healthy Eating Index 2010; AMED=Alternate Mediterranean Diet; DASH=Dietary Approach to Stop Hypertension; NHS=Nurses Health Study; HPFS=Health Professionals Follow-up Study. Histograms and bars are coefficients and 95% CIs for interactions between genetic risk score (per 10 risk allele) and changes in diet quality scores and dietary components (per 1 SD increment) on BMI change. Value of 1 SD: AHEI-2010: 8.38; DASH: 3.71; AMED: 1.72; fruits (servings/d): 1.12; vegetables (servings/d): 2.06; long chain (n-3) fats (mg/d): 300.7; whole grains (g/d): 17.34; low fat dairy (servings/d): 0.88; legumes (servings/d): 0.27; fish (servings/d): 0.38; alcohol (drinks/d): 0.70; sodium (mg/d): 3.10; red and processed meats (servings/d): 0.26; nuts (servings/d): 0.52; ratio of monounsaturated to saturated fat: 0.21; polyunsaturated fatty acids (% of energy): 1.68; sugar sweetened drinks and fruit juice (servings/d): 0.92; trans fat (% of energy): 0.01. Data were derived from repeated measurements analyses for women in Nurses Health Study (five intervals of four years from 1986 to 2006) and men in Health Professionals Follow-up Study (five intervals of four years from 1986 to 2006). Results were adjusted for same set of variables as in table 2. Results for two cohorts were pooled by means of inverse variance weighted fixed effects meta-analysis

In participants younger than 65 years and in those who had never smoked throughout the follow-up period, we observed similar but weaker results for genetic associations and interactions between the genetic risk score and changes in diet quality scores on change in body mass index (supplementary tables F and G). Moreover, analyses using the genetic risk score comprising 97 SNPs yielded consistent results (supplementary table H).

In this study, we found consistent interactions between changes in diet quality scores and genetic predisposition related to long term changes in body mass index and body weight in two independent prospective cohorts of US women and men. Our findings show that improving adherence to healthy dietary patterns assessed according to the AHEI-2010 and DASH could significantly attenuate the genetic association with increases in body mass index and body weight. Viewed differently, improving diet quality over time was associated with decreases in body mass index and body weight, and such favorable effect was more prominent in people at high genetic risk for obesity than in those with low genetic risk.

The dramatic alternations in dietary patterns over the past decades have paralleled the rapid rise in the prevalence of obesity in the US.34 Emerging evidence supports a protective effect of improved adherence to healthy dietary patterns on weight gain and other health outcomes such as cardiovascular disease and total and cardiovascular disease mortality.1112133031 In previous studies, we have shown that dietary factors such as sugar sweetened drinks and fried foods could amplify the genetic associations with elevated body mass index.56 Similar interactions have also been reported by another group.32 Our findings in this study are consistent with these previous reports and for the first time indicate that improving adherence to healthy dietary patterns might diminish the genetic association with weight gain. Here, we evaluated healthy dietary patterns by diet quality scores. Instead of considering individual diets in isolation, diet quality scores provide comprehensive measures of diets incorporating nutrients and foods and therefore represent a broader picture of dietary intake.3334 In this study, the AHEI-2010 showed the most significant interaction with genetic predisposition to obesity on changes in body mass index and body weight, and we also found a similar interaction pattern for DASH but not for AMED. When evaluating changes over time, the continuous scale and wider range of the AHEI-2010 may allow for greater sensitivity to differentiate dietary changes; in contrast, the wider scale and narrower range of AMED may limit its ability to detect the differences in dietary changes. Additionally, the AHEI-2010 captured all four dietary components (fruits, vegetables, long chain (n-3) fats, and trans fat) that contributed to significant interactions with the genetic risk score at a nominal significance threshold, whereas DASH and AMED each captured two, which might also account for the observed differences between the three diet quality scores.

From another point of view, our findings indicate that people with a greater genetic predisposition seem to be more susceptible to the favorable effect of improving diet quality on weight management. Our results are in line with the findings of a meta-analysis (including 6951 participants from 10 studies) showing that people carrying the homozygous FTO allele predisposing to obesity may lose more weight than non-carriers through diet and lifestyle interventions.35 In a more recent meta-analysis of 9563 participants from eight randomized controlled trials, each copy of the FTO obesity predisposing allele was associated with non-significant reductions in body mass index (0.02, 95% confidence interval 0.13 to 0.09) and body weight (0.04, 0.34 to 0.26, kg) (indicative of gene by treatment interactions) after weight loss intervention in the treatment versus control arm.36 Of note, the effect sizes of gene by treatment (dietary, physical activity, or drug based intervention) interaction in this meta-analysis are in similar ranges to the effect sizes of gene by dietary patterns interaction shown in our study, supporting the generalization of the effect sizes yielded by our study.

The precise mechanisms underlying the observed interactions remain unclear. The beneficial bioactivities of healthy dietary patterns, such as balancing energy intake, regulating metabolism, and reducing cardiometabolic risk,3738 may partly explain their modifying effect on genetic predisposition to weight gain. In addition, several genes associated with body mass index have been shown to be involved in central appetite regulation and energy homeostasis,26 which may also be responsible for the observed interactions. However, we cannot exclude the involvement of other biological pathways, and future functional studies are needed to provide biological insights into the gene by diet interactions on weight change.

The strengths of our study include the cross validation from two independent prospective cohorts of men and women, the well validated measures of dietary factors and body weight within five repeated four year periods of a 20 year follow-up, and the reliable findings improved by several sensitivity analyses. Notably, we evaluated changes in diet quality scores and changes in body mass index and body weight during the same four year intervals in discrete periods, because this change-on-change analytic approach has been shown to generate more robust, consistent, and biologically plausible relations between diet and long term weight change than the approaches of prevalent diet with weight change (prevalent analysis) or change in diet with weight change in the subsequent four years (lagged changes analysis).39

Our study also has several potential limitations. Firstly, although we have carefully controlled for baseline and concurrent changes of lifestyle and dietary factors in the analyses, unmeasured or unknown confounders may also exist. Secondly, because adherence to healthy dietary patterns was not randomized, the association between dietary factors and weight change may not imply a causal relation. Thirdly, the results could be underestimated by potential reverse causality; for example, people who gained weight might tend to adopt healthier eating patterns to lose weight. Fourthly, our study was restricted to health professionals of European descent in the US, and the generalizability of our findings should be tested in other demographic and racial/ethnic populations.

Our results suggest that weight gain associated with genetic predisposition can be at least partly counteracted by improving adherence to healthy dietary patterns. Importantly, for people who are genetically predisposed to obesity, improving adherence to a healthy diet is more likely to lead to greater weight loss. Our findings support recommendation of adherence to healthy dietary patterns,37 particularly for people at high genetic risk of obesity. The observed genetic effects were modest in magnitude, compared with lifestyle risk factors. Of note, the changes in body mass index and body weight reported in our study were changes per four years. Because changes in body mass index and body weight are essentially cumulative during the life course, the long term effect size would be substantial. Furthermore, long term, dramatic weight loss is difficult to achieve, even in the context of weight loss interventions. Therefore, even modest weight loss or simply maintaining weight from adulthood onward, compared with gaining weight, may have a substantial effect on population health.

Our study provides reproducible evidence from two prospective cohorts of US men and women that improving adherence to healthy dietary patterns could attenuate the genetic association with body mass index increment and weight gain, and the beneficial effect of improving diet quality on weight management was more prominent in people at high genetic risk. Our findings highlight the importance of improving adherence to a healthy diet in the prevention of weight gain, particularly in people genetically predisposed to obesity.

Improving adherence to healthy dietary patterns, as assessed by various diet scores, has been associated with weight loss in several studies

No study has assessed the interactions between changes in these diet quality scores and genetic predisposition to obesity in relation to long term changes in body mass index and body weight

Improving adherence to healthy dietary patterns as assessed by the Alternate Healthy Eating Index 2010 and Dietary Approach to Stop Hypertension can counteract part of gene related, long term weight gain

People at high genetic risk for obesity are more susceptible to the beneficial effect of improving diet quality on weight loss

This underlines the importance of improving adherence to healthy dietary patterns in the prevention of weight gain, especially in people with greater genetic predisposition to obesity

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Discover how to modify your balanced healthy diet for long term effective weight loss.

No matter where it comes from, a calorie is a calorie, and it takes 3,500 calories to gain or lose a pound. Want to shed a perfectly respectable 1 pound per week? Carve 500 calories off your day by thinking through your healthy food choices and upping your exercise.

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Cut out the specific items in whatever categorycarbs, sweets, meatgives you difficulty without cutting out the nutrition. Give pretzels the heave-ho but don't dismiss whole-grain breads. Has ice cream become a problem? Instead, snack on single-serving portions of yogurt.

The best way to achieve that same clarity when you're trying to lose weight is to set some rules. Find yourself snacking on cereal at night? Make an only-for-breakfast rule. If you slip, no cereal in your house for a month! Tend to dive into the breadbasket as soon as the waiter brings it around? Set a one-starchy-carb-per-restaurant-meal rule. If you want the bread, tell yourself before you head out that you'll skip the potato or pasta that comes with your meal. To make the rules official, write them down.

Discover three more tips from Shape about a balanced healthy diet strategy that will help lead to effective long term weight loss.

[header = Find more long term weight loss tips for your balanced healthy diet at Shape.]

Fill up on wholesome, fiber-rich, water-filled healthy foods like vegetables, fruits, whole grains and beans, which fill you up faster for longer on fewer calories. And how you eat is as important as what you eat. A growing body of research shows that the best way to keep your metabolism revved and body-fat levels low is to feed yourself in small amounts. Eat airline-size (rather than restaurant-size) portions of healthy foods like meat, fish, pasta, grains and desserts. And eat every three to four hours, for a total of five mini-meals per day.

You're much more likely to stick with a diet if your food looks, tastes and smells delicious. Feeling deprived will only backfire. Make a plan you can live with by livening up healthy foods with herbs and spices like basil, cilantro, curry and ginger; aromatic veggies like garlic and onions; and condiments like mustard, hot pepper sauce or salsa. Experiment with new nutritious foods: Tantalize your taste buds with two new fruits or vegetables at each meal. Try different cold/hot cereals and breads. Don't declare high-fat favorites "off limits"; savor them in small amounts to maintain a balanced healthy diet.

For energy, satisfaction, staying power and good health, aim to eat a healthy balance of protein (15-20 percent of your total daily calories), fat (less than 30 percent of your total daily calories) and carbohydrate (50-55 percent of your total daily calories) each day. Rule of thumb: Fill three-quarters of your plate with plant foods, leaving the rest for small amounts of fish, nonfat milk products and nuts or seeds.

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In 2005, Colin and his son Tom, now a physician, shared those findings with the world in The China Study, hailed as one of the most important books about diet and health ever written.

Featuring brand new content, this heavily expanded edition of Colin and Toms groundbreaking book includes the latest undeniable evidence of the power of a plant-based diet, plus updated information about the changing medical system and how patients stand to benefit from a surging interest in plant-based nutrition.

The China StudyRevised and Expanded Edition presents a clear and concise message of hope as it dispels a multitude of health myths and misinformation. The basic message is clear. The key to a long, healthy life lies in three things: breakfast, lunch, and dinner.

Read more here:
The China Study: Revised and Expanded Edition: The Most ...

In the last few years a lot of diet gurus have tried to argue that calories dont count And to be honest I understand why. Its what we all want to hear!...

But to be blunt Its also the biggest lie in weight loss...

Ignore for a moment all the fancy weight loss theories youve heard. Some of them may be true. Some completely bogus. And others so weak they dont make a difference in your real results.

However there is one undeniable truth about weight loss...

This one thing may not be popular. But it MUST happen, no matter what the diet gurus pretend. Here it is

To lose weight you must eat below a certain threshold of calories.

Now, stick with me for a second, ok? I know youre probably thinking

How is this any different from what Ive already heard?...

Youll see in a moment why this is totally different. First...

Lets define a calorie...

Basically its a way of talking about the energy stored in the food you eat. Its also used to talk about the energy your body burns to live and to do whatever activities you do throughout your day.

Now I know this probably isnt going to be popular advice. However...

Even though you NEVER have to count a single calorie I just dont have a magic formula that allows you to eat as many calories as you want and still lose weight. And

If someone claims you can do that run as fast as you can in the opposite direction!

And second I said you need to eat below a certain threshold of food.

The trick is knowing what your level of calories is and getting below it. However...

You dont have to do it every day. Theres a simple strategy that allows you to stay below your personal threshold WITHOUT daily discipline, precise calorie counting, or giving up any of your favorite foods.

And using this simple strategy is what helps clean out your body even at the deepest level of your cells so that you can actually turn back the clock, look younger and feel more energy than folks half your age

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Eat - STOP - Eat

You want to lose weight and keep it off for good. These five strategies will help you do just that.

Most people trying to lose weight only focus on their ultimate goal: dropping pounds. But it's important not to lose sight of the diet and exercise changes that will get you there.

Choose two or three diet and exercise goals at a time that you are willing to take on. And make sure they are specific and realistic.

For example, "exercise more" is a wonderful goal, but it's not specific. "Walk 5 miles every day" is specific and measurable. But is it realistic if you're just starting out?

"Walk 30 minutes every day" is better, but what happens if work or weather interferes? "Walk 30 minutes for 5 days each week" is specific and realistic.

Are there situations that make you want to eat more? Start noticing them. For example, you may learn that you're more likely to overeat while you're bored or stressed.

Then figure out ways to get around those triggers. Do something else to soothe your stress, for instance.

Also, you might want to put treats away. You're more likely to eat them if they're visible and easy to get to.

That's right: You should feel full. But how you do that might surprise you.

It's mostly about time: 15 minutes, to be specific. You need at least that much time to feel full. So eat slower, giving your brain enough time to notice that you've eaten.

What you eat can also help. Think fiber (like fruits and veggies) to fill up.

Another trick is to use smaller plates so that small portions do not appear too small.

Also, changing your eating schedule can help you reach your goal, especially if you tend to skip or delay meals and overeat later.

A good reward is something that is desirable, timely, and depends on meeting your goal.

Rewards may include treating yourself to a movie or massage, taking an afternoon off from work, or giving an hour of time to yourself.

Keep in mind that many small rewards, given for meeting small goals, can work better than bigger rewards for long, difficult goals.

Jot down things like how much you exercise and what you eat. There are many apps that can help.

Doing this can really open your eyes to what you are doing and what you need to do to meet your weight loss goals.

SOURCES:

Academy of Nutrition and Dietetics.

Weight Watchers.

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Long-Term Weight Loss - webmd.com

There's no lack of people willing to sell you on the newest and best way to lose weight. But let the true experts -- ordinary people who have lost weight and kept it off -- share their recipe for success. Then you can take the first few baby steps to being and "thinking" thin.

Thinking thin is all about small, simple changes you make on a daily basis, not about dropping 20 pounds by year's end.

"Thinking thin in a world that would have us be fat as barrels is no easy task," says Catherine Fitzgerald, RD, director of the health promotion division in the University of Michigan Health System.

"Food is everywhere, so you have to develop a personal lifestyle, sooner rather than later in life, that is compatible with your long-term weight goals. People should focus their efforts on weight loss as a means of staying healthy, not reaching some unreachable ideal of beauty that our culture puts out there."

The University of Colorado's National Weight Control Registry set out to examine everyday people who have achieved long-term weight loss. Set up by professor James O. Hill and his colleagues nearly 20 years ago, the registry includes information about more than 3,000 people who have, on average, lost more than 60 pounds and kept if off for more than five years.

After studying the registry's participants, Hill identified four common behaviors among those who have successfully maintained their weight loss:

Most weight-management experts would counsel against weighing yourself daily because it may be counterproductive and could lead to disappointment. And yet it works, according to the registry researchers.

Here's how the participants said they maintained their weight loss:

Fitzgerald says that a major part of keeping a focus on weight loss or weight management is as simple as staying positive.

"It's always better to go with what we can do, rather than what we can't do," she says. "Make reachable goals, like eating an extra serving of fruits or vegetables. You also can make healthier choices."

Many fast food restaurants are including healthier items on their menus. For example, Burger King's vegetable burgers and Wendy's salads, Fitzgerald says.

"A healthy choice is just as easy to make today as an unhealthy one," she says.

What role does your family play? If you come from a family with a history of weight problems, does that mean you are fighting a losing battle?

"Genetics plays a role in increasing your susceptibility to becoming obese, but genetics alone does not determine whether your body does or does not store fat," says David Schteingart, MD, professor of endocrinology and director of the obesity rehabilitation program at the University of Michigan. "In particular, there have been a number of studies that have shown that a person's weight and manner of fat storage is most closely linked to that of his or her biological mother."

Still, a family history of obesity can't be used as reason to give up.

Most of these studies show that genetics is responsible for only 25% of your risk of being obese, says Schteingart. "The other 75% then includes many facets, such as cultural influences, personal lifestyle, and availability of food, among others."

"Behaviors and lifestyle can be extremely difficult things to change, especially as we age," says Schteingart. "But simple steps maintained over time are what works."

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Thinking Thin: Recipe for Success for Long-Term Weight Loss

If long-term weight loss were impossible, would it even be worth trying to lose weight?

Well, bad news. Areport that hit headlines recently suggests that permanent weight loss is near impossible. Decades of clinical research, public health initiatives and personal attempts at diet and exercise have yielded a net sum of zero. Sure, people lose weight all the time; thats pretty easy to do but they cant keep it off.

A review of the scientific literature shows that virtually every participant of structured weight-loss programs regains all of their weight loss within five years. Those who managed to keep the weight off averaged a weight loss of 6.6 pounds and a reduced weight of less than 3% of their initial body weight. That means that if you were a 250-pound overweight dieter, after five years of watching your weight, youd be a sleek 243 pounds. That may not sound like a lot, but it has some scientists impressed. Take Weight Watchers, for example. According to a study paid for by Weight Watchers, half of all dieters who reached their goal weight through their program were still at least 5% lighter after five years. The starting weight was 165 pounds overweight, but not obese. The dieters lost about 22 pounds, or 13.3%, by restricting calories, but then regained an average of 11 pounds five years later. Next to the near-zero success rate of hospital and university-based studies, Weight Watcher results were considered a major victory. At this point, just being able to stop people from gaining more weight is considered a success.

A long-term weight loss effort maintained anywhere from one to five years is considered successful if youre 5 to 10% lighter than you were initially. Setting the bar so low means that, in reality, successful losers go from obese to overweight not from overweight to thin. From a public health perspective, obesity is classified as a Body Mass Index (BMI) over 30. If youre a regular reader of AskMen, youll know that BMI is a measure of a persons weight in relation to their height, not an indicator of body fat. Bodybuilders with low body fat will invariably be classified as obese since muscle weighs more than fat. From a global perspective, however, we know that nations are not populated by Spartan Warriors (their descendents, the Greeks, are now Europes most overweight country), so using BMI is a fine way to measure obesity at a national level.

By now, it wont surprise anyone to hear that the world is fatter than ever. In 2010, there were 1.5 billion people worldwide who were obese, and the trend is growing. Obesity is behind 3.4 million deaths and 3.9% of years of lives lost a substantial increase from previous decades that makes obesity a major global health issue, perhaps more important than malnutrition and infectious disease. In the past 33 years, no country has had a success story in curbing their obesity epidemic. Some countries in the Middle East (Kuwait, Libya, and Qatar) and the Pacific (Tonga Kiribati, Federated States of Micronesia, Tonga and Samoa) now have more than half of their population classified as obese. In the United States, more than one-third and 17% of youth are obese. As a result, as many as 40% of women and 24% of men in America are trying to lose weight at any given time; many have tried a variety of methods such as diets, exercise, behavior modification, and drugs. Even those who are not overweight particularly young women are trying to lose weight. We know that obesity is a complex issue; it reflects inherited, environmental, cultural, socioeconomic, and psychological conditions. How to reverse the process, on the other hand, is beyond our understanding. At least, thats what the science is suggesting.

So what about the guy or girl you see in those Before and After photos in weight loss infomercials those who completely transform their bodies through diet and exercise? Either theyll regain all the weight in a few years or theyre one of those exceptional individuals that are rarely encountered like that friend of a friend you heard who lost 50 pounds and completed a marathon. If they did it, the mind convinces us, so can we. But the math is against us. If only two out of 1,000 Weight Watchers customers actually maintain large weight loss permanently, you cant expect such simple advice as Eat less, exercise more to actually work. In todays world of surplus calories and sedentariness, eating less and exercising more takes willpower, and lets admit it, willpower doesnt work.

The main reason dieting fails is because many of us still believe that cutting calories is the best way to lose weight. You will indeed lose weight but wait and see how long it takes for the starvation mechanism to kick in and for your brain to betray you with food urges that are impossible to resist. For a formerly fat person, this is what it feels like all the time. The part of the brain that controls hunger and appetite the hypothalamus is continually turned on. That means that the brain of a 175-pound man who used to be overweight is quite different than the brain of a man who was always 175 pounds. The reason we cant lose weight is because our brains think were not overweight, and might actually think that were underweight. The biochemistry of how our brain regulates bodyweight is covered in my earlier AskMen article on how to maintain weight loss.

While science has had dismal success in keeping the weight off people, it has recently shed light on why peoples brains make them gain weight. Our bodies are fine-tuned machines that keep everything in balance a process termed homeostasis. The brain regulates the amount of body fat by adjusting our energy levels, appetite and digestive efficiency. It is counter-evolutionary to carry around too little or too much fat. If obesity occurs, it means that theres a breakdown in the system caused by an imbalance in brain chemistry, mirrored by an imbalance in our environment.

Food and other things we put in our mouth (let your imagination run wild) is the closest exposure we have to our environment we literally place stuff from the outside into our insides. Its no surprise, then, to learn that diet has an enormous effect on our body and its chemistry. A recent study shows that years of eating and overeating the typical American diet actually damages the brain. More specifically, it damages the signalling pathways in the hypothalamus the part of the brain that regulates metabolism and appetite.

Two hormones have been recognized to have a major influence on appetite and energy balance: leptin and ghrelin. Leptin is a hormone that signals to the brain how much fat were carrying and can suppress appetite and energy intake. Ghrelin does the opposite its a fast-acting hormone that plays a role in increasing appetite. We can take a guess at how the brain of a former fat person works. Their brains are resistant to the appetite-suppressing effects of leptin and more sensitive to appetite-stimulating ghrelin. It cant tell how much fat is stored in the body and you cant trust the messages its sending you about appetite, hunger and fullness.

So what dietary factors in the typical American diet cause such damage to the brain? Its the fat and simple carbs. A fatty, high-carb diet causes alterations in structural plasticity, i.e. brain changes. The underlying mechanism involves inflammation and damage to the nerves, suggesting that our bodies were not designed to thrive on modern diets. They were designed for whole foods.

In one of my university nutrition classes, the professor asked us: What is the sweetest food found in nature? The answers ranged from honey and maple syrup to fruit. All of these, he noted, were seasonal only available for a few months or days out of the year. He then asked, What is the fattiest food? Animals were the correct answer. The final question What food found in nature is both high in fat and high in sugar? was too tough to answer. We couldnt think of a single one. Fruits are fat-free and animals are low-carb. Yet every single processed food we find in the grocery aisles are high in both sugar and fat and, oftentimes, salt. These three nutrients are highly addictive to humans simply because they were crucial for our survival in the wilderness.

Our bodies havent evolved as fast as the food market industry, who were quick to recognize that tasty food sells. In our fight against fat, it is plainly a fight between them and us. Fatty high-carb foods are too delicious, too tempting, and too plentiful for us to resist. Our own genes drive us towards overeating these foods, and once the weight creeps on, many of us turn to fat-free or low-carb foods that are marketed as weight-loss aids. Ironically, many of these diet shakes, diet bars, and diet packs are themselves highly processed foods.

Change your diet, and change it fast. In the words of Underground Wellness Sean Croxton, JERF just eat real food. Wholesome real food is not processed and has the closest macronutrient balance that our bodies were designed to digest and metabolise. While some damage to the hypothalamus may be permanent, it may be possible to reverse much of it. Whether you adopt the Paleo or the Mediterranean diet, choose a way of eating that works for you but that includes lean quality meats, seafood, plenty of vegetables, fruit, nuts, and seeds. Say goodbye to fast food and junk food and never, ever let yourself go hungry for the sake of losing weight. If youve been battling weight for a while, make sure to eat fish. Omega-3 fats are possibly the most potent anti-inflammatory agent in your diet and they also appear to modulate the negative effects of a fatty, high-carb diet. Even better news, fish oil is fantastic for memory and brain health, and can make developing Alzheimers far less likely.

Permanent weight loss takes time. Dont think for a second that losing weight Biggest Loser-style is the way to go. Many of those who dropped massive amounts of weight on the show have gained most of it back again within a year or two. You need to heal your brain. And unlike a scratch or a broken bone, healing your brain takes time. Be patient and keep it simple. Just eat real food.

Permanent weight loss does not work with inane methods of loss and maintenance. Dieting is typically viewed as an undertaking of severe vigilance on calorie intake and expenditure. Picture the dieter who is on a highly restrictive diet, denying their ability to use food for comfort or celebration, establishing a surreal marathon-type goal, and nail-biting their way through hunger and cravings. Theyve chosen suffering as their weight management method. No matter how much you want to lose weight, people arent built for long-term relentless suffering. To be successful, you need to find a way to enjoy your journey. Eat simply and avoid fatty, high-carb foods. The global obesity epidemic would reverse its course if traditional foods and eating habits (eating dinner as a family, for example), were preserved. Unfortunately, whether by choice or necessity (inaccessible, unaffordable, or unavailable food), inexpensive processed market foods have largely replaced indigenous cuisines. Theres no easy solution to curing obesity. However, despite what statistics show, permanent weight loss is not incurable. We just need to heal our brains first.

Read more:
Is Long Term Weight Loss Possible? - AskMen

Theres no one-size-fits-all weight loss plan, but taking on a consistent strategy to dropping pounds that can be repeated, rather than a quick approach as with crash diets, may be the key to slimming down for good.

In a new study conducted at Drexel University, psychologists investigatedwhy some people have success with weight loss programs, but others dont.

It seems that developing stable, repeatable behaviors related to food intake and weight loss early on in a weight control program is really important for maintaining changes over the long term, lead author Emily Feig, who conducted the researchas a doctoral student at Drexel, said in a statement.

The study, published in the journal Obesity, involved 183 overweight or obese adults, a majority of whom were white females living in the Philadelphia area. The researchers enrolled all of the adults into one of three different year-longweight loss programsinvolving behavioral treatment, such as setting goals for increasing physical activity and monitoring their calorie intake. One group was instructed to use two meal replacements each day during the first sixmonths and another group was told to eat less energy-dense foods while having more protein and fiber.

Each week, the participants weights were recorded. Additionally, they self-reported their attitudes and behaviors regarding cravings, emotional eating, and binge eating.

Feig and her colleagues found that those who had consistent weight loss in the first six weeks were more likely to keep off the unwanted pounds in the long-term compared to those whose weights varied each week.

This study goes even further in supporting the importance of early weight changes by showing that weekly variability in weight, above and beyond how much weight is lost, predicts weight loss maintenance up to two years later, Feig told CNN. So it seems that both success and consistency in weight loss at the beginning of a program is important for long-term success.

The findings add to priorstudies showing that the amount of weight a person loses early on in a weight loss program can predict how much they lose down the road, Feig pointed out.

The research also revealed in a twist that participants who reported lessemotional eating andbinging, and who wereless preoccupied with food at the beginning of the study, were more likely to have greater weight fluctuations and less weight loss overall. So success isn't predicated on someone's relationship to food so much as the early habits the dieter establishes in the beginning, the statement notes.

The study cant confirm why some peoples weights widely fluctuate during weight loss programs, but the researchers plan to further explore the topic. Still, principal investigator Michael Lowesays the findings highlight a possible strategy for maintaining weight loss.

Settle on a weight loss plan that you can maintain week in and week out, even if that means consistently losing of a pound each week, Lowe, a psychology professor at Drexel, said in thestatement.

The bottom line: Losing weight consistently, even if it's not a lot, may be more effective then attempting to achieve long-term success from a risky crash diet.

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Long-Term Weight Loss Success May Rely On Consistency ...

September 6, 2017

The more you exercise, the more those pounds should just melt off, right?

Not always this according to a recent exercise study out of the United Kingdom.

Conducted by scientists from Loughborough University in Britain, the study concludes that exercise as a weight-loss strategy is tricky, complex and not as relational as one might think.

To provide a deeper understanding of the nature of weight loss, ASU Now turned to Glenn A. Gaesser, an Arizona State University professor of exercise and health promotion in the College of Health Solutions.

Glenn A. Gaesser

Question: A recently published by the Journal of Endocrinology shows that exercise isnt always a foolproof weight-loss strategy in large part because exercise makes you hungrier and many people wind up consuming more calories than they normally would. What is your philosophy?

Answer: This was a short-term study, only looking at a few hours after exercise. The real issue is what happens long-term. Most studies show that weight loss from exercise training of any type is far less than what is expected on the basis of the cumulative calories burned during all exercise sessions combined.

This is because the human body tends to defend its set-point weight, much the same way a thermostat is designed to maintain a set temperature. This involves a number of physiological and hormonal responses that essentially prevent chronic exercise from reducing body weight to unhealthy levels. The same is true when people diet.

Adaptive thermogenesis prevents most people from losing weight and/or maintaining weight loss. Set-point is an individual thing, determined largely by genes but also environment. It also tends to increase with age.

Q: How do different types of exercise affect appetite?

A: This is a tough one. Higher-intensity exercise (think sprint-type interval exercise) typically suppresses appetite at least initially. But the real issue is, as I mentioned earlier, what happens in the long term? Eventually, hunger comes back and we eat. That is why virtually every study that has been published on exercise training and weight loss shows minimal effects.

Q: Are there any good non-exercise habits or methods that blunt appetite?

A: Good luck with that one. Trying to blunt appetite is essentially trying to battle biology, and biology inevitably wins. For individuals trying to lose some weight via exercise, I would suggest assessing progress fairly frequently with the scale and making adjustments accordingly.

We also published an article in the New York Times a couple of years ago showing that weight loss early on during an exercise program was also a significant predictor of weight (and fat) loss at the end of the exercise program.

Q: Ive heard that chocolate milk is the best thing to have after a workout. True or false?

A: Chocolate milk is fine I love it. Its got carbs and protein, but not necessarily the best. The overall 24-hour dietary intake is far more important than what you eat right after a workout.

Top photo courtesy of Pixabay

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ASU fitness expert says new study underscores tricky nature of weight loss - Arizona State University

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