Intake of macronutrients as predictors of 5-y changes in waist circumference.

Abstract

BACKGROUND:

The diet may influence the development of abdominal obesity, but the few studies that have prospectively examined the relations between diet and changes in waist circumference (WC) have given inconsistent results.

OBJECTIVE:

Associations between total energy intake, energy intake from macronutrients, and energy intake from macronutrient subgroups based on different food sources and 5-y differences in WC (DWC) were investigated.

DESIGN:

A Danish cohort of 22 570 women and 20 126 men aged 50-64 y with baseline data on WC, diet, BMI, and potential confounders reported their WC 5 y later. Associations of baseline diet with DWC were assessed by multiple linear regression analysis.

RESULTS:

Neither total energy intake nor energy intake from each of the macronutrients was associated with DWC, except for an inverse association with protein, especially animal protein. In women, positive associations with DWC were seen for carbohydrate from refined grains and potatoes and from foods with simple sugars, whereas carbohydrate from fruit and vegetables was inversely associated and significantly different from any other carbohydrate subgroup. The results for men resembled those for women, although none were significant. Vegetable fat was positively associated with DWC for both men and women in a combined analysis. A U-shaped association between alcohol from wine and DWC was present for both sexes, and alcohol from spirits was positively associated with DWC in women.

CONCLUSIONS:

Although no significant associations with total energy or energy from fat, carbohydrate, or alcohol were observed, protein intake was inversely related to DWC, and some macronutrient subgroups were significantly associated with DWC.

Quality protein intake is inversely related with abdominal fat

Abstract

Dietary protein intake and specifically the quality of the protein in the diet has become an area of recent interest. This study determined the relationship between the amount of quality protein, carbohydrate, and dietary fat consumed and the amount of times the ~10 g essential amino acid (EAA) threshold was reached at a meal, with percent central abdominal fat (CAF). Quality protein was defined as the ratio of EAA to total dietary protein. Quality protein consumed in a 24-hour period and the amount of times reaching the EAA threshold per day was inversely related to percent CAF, but not for carbohydrate or dietary fat. In conclusion, moderate to strong correlations between variables indicate that quality and distribution of protein may play an important role in regulating CAF, which is a strong independent marker for disease and mortality.

Introduction

Dietary protein intake and specifically the quality of the protein in the diet has become an area of recent interest, particularly when combined with resistance training (for a thorough review the reader is directed to ref. [1]). Quality of protein is defined as the ratio of essential amino acids (EAA) to dietary protein in grams. The dietary reference intake (DRI) includes no specific recommendation regarding the type of dietary protein consumed or distribution of that dietary protein throughout the day. Approximately 10 g of EAA, at a meal, maximally stimulates muscle protein synthesis (MPS) [2]. EAA intake beyond this level does not appear to result in an additional anabolic response [3].

Studies have demonstrated that the consumption of dietary protein above the DRI has been associated with favorable changes in body composition [4]. Proposed mechanisms include the maintenance or accretion of lean mass and/or increased thermogenesis and satiety [5]. A 5-year prospective study found that protein intake was inversely related to changes in waist circumference [6]. Waist circumference is a surrogate marker for abdominal obesity, and this type of obesity is associated with significant risks of developing type 2 diabetes, coronary artery disease, stroke, and a higher risk of mortality, even after adjustments for general obesity [6]. However, the quality of the protein source consumed and the distribution of that protein throughout the day with respect to central abdominal fat (CAF) have not been investigated in free living conditions.

We sought to determine the relationship between the amount of quality protein consumed in 24-hours and the amount of times the ~10 g EAA threshold was reached at a meal, with respect to percent CAF. This is a secondary analysis using a data set from a previously reported paper on quality protein, overall body composition (lean mass and total body fat), and bone health [7].

Weight loss maintenance in overweight subjects on ad libitum diets with high or low protein content and glycemic index: the DIOGENES trial 12-month results

Abstract

BACKGROUND:

A high dietary protein (P) content and low glycemic index (LGI) have been suggested to be beneficial for weight management, but long-term studies are scarce.

OBJECTIVE:

The DIOGENES randomized clinical trial investigated the effect of P and GI on weight loss maintenance in overweight or obese adults in eight centers across Europe. This study reports the 1-year results in two of the centers that extended the intervention to 1 year.

METHOD:

After an 8-week low-calorie diet (LCD), 256 adults (body mass index >27 kg m(-)(2)) were randomized to five ad libitum diets for 12 months: high P/LGI (HP/LGI), HP/high GI (HP/HGI), low P/LGI (LP/LGI), LP/HGI and a control diet. During the first 6 months, foods were provided for free through a shop system and during the whole 12-month period, subjects received guidance by a dietician. Primary outcome variable was the change in body weight over the 12-month intervention period.

RESULTS:

During the LCD period, subjects lost 11.2 (10.8, 12.0) kg (mean (95% confidence interval (CI))). Average weight regain over the 12-month intervention period was 3.9 (95% CI 3.0-4.8) kg. Subjects on the HP diets regained less weight than subjects on the LP diets. The difference in weight regain after 1 year was 2.0 (0.4, 3.6) kg (P=0.017) (completers analysis, N=139) or 2.8 (1.4, 4.1) kg (P<0.001) (intention-to-treat analysis, N=256). No consistent effect of GI on weight regain was found. There were no clinically relevant differences in changes in cardiometabolic risk factors among diet groups.

CONCLUSION:

A higher protein content of an ad libitum diet improves weight loss maintenance in overweight and obese adults over 12 months.

High protein intake sustains weight maintenance after body weight loss in humans

Abstract

BACKGROUND:

A relatively high percentage of energy intake as protein has been shown to increase satiety and decrease energy efficiency during overfeeding.

AIM:

To investigate whether addition of protein may improve weight maintenance by preventing or limiting weight regain after weight loss of 5-10% in moderately obese subjects.

DESIGN OF THE STUDY:

In a randomized parallel design, 148 male and female subjects (age 44.2 +/- 10.1 y; body mass index (BMI) 29.5 +/- 2.5 kg/m2; body fat 37.2 +/- 5.0%) followed a very low-energy diet (2.1 MJ/day) during 4 weeks. For subsequent 3 months weight-maintenance assessment, they were stratified according to age, BMI, body weight, restrained eating, and resting energy expenditure (REE), and randomized over two groups. Both groups visited the University with the same frequency, receiving the same counseling on demand by the dietitian. One group (n=73) received 48.2 g/day additional protein to their diet. Measurements at baseline, after weight loss, and after 3 months weight maintenance were body weight, body composition, metabolic measurements, appetite profile, eating attitude, and relevant blood parameters.

RESULTS:

Changes in body mass, waist circumference, REE, respiratory quotient (RQ), total energy expenditure (TEE), dietary restraint, fasting blood-glucose, insulin, triacylglycerol, leptin, beta-hydroxybutyrate, glycerol, and free fatty acids were significant during weight loss and did not differ between groups. During weight maintenance, the 'additional-protein group' showed in comparison to the nonadditional-protein group 18 vs 15 en% protein intake, a 50% lower body weight regain only consisting of fat-free mass, a 50% decreased energy efficiency, increased satiety while energy intake did not differ, and a lower increase in triacylglycerol and in leptin; REE, RQ, TEE, and increases in other blood parameters measured did not differ.

CONCLUSION:

A 20% higher protein intake, that is, 18% of energy vs 15% of energy during weight maintenance after weight loss, resulted in a 50% lower body weight regain, only consisting of fat-free mass, and related to increased satiety and decreased energy efficiency.

A high-protein diet induces sustained reductions in appetite, ad libitum caloric intake, and body weight despite compensatory changes in diurnal plasma leptin and ghrelin concentrations

Abstract

Background: Ad libitum, low-carbohydrate diets decrease caloric intake and cause weight loss. It is unclear whether these effects are due to the reduced carbohydrate content of such diets or to their associated increase in protein intake.

Objective: We tested the hypothesis that increasing the protein content while maintaining the carbohydrate content of the diet lowers body weight by decreasing appetite and spontaneous caloric intake.

Design: Appetite, caloric intake, body weight, and fat mass were measured in 19 subjects placed sequentially on the following diets: a weight-maintaining diet (15% protein, 35% fat, and 50% carbohydrate) for 2 wk, an isocaloric diet (30% protein, 20% fat, and 50% carbohydrate) for 2 wk, and an ad libitum diet (30% protein, 20% fat, and 50% carbohydrate) for 12 wk. Blood was sampled frequently at the end of each diet phase to measure the area under the plasma concentration versus time curve (AUC) for insulin, leptin, and ghrelin.

Results: Satiety was markedly increased with the isocaloric high-protein diet despite an unchanged leptin AUC. Mean (±SE) spontaneous energy intake decreased by 441 ± 63 kcal/d, body weight decreased by 4.9 ± 0.5 kg, and fat mass decreased by 3.7 ± 0.4 kg with the ad libitum, high-protein diet, despite a significantly decreased leptin AUC and increased ghrelin AUC.

Conclusions: An increase in dietary protein from 15% to 30% of energy at a constant carbohydrate intake produces a sustained decrease in ad libitum caloric intake that may be mediated by increased central nervous system leptin sensitivity and results in significant weight loss. This anorexic effect of protein may contribute to the weight loss produced by low-carbohydrate diets.

Postprandial thermogenesis is increased 100% on a high-protein, low-fat diet versus a high-carbohydrate, low-fat diet in healthy, young women.

Abstract

OBJECTIVE:

The recent literature suggests that high-protein, low-fat diets promote a greater degree of weight loss compared to high-carbohydrate, low-fat diets, but the mechanism of this enhanced weight loss is unclear. This study compared the acute, energy-cost of meal-induced thermogenesis on a high-protein, low-fat diet versus a high-carbohydrate, low-fat diet.

METHODS:

Ten healthy, normal weight, non-smoking female volunteers aged 19-22 years were recruited from a campus population. Using a randomized, cross-over design, subjects consumed the high-protein and the high-carbohydrate diets for one day each, and testing was separated by a 28- or 56-day interval. Control diets were consumed for two days prior to each test day. On test day, the resting energy expenditure, the non-protein respiratory quotient and body temperature were measured following a 10-hour fast and at 2.5-hour post breakfast, lunch and dinner. Fasting blood samples were collected test day and the next morning, and complete 24-hour urine samples were collected the day of testing.

RESULTS:

Postprandial thermogenesis at 2.5 hours post-meal averaged about twofold higher on the high protein diet versus the high carbohydrate diet, and differences were significant after the breakfast and the dinner meals (p < 0.05). Body temperature was slightly higher on the high protein diet (p = 0.08 after the dinner meal). Changes in the respiratory quotient post-meals did not differ by diet, and there was no difference in 24-hour glomerular filtration rates by diet. Nitrogen balance was significantly greater on the high-protein diet compared to the high-carbohydrate diet (7.6 +/- 0.9 and -0.4 +/- 0.5 gN/day, p < 0.05), and at 24-hour post-intervention, fasting plasma urea nitrogen concentrations were raised on the high protein diet versus the high-carbohydrate diet (13.9 +/- 0.9 and 11.2 +/- 1.0 mg/dL respectively, p < 0.05).

CONCLUSIONS:

These data indicate an added energy-cost associated with high-protein, low-fat diets and may help explain the efficacy of such diets for weight loss.

Gluconeogenesis and energy expenditure after a high-protein, carbohydrate-free diet.

Abstract

BACKGROUND:

High-protein diets have been shown to increase energy expenditure (EE).

OBJECTIVE:

The objective was to study whether a high-protein, carbohydrate-free diet (H diet) increases gluconeogenesis and whether this can explain the increase in EE.

DESIGN:

Ten healthy men with a mean (+/-SEM) body mass index (in kg/m(2)) of 23.0 +/- 0.8 and age of 23 +/- 1 y received an isoenergetic H diet (H condition; 30%, 0%, and 70% of energy from protein, carbohydrate, and fat, respectively) or a normal-protein diet (N condition; 12%, 55%, and 33% of energy from protein, carbohydrate, and fat, respectively) for 1.5 d according to a randomized crossover design, and EE was measured in a respiration chamber. Endogenous glucose production (EGP) and fractional gluconeogenesis were measured via infusion of [6,6-(2)H(2)]glucose and ingestion of (2)H(2)O; absolute gluconeogenesis was calculated by multiplying fractional gluconeogenesis by EGP. Body glycogen stores were lowered at the start of the intervention with an exhaustive glycogen-lowering exercise test.

RESULTS:

EGP was lower in the H condition than in the N condition (181 +/- 9 compared with 226 +/- 9 g/d; P < 0.001), whereas fractional gluconeogenesis was higher (0.95 +/- 0.04 compared with 0.64 +/- 0.03; P < 0.001) and absolute gluconeogenesis tended to be higher (171 +/- 10 compared with 145 +/- 10 g/d; P = 0.06) in the H condition than in the N condition. EE (resting metabolic rate) was greater in the H condition than in the N condition (8.46 +/- 0.23 compared with 8.12 +/- 0.31 MJ/d; P < 0.05). The increase in EE was a function of the increase in gluconeogenesis (DeltaEE = 0.007 x Deltagluconeogenesis - 0.038; r = 0.70, R(2) = 0.49, P < 0.05). The contribution of Deltagluconeogenesis to DeltaEE was 42%; the energy cost of gluconeogenesis was 33% (95% CI: 16%, 50%).

CONCLUSIONS:

Forty-two percent of the increase in energy expenditure after the H diet was explained by the increase in gluconeogenesis. The cost of gluconeogenesis was 33% of the energy content of the produced glucose.

The effects of consuming frequent, higher protein meals on appetite and satiety during weight loss in overweight/obese men.

Abstract

The purpose of this study was to determine the effects of dietary protein and eating frequency on perceived appetite and satiety during weight loss. A total of 27 overweight/obese men (age 47 ± 3 years; BMI 31.5 ± 0.7 kg/m(2)) were randomized to groups that consumed an energy-restriction diet (i.e., 750 kcal/day below daily energy need) as either higher protein (HP, 25% of energy as protein, n = 14) or normal protein (NP, 14% of energy as protein, n = 13) for 12 weeks. Beginning on week 7, the participants consumed their respective diets as either 3 eating occasions/day (3-EO; every 5 h) or 6 eating occasions/day (6-EO; every 2 h), in randomized order, for 3 consecutive days. Indexes of appetite and satiety were assessed every waking hour on the third day of each pattern. Daily hunger, desire to eat, and preoccupation with thoughts of food were not different between groups. The HP group experienced greater fullness throughout the day vs. NP (511 ± 56 vs. 243 ± 54 mm · 15 h; P < 0.005). When compared to NP, the HP group experienced lower late-night desire to eat (13 ± 4 vs. 27 ± 4 mm, P < 0.01) and preoccupation with thoughts of food (8 ± 4 vs. 21 ± 4 mm; P < 0.01). Within groups, the 3 vs. 6-EO patterns did not influence daily hunger, fullness, desire to eat, or preoccupation with thoughts of food. The 3-EO pattern led to greater evening and late-night fullness vs. 6-EO but only within the HP group (P < 0.005). Collectively, these data support the consumption of HP intake, but not greater eating frequency, for improved appetite control and satiety in overweight/obese men during energy restriction-induced weight loss.

Protein intake and energy balance.

Abstract

Maintaining energy balance in the context of body-weight regulation requires a multifactorial approach. Recent findings suggest that an elevated protein intake plays a key role herein, through (i) increased satiety related to increased diet-induced thermogenesis, (ii) its effect on thermogenesis, (iii) body composition, and (iv) decreased energy-efficiency, all of which are related to protein metabolism. Supported by these mechanisms, relatively larger weight loss and subsequent stronger body-weight maintenance have been observed. Elevated thermogenesis and GLP-1 appear to play a role in high protein induced satiety. Moreover, a negative fat-balance and positive protein-balance is shown in the short-term, whereby fat-oxidation is increased. Furthermore, a high protein diet shows a reduced energy efficiency related to the body-composition of the body-weight regained, i.e. favor of fat free mass. Since protein intake is studied under various energy balances, absolute and relative protein intake needs to be discriminated. In absolute grams, a normal protein diet becomes a relatively high protein diet in negative energy balance and at weight maintenance. Therefore 'high protein negative energy balance diets' aim to keep the grams of proteins ingested at the same level as consumed at energy balance, despite lower energy intakes.

Effects of food form and timing of ingestion on appetite

Effects of food form and timing of ingestion on appetite and energy intake in lean young adults and in young adults with obesity.

Abstract

OBJECTIVE:

Overweight and obesity have been attributed to increased eating frequency and the size of eating events. This study explored the influence of the timing of eating events and food form on appetite and daily energy intake.

DESIGN:

Crossover, clinical intervention where participants consumed 300-kcal loads of a solid (apple), semisolid (apple sauce), and beverage (apple juice) at a meal or 2 hours later (snack).

SUBJECTS:

Twenty normal-weight (body mass index 22.6+/-1.8) and 20 obese (body mass index 32.3+/-1.5) adults. There were 10 men and 10 women within each body mass index group.

MEASUREMENTS:

On six occasions, participants reported to the laboratory at their customary midday mealtime. Appetite questionnaires and motor skills tests were completed upon arrival and at 30-minute intervals for the 2 hours participants were in the laboratory and at 30-minute intervals for 4 hours after leaving the laboratory. Diet recalls were collected the next day. Data were collected between January 2006 and March 2007.

RESULTS:

Whether consumed with a meal or alone as a snack, the beverage elicited the weakest appetitive response, the solid food form elicited the strongest appetitive response and the semisolid response was intermediate. The appetite shift was greatest for the solid food when consumed as a snack. The interval between test food consumption and the first spontaneous eating event >100 kcal was shortest for the beverage. No significant treatment effects were observed for test day energy intake or between lean individuals and individuals with obesity.

CONCLUSIONS:

Based on the appetitive findings, consumption of an energy-yielding beverage either with a meal or as a snack poses a greater risk for promoting positive energy than macronutrient-matched semisolid or solid foods consumed at these times.

 

Greater fructose consumption is associated with cardiometabolic risk markers

Greater fructose consumption is associated with cardiometabolic risk markers and visceral adiposity in adolescents.

Abstract

Though adolescents consume more fructose than any other age group, the relationship between fructose consumption and markers of cardiometabolic risk has not been established in this population. We determined associations of total fructose intake (free fructose plus one-half the intake of free sucrose) with cardiometabolic risk factors and type of adiposity in 559 adolescents aged 14-18 y. Fasting blood samples were measured for glucose, insulin, lipids, adiponectin, and C-reactive protein. Diet was assessed with 4-7 24-h recalls and physical activity (PA) was determined by accelerometry. Fat-free soft tissue (FFST) mass and fat mass were measured by DXA. The s.c. abdominal adipose tissue (SAAT) and visceral adipose tissue (VAT) were assessed using MRI. Multiple linear regression, adjusting for age, sex, race, Tanner stage, FFST mass, fat mass, PA, energy intake, fiber intake, and socioeconomic status, revealed that fructose intake was associated with VAT (β = 0.13; P = 0.03) but not SAAT (P = 0.15). Significant linear upward trends across tertiles of fructose intake were observed for systolic blood pressure, fasting glucose, HOMA-IR, and C-reactive protein after adjusting for the same covariates (all P-trend < 0.04). Conversely, significant linear downward trends across tertiles of fructose intake were observed for plasma HDL-cholesterol and adiponectin (both P-trend < 0.03). When SAAT was added as a covariate, these trends persisted (all P-trend < 0.05). However, when VAT was included as a covariate, it attenuated these trends (all P-trend > 0.05). In adolescents, higher fructose consumption is associated with multiple markers of cardiometabolic risk, but it appears that these relationships are mediated by visceral obesity.

 

Effect of Fructose Overfeeding and Fish Oil

Effect of Fructose Overfeeding and Fish Oil Administration on Hepatic De Novo Lipogenesis and Insulin Sensitivity in Healthy Men

Abstract

High-fructose diet stimulates hepatic de novo lipogenesis (DNL) and causes hypertriglyceridemia and insulin resistance in rodents. Fructose-induced insulin resistance may be secondary to alterations of lipid metabolism. In contrast, fish oil supplementation decreases triglycerides and may improve insulin resistance. Therefore, we studied the effect of high-fructose diet and fish oil on DNL and VLDL triglycerides and their impact on insulin resistance. Seven normal men were studied on four occasions: after fish oil (7.2 g/day) for 28 days; a 6-day high-fructose diet (corresponding to an extra 25% of total calories); fish oil plus high-fructose diet; and control conditions. Following each condition, fasting fractional DNL and endogenous glucose production (EGP) were evaluated using [1-¹³C]sodium acetate and 6,6-²H₂ glucose and a two-step hyperinsulinemic-euglycemic clamp was performed to assess insulin sensitivity. High-fructose diet significantly increased fasting glycemia (7 ± 2%), triglycerides (79 ± 22%), fractional DNL (sixfold), and EGP (14 ± 3%, all P < 0.05). It also impaired insulin-induced suppression of adipose tissue lipolysis and EGP (P < 0.05) but had no effect on whole- body insulin-mediated glucose disposal. Fish oil significantly decreased triglycerides (37%, P < 0.05) after high-fructose diet compared with high-fructose diet without fish oil and tended to reduce DNL but had no other significant effect. In conclusion, high-fructose diet induced dyslipidemia and hepatic and adipose tissue insulin resistance. Fish oil reversed dyslipidemia but not insulin resistance.

How bad is fructose?

George A Bray

This issue of the Journal contains another disturbing article on the biology of fructose (1). Why is fructose of concern? First, it is sweeter than either glucose or sucrose. In fruit, it serves as a marker for foods that are nutritionally rich. However, in soft drinks and other “sweets,” fructose serves to reward sweet taste that provides “calories,” often without much else in the way of nutrition. Second, the intake of soft drinks containing high-fructose corn syrup (HFCS) or sucrose has risen in parallel with the epidemic of obesity, which suggests a relation (2). Third, the article in this issue of the Journal (1) and another article published elsewhere last year (3) implicate dietary fructose as a potential risk factor for cardiovascular disease.

The intake of dietary fructose has increased significantly from 1970 to 2000. There has been a 25% increase in available “added sugars” during this period (4). The Continuing Survey of Food Intake by Individuals from 1994 to 1996 showed that the average person had a daily added sugars intake of 79 g (equivalent to 316 kcal/d or 15% of energy intake), approximately half of which was fructose. More important, persons who are ranked in the top one-third of fructose consumers ingest 137 g added sugars/d, and those in the top 10% consume 178 g/d, with half of that amount being fructose. If there are health concerns with fructose, then this increased intake could aggravate those problems.

Before the European encounter with the New World 500 y ago and the development of the worldwide sugar industry, fructose in the human diet was limited to a few items. For example, honey, dates, raisins, molasses, and figs have a content of >10% of this sugar, whereas a fructose content of 5–10% by weight is found in grapes, raw apples, apple juice, persimmons, and blueberries. Milk, the main nourishment for infants, has essentially no fructose, and neither do most vegetables and meats, which indicates that human beings had little dietary exposure to fructose before the mass production of sugar.

Most fructose in the American diet comes not from fresh fruit, but from HFCS or sucrose (sugar) that is found in soft drinks and sweets, which typically have few other nutrients (2). Soft drink consumption, which provides most of this fructose, has increased dramatically in the past 6 decades, rising from a per-person consumption of 90 servings/y (≈2 servings/wk) in 1942 to that of 600 servings/y (≈2 servings/d) in 2000 (5). More than 50% of preschool children consume some calorie-sweetened beverages (6). Children of this age would not normally be exposed to fructose, let alone in these high amounts. Because both HFCS and sucrose are “delivery vehicles for fructose,” the load of fructose has increased in parallel with the use of sugar.

Fructose is an intermediary in the metabolism of glucose, but there is no biological need for dietary fructose. When ingested by itself, fructose is poorly absorbed from the gastrointestinal tract, and it is almost entirely cleared by the liver—the circulating concentration is ≈0.01 mmol/L in peripheral blood, compared with 5.5 mmol/L for glucose.

Fructose differs in several ways from glucose, the other half of the sucrose (sugar) molecule (4). Fructose is absorbed from the gastrointestinal tract by a different mechanism than that for glucose. Glucose stimulates insulin release from the isolated pancreas, but fructose does not. Most cells have only low amounts of the glut-5 transporter, which transports fructose into cells. Fructose cannot enter most cells, because they lack glut-5, whereas glucose is transported into cells by glut-4, an insulin-dependent transport system. Finally, once inside the liver cell, fructose can enter the pathways that provide glycerol, the backbone for triacylglycerol. The growing dietary amount of fructose that is derived from sucrose or HFCS has raised questions about how children and adults respond to fructose alone or when it is accompanied by glucose. In one study, the consumption of high-fructose meals reduced 24-h plasma insulin and leptin concentrations and increased postprandial fasting triacylglycerols in women, but it did not suppress circulating ghrelin, a major appetite-stimulating hormone (4).

Fructose is metabolized, primarily in the liver, by phosphorylation on the 1-position, a process that bypasses the rate-limiting phosphofructokinase step (4). Hepatic metabolism of fructose thus favors lipogenesis, and it is not surprising that several studies have found changes in circulating lipids when subjects eat high-fructose diets (4). In the study conducted by Aeberli et al (1), dietary factors, especially fructose, were examined in relation to body mass index, waist-to-hip ratio, plasma lipid profile, and LDL particle size in 74 Swiss schoolchildren who were 6–14 y old. In that study, plasma triacylglycerols were higher, HDL-cholesterol concentrations were lower, and lipoprotein (LDL) particle size was smaller in the overweight children than in the normal-weight children. Fatter children had smaller LDL particle size, and, even after control for adiposity, dietary fructose intake was the only dietary factor related to LDL particle size. In this study, it was the free fructose, and not sucrose, that was related to the effect of LDL particle size. Studies in rodents, dogs, and nonhuman primates eating diets high in fructose or sucrose consistently show hyperlipidemia (4). The current report by Aeberli et al suggests that the higher intake of fructose by school-age children may have detrimental effects on their future risk of cardiovascular disease by reducing LDL particle size. It is interesting that this study did not find a relation of dietary fructose with triacylglycerols but did find a relation with the more concerning lipid particle, LDL cholesterol. Another recent report has proposed a hypothesis relating fructose intake to the long-known relation between uric acid and heart disease (3). The ADP formed from ATP after phosphorylation of fructose on the 1-position can be further metabolized to uric acid. The metabolism of fructose in the liver drives the production of uric acid, which utilizes nitric oxide, a key modulator of vascular function (3). The studies by Aeberli et al and Nakagawa et al suggest that the relation of fructose to health needs reevaluation.

Adverse metabolic effects of dietary fructose

 

Adverse metabolic effects of dietary fructose: results from the recent epidemiological, clinical, and mechanistic studies

 

Abstract

PURPOSE OF REVIEW:

The effects of dietary sugar on risk factors and the processes associated with metabolic disease remain a controversial topic, with recent reviews of the available evidence arriving at widely discrepant conclusions.

RECENT FINDINGS:

There are many recently published epidemiological studies that provide evidence that sugar consumption is associated with metabolic disease. Three recent clinical studies, which investigated the effects of consuming relevant doses of sucrose or high-fructose corn syrup along with ad libitum diets, provide evidence that consumption of these sugars increase the risk factors for cardiovascular disease and metabolic syndrome. Mechanistic studies suggest that these effects result from the rapid hepatic metabolism of fructose catalyzed by fructokinase C, which generates substrate for de novo lipogenesis and leads to increased uric acid levels. Recent clinical studies investigating the effects of consuming less sugar, via educational interventions or by substitution of sugar-sweetened beverages for noncalorically sweetened beverages, provide evidence that such strategies have beneficial effects on risk factors for metabolic disease or on BMI in children.

SUMMARY:

The accumulating epidemiological evidence, direct clinical evidence, and the evidence suggesting plausible mechanisms support a role for sugar in the epidemics of metabolic syndrome, cardiovascular disease, and type 2 diabetes.

 

Why Lose Belly Fat? Central Obesity and Health

Obesity is a condition characterized by excessive accumulation of body fat and increased body weight.
Scientific studies have revealed that obesity is associated with negative effects on health and reduced life expectancy.
Obesity is most often defined as a body mass index (BMI) above 30. High BMI is associated with increased risk of high blood pressure, lipid disorders, type 2 diabetes and cardiovascular disease.
However, the definition of BMI has several problems. It doesn’t account for different body frames, and it doesn’t differentiate between muscle and fat.
Many individuals with high BMI don’t have the metabolic abnormalities associated with obesity and will not develop the typical complications of this disorder.
Furthermore, many normal weight individuals suffer from the same metabolic abnormalities that are usually associated with obesity. These subjects are often defined as metabolically obese, normal-weight (MONW) (1).

Visceral Obesity

Many studies have shown that body shape and the regional distribution of fat may be more important for health than the total amount of body fat. Most importantly, it has been shown that the accumulation of fat around the internal organs may play a key role. This phenomenon is often termed visceral obesity.
The term visceral obesity defines excessive fat accumulation around the organs within the abdominal cavity.
The terms central or abdominal obesity, or belly fat, describe fat accumulation in the upper part of the body and don’t differentiate between visceral or subcutaneous fat accumulation. Usually, belly fat is a combination of both.
Evidence that visceral fat tissue is more damaging to health than subcutaneous abdominal fat is rapidly emerging. Research suggests that obese individuals with excess visceral obesity have a higher risk of diabetes, lipid disorders, and cardiovascular disease than those with less visceral fat accumulation (2).

History

In 1947, Professor Jean Vague from the University of Marseille, was the first to recognize that the regional distribution of body fat was a more important predictor of risk and metabolic abnormalities than excess fatness in general (3).
Vague defined two different body shapes. Android obesity or apple shape refers to the accumulation of fat in the upper body are. Gynoid obesity or pear shape refers to the accumulation of fat on the hips and thighs. The latter is more common among women than men.
Although Vague’s ideas were initially met with skepticism, they were later confirmed by scientific studies.
In 1984, the results of a large Swedish epidemiological study showed that an increased abdominal waistline among middle-aged men and women was strongly predictive of higher risk of coronary heart disease later in life (4,5). Later these same investigators showed that central obesity was strongly associated with increased risk of diabetes.

Central Obesity and Health

Studies have shown that the accumulation of belly fat is associated with several disease conditions such as type 2 diabetes, lipid disorders, high blood pressure, cardiovascular disease and some types of cancer. Most of these studies have used waist circumference to define central obesity although some have directly assessed visceral fat by using modern imaging techniques.

Insulin Resistance and Type 2 Diabetes

Insulin resistance is defined as a diminished response to a given concentration of insulin and is associated with increased risk of type 2 diabetes.
Insulin resistance and type 2 diabetes are key features among people with central obesity. In fact, central obesity appears to be a better predictor of type 2 diabetes than general obesity assessed by BMI (6).

Lipid Disorders

Lipid abnormalities commonly associated with central obesity include high levels of triglycerides and low levels of HDL-cholesterol. Consequently, the triglyceride/HDL cholesterol ratio is elevated.
People with central obesity often have normal total cholesterol and relatively normal levels of LDL-cholesterol. However, they often have high number of LDL particles that can be measured by raised levels of LDL-P and Apolipoprotein B. A high number of LDL-particles is associated with increased risk of atherosclerosis and cardiovascular risk in general.
Central obesity is often associated with small and dense LDL particles. Small LDL particles bind weakly with LDL-receptors making their clearance from the circulation less efficient. Therefore, small LDL particles are likely to circulate for a longer time, increasing the total number of LDL particles available. Furthermore, insulin resistance worsens the clearance of LDL particles from the circulation (7).
The combination of high triglycerides, low HDL cholesterol, and small, dense LDL particles, often termed the “atherogenic lipid triad”, is strongly associated with the risk of cardiovascular disease.

High Blood Pressure

High blood pressure (hypertension) is a well-known risk factor for heart disease and stroke. Hypertension is more common in obese people than normal weight individuals.
Studies have found that central obesity assessed by waist circumference is associated with increased risk of hypertension (8).

Cardiovascular Disease 

Central obesity is a predictor of cardiovascular disease and mortality, independent of traditional risk factors and BMI (9). Thus, abdominal obesity appears to be a stronger risk factor for cardiovascular disease than general obesity in itself.
Interestingly, the Nurses’ Health Study found the cardiovascular risk of overweight/obese women without central obesity was similar to that of normal weight women with central obesity (10).
The large INTERHEART study indicated that central obesity was a stronger predictor of heart attack (myocardial infarction) than general obesity assessed by BMI.

Cancer

Epidemiological data have showed an association between obesity assessed by BMI and increased risk of several types of cancer (11).
Similar data also indicate that central obesity may be associated with increased risk of cancer of the colon and rectum, breast cancer in women, prostate cancer in men, and cancer of the esophagus.

Why Do We Accumulate Belly Fat?

The mechanisms behind central obesity are complicated. Why do some individuals accumulate fat within the abdominal cavity while others don’t?
Age and gender clearly play a role. Young individuals are more likely to store excess fat under their skin (subcutaneous fat) than around the organs of the abdominal cavity.
The ratio of visceral to subcutaneous abdominal fat tends to increase with age. Furthermore, women tend to have much higher proportion of subcutaneous than visceral fat compared with men of same age.
Men are much more likely to accumulate fat in the upper body, whereas women often accumulate fat in the lower parts of the body, on the hips and thighs.
Sex hormones appear to play a role. Men with low testosterone levels tend to have more central obesity than those with normal levels. Estrogen treatment of female-to-male transsexuals appears to increase subcutaneous fat depots in all areas.
Studies have clearly shown aggregation of visceral obesity in some families (12). Thus, genetic factors appear to influence how much fat is stored under the skin compared with around the visceral organs.

Nutritional Factors

Very few studies have assessed nutritional factors that may underlie central obesity.
Recently published data from the PREDIMED study revealed that a Mediterranean diet supplemented with nuts was associated with less central obesity, lower triglyceride levels, less small and dense LDL particles and lower LDL particle number (13).
Consumption of sugar sweetened-beverages is associated with increased risk of obesity and type 2 diabetes. Intake of fructose raises triglyceride levels and blood sugar.
In fact, data suggests that the intake of fructose stimulates visceral fat accumulation more than the intake of other simple sugars (14).

Physical Inactivity

Although it has not been proven that a sedentary lifestyle predisposes to the accumulation of belly fat, there is evidence that regular exercise is associated with less central obesity.
A systematic review found that regular physical activity was associated with a marked reduction in central obesity, even in studies not reporting reductions in body weight (15).

Why Should We, and How Can We Lose Belly Fat?

The strong association between central obesity and diverse disease conditions suggests that avoiding the accumulation belly fat, or losing belly fat if present, may reduce risk and improve health.
Any intervention that will induce weight loss is likely to reduce belly fat.
In theory, weigh loss interventions that target visceral fat preferentially may improve health without the need for general weight loss. However, the principal finding of a recent review (16) was that there are no effective interventions available that target visceral fat preferentially.
So, if somebody claims that a certain approach will reduce belly fat more than other fat, you can be certain that this intervention is not supported by scientific evidence.
Restricting carbohydrates may help lower triglyceride levels.  This may improve lipid profile by increasing LDL particle size, and reducing LDL particle number and apoliporotein B levels. In fact, the positive effects of dietary carbohydrate restriction in people with insulin resistance and type 2 diabetes may have been underestimated (17).
As mentioned previously, a Mediterranean-type diet may reduce belly fat and improve some of the metabolic abnormalities associated with central obesity.
Many experts believe that physical exercise is not effective when it comes to losing weight. However, failure to recognize the benefits of exercise, independent of weight loss, is misguided.
Obese individuals can improve their health without losing weight. In my opinion, regular physical exercise should play a key role for the treatment of central obesity.

Metabolic obesity: the paradox between visceral and subcutaneous fat.

Abstract

In contrast to the accumulation of fat in the gluteo-femoral region, the accumulation of fat around abdominal viscera and inside intraabdominal solid organs is strongly associated with obesity-related complications like Type 2 diabetes and coronary artery disease. The association between visceral adiposity and accelerated atherosclerosis was shown to be independent of age, overall obesity or the amount of subcutaneous fat. Recent evidence revealed several biological and genetic differences between intraabdominal visceral-fat and peripheral subcutaneous-fat. Such differences are also reflected in their contrasting roles in the pathogenesis of obesity-related cardiometabolic problems, in either lean or obese individuals. The functional differences between visceral and the subcutaneous adipocytes may be related to their anatomical location. Visceral adipose tissue and its adipose-tissue resident macrophages produce more proinflamatory cytokines like tumor necrosis factor-alpha (TNF-alpha) and interleukin-6 (IL-6) and less adiponectin. These cytokines changes induce insulin resistance and play a major role in the pathogenesis of endothelial dysfunction and subsequent atherosclerosis. The rate of visceral fat accumulation is also different according to the individual's gender and ethnic background; being more prominent in white men, African American women and Asian Indian and Japanese men and women. Such differences may explain the variation in the cardiometabolic risk at different waist measurements between different populations. However, it is unclear how much visceral fat reduction is needed to induce favorable metabolic changes. On the other hand, peripheral fat mass is negatively correlated with atherogenic metabolic risk factors and its selective reduction by liposuction does improve cardiovascular risk profile. The increasing knowledge about body fat distribution and its modifiers may lead to the development of more effective treatment strategies for people with/or at high risk for Type 2 diabetes and coronary artery disease. These accumulating observations also urge our need for a new definition of obesity based on the anatomical location of fat rather than on its volume, especially when cardiometabolic risk is considered. The term "Metabolic Obesity", in reference to visceral fat accumulation in either lean or obese individuals may identify those at risk for cardiovascular disease better than the currently used definitions of obesity.

The "metabolically-obese," normal-weight individual.

Abstract

A great many disorders including maturity-onset (type II) diabetes, hypertension, and hypertriglyceridemia are frequently associated with adult-onset obesity and improve with caloric restriction. It is the premise of this brief review that there are patients with these disorders who are not obese according to standard weight tables or other readily-available criteria; but who would also respond favorably to caloric restriction. It is proposed that such individuals might be characterized by hyperinsulinism and possibly an increase in fat cell size compared to patients of similar age, height, and weight and/or to themselves at an earlier time. The possibility is also discussed that inactivity is a contributing factor in some of these individuals and that for them, the appropriate therapy might be exercise.

Prevalence of metabolic syndrome

Prevalence of metabolic syndrome among adults 20 years of age and over, by sex, age, race and ethnicity, and body mass index: United States, 2003-2006.

Abstract

OBJECTIVE:

The purpose of this study was to examine the prevalence of individual risk factors for metabolic syndrome as well as the prevalence of metabolic syndrome in the National Health and Nutrition Examination Survey (NHANES) 2003-2006.

METHODS:

The analytic sample consisted of 3,423 adults, 20 years of age and over, from NHANES 2003-2006. The National Cholesterol Education Program's Adult Treatment Panel III (NCEP/ATP III) guidelines were used to identify adults who met their criteria for metabolic syndrome. Prevalence estimates were calculated for each risk factor for metabolic syndrome in addition to the prevalence of metabolic syndrome. Prevalence estimates and odds ratios were analyzed by sex and by age group, race and ethnicity, and body mass index (BMI) stratified by sex.

RESULTS:

Approximately 34% of adults met the criteria for metabolic syndrome. Males and females 40-59 years of age were about three times as likely as those 20-39 years of age to meet the criteria for metabolic syndrome. Males 60 years of age and over were more than four times as likely and females 60 years of age and over were more than six times as likely as the youngest age group to meet the criteria. Non-Hispanic black males were about one-half as likely as non-Hispanic white males to meet the criteria for metabolic syndrome, while non-Hispanic black and Mexican-American females were about 1.5 times as likely as non-Hispanic white females to meet the criteria. Overweight males were about six times as likely and obese males were about 32 times as likely as normal weight males to meet the criteria. Overweight females were more than five times as likely and obese females were more than 17 times as likely as normal weight females to meet the criteria.

CONCLUSIONS:

These results demonstrate that metabolic syndrome is prevalent and that it increases with age and with BMI. The prevalence varied by race and ethnicity but the pattern was different for males and females.