Indications for an Association between Higher PUFA Intake with Improved Lean Mass and Reduced Adiposity in Children
This article at a glance 
Obesity is defined by an excessive accumulation of white adipose tissue. Obesogenic adipose tissue growth is different from the development of fat tissue in normal development; both the formation of new adipocytes that differentiate from adipose precursor cells present in adipose tissue, as well as the size of adipocytes is increased, compared to adipose tissue in lean persons. Whereas storage of energy in the form of fat is a physiological process, dealing with excess energy triggers adaptations in adipose tissue, which can become pathological. Obesity in adults is associated with a markedly increased risk of other diseases such as type 2 diabetes and cardiovascular disorders. Also in children obesity has been associated with different aspects of metabolic syndrome, although a definition of metabolic syndrome in children proves difficult to establish. Furthermore, a high body mass index (BMI), gains in BMI, and obesity during childhood furthermore confer higher risks of obesity-associated comorbidities during adulthood. Therefore, reducing obesity during childhood is considered to be critical in order to lower adverse health risks later in life. It needs to be mentioned that childhood obesity-associated risks are not irreversible, and attaining a normal weight during adulthood is associated with a risk that is comparable to that of adults who have not been obese or overweight during their childhood. Identification of the relevant factors that drive pediatric obesity, especially those influences that can be reversed, is likely to be helpful in addressing this epidemic. 
Many factors are considered to play a role in the advance of obesity in youth, such as: increased accessibility to affordable food in general, and refined carbohydrate-containing food specifically, the promotion of sweet preference by the use of sweeteners in calorie-rich food and beverages, the use of visual cues that promote acquisition of calorie-rich food, and increased portion size. These factors are believed to find their main cause in living in an increasingly calorie-replete environment. A major contributor has also been a reduction in exercise and increase in sedentary behavior as a result of increased use of indoor activities (computer/games) by children. A relatively new idea explaining the obesity epidemic is that body weight is to a major extent under external control, i.e. our brain does not exert an inhibitory control over eating under most circumstances, and we engage in appetitive behavior unless the financial or physical cost of access to food is high. As a result of increased access to food in general, eating and body weight will increase by default. A further line of thinking is that a decreased hippocampal-mediated feedback on energy signals, caused by a Westernized diet with too high intake of saturated fatty acids and total energy, and a lack of specific beneficial nutrients that support hippocampal regulation of food intake and metabolism, may underlie a cognitive defect that allows overconsumption and the development of the overweight state. The hippocampus exerts an important controlling function in the neurocognitive control over food intake, in particular in the learned control over eating behavior. Habitual omega-3 dietary intake and higher DHA levels in primary school-age children have been linked to higher hippocampal relational memory, whereas saturated fatty acid and sugar intake is negatively related to hippocampal function. Nutrient quality may be of crucial importance to maintain normal neurophysiological control over food choices, intake level and proper metabolic responses to energy intake, including post-ingestive inhibitory influence that limits further food intake. In other words, disturbances in the normal neuro-physiological relationship between taste and energy content could contribute to increased food and energy intake in the context of a poor and energy-replete diet, allowing passive overconsumption and leading to overweight. Specific but poorly defined technological and economic developments over the past decades that affect all socio-demographic groups worldwide have also been suggested to affect people globally and drive the obesity epidemic. Changes in the accessibility of specific dietary nutrients have occurred in parallel with a significantly increased dietary use of vegetable seed oils responsible for a substantially higher intake of linoleic acid. An essential relation between the dietary intake of specific PUFA and risk for developing obesity has been postulated. Exploratory studies in children have found associations between obesity, disturbances in energy metabolism, and low blood levels of EPA/DHA. Some studies have provided indications that in obese children omega-3 LCPUFA levels in blood may be lower than in lean children, but not all studies are supportive. Currently, no conclusive evidence is available that support an unambiguous link between tissue levels of EPA/DHA and alterations in blood lipid profile, insulin sensitivity, and blood pressure in obese children. In order to establish if any relationship between PUFA intake and obesity in children exists at all, Cardel and colleagues have determined the associations between self-reported fatty acid intake and several indices of adiposity in children age 7-12 years. The study was performed at the Department of Pediatrics and the Anschutz Health and Wellness Center of the School of Medicine at the University of Colorado Denver in Aurora, CO, and the Department of Nutrition Sciences and the Nutrition Obesity Research Center at the University of Alabama, Birmingham, AL, USA. Furthermore, the associations between the ratio of PUFA to saturated fatty acid intakes were assessed in order to determine if higher saturated fatty acid intake in combination with lower PUFA intake might be associated with higher adiposity. Body composition and dietary intake were determined in 311 children with a racially-diverse background (European American, African American and Hispanic American backgrounds, 37, 34 and 27%, respectively). The racial diversity of the study sample is an important aspect since previous studies in this area had focused on study groups with limited population diversity. 
Of the children, nearly half were girls (47%), and none had any medical diagnosis or received medication. The mean age of the children was 9.6 years and they were in a peri-pubertal stage. All children were weighed, their height measured, and their fat mass, lean mass, and percentage body fat measured by dual-energy X-ray absorptiometry. Abdominal adiposity was measured by computed tomography scanning (in two-thirds of the children), permitting quantification of intra-abdominal adipose tissue, sub-cutaneous abdominal adipose tissue, and total abdominal adipose tissue. Over half of the children were of normal weight, 23% were overweight and 10% obese. The children were asked to report their dietary intake of different food items by means of two 24-hour recalls taken at two study visits in a one-month period (in the presence of one of their parents). Among the various calculations made from the recall measurements were macronutrient composition, total PUFAs, saturated fatty acids, omega-3 PUFAs, omega-6 PUFAs, and total energy intake. Dietary intake of nutrients was corrected for daily energy intake. The researchers acknowledge the limitations associated with a dietary recall approach to calculating energy intake. Of interest, resting energy expenditure and daily physical activity of all children were also determined. Resting energy expenditure represents most of the daily energy expenditure of children. Socioeconomic status, pubertal status, and genetic admixture were determined for each child as additional covariates. In order to assess if PUFA intake had any relationship to demographic or specific dietary variables, the researchers first carried out a comparison of the children with a total daily PUFA intake above the mean (13.5 ± 6.7 g/d) with those below the mean. Children with higher total PUFA intake (17.2 ± 7.2 g/d) had significantly lower carbohydrate intake, higher total fat intake, and higher PUFA intake as a percentage of energy. They also ingested significantly higher amounts of omega-3 LCPUFA, alpha-linolenic acid, EPA, DHA, linoleic acid, and arachidonic acid. The ratio of total PUFA to saturated fatty acid intake was nearly double compared to children with a total daily PUFA intake below the average. Importantly, the average daily energy intake, resting energy expenditure, or daily physical activity, was not different between the children with lower or higher total PUFA intake. Associations between individual dietary variables and measures of body composition and adiposity were determined by multivariate linear regression analysis. Total PUFA intake was found to be positively associated with lean body mass, and negatively associated with the percentage of body fat and intra-abdominal tissue. A higher ratio of PUFA to saturated fatty acid intake was associated with higher lean mass, lower percentage body fat, and lower intra-abdominal fat. Higher intake of both omega-3 LCPUFA and omega-6 LCPUFA was associated with higher lean mass, but not with any measures of adiposity. The ratio of omega-6 to omega-3 PUFA intake was found to be negatively associated with intra-abdominal adiposity, but not with other measures of body composition. All analyses were adjusted for a number of potential confounders such as pubertal stage, sex, socioeconomic status, genetic admixture, and total energy intake (and for height in the case of lean mass). The results of this study suggest that in a racially diverse group of US American school-age children, a higher self-reported intake of PUFAs and a higher ratio of PUFAs to saturated fatty acids is positively associated with lean mass, and negatively associated with visceral adiposity and the percentage of body fat. It needs to be noted that the results of this study are obtained on a background daily intake of EPA plus DHA that is very low; even in the children with total PUFA intake above the mean, less than 20% met recommended intake levels. In this context, both omega-6 and omega-3 LCPUFA intake was associated with increased lean mass, but not with any measure of adiposity. Perhaps unexpectedly, the ratio of omega-6 to omega-3 intake was found to be negatively associated with intra-abdominal fat mass. Several research groups have found that omega-6 PUFA and omega-3 PUFA play a role in determining whether adipose tissue displays a metabolically healthy phenotype or an inflammatory phenotype that may drive aspects of the metabolic syndrome. A higher omega-6 to omega-3 PUFA ratio in the Western diet has been implicated as causing greater fat mass accumulation and thus contributes to increased pediatric obesity prevalence. In adult women who were initially of normal weight, the omega-6 PUFA level in red blood cells has been positively associated with developing overweight over a 10-year period. In contrast, adults receiving a diet rich in omega-6 PUFA displayed lower hepatic fat accumulation. The authors of the present study suggest that the role of omega-6 PUFA has not been sufficiently well studied with respect to childhood obesity, and that much of what we know about the role of individual fatty acids in obesity is derived from mechanistic studies carried out on rodents. 
As recognized by the authors in this report, the measurement of energy intake from self-reported estimates is problematic. The individual variation in actual energy intake from that calculated from self-reported dietary intake is very large, and it has been argued that dietary energy intake cannot be reliably determined at all from recall measurements. Whether energy intake from self-reported 24-h recall may be less variable in children than in adults is not known. Although not statistically significant, the high PUFA group did exercise more (in minutes). However, no adjustment in the analysis was made for moderate and vigorous physical activity. In order to gather additional support for the validity of the results of this study, replication is needed, as well as the use of more reliable methods for measuring energy intake. The results of this study reveal statistically significant associations, but no further analyses were carried out to minimize random sampling errors (significance levels were not adjusted for multiple comparisons to counteract the increasing error rates associated with multiple comparisons). As indicated by the authors, the results are exploratory, and additional research studies are required. The important message from this study is that higher PUFA intake, and the ratio of PUFA to saturated fatty acid intake, may be characteristic of children that are less obese and leaner. The strengths of this study are the use of advanced techniques for measuring body composition and adiposity, instead of only BMI, as well as the correction for a number of confounding factors that have not been measured in previous studies, such as ethnic background and energy expenditure. Further well-designed intervention studies are now needed to show a causal relationship between loss of leanness due to low dietary intake of PUFA and/or excess of saturated fatty acid intake in school-age children. The results of this study lend support to the idea that dietary deficiencies and excesses of specific fatty acids may be related to development of adiposity in children. The age group studied here follows a critical age period (5-7 years) in which obesity as part of chronic disease programming becomes more evident. This study represents one further step in assessing if the quality of a child’s diet constitutes an important factor contributing to pediatric obesity, particularly in line with the potential to address overweight and obesity by regaining control over food-related cognitive processing. Cardel M, Lemas DJ, Jackson KH, Friedman JE, Fernandez JR. Higher intake of PUFAs Is associated with lower total and visceral adiposity and higher lean mass in a racially diverse sample of children. J. Nutr. 2015;145(9):2146-2152. [PubMed] Worth Noting Aller EE, Abete I, Astrup A, Martinez JA, van Baak MA. Starches, sugars and obesity. Nutrients 2011;3(3):341-369. [PubMed] Anschutz Health and Wellness Center: http://www.anschutzwellness.com/ Baym CL, Khan NA, Monti JM, Raine LB, Drollette ES, Moore RD, Scudder MR, Kramer AF, Hillman CH, Cohen NJ. Dietary lipids are differentially associated with hippocampal-dependent relational memory in prepubescent children. Am. J. Clin. Nutr. 2014;99(5):1026-1032. [PubMed] Bellisle F. Intense sweeteners, appetite for the sweet taste, and relationship to weight management. Curr. Obes. Rep. 2015;4(1):106-110. [PubMed] Benoit SC, Davis JF, Davidson TL. Learned and cognitive controls of food intake. Brain Res. 2010;1350:71-76. [PubMed] Berry R, Jeffery E, Rodeheffer MS. Weighing in on adipocyte precursors. Cell Metab. 2014;19(1):8-20. [PubMed] Burrows T, Collins CE, Garg ML. Omega-3 index, obesity and insulin resistance in children. Int. J. Pediatr. Obes. 2011;6(2-2):e532-539. [PubMed] Childhood Obesity Intervention Cost Effectiveness Study: http://choicesproject.org/ Cole TJ, Bellizzi MC, Flegal KM, Dietz WH. Establishing a standard definition for child overweight and obesity worldwide: international survey. BMJ 2000;320(7244):1240-1243. [PubMed] Davidson TL, Martin AA. Obesity: Cognitive impairment and the failure to 'eat right'. Curr. Biol. 2014;24(15):R685-687. [PubMed] Elberg J, McDuffie JR, Sebring NG, Salaita C, Keil M, Robotham D, Reynolds JC, Yanovski JA. Comparison of methods to assess change in children's body composition. Am. J. Clin. Nutr. 2004;80(1):64-69. [PubMed] Jeffery E, Church CD, Holtrup B, Colman L, Rodeheffer MS. Rapid depot-specific activation of adipocyte precursor cells at the onset of obesity. Nat. Cell Biol. 2015;17(4):376-385. [PubMed] Juonala M, Magnussen CG, Berenson GS, Venn A, Burns TL, Sabin MA, Srinivasan SR, Daniels SR, Davis PH, Chen W, Sun C, Cheung M, Viikari JS, Dwyer T, Raitakari OT. Childhood adiposity, adult adiposity, and cardiovascular risk factors. N. Engl. J. Med. 2011;365(20):1876-1885. [PubMed] Lassandro C, Banderali G, Radaelli G, Borghi E, Moretti F, Verduci E. Docosahexaenoic acid levels in blood and metabolic syndrome in obese children: Is there a link? Int. J. Mol. Sci. 2015;16(8):19989-20000. [PubMed] Mishra AK, Dubey V, Ghosh AR. Obesity: An overview of possible role(s) of gut hormones, lipid sensing and gut microbiota. Metabolism 2016;65(1):48-65. [PubMed] Naughton SS, Mathai ML, Hryciw DH, McAinch AJ. Australia's nutrition transition 1961-2009: a focus on fats. Br. J. Nutr. 2015;114(3):337-346. [PubMed] Ng M, Fleming T, Robinson M, Thomson B, Graetz N, et al. Global, regional, and national prevalence of overweight and obesity in children and adults during 1980-2013: a systematic analysis for the Global Burden of Disease Study 2013. Lancet 2014;384(9945):766-781. [PubMed] Ogden CL, Carroll MD, Kit BK, Flegal KM. Prevalence of childhood and adult obesity in the United States, 2011-2012. JAMA 2014;311(8):806-814. [PubMed] Petkeviciene J, Klumbiene J, Kriaucioniene V, Raskiliene A, Sakyte E, Ceponiene I. Anthropometric measurements in childhood and prediction of cardiovascular risk factors in adulthood: Kaunas cardiovascular risk cohort study. BMC Public Health 2015;15:218. [PubMed] Rolland-Cachera MF, Deheeger M, Maillot M, Bellisle F. Early adiposity rebound: causes and consequences for obesity in children and adults. Int. J. Obes. (Lond) 2006;30 Suppl 4:S11-17. [PubMed] Sabin MA, Kao KT, Juonala M, Baur LA, Wake M. Viewpoint article: Childhood obesity--looking back over 50 years to begin to look forward. J. Paediatr. Child Health 2015;51(1):82-86. [PubMed] Schoeller DA, Thomas D, Archer E, Heymsfield SB, Blair SN, Goran MI, Hill JO, Atkinson RL, Corkey BE, Foreyt J, Dhurandhar NV, Kral JG, Hall KD, Hansen BC, Heitmann BL, Ravussin E, Allison DB. Self-report-based estimates of energy intake offer an inadequate basis for scientific conclusions. Am. J. Clin. Nutr. 2013;97(6):1413-1415. [PubMed] Siebelink E, Geelen A, de Vries JH. Self-reported energy intake by FFQ compared with actual energy intake to maintain body weight in 516 adults. Br. J. Nutr. 2011;106(2):274-281. [PubMed] Simopoulos AP. An Increase in the omega-6/omega-3 fatty acid ratio increases the risk for obesity. Nutrients 2016;8(128):1-17. [PubMed] Swithers SE, Ogden SB, Davidson TL. Fat substitutes promote weight gain in rats consuming high-fat diets. Behav. Neurosci. 2011;125(4):512-518. [PubMed] van Beek L, Lips MA, Visser A, Pijl H, Ioan-Facsinay A, Toes R, Berends FJ, Willems van Dijk K, Koning F, van Harmelen V. Increased systemic and adipose tissue inflammation differentiates obese women with T2DM from obese women with normal glucose tolerance. Metabolism 2014;63(4):492-501. [PubMed] Wang L, Manson JE, Rautiainen S, Gaziano JM, Buring JE, Tsai MY, Sesso HD. A prospective study of erythrocyte polyunsaturated fatty acid, weight gain, and risk of becoming overweight or obese in middle-aged and older women. Eur. J. Nutr. 2016;55(2):687-697. [PubMed] Ward ZJ, Long MW, Resch SC, Gortmaker SL, Cradock AL, Giles C, Hsiao A, Wang YC. Redrawing the US obesity landscape: bias-corrected estimates of state-specific adult obesity prevalence. PLoS One 2016;11(3):e0150735. [PubMed] Weiss R, Bremer AA, Lustig RH. What is metabolic syndrome, and why are children getting it? Ann. N.Y. Acad. Sci. 2013;1281:123-140. [PubMed] Yanovski JA. Pediatric obesity. An introduction. Appetite 2015;93:3-12. [PubMed] Zandian M, Bergh C, Ioakimidis I, Esfandiari M, Shield J, Lightman S, Leon M, Södersten P. Control of body weight by eating behavior in children. Front. Pediatr. 2015;3:89. [PubMed]
- This study addressed if any associations exist between self-reported dietary intake of polyunsaturated fatty acids and obesity in 7-12 year old US American children from a racially diverse background.
- Associations were identified between higher total PUFA intake and lower body fat and intra-abdominal adipose tissue.
- Total dietary PUFA intake, as well as the ratio of PUFA to saturated fatty acid intake, as reported by the children, was positively correlated with lean mass.
Obesity is defined by an excessive accumulation of white adipose tissue. Obesogenic adipose tissue growth is different from the development of fat tissue in normal development; both the formation of new adipocytes that differentiate from adipose precursor cells present in adipose tissue, as well as the size of adipocytes is increased, compared to adipose tissue in lean persons. Whereas storage of energy in the form of fat is a physiological process, dealing with excess energy triggers adaptations in adipose tissue, which can become pathological. Obesity in adults is associated with a markedly increased risk of other diseases such as type 2 diabetes and cardiovascular disorders. Also in children obesity has been associated with different aspects of metabolic syndrome, although a definition of metabolic syndrome in children proves difficult to establish. Furthermore, a high body mass index (BMI), gains in BMI, and obesity during childhood furthermore confer higher risks of obesity-associated comorbidities during adulthood. Therefore, reducing obesity during childhood is considered to be critical in order to lower adverse health risks later in life. It needs to be mentioned that childhood obesity-associated risks are not irreversible, and attaining a normal weight during adulthood is associated with a risk that is comparable to that of adults who have not been obese or overweight during their childhood. Identification of the relevant factors that drive pediatric obesity, especially those influences that can be reversed, is likely to be helpful in addressing this epidemic. Many factors are considered to play a role in the advance of obesity in youth, such as: increased accessibility to affordable food in general, and refined carbohydrate-containing food specifically, the promotion of sweet preference by the use of sweeteners in calorie-rich food and beverages, the use of visual cues that promote acquisition of calorie-rich food, and increased portion size. These factors are believed to find their main cause in living in an increasingly calorie-replete environment. A major contributor has also been a reduction in exercise and increase in sedentary behavior as a result of increased use of indoor activities (computer/games) by children. A relatively new idea explaining the obesity epidemic is that body weight is to a major extent under external control, i.e. our brain does not exert an inhibitory control over eating under most circumstances, and we engage in appetitive behavior unless the financial or physical cost of access to food is high. As a result of increased access to food in general, eating and body weight will increase by default. A further line of thinking is that a decreased hippocampal-mediated feedback on energy signals, caused by a Westernized diet with too high intake of saturated fatty acids and total energy, and a lack of specific beneficial nutrients that support hippocampal regulation of food intake and metabolism, may underlie a cognitive defect that allows overconsumption and the development of the overweight state. The hippocampus exerts an important controlling function in the neurocognitive control over food intake, in particular in the learned control over eating behavior. Habitual omega-3 dietary intake and higher DHA levels in primary school-age children have been linked to higher hippocampal relational memory, whereas saturated fatty acid and sugar intake is negatively related to hippocampal function. Nutrient quality may be of crucial importance to maintain normal neurophysiological control over food choices, intake level and proper metabolic responses to energy intake, including post-ingestive inhibitory influence that limits further food intake. In other words, disturbances in the normal neuro-physiological relationship between taste and energy content could contribute to increased food and energy intake in the context of a poor and energy-replete diet, allowing passive overconsumption and leading to overweight. Specific but poorly defined technological and economic developments over the past decades that affect all socio-demographic groups worldwide have also been suggested to affect people globally and drive the obesity epidemic. Changes in the accessibility of specific dietary nutrients have occurred in parallel with a significantly increased dietary use of vegetable seed oils responsible for a substantially higher intake of linoleic acid. An essential relation between the dietary intake of specific PUFA and risk for developing obesity has been postulated. Exploratory studies in children have found associations between obesity, disturbances in energy metabolism, and low blood levels of EPA/DHA. Some studies have provided indications that in obese children omega-3 LCPUFA levels in blood may be lower than in lean children, but not all studies are supportive. Currently, no conclusive evidence is available that support an unambiguous link between tissue levels of EPA/DHA and alterations in blood lipid profile, insulin sensitivity, and blood pressure in obese children. In order to establish if any relationship between PUFA intake and obesity in children exists at all, Cardel and colleagues have determined the associations between self-reported fatty acid intake and several indices of adiposity in children age 7-12 years. The study was performed at the Department of Pediatrics and the Anschutz Health and Wellness Center of the School of Medicine at the University of Colorado Denver in Aurora, CO, and the Department of Nutrition Sciences and the Nutrition Obesity Research Center at the University of Alabama, Birmingham, AL, USA. Furthermore, the associations between the ratio of PUFA to saturated fatty acid intakes were assessed in order to determine if higher saturated fatty acid intake in combination with lower PUFA intake might be associated with higher adiposity. Body composition and dietary intake were determined in 311 children with a racially-diverse background (European American, African American and Hispanic American backgrounds, 37, 34 and 27%, respectively). The racial diversity of the study sample is an important aspect since previous studies in this area had focused on study groups with limited population diversity. Of the children, nearly half were girls (47%), and none had any medical diagnosis or received medication. The mean age of the children was 9.6 years and they were in a peri-pubertal stage. All children were weighed, their height measured, and their fat mass, lean mass, and percentage body fat measured by dual-energy X-ray absorptiometry. Abdominal adiposity was measured by computed tomography scanning (in two-thirds of the children), permitting quantification of intra-abdominal adipose tissue, sub-cutaneous abdominal adipose tissue, and total abdominal adipose tissue. Over half of the children were of normal weight, 23% were overweight and 10% obese. The children were asked to report their dietary intake of different food items by means of two 24-hour recalls taken at two study visits in a one-month period (in the presence of one of their parents). Among the various calculations made from the recall measurements were macronutrient composition, total PUFAs, saturated fatty acids, omega-3 PUFAs, omega-6 PUFAs, and total energy intake. Dietary intake of nutrients was corrected for daily energy intake. The researchers acknowledge the limitations associated with a dietary recall approach to calculating energy intake. Of interest, resting energy expenditure and daily physical activity of all children were also determined. Resting energy expenditure represents most of the daily energy expenditure of children. Socioeconomic status, pubertal status, and genetic admixture were determined for each child as additional covariates. In order to assess if PUFA intake had any relationship to demographic or specific dietary variables, the researchers first carried out a comparison of the children with a total daily PUFA intake above the mean (13.5 ± 6.7 g/d) with those below the mean. Children with higher total PUFA intake (17.2 ± 7.2 g/d) had significantly lower carbohydrate intake, higher total fat intake, and higher PUFA intake as a percentage of energy. They also ingested significantly higher amounts of omega-3 LCPUFA, alpha-linolenic acid, EPA, DHA, linoleic acid, and arachidonic acid. The ratio of total PUFA to saturated fatty acid intake was nearly double compared to children with a total daily PUFA intake below the average. Importantly, the average daily energy intake, resting energy expenditure, or daily physical activity, was not different between the children with lower or higher total PUFA intake. Associations between individual dietary variables and measures of body composition and adiposity were determined by multivariate linear regression analysis. Total PUFA intake was found to be positively associated with lean body mass, and negatively associated with the percentage of body fat and intra-abdominal tissue. A higher ratio of PUFA to saturated fatty acid intake was associated with higher lean mass, lower percentage body fat, and lower intra-abdominal fat. Higher intake of both omega-3 LCPUFA and omega-6 LCPUFA was associated with higher lean mass, but not with any measures of adiposity. The ratio of omega-6 to omega-3 PUFA intake was found to be negatively associated with intra-abdominal adiposity, but not with other measures of body composition. All analyses were adjusted for a number of potential confounders such as pubertal stage, sex, socioeconomic status, genetic admixture, and total energy intake (and for height in the case of lean mass). The results of this study suggest that in a racially diverse group of US American school-age children, a higher self-reported intake of PUFAs and a higher ratio of PUFAs to saturated fatty acids is positively associated with lean mass, and negatively associated with visceral adiposity and the percentage of body fat. It needs to be noted that the results of this study are obtained on a background daily intake of EPA plus DHA that is very low; even in the children with total PUFA intake above the mean, less than 20% met recommended intake levels. In this context, both omega-6 and omega-3 LCPUFA intake was associated with increased lean mass, but not with any measure of adiposity. Perhaps unexpectedly, the ratio of omega-6 to omega-3 intake was found to be negatively associated with intra-abdominal fat mass. Several research groups have found that omega-6 PUFA and omega-3 PUFA play a role in determining whether adipose tissue displays a metabolically healthy phenotype or an inflammatory phenotype that may drive aspects of the metabolic syndrome. A higher omega-6 to omega-3 PUFA ratio in the Western diet has been implicated as causing greater fat mass accumulation and thus contributes to increased pediatric obesity prevalence. In adult women who were initially of normal weight, the omega-6 PUFA level in red blood cells has been positively associated with developing overweight over a 10-year period. In contrast, adults receiving a diet rich in omega-6 PUFA displayed lower hepatic fat accumulation. The authors of the present study suggest that the role of omega-6 PUFA has not been sufficiently well studied with respect to childhood obesity, and that much of what we know about the role of individual fatty acids in obesity is derived from mechanistic studies carried out on rodents. As recognized by the authors in this report, the measurement of energy intake from self-reported estimates is problematic. The individual variation in actual energy intake from that calculated from self-reported dietary intake is very large, and it has been argued that dietary energy intake cannot be reliably determined at all from recall measurements. Whether energy intake from self-reported 24-h recall may be less variable in children than in adults is not known. Although not statistically significant, the high PUFA group did exercise more (in minutes). However, no adjustment in the analysis was made for moderate and vigorous physical activity. In order to gather additional support for the validity of the results of this study, replication is needed, as well as the use of more reliable methods for measuring energy intake. The results of this study reveal statistically significant associations, but no further analyses were carried out to minimize random sampling errors (significance levels were not adjusted for multiple comparisons to counteract the increasing error rates associated with multiple comparisons). As indicated by the authors, the results are exploratory, and additional research studies are required. The important message from this study is that higher PUFA intake, and the ratio of PUFA to saturated fatty acid intake, may be characteristic of children that are less obese and leaner. The strengths of this study are the use of advanced techniques for measuring body composition and adiposity, instead of only BMI, as well as the correction for a number of confounding factors that have not been measured in previous studies, such as ethnic background and energy expenditure. Further well-designed intervention studies are now needed to show a causal relationship between loss of leanness due to low dietary intake of PUFA and/or excess of saturated fatty acid intake in school-age children. The results of this study lend support to the idea that dietary deficiencies and excesses of specific fatty acids may be related to development of adiposity in children. The age group studied here follows a critical age period (5-7 years) in which obesity as part of chronic disease programming becomes more evident. This study represents one further step in assessing if the quality of a child’s diet constitutes an important factor contributing to pediatric obesity, particularly in line with the potential to address overweight and obesity by regaining control over food-related cognitive processing. Cardel M, Lemas DJ, Jackson KH, Friedman JE, Fernandez JR. Higher intake of PUFAs Is associated with lower total and visceral adiposity and higher lean mass in a racially diverse sample of children. J. Nutr. 2015;145(9):2146-2152. [PubMed] Worth Noting Aller EE, Abete I, Astrup A, Martinez JA, van Baak MA. Starches, sugars and obesity. Nutrients 2011;3(3):341-369. [PubMed] Anschutz Health and Wellness Center: http://www.anschutzwellness.com/ Baym CL, Khan NA, Monti JM, Raine LB, Drollette ES, Moore RD, Scudder MR, Kramer AF, Hillman CH, Cohen NJ. Dietary lipids are differentially associated with hippocampal-dependent relational memory in prepubescent children. Am. J. Clin. Nutr. 2014;99(5):1026-1032. [PubMed] Bellisle F. Intense sweeteners, appetite for the sweet taste, and relationship to weight management. Curr. Obes. Rep. 2015;4(1):106-110. [PubMed] Benoit SC, Davis JF, Davidson TL. Learned and cognitive controls of food intake. Brain Res. 2010;1350:71-76. [PubMed] Berry R, Jeffery E, Rodeheffer MS. Weighing in on adipocyte precursors. Cell Metab. 2014;19(1):8-20. [PubMed] Burrows T, Collins CE, Garg ML. Omega-3 index, obesity and insulin resistance in children. Int. J. Pediatr. Obes. 2011;6(2-2):e532-539. [PubMed] Childhood Obesity Intervention Cost Effectiveness Study: http://choicesproject.org/ Cole TJ, Bellizzi MC, Flegal KM, Dietz WH. Establishing a standard definition for child overweight and obesity worldwide: international survey. BMJ 2000;320(7244):1240-1243. [PubMed] Davidson TL, Martin AA. Obesity: Cognitive impairment and the failure to 'eat right'. Curr. Biol. 2014;24(15):R685-687. [PubMed] Elberg J, McDuffie JR, Sebring NG, Salaita C, Keil M, Robotham D, Reynolds JC, Yanovski JA. Comparison of methods to assess change in children's body composition. Am. J. Clin. Nutr. 2004;80(1):64-69. [PubMed] Jeffery E, Church CD, Holtrup B, Colman L, Rodeheffer MS. Rapid depot-specific activation of adipocyte precursor cells at the onset of obesity. Nat. Cell Biol. 2015;17(4):376-385. [PubMed] Juonala M, Magnussen CG, Berenson GS, Venn A, Burns TL, Sabin MA, Srinivasan SR, Daniels SR, Davis PH, Chen W, Sun C, Cheung M, Viikari JS, Dwyer T, Raitakari OT. Childhood adiposity, adult adiposity, and cardiovascular risk factors. N. Engl. J. Med. 2011;365(20):1876-1885. [PubMed] Lassandro C, Banderali G, Radaelli G, Borghi E, Moretti F, Verduci E. Docosahexaenoic acid levels in blood and metabolic syndrome in obese children: Is there a link? Int. J. Mol. Sci. 2015;16(8):19989-20000. 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