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The prevalence of obesity has become an epidemic. It is estimated that in the United States, 64.5% of the general population is either overweight, defined by body mass index [BMI, body weight (kg)/height (m)2] between 25.0 and 29.9 kg/m2, or obese (BMI > 30.0 kg/m2).1 The major medical complications associated with obesity include metabolic syndrome, type 2 diabetes, cardiovascular disease, hypertension, and certain types of cancer,2 to name a few. Cancers strongly associated with obesity include kidney, esophagus, colon, gallbladder, pancreas, endometrial, ovary, and postmenopausal breast cancer.3,4

There are several potential mechanisms connecting obesity with the increased risk of cancer:

(1) Elevated blood estrogen levels. Adipose tissue is an extragonadal source of estrogen that can convert androgen into estrogen. With large amounts of adipose tissue mass in obese individuals, the amount of estrogen circulating in these individuals is higher than normal. Estrogen is known to stimulate tumorigenesis and thus increase the risk of cancer, especially estrogen receptor (ER)-positive breast


(2) Hyperinsulinemia/insulin resistance. Hyperinsulinemia and insulin resistance are the cornerstones of metabolic syndrome and are commonly seen in obese individuals.7 Hyperinsulinemia/insulin resistance reduces the production of insulinlike-growth factor binding protein-1 (IGFBP-1) and IGFBP-2, thus increases the level of free insulin-like growth factor-1 (IGF-1).8 Insulin and IGF-1 are known to stimulate mitogenesis and angiogenesis and therefore may increase the risk of cancer.8-10 In addition, hyperinsulinemia is correlated with reduced production of sex hormone-binding globulin.11 The net effect of increased estrogen production and reduced sex hormone-binding globulin production is elevated levels of free estrogen in blood circulation. As a result, the risk for breast cancer is increased. Patients with metabolic syndrome or elevated levels of insulin and IGF-1 also have an increased risk for colon cancer.12,13 Other metabolic abnormalities observed in obesity as part of the metabolic syndrome include high levels of total cholesterol, low-density-lipoprotein cholesterol (LDL-C) and triglyceride, low levels of high-density-lipoprotein cholesterol (HDL-C), and hypertension.7 A low HDL-C has been shown to be associated with high levels of blood estrogen, leptin, and insulin, and thus may serve as a marker for breast cancer risks in postmenopausal women.14-16

(3) Other metabolic alterations. Obesity is characterized with elevated blood leptin levels.17,18 Leptin, the protein product of the ob gene, is secreted by adipose tissue and is directly correlated to total adipose tissue mass in the body.18 Leptin has been reported to be angiogenic19,20 and has been postulated to be the link between obesity and prostate cancer,21,22 breast cancer,23,24 colon cancer,25 as well as cancer in other sites.26


Obesity is not only a risk factor for cancer occurrence, but also a risk factor for cancer recurrence,27,28 poor prognosis for survival,29-33 and increased risk of cancer mortality.34 Weight gain after diagnosis can also adversely affect cancer prognosis and survival.33 Weight gain is common in breast cancer patients, especially in those who are receiving adjuvant chemotherapy or are younger than 60 years of age.35-37 This weight gain after breast cancer diagnosis may be attributed to reduced physical activity38 and altered dietary patterns.39 It is interesting to note that some studies did not detect a change in body weight. However, a change in body composition, mainly an increase in adipose tissue mass and reduction or no change in lean body mass, has been observed in these studies.40,41


With a poorer prognosis for survival, it is expected that obese cancer survivors should have enhanced motivation to lose weight in order to prevent cancer recurrence or to prolong cancer-free life. Different dietary regimens have been deployed to assist cancer survivors in losing weight. Dietary intervention trials aimed at increased intakes of fruit, vegetable, and fiber, and reduced fat intake were usually effective in achieving short-term goals, and resulted in weight loss during the first 6 months of the trial.42 However, the long-term effectiveness of these interventions is debatable. Thomson et al. reported that at the end of 4 years, the body weight, BMI, and body composition of the breast cancer survivors were not significantly different from the baseline levels.43 Thus, even though the intakes of fruit, vegetable, and fiber were still increased compared to baseline level, reduction in energy intake is still necessary in order to maintain the weight loss observed during the early post-diagnostic period.44 In a population-based study, Coups and Ostroff reported that without any intervention, there was no difference in dietary intake patterns in terms of fruit, vegetable, and fat intakes between cancer survivors and non-cancer controls.45 However, Blanchard et al. reported that 47% of the cancer survivors did improve their dietary quality.44,46

We have employed different weight loss regimens to compare the effectiveness of weight loss and maintenance in breast cancer survivors.47,48 In this study, the participants were randomized into four treatment groups:

(1) Control group: Participants were only given the National Cancer Institute's "Action Guide to Healthy Eating" and the "Food Guide Pyramid" without any other dietary or exercise instruction;

(2) Weight Watchers group: Participants were provided with free coupons to attend weekly Weight Watchers group meetings with no further dietary or exercise instructions;

(3) Individualized group: Participants met with a registered dietitian (RD) for weekly one-on-one counseling for the first 3 months, biweekly for the next 3 months, and monthly for the last 6 months. They were free to call the RD at any time if they need more nutritional counseling. They were required to keep diet and exercise records; and

(4) Comprehensive group: Participants in this group were provided with free coupons to attend Weight Watchers weekly meetings and also received individualized dietary counseling. They were required to keep diet and exercise records.

At the end of 12 months, the three intervention groups lost weight. However, only the Individualized and Comprehensive groups had statistically significant weight loss as compared to their baseline weight (Table 1), and only the Comprehensive group reduced a significant amount of body fat percent. Participants in the Comprehensive group also showed the most improvement in metabolic parameters, such as an increase in HDL-C and reduction in LDL-C and leptin levels. Thus, even in breast cancer survivors for whom losing weight is beneficial, it is unlikely that weight loss will be achieved without any intervention. Furthermore, it appears that intensive individualized diet counseling and group support are required to achieve significant weight loss. Demark-Wahnefried et al. also reported that to date, all the dietary interventions were resource intensive.49 In addition, dietary interventions may achieve the goal of increasing fruit and vegetable intake and reducing fat intake in

Table 1. Anthropometric and Dietary Changes from Baseline to the End of 12 Months of four Groups of Subjects

Table 1. Anthropometric and Dietary Changes from Baseline to the End of 12 Months of four Groups of Subjects


Weight watchers




Body weight (kg)

1.1 i 1.7a

-2.7 ± 2.1ac

-8.0 i 1.9bc*

-9.5 i 2.7b*


BMI (kg/m2)

0.5 i 0.9a

-1.5 ± 1.0ac

-3.0 i 1.3bc*

-3.7 i 0.8bc*


Body fat (%)

0.23 i 0.6a

-0.99 ± 0.08ac

-3.17 i 0.8bc

-3.65 i 1.1bf


Energy intake (kcal)

-145 i 179

-570 ± 58 f

-515 i 118*

-393 i 163*


Dietary fat intake (%)

5.4 i 3.7*

-2.6 ± 2.8*

-4.8 i 1.5*

0.9 i 3.4


Adopted from Jen et al.47 with permission. Numbers with different superscripts were significantly different from each other.

^Significantly different from its baseline value at p < 0.05; f significantly different from its baseline value at p < 0.01; ns, not significant.

Adopted from Jen et al.47 with permission. Numbers with different superscripts were significantly different from each other.

^Significantly different from its baseline value at p < 0.05; f significantly different from its baseline value at p < 0.01; ns, not significant.

breast cancer survivors, but without energy restriction, weight loss is still not likely to be achieved.43

Since weight loss can prevent cancer incidence and recurrence, as well as other chronic diseases,50 weight loss has been attempted by obese individuals as well as cancer survivors. However, weight loss maintenance is very difficult to achieve. It has been reported that less than 10% of formerly obese patients are able to maintain significant weight loss for an extended period of time, and weight regain is fast.51 For many obese individuals, this weight loss/regain cycle repeats many times thus producing a weight yo-yo or weight cycling phenomena. We have previously reported that animals experiencing this kind of weight cycling showed insulin resistance.52 Moreover, at sacrifice time, animals which went through five cycles of weight cycling had similar body weights as the control animals that maintained a constant body weight throughout the study.53 However, the weight-cycled rats still had elevated levels of 5-hydroxymethyl-2'-deoxyuridine as compared to the control animals. 5-hydroxymethyl-2'-deoxyuridine, an oxidized thymidine residue, is an indicator of oxidized DNA damage and serves as a marker for breast cancer risk.54 Thus, these animal data indicated the potential of weight cycling to induce breast cancer. However, we also observed that when insulin resistance was not produced, weight cycling did not increase the risk of breast cancer.55 Therefore, it may be the insulin resistance per se, not the weight cycling itself, that increases cancer risks. Cleary et al. reported that weight cycling reduced the incidence of mammary tumors.56 However, no data on insulin resistance in these mice were reported. It is possible that no insulin resistance was produced in their animals asjudged by the fact that weight-cycled mice had similar body weight, fat pad weight, and IGF-1 levels as the ad-libitum fed mice. Since weight gain/obesity is positively associated with insulin resistance and weight loss improves insulin sensitivity, weight loss or maintenance should be strongly encouraged in cancer survivors.


Body weight regulation is determined by energy balance: energy intake and energy expenditure. In order to lose weight, a negative energy balance (energy intake less than energy expenditure) must be achieved. Generally speaking, there are two dietary strategies to reduce energy intake: (1) altering dietary composition; and (2) reducing food intake and eating a balanced diet, thus reducing energy intake.

5.0. ALTERING DIETARY COMPOSITION 5.1. Low Carbohydrate (CHO), High Protein/Fat Diets

This type of diet has enjoyed widespread popularity in recent years. The most famous representatives of this type are "Dr. Atkin's Diet Revolution" in the 1970s and his "Dr. Atkin's New Diet Revolution" in the 1990s. This type of diet proclaims that high CHO induces postprandial hyperglycemia, and thus elevates insulin secretion. This increased insulin secretion not only enhances lipogenesis by increasing glucose uptake by the fat cells, but also triggers hunger due to reduced blood glucose levels.57-59 In addition, elevated insulin levels inhibit the release of the brain satiety hormone serotonin.60 Thus, consuming a high CHO diet will make individuals even hungrier and desire to eat even more CHO, and the elevated blood insulin levels will cause insulin resistance.57-59 As stated previously, insulin resistance reduces the secretion of sex hormone binding globulin and IGFBP-1, thus producing more free-circulating IGF and estrogen. As a result, cancer risk is increased. The low CHO diets claim that by reducing CHO intake, blood insulin secretion will be blunted and the possibility of insulin resistance will be reduced. When individuals start a low CHO diet, weight loss is faster when compared to individuals on a high CHO diet at the end of 6 months. At the end of 1 year, the amount of weight lost is similar for people on the high and low CHO diets.61,62 The rapid weight loss at the beginning of a low CHO diet is mostly due to loss of body water and muscle and liver glycogen. A significantly higher amount of lean body mass loss has also been observed with low CHO/high fat diet as compared to high CHO/low fat diet.63 Low CHO diets also generate ketones because of incomplete fat catabolism.64 Ketones may suppress appetite, a mechanism proposed by Atkins as desirable. Nevertheless, the long-term health effects of elevated ketone levels in adults have not been examined.65

The effects of a low CHO diet on appetite depend on whether the diet is high in fat or protein. A reduction in perceived hunger from baseline levels in individuals consuming the low CHO/high protein diet, but not the high CHO diet, for 6 weeks has been observed.66 However, the long-term effects of a low CHO/high protein diet on hunger perception warrants further investigation. High fat diets, on the other hand, have weak satiety value, and thus may lead to overconsumption.67 The long-term consequence of consuming a high fat diet could be increased weight gain and obesity.

The improvement of blood triglyceride and HDL-C seen in individuals on the low CHO diets has been proclaimed as evidence that a low CHO diet is superior to a high CHO diet.61,62 This improvement may be explained by the weight loss. Since individuals consuming low CHO diets lost more weight at the beginning of the diet,61,68 it is not surprising to see a better lipid profile than that of people on a high CHO diet. However, a low CHO diet can also result in increased total cholesterol and LDL-C levels.61,68,69 Therefore, the health benefit of long-term consumption of this type of diet is still questionable.

Other adverse effects of low CHO diets include increased urinary calcium excretion,70 foul taste in the mouth,71 weakness,71 constipation,72 and headache and dizziness,73 to name a few. Many of these symptoms are similar to those cancer survivors reported during and/or following radiation and various types of chemotherapy.74,75 Increased urinary calcium excretion may increase the risk of developing osteoporosis.76 Treatment for breast and prostate cancer will also increase the risk of osteoporosis,77 suggesting that a high protein/fat diet may be con-traindicated for cancer survivors. However, we have observed that in postmenopausal women, breast cancer survivors had significantly higher proximal radial Z scores (age and ethnicity-adjusted bone density) than controls while there was no difference between cases and controls in premenopausal women.78 The Z score was also significantly higher in African American cases than in African American women in the control group. No such difference was identified in Caucasian women.78 These inconsistent results point to the need for further study to examine the relationship between high protein/fat intake, osteoporosis and cancer occurrence and recurrence. Before a definitive answer is derived, it would be a good practice not to consume a high protein/fat diet because of its association with other chronic diseases.

High protein/fat diets allow for unlimited quantities of meat, cheese, eggs, and other high protein/fat foods while severely restricting fruit and vegetable intakes. Yang et al.79 reported that in Japan, the incidence of colorectal cancer was positively correlated with the intakes of animal protein, fat, and oil, but was negatively associated with plant protein consumption. High fat/high protein diets are also correlated with renal cell carcinoma.80 Nagle et al.81 observed that cancer survival was negatively associated with the intake of red meat, white meat, and protein, but positively correlated with vegetable intake, especially cruciferous vegetables.

Even though there is no research specifically examining the relationship between high fat/protein intake and cancer recurrence at this point, given the fact that cancer patients are more likely to develop other chronic diseases82 that are associated with high fat/protein intake, it seems advisable for the cancer survivors to avoid diets high in protein or fat.

5.2. High CHO Diets

High CHO diets have moderate protein content and low fat content (usually between 10 and 20%). The representative diets are Dr. Pritikin's diet83,84 and Ornish's diet.85,86 Barnard87 reported that for subjects who were in the Pritikin Longevity Center for 3 weeks, medically supervised with daily aerobic exercise, and fed the Pritikin diet, there was a 5.5% decrease in body weight in men and a 4.4% decrease in women.87,88 However, Barnard's studies omit information on total caloric intake or energy expenditure. Pritikin did recommend 1000-1200 kcal/day, which would suggest that they consumed a low-calorie diet. Ornish et al.8 reported that results from the Lifestyle Heart Trial indicated that there was a significant difference in the amount of fat intake and weight loss between the experimental group following the Ornish diet and their Control group: 10.9 kg weight loss at l year with a sustained weight loss of 5.8 kg at 5 years in the experimental group, compared to no change in the control group. Havel et al.90 reported that for women with a family history of diabetes, consumption of a low fat diet for 6 months was predictive of weight loss and fat loss. A meta-analysis conducted by Astrup et al. revealed that an ad-libitum low fat/high CHO diet induced a significant weight loss.91 It is worth mentioning that many of the studies examining the effects of a low fat/high CHO diet on body weight regulation observed a reduction in energy intake, even though energy reduction was never intended.92,91 Thus, one advantage of the high CHO diets is lowered energy intake due to low energy density in this type of diet.

However, not all studies have reported a greater weight loss for individuals on high CHO diets as compared to those on conventional low caloric diets or low CHO diets.61 Nordmann et al. analyzed five randomized clinical trials comparing low CHO versus high CHO diets. They concluded that after 6 months, individuals randomized to the low CHO diet lost more weight than those randomized to low fat/high CHO diet.93 Nevertheless, the difference between the diets disappeared at the end of 1 year.

The major focus of this dietary approach is to focus on the "type" of calories and "caloric density" rather than "counting total calories" directly. The focus is really based on the promotion of eating more high complex carbohydrates and high fiber foods to lose weight—specially to eat more fruits, vegetables, whole grains, and beans, while trying to omit sugar and white flour (note: Ornish's diet is vegetarian, while Pritikin allows for a limited amount of low fat animal protein daily: no more than 3.5 ounces/day).94 Foods high in fruits and vegetables are usually low in energy density.95 The energy densities of foods have been shown to be associated with body weight and BMI.95,96 It has been reported that overweight subjects who consume a low fat, high CHO diet do eat fewer calories and lose weight and body fat.68,90, 97-99 Nevertheless, Raben et al.100 and Prewitt et al.101 both reported that the consumption of a low fat diet resulted in an increase in caloric intake but a decrease in body weight. Hays et al.102 reported that a diet rich in complex carbohydrates resulted in an increase in lean body mass and a decrease in fat mass among 34 subjects with impaired glucose tolerance.

The Iowa Women's Health Study has observed that postmenopausal women who were less overweight and consumed less fat had higher rate of survival after breast cancer diagnosis than those who were overweight and consuming higher fat.103 In order to evaluate the efficacy of a low fat/high complex CHO diet on breast cancer recurrence, two multicenter randomized controlled trials of dietary interventions have been funded by the National Cancer Institute: the Women's Intervention Nutrition Study (WINS) and the Women's Healthy Eating and Living Study (WHELS). The Women's Healthy Eating and Living Study is a part of the Women's Health Initiative. The WINS study was designed to investigate the effects of reducing dietary fat intake with adjuvant systemic therapy on cancer recurrence rates in postmenopausal women with early stage, surgically treated breast cancer.104 The primary aim of the WHELS is to evaluate the effects of a high-vegetable, low fat diet in reducing breast cancer recurrence and mortality.105 Although weight loss was not the goal of these programs, some weight loss in the intervention groups have been observed in some reports106,107 although not in others.43,44

There have been concerns regarding the impact of the consumption of high CHO, low fat diets on blood glucose, lipids, insulin, and leptin levels. Most studies have reported that these diets usually result in decreased energy intake, blood glucose, and insulin levels.84,88,108,109 The effects of high CHO diets on blood lipid levels are controversial. Gerhard et al. reported that a low fat/high CHO diet significantly reduced body weight as compared to a diet high in monounsaturated fat diet. However, there was no difference between these diets in the levels of blood lipids nor in glycemic control and insulin sensitivity.110 On the other hand, high CHO diets have been reported to increase blood triglyceride levels.61,62,68 Noakes et al. reported that individuals on an energy-restricted, high-protein diet had metabolic profiles as good as or even better than those on a high CHO diet.109 Kasim-Karakas et al. observed that when individuals on an high CHO diet ad-libitum, they lost weight but maintained their normal blood triglyceride levels.99 However, when individuals were put on an euenergetic high CHO diet to maintain their body weight, their blood triglyceride levels elevated. Similar findings have been noticed by others. Schaefer et al. reported that effects of a high CHO diet on blood lipid levels were related to the body weight change.111 When body weight was kept constant, the high CHO diet lowered total cholesterol, LDL-C, and HDL-C, as well as elevated triglyceride levels. When the high CHO diet was consumed ad-libitum, these individuals lost weight and lowered their LDL-C without any adverse effects on blood triglyceride levels and TC/HDL-C ratios.111 Thus, the effects of high CHO diets can be modulated by the energy intake or body weight change.

Many of the controversies regarding the effects of high CHO diets on blood lipid levels may also be related to the CHO used. When high CHO diets are high in fruits and vegetables (and thus are high in fiber), the diet's adverse effects on blood lipid levels may be alleviated.112,113 Many of the "low fat" food products on the market, on the other hand, are high in simple CHO, as demonstrated in Table 2.

Table 2. Energy and Macronutrient Content of Regular and Fat-Reduced Peanut Butter of a National Brand (Serving Size: 2 Tablespoons)

Regular fat

Reduced fat

Energy (kcal)



Fat (g)



Fat (kcal)



Carbohydrate (g)



Sugar (g)



Protein (g)



With the added simple CHO, there is no reduction in caloric content, even though the fat content is reduced. The added simple CHO also elevates blood lipid levels. Thus, these "reduced-fat" products offer no health benefits. Considering the fact that the current dietary guidelines for cancer prevention include a high consumption of fruits and vegetables and a reduced intake of fat,114 the low fat, high CHO diets rich in fruits and vegetables should also be recommended for cancer survivors and for all individuals in order to reduce the risks for other chronic diseases.

Studies investigating the satiety of high CHO, low fat diets have reported that low fat diets received higher hedonic ratings compared to high-fat diets.98 The exposure to high CHO containing foods can result in a marked restraining effect on the expression of appetite.115

There are data to support that individuals who consume a low fat, high CHO diet are perhaps more successful at maintaining weight loss.116-118 The responses of insulin and leptin levels to dietary CHO may play a role in the weight-maintaining effects of these dietary regimens. Weigle et al.119 have reported that there was no difference in the area under the curve (AUC) for blood leptin levels between high CHO and low CHO diet consumption in the short-term. However, after 12 weeks on the high CHO diet, the AUC for leptin in that group was significantly higher than that observed for the low CHO diet. Therefore, one of the mechanisms for the maintenance of weight loss in high CHO diets may be attributed to the elevated leptin levels.

5.3. Balanced, Energy-Reduced Diets

Diets in this category are represented by the Dietary Approaches for the Stop of Hypertension (DASH) diet,120 the National Cholesterol Education Program Step I Diet (NCEP),121 and the 2002 National Academy of Science's Institute of Medicine (IOM) dietary guidelines.122 Several studies have reported that total caloric content was more important than diet composition for weight loss,123,124 and the percent of calories from fat (15-35%) did not seem to influence the amount of weight loss. Based on the analysis of four popular diets with very different diet compositions by Dansinger et al.,69 it is apparent that there is not one specific macronutrient that induces weight loss. Rather, it is the reduction in total energy intake and the degree of adherence to the diet that produces the weight loss. Without reduction in energy intake, even diets with high fruits and vegetable content would not achieve weight loss.43,44 The best strategy to reduce energy intake is to reduce portion size and to reduce the consumption of energy-dense foods.

Since the degree of adherence determines the amount of weight loss, the best diet to reduce body weight would be a diet that is nutritionally balanced and easy

Nutrition and Weight Management in Cancer Survivors 277 Table 3. Low-Calorie Step I Diet to Reduce Body Weight in Obese Individuals125


Recommended intake

Calories Total fat

Saturated fatty acids

Monounsaturated fatty acids

Polyunsaturated fatty acids




Sodium chloride

Calcium Fiber

Approximately a 500 to 1000 kcal/day reduction from usual intake 30% or less

8-10% of total calories Up to 15% of total calories Up to 10% of total calories <300 mg/day

Approximately 15% of total calories 55% or more of total calories

No more than 1000 mmol/mol/day (approximately 2.4 g of sodium or 6 g sodium chloride) 1000-1500 mg/day 20-30 mg/day to adhere to for long periods of time. A diet that severely restricts one type of food to the extreme may produce desired short-term weight loss, but long-term success may be difficult to achieve.69 Dietary recommendations for weight loss should be based on the "Clinical Guidelines on the Identification, Evaluation, and Treatment of Overweight and Obesity in Adults."125 The key element of these guidelines is the use of a moderate decrease in caloric intake to achieve a slow but progressive weight loss. The dietary composition goals of these guidelines are shown in Table 3. Another recommendation for a balanced, low-energy diet plan is the USDA's Dietary Guidelines for Americans 2005 (http:,/ which include adopting a balanced eating plan based on the USDA Food Guide or the DASH eating plan (Table 4). The DASH diet emphasizes fruits, vegetables, and low fat dairy products. American Institute for Cancer Research also established "AICR Diet and Health Guidelines for Cancer Prevention" which again emphasizes choosing plant-based diet plans, consuming plenty of fruits and vegetables, and maintaining a healthy body weight, among other recommendations (http:,/,

From the research evidence collected thus far, it is clear that in order to prevent cancer occurrence/recurrence, maintaining a healthy body weight and consuming enough fresh fruits and vegetables are critical. Therefore, the optimal dietary plan would be to follow the NCEP's Step I diet plan. The goals of this diet plan are as follows.

Table 4. The DASH Diet Recommendations

Type of food Number of servings for 1600-3100 kcal diets

Grains and grain products (include at least three 6-12

whole grain foods each day)

Fruits 4-6

Vegetables 4-6

Low fat or nonfat dairy foods 2-4

Lean meats, fish, poultry 1.5-2.5

Nuts, seeds, and legumes 3-6 per week

Fats and sweets 2-4

(1) To reduce energy intake. By reducing energy intake by 500 kcal to 1000 kcal, a weight loss of 1 to 2 lb/week will be produced, since a pound of fat is about 3500 kcal. This reduction in energy intake can be easily achieved by reducing the portion size without any major alteration in eating plan. The portion sizes for commonly consumed foods are presented in Table 5.

(2) To reduce daily fat intake to about 30% of energy intake, to replace saturated fatty acids with mono or polyunsaturated fatty acids, and to reduce cholesterol intake. It has been shown that not only the quantity but also the quality of dietary fat is important for general health. Saturated fats and trans fats are associated with hyperinsulinemia and insulin resistance, which could in turn increase the risk for cancer.126,127 Omega-3 («-3) fatty acids improve insulin sensitivity, and thus may reduce cancer risk.128,129 However, a recent meta-analysis of the effects of dietary fatty acids on cancer risks showed no consistent connection between «-3 fatty acids and cancer incidence.130 Nevertheless, considering the fact that cancer patients are at higher risk of other chronic diseases and ^-3 fatty acids are known to be protective of cardiovascular diseases,127,131 replacing saturated fatty acids with ^-3 fatty acids may still be advisable. Foods rich in ^-3 fatty acids are fatty fish such as mackerel, salmon, herring, tuna, as well as canola and soybean oils, walnuts, flaxseeds.

Table 5. USDA's Daily Food Guide and Serving Sizes134

Bread, Cereals, and other grain products: 6 to 11 servings/day

One serving: 1 slice bread t/2 cup cooked cereal, rice or pasta (looks like / baseball) 1 oz ready-to-eat cereal V2 bun, bagel or English muffin 1 small roll, biscuit, or muffin

3 to 4 small or 2 large crackers

Vegetables: 3 to 5 servings/day

One serving: 1/2 cup cooked or raw vegetables (looks like 1/2 baseball or rounded handful for adult) 1 cup leafy raw vegetable (looks like 1 baseball or fist of an average adult)

1/2 cup cooked legumes 3/4 cup vegetable juice

Fruits: 2 to 4 servings/day

One serving: 1 medium apple, banana, or orange (looks like a baseball) 1/2 grape fruit

1 melon wedge

3/4 cup juice 1/2 cup berries

1/2 cup diced, cooked, or canned fruit 1/4 cup dried fruit (looks like 1 golf ball)

Meat, poultry, fish, and alternates: 2 to 3 servings/day

One serving: 2 to 3 oz lean, cooked meat, poultry, or fish (looks like a deck of cards) 1 egg

1/2 cup cooked legumes (looks like 1/2 baseball)

4 oz tofu

1/3 cup nuts or seeds (level handful for average adult)

2 tablespoons peanut butter (as 1 oz meat, look like a marshmallow)

Milk, cheese, and yogurt: 2 servings/day

One serving: 1 cup milk or yogurt

2 oz processed cheese food 1 1/2 oz cheese (1 oz looks like 4 dice)

(3) To consume plant-based protein and lean meats as the main protein source of the diet. These types of foods contain no or low amount of cholesterol and saturated fatty acids. They not only provide adequate amount of protein, but also reduce the risk of cardiovascular disease and cancers.

(4) To use complex carbohydrates, such as fruits, vegetables, and whole grains as the carbohydrate sources as suggested for the DASH diet.125 These complex carbohydrates contain not only adequate amounts of fibers, but also micronutrients that have been shown to reduce cancer risk.129 These micronutrients include vitamins C and E, folate, carotinoids, calcium, and phytochemicals. Consuming whole foods is preferable over supplements, since the micronutrients in whole foods may have synergistic effects to provide maximal protection. Foods rich in the colors red (tomatoes, red peppers, red onions, beets, strawberries, raspberries, watermelon, etc), green (broccoli, green leafy vegetables, green pepper, green grapes, honey dew, etc), blue/purple (blueberries, blackberries, eggplant, purple grapes, etc), orange/yellow (carrots, pumpkin, sweet corn, butternut squash, sweet potatoes, oranges, cantaloupes, nectarines, papayas, etc) and white (cauliflower, onions, garlic, potatoes, mushrooms, pears, bananas, etc) are the best sources of these mi-cronutrients and are strongly recommended to reduce the risk of cancer occurrence and recurrence. For more detailed fruit and vegetable choices, please visit If fresh fruits and vegetables are not readily available, frozen or canned varieties are suitable substitutes.132 For some cancer survivors with compromised immune systems, consuming raw vegetables may not be advisable132 because the pathogens attached to these foods may increase the risk of infection.

In summary, evidence suggests that in order to reduce the risk of cancer recurrence, cancer survivors should try to maintain a healthy body weight. Obese cancer survivors should follow the NCEP's Step I diet to reduce energy intake and thus body weight. Following the DASH diet simultaneously will ascertain that adequate fruits and vegetables are consumed to take advantage of the phytochemicals and dietary fibers contained in this type of diet in order to reduce the risk of cancer occurrence/recurrence.

The other side of the equation for body weight regulation is energy expenditure. The major components of energy expenditure are basal metabolic rate, the thermic effects of foods (energy used to process food consumed), and physical activity. The only component of energy expenditure that individuals have control over is physical activity. How physical activity can reduce the risk of cancer and prevent cancer recurrence is presented in Chapter 15 of this book.


Major strides have been made in identifying the mechanisms of carcinogenesis and effective treatment regimens. Coupled with early detection, cancer mortality rates have been declining continuously.133 As a result, the number of cancer survivors has increased significantly. However, there are major gaps in the knowledge regarding the long-term efficacy of dietary regimen to prevent cancer recurrence and/or prolong cancer-free life. Future research in nutrition and cancer survivors should be focused on the following as summarized in Table 6.

Table 6. Future Research Needs for Cancer Survivors


To collect long-term data from dietary intervention trials

To develop plans to disseminate nutrition knowledge about high CHO/lowfat diets

To establish policies to make fresh fruits and vegetables and whole grain foods available and affordable

To encourage a healthy lifestyle


To establish that Step 1 diet and DASH diet are effective in weight loss and maintenance, and in preventing cancer occurrence/recurrence To make general public and cancer survivors aware the health benefits of the high CHO/low fat diets and how to adhere to these dietary plans To make fresh fruits, vegetables and whole grain foods the major component of daily meals

To use nutritional and behavioral strategies to reduce the risk of cancer occurrence/recurrence

(1) Collecting data from long-term dietary intervention trials to further establish the efficacy of Step I diet plus DASH diet (low fat/high CHO rich in complex CHO) in cancer survivors (as well as general public) on reducing body weight and maintaining the weight loss, as well as on preventing cancer recurrence. These dietary plans have to be innovative and easy to follow so individuals can adhere to them for a lifetime. The AICR's "The New American Plate" ( is one of the fresh and easy ways to help individuals to consume more plant-based foods.

(2) Developing plans to disseminate knowledge regarding the health benefits of high CHO/low fat diets to general public, especially to cancer survivors.

(3) Establishing policies to make fresh fruits and vegetables, and whole grain foods readily available and affordable to the general public.

(4) Encouraging cancer survivors and general public to follow a healthy lifestyle, including maintaining a healthy body weight, consuming a balanced, plant-based diet with reduced energy intake, and engaging in daily physical activities.

Since the Step I diet and DASH diet have been proven to be safe and less expensive than drugs, consuming these diets may prove to be a viable alternative for reducing the risk of cancer occurrence/recurrence.


1. Flegal, K., Carroll, M., Ogden, C., and Johnson, C. Prevalence and trends in obesity among US adults, 1999-2000. JAMA 2002; 288: 1723-7.

2. Bray, G. Medical consequences of obesity. J. Clin. Endocrinol. Metab. 2004; 89: 2583-9.

3. Lukanova, A., Bjor, O., Kaaks, R., et al. Body mass index and cancer: Results from the Northern Sweden Health and Disease Cohort. Int. J. Cancer 2006; 118: 458-66.

4. Bianchini, F., Kaaks, R., and Vainio, H. Overweight, obesity, and cancer risk. Lancet Oncol. 2002; 3: 565-74.

5. Clemons, M., and Goss, P. Estrogen and the risk of breast cancer. N. Engl. J. Med. 2001; 344: 276-85.

6. Key, T. Serum oestradiol and breast cancer risk. Endocrinol. Relat. Cancer 1999; 6: 175-80.

7. Reaven, G. Are insulin resistance and/or compensatory hyperinsulinemia involved in the etiology and clinical course of patients with hypertension? Int. J. Obes. 1995; 19(Suppl 1): S2-5.

8. Kaaks, R., Lukanova, A., and Kurzer, M. Obesity, endogenous hormones, and endometrial cancer risk: A synthetic review. Cancer Epidemiol. Biomarkers Prev. 2002; 11: 1531-43.

9. Khandwala, H., McCutcheon, I., Flyvbjerg, A., and Friend, K. The effects of insulin-like growth factors on tumorigenesis and neoplastic growth. Endocr. Reb. 2000; 21: 215-44.

10. Hammarsten, J., and Hogstedt, B. Hyperinsulineaemia: A prospective risk factor for lethal clinical prostate cancer. Eur. J. Cancer 2005; 41: 2887-95.

11. Persson, I. Estrogens in the causation of breast, endometrial and ovarian cancers: Evidence and hypotheses from epidemiological findings. J. Steroid Biochem. Mol. Biol. 2000; 74: 357-64.

12. Giovannucci, E. Insulin, insulin-like growth factors and colon cancer: A review of the evidence. J. Nutr. 2001; 131: 3109S-3120S.

13. Morita, T., Tabata, S., Mineshita, M., Mizoue, T., Moore, M., and Kono, S. The metabolic syndrome is associated with increased risk of colorectal adenoma development: The Self-Defense Forces Health Study. Asian Pac. J. Cancer Prev. 2005; 6: 485-9.

14. Furberg, A.-S., Veierod, M. Wilsgaard, T., Bernstein, L., andThune, I. Serum high-density lipoprotein cholesterol, metabolic profile, and breast cancer risk. J. Natl. Cancer Inst. 2004; 96: 1152-60.

15. Furberg, A.-S.,Jasienska, G., Bjurstam, N., etal. Metabolic and hormonal profiles: HDL cholesterol as a plausible biomarker of breast cancer risk. The Norwegian EBBA Study. Cancer Epidemiol. Biomarkers Prev. 2005; 14: 33-40.

16. Ray, G., and Husain, S. Role of lipids, lipoproteins and vitamins in women with breast cancer. Clin. Biochem. 2001; 34: 71-6.

17. Caro,J., Sinha, M., Kolaczynski, J., Zhang, P., and Considine, R. Leptin: The tale of an obesity gene. Diabetes 1996; 45: 1455-62.

18. Considine, R., Sinha, M., Heiman, M., etal. Serum immunoreactive-leptin concentrations in normal-weight and obese humans. N. Eng. J. Med. 1996; 334: 292-5.

19. Sierra-Honigmann, M., Nath, A., Murakami, C., et al. Biological action of leptin as an angiogenic factor. Science 1998; 281: 1683-6.

20. Bouloumie, A., Drexler, H., Lafontan, M., and Busse, R. Leptin, the product ofOb gene, promotes angiogenesis. Circ. Res. 1998; 83: 1059-66.

21. Ribeiro, R., Lopes, C., and Medeiros, R. The link between obesity and prostate cancer: The leptin pathway and therapeutic perspectives. Prostate Cancer Prostatic Dis. 2006; 9: 19-24.

22. Stattin, P., Soderberg, S., Hallmans, G., et al. Leptin associated with increased prostate cancer risk: A nested case-referent study. J. Clin. Endocrinol. Metab. 2001; 86: 1341-5.

23. Cleary, M., Phillips, F., Getzin, S., etal. Genetically obese MMTV-TGF-alpha/Lep(ob)Lep(ob) female mice do not develop mammary tumors. Breast Cancer Res. Treat. 2003; 77: 205-15.

24. Ishikawa, M., Kitayama, J., and Nagawa, H. Enhanced expression of leptin and leptin receptor (OB-R) in human breast cancer. Clin. Cancer Res. 2004; 10: 4325-31.

25. Hardwick, J., Van Den Brink, G., Offerhaus, G., Van Deventer, S., Peppelenbosch, M. Leptin is a growth factor for colonic epithelial cells. Gastroenterology 2001; 121: 79-90.

26. Garofalo, C., and Surmacz, E. Leptin and cancer. J. Cell Physiol. 2006; 207: 12-22.

27. Goodwin, P., and Boyd, N. Body size and breast cancer prognosis: A critical review of the evidence. Breast Cancer Res. Treat. 1990; 16: 205-14.

28. Rock, C., and Demark-Wahnefried, W. Nutrition and survival after the diagnosis of breast cancer: A reveiwof the evidence. J.Clin. Oncol. 2002; 20: 3302-16.

29. Bastarrachea, J., Hortobagyi, G., Smith, T., Kau, S.-W, and Buzdar, A. Obesity is an adverse prognostic factor for patients receiving adjuvant chemotherapy for breast cancer. Ann. Intern. Med. 1993; 119: 18-25.

30. Chlebowski, R., Aiello, E., and McTieman, A. Weight loss in breast cancer patient management. J.Clin. Oncol. 2002; 20: 1128-43.

31. Ballard-Barbash, R. Anthropometry and breast cancer. Cancer 1994; 74: 1090-1100.

32. Amling, C. The association between obesity and the progression of prostate and renal cell carcinoma. Urol. Oncol. 2004; 22: 478-84.

33. Kroenke, C., Chen, W., Rosner, B., and Holmes, M. Weight, weight gain, and survival after breast cancer diagnosis. J. Clin. Oncol. 2005; 23: 1345-7.

34. Calle, E., Rodriquez, C., Walker-Thurmond, K., and Thun, M. Overweight, obesity and mortality from cancer in a prospectively studied cohort of US adults. N. Engl. J. Med. 2003; 348: 162538.

35. Demark-Wahnefried, W., Rimer, B., and Winer, E. Weight gain in women diagnosed with breast cancer. J.Am. Diet. Assoc. 1997; 97: 519-29.

36. Chlebowski, R., Weiner, J., Reynolds, R., Luce, J., Bulcavage, L., and Bateman, J. Long-term survival following relapse after 5-FU but not CMF adjuvant breast cancer therapy. Breast Cancer Res. Treat. 1986; 7: 23-9.

37. Caan, B., Sternfeld, B., Gunderson, E., Coates, A., Quesenberry, C.J., and Slattery, M. Life After Cancer Epidemiology (LACE) Study: A cohort of early stage breast cancer survivors (United States). Cancer Causes Control 2005; 16: 545-56.

38. Irwin, M., Crumley, D., McTiernan, A., et al. Physical activity levels before and after a diagnosis of breast carcinoma: The Health, Eating, Activity, and Lifestyle (HEAL) study. Cancer 2003; 97: 1746-57.

39. Rock, C., Mc Eligot, A., Flatts, S., et al. S. Eating pathology and obesity in women at risk for breast cancer recurrence. Int. J. Eat. Disord. 2000; 27: 172-9.

40. Demark-Wahnefried, W., Peterson, B., Winer, E., etal. Changes in weight, body composition, and factors in influencing energy balance among premenopausal breast cancer patients receiving adjuvant chemotherapy. J. Clin. Oncol. 2001; 19: 2381-9.

41. Aslani, A., Smith, R., Allen, B., Pavlakis, N., Levi, J. Changes in body composition during breast cancer chemotherapy with the CMF-regimen. Breast Cancer Res. Treat. 1999; 57: 285-90.

42. Pierce, J., Newman, V., Flatt, S., et al. Telephone counseling intervention increases intakes of micronutrient- and phytochemical-rich vegetables, fruit and fiber in breast cancer survivors. J.Nutr. 2004; 134: 452-8.

43. Thomson, C., Rocs Giuliano, A., Newton, T., Gui, H., Reid, P., Green, T., and Alberts, D. Women's Healthy Eating & Living Study Group. Longitudinal changes in body weight and body composition among women previously treated for breast cancer consuming a high-vegetable, fruit and fiber, low fat diet. Eur. J.Nutr. 2005; 44: 18-25.

44. Rock, C., Flatt, S., Thomson, C., et al. Effects of a high-fiber, low-fat diet intervention on serum concentrations of reproductive steroid hormones in women with a history of breast cancer. J. Clin. Oncol. 2004; 22: 2379-87.

45. Coups, E., and Ostroff, J. A population-bsed estimate of the prevalence of behavioral risk factors maong adult cancer surviviors and noncancer controls. Prev. Med. 2005; 40: 702-11.

46. Blanchard, C., Denniston, M., Baker, F., et al. Do adults change their lifestyle behaviors after a cancer diagnosis? Am. J. Health Behav. 2003; 27: 246-56.

47. Jen, K.-L.C., Djuric, Z., DiLaura, N., et al. Improvement of metabolism among obese breast cancer survivors in differing weight loss regimens. Obes. Res. 2004; 12: 306-12.

48. Djuric, Z., DiLaura, N., Jenkins, I., et al. Combining weight-loss counseling with Weight Watchers Plan for obese breast cancer survivors. Obes. Res. 2002; 10: 657-65.

49. Demark-Wahnefried, W., Aziz, N., Rowland, J., and Pinto, B. Riding the crest of the teachable moment: Promoting long-term health after the diagnosis of cancer. J. Clin. Oncol. 2005; 23: 581430.

50. Bray, G. Health hazards of obesity. Endocrinol. Metab. Clin. N. Am. 1996; 25: 907-19.

51. Goodrick, G., and Foreyt, J. Why treatment for obesity don't last? J. Am. Diet. Assoc. 1991; 91: 1243-7.

52. Lu, H., Buison, A., Uhley, V., Jen, K.-L.C. Long-term weight cycling in female Wistar rats: Effects on metabolism. Obes. Res. 1995; 3: 521-30.

53. Uhley, V., Pellizzon, M., Buison, A., Guo, F., Djuric, Z., Jen, K.-L. Chronic weight cycling increases oxidative DNA damage levels in mammary gland of female rats fed a high-fat diet. Nutr. Cancer 1997; 29: 55-9.

54. Djuric, Z., Heilbrun, L., Simon, M., et al. Levels of 5-hydroxymethly-2'-deoxyuridine in DAN from blood as a marker of breast cancer. Cancer 1996; 77: 691-6.

55. Buison, A., Pellizzon, M., Brogan, K., Baranes, M., Jen, K.-L.C. Weight cycling did not increase tumor incidence in high fat-fed rats treated with a low-dose 7,12-dimethylbenzyl(1)anthracene. Nutr. Res. 2005; 25: 1097-108.

56. Cleary, M., Jacobson, M., Phillips, F., Getzin, S., Grande, J., and Maihle, N. Weight-cycling decreases incidence and increases latency of mammary tumores to a greater extent than does chronic caloric restriction in mouse mammary tumor virus-transforming growth factor-a female mice. Cancer Epidemiol. Biomarkers Prev. 2002; 11: 836-43.

57. Atkins, R. Dr. Artkins'New Diet Revolution. Simon & Schuster: New York, 1998.

58. Steward, H., Bethea, M., Andrew, S., and Balart, L. Sugar Busters! Ballantine Books: New York, 1995.

59. Eades, M., and Eades, M. Protein Power. Bantam Books, NY, 1996.

60. Heller, R., and Heller, R. The Carbohydrate Addict's Diet. Penguin Books: New York, 1991.

61. Foster, G., Wyatt, H., Hill, J., et al. A randomized trial of a low-carbohydrate diet for obesity. N. Engl. J.Med. 2003; 348: 2082-90.

62. Stern, L., Iqbal, N., Seshadri, P., et al. The effects of low-carbohydrate versus conventional weight loss diets in severely obese adults: One-year follow-up of a randomized trial. Ann. Intern. Med. 2004; 140: 778-85.

63. Meckling, K., O'Sullivan, C., and Saari, D. Comparison of a low-fat diet to a low-carbohydrate diet on wieght loss, body composition, and risk factors for diabetes and cardiovascular disease in free-living, overweight men and women. J. Clin. Endocrinol. Metab. 2004; 89: 2717-23.

64. Astrup, A., Larsen, T., and Harper, A. Atkins and other low-carbohydrate diets: Hoax or an effective tool for weight loss? Lancet 2004; 364: 897-9.

65. St. Jeor, S., Howard, B., Prewitt, E., et al. Dietary protein and weight reduction. A statement for Healthcare Professionals from the Nutrition Committee of the Council on Nutrition, Physical Activity, and Metabolism of the American Heart Association. Circulation 2001; 104: 1869-74.

66. Nickols-Richardson, S., Coleman, M., Volpe, J., and Hosig, K. Perceived hunger is lower and weight loss is greater in overweight premenopausal women consuming a low-carbohydrate/high-protein vs high-carbohydrate/low-fat diet. J. Am. Diet Assoc. 2005; 105: 1433-7.

67. Blundell, J., and Macdiarmid, J. Fat as a risk factor for overconsumption: Satiation, satiety, and patterns of eating. J.Am. Diet Assoc. 1997; 97(Suppl): S63-S69.

68. Yancy, W.,Jr., Olsen, M., Guyton, J., Bakst, R., and Westman, E. A low-carbohydrate, ketogenic diet versus a low-fat diet to treat obesity and hyperlipidemia: A randomized, controlled trial. Ann. Intern. Med. 2004; 140: 769-77.

69. Dansinger, M., Gleason,J., Griffith, J., Selker, H., and Schaefer, E. Comparison of the Atkins, Omish, Weight Watchers, and Zone diets for weight loss and heart disease risk reduction. JAMA 2005; 293: 43-53.

70. Denke, M. Metabolic effects of high-protein, low-carbohydrate diets. Am. J. Cardiol. 2001; 88: 5961.

71. LaRosa,J., Gordon, A., Muesing, R., and Rosing, D. Effects of high-protein, low-carbohydrate dieting on plasma lipoproteins and body weight. J. Am. Diet Assoc. 1980; 77: 264-70.

72. Baron, J., Schori, A., Crow, B., Carter, R., and Mann, J. A randomized controlled trial of low carbohydrate and low fat/high fiber diets for weight loss. Am. J. Public Health 1986; 76: 1293-6.

73. Worthington, B., and Taylor, L. Balanced low-calorie vs high-protein-low carbohydrate reducing diets. II. Biochemical changes. J. Am. Diet. Assoc. 1974; 64: 52-5.

74. National Institutes ofHealth Consensus Development Panel. National Institute ofHealth Consensus Development Conference statement: Adjuvant therapy for breast cancer., November 1-2, 2000. J.Natl. Cancer Inst. Monogr. 2001; (30): 5-15.

75. Kayl, A., and Meyers, C. Side-effects of chemotherapy and quality of life in ovarian and breast cancer patients. Curr. Opin. Obstet. Gynecol. 2006; 18: 24-8.

76. Barzel, U., and Massey, L. Excess dietary protein can adversely affect bone. J.Nutr. 1998; 128:1051-3.

77. Theriault, R. Pathophysiology and implications of cancer treatment-induced bone loss. Oncology 2004; 18(Suppl 3): 11-15.

78. Jen, K.-L.C., Buison, A., Darga, L., and Nelson, D. The relationship between blood leptin levela nd bone density is specific to ethnicity and menopausal status. J. Lab. Clin. Med. 2005; 146: 18-24.

79. Yang, C., Kuroishi, T., Huang, X., Inoue, M., and Tajima, K. Correlation between food consumption and colorectal cancer: An ecological analysis in Japan. Asian Pac. J. Cancer Prev. 2002; 3: 77-83.

80. Handa, K., and Kreiger, N. Diet patterns and the risk of renal cell carcinoma. Public Health Nutr. 2002; 5: 757-67.

81. Nagle, C., Purdie, D., Webb, P., Green, A., Harvey, P., and Bain, C. Dietary influences on survival after ovarian cancer. Int. J. Cancer 2003; 106: 264-9.

82. Hewitt, M., Rowland, J., and Yancik, R. Cancer survivors in the United States: Age, health, and disability. J. Gerontol. A Biol. Sci. Med. Sci. 2003; 58: 82-91.

83. Pritikin, R. The New Pritikin Program. Simon & Schuster Inc.: New York, 1990.

84. Pritikin, R. The Pritikin Principle. Time Life Books: Alexandria, VA, 2000.

85. Ornish, D. Dr. Ornish's Program for Reversing Heart Disease. Ballentine Books: New York, 1990.

86. Ornish, D. Eat More, Weight Less. Harper Paperbacks: New York, 1993.

87. Barnard, R. Effects of life-style modification on serum lipids. Arch. Intern. Med. 1991; 151: 1389-94.

88. Barnard, R., Ugianskis, E., Martin, D. Inkel, S. Role of diet and exercise in the management of hyperinsulinemia and associated atherosclerotic risk factors. Am. J. Cardiol. 1992; 69: 440-4.

89. Ornish, D., Scherwitz, L.B., J.H., Brown S, et al. Intensive lifestyle changes for reversal of coronary heart disease. JAMA 1998; 280: 2001-7.

90. Havel, P., Kasim-Karakas, S., Mueller, W., Johnson, P., Gingerich, R., and Stern, J. Relationship of plasma leptin to plasma insulin and adiposity in normal weight and overweight women: Effects of dietary fat content and sustained weight loss. J. Clin. Endocrinol. Metab. 1996; 81: 4406-13.

91. Astrup, A., Grunwald, G., Melanson, E., Saris, W., and Hill, J. The role of low-fat diets in body weight control: A meta-analysis of ad libitum dietary intervention studies. Int. J. Obes. 2000; 24: 1545-52.

92. Lara-Castro, C., and Garvey, W. Diet, insulin resistance, and obesity: Zoning in on data for Atkins dieters living in South Beach. J. Clin. Endocrinol. Metab. 2004; 89: 4197-205.

93. Nordmann, A., Nordmann, A., Briel, M., et al. Effects of low-carbohydrate vs low-fat diets on weight loss and cardiovascular risk factors: A meta-analysis of randomized controlled trials. Arch. Intern. Med. 2006; 166: 285-93.

94. Schaefer, E., Gleason, J., and Dansinger, M. The effects oflow-fat, high-carbohydrate diets on plasma lipoprotein, weight loss, and heart disease risk reduction. Curr. Atheroscler. Rep. 2005; 7: 421-7.

95. Kant, A., and Graubard, B. Energy density of diets reproted by American adults: Association with food group intake, nutrient intake, and body weight. Int. J. Obes. Relat. Metab. Disord. 2005; 29: 950-6.

96. Drewnowski, A., Almiron-Roig, E., Marmonier, C., and Lluch, A. Dietary energy density and body weight: Is there a relationship? Nutr. Rev. 2004; 62: 403-13.

97. Powell, J., Tucker, L., Fisher, A., and Wilcox, K. The effects of different percentages of dietary fat intake, exercise, and calorie restriction on body composition and body weight in obese females. Am. J. Health Promot. 1994; 8: 442-8.

98. Djuric, Z., Uhley, V.D., Depp. J.B., Brooks, K., Lababidi, S., and Heilbrun, L. A clinical trial to selectively change dietary fat and/or energy intake in women: The Women's Diet Study. Nutr. Cancer 1999; 34: 27-35.

99. Kasim-Karakas, S., Almario, R., Mueller, W., and Peerson, J. Changes in plasma lipoproteins during low-fat, high-carbohydrate diets: Effects of energy intake. Am. J. Clin. Nutr. 2000; 71: 1439-47.

100. Raben, A., Jensen, N.D., Marckmann, P., Sandstrom, B., and Astrup, A. Spontaneous weight loss during 11 weeks' ad libitum intake of a low fat/high fiber diet in young, normal weight subjects. Int. J. Obes. 1995; 19: 916-23.

101. Prewitt, T., Schmeisser, D., Bowen, P., et al. Changes in body weight, body composition, and energy intake in women fed high- and low-fat diets. Am. J. Clin. Nutr. 1991; 54: 304-10.

102. Hays, N., Starling, R. Li, X., Sullivan, D., Trappe, T., Fluckey, J., and Evans, W. Effects of an ad libitum low-fat, high-carbohydrate diet on body weight, body composition, and fat distribution in older men and women: A randomized controlled trial. Arch. Intern. Med. 2004; 164: 210-17.

103. Zhang, S., Folsom, A., Sellers, T., Kushi, L., and Potter, J. Better breast cancer survival for post-menopausal women who are less overweight and eat less fat. Cancer 1995; 76: 275-83.

104. Chlebowski, R., Blackburn, G., Buzzard, I., etal. Adherence to dietary fat intake reduction program in postmenopausal women receiving therapy for early stage breast cancer. The Women's Intervention nutrition Study. J. Clin. Oncol. 1993; 11: 2072-80.

105. Pierce, J., Faerber, S., Wright, F., et al. A randomized trial of the effect of a plant-based dietary pattern on additional breast cancer events and survival: The Women's Healthy Eating and Living (WHEL) Study. Control Clin. Trials 2002; 23: 728-56.

106. Chlebowski, R., and Grosvenor, M. The scope of nutrition intervention trials with cancer-related endpoints. Cancer 1994; 74: 2734-8.

107. Kristal, A., Shattuck, A., Bowen, D., Sponzo, R., and Nixon, D. Feasibility of using volunteer research staff to deliver and evaluate a low-fat dietary intervention: The American Cancer Society Breast Cancer Dietary Intervention Project. Cancer Epidemiol. Biomarkers Prev. 1997; 6: 459-67.

108. Sargrad, K., Homko, C., Mozzoli, M., and Boden, G. Effect of high protein vs high carbohydrate intake on insulin sensitivity, body weight, hemoglobin A1C, and blood pressure in patients with type 2 diabetes mellitus. J.Am. Diet. Assoc. 2005; 105: 573-80.

109. Noakes, M., Leogh, J., Foster, P., and Clifton, P. Effect of an energy-restricted, high-protein, low-fat diet relative to a conventional high-carbohydrate, low-fat diet on weight loss, body composition, nutritional status, and markers of cardiovascular health in obese women. Am. J. Clin. Nutr. 2005; 81: 1298-1306.

110. Gerhard, G., Ahmann, A., Meeuws, K., McMurry, M., Duell, P., and Connor, W. Effects of a low-fat diet compared with those of a high-monounsaturated fat diet on body weight, plasma lipids and lipoproteins, and glycemic control in type 2 diabetes. Am. J. Clin. Nutr. 2004; 80: 668-73.

111. Schaefer, E., Lichtenstein, A., Lamon-Fava, S., i Body weight and low-density lipoprotein cholesterol changes after consumption of a low-fat ad libitum diet. JAMA 1995; 274: 1450-5.

112. Wolever, T., andMehling, C. High-carbohydrate-low-glycaemic index dietary advice improves glucose disposition index in subjects with imparied glucose tolearnce. Br. J. Nutr. 2002; 87: 477-87.

113. Anderson, J., Chen, W., and Sieling, B. Hypolipidemic effect of high-carbohydrate, high-fiber diet. Metabolism 1980; 29: 827-31.

114. Byers, T., Nestle, M., McTieman, A., et al. American cancer Society guidelines on nutrition and physical activity for cancer prevention: Reducing the risk of cancer with healthy food choices and physical activity. CA Cancer J. Clin. 2002; 52: 92-119.

115. Blundell, J., Green, S., and Burley, V. Carbohydrates and human appetite. Am. J. Clin. Nutr. 1994; 59(Suppl 3): 728S-734S.

116. McGuire, M., Wing, R., Klem, M., and Hill, J. Behavioral strategies of individual who have maintained long-term weight losses. Obes. Res. 1999; 7: 334-41.

117. Leser, M., Yanovski, S.Y., and Janovski, A. A low-fat intake and greater activity level are associated with lower weight regain 3 years after completing a very-low-calorie diet. J. Am. Diet. Assoc. 2002; 102: 1252-6.

118. Wing, R., and Phelan, S. Long-term weight loss maintenance. Am. J. Clin. Nutr. 2005; 82(1 Suppl): 222S-225S.

119. Weigle, D., Cummings, D.N., Newby, P.D., Breen, P., Frayo, R., Matthys, C.C., H.S., and Purnell, J. Roles of leptin and ghrelin in the loss of body weight casued by a low fat, high carbohydrate diet. J. Clin. Endocrinol. Metab. 2003; 88: 1577-86.

120. Appel, L., Moore, T., Obazanek, E., et al. A clinical trial of the effects of dietary patterns on blood pressure. DASH Collaborative Research Group. N. Engl. J. Med. 1997; 336: 1117-24.


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