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Clinical Director, Kansas City University of Medicine and Biosciences College of Osteopathic Medicine

Altogether, these four studies included approximately 62,500 subjects with a mean follow-up ranging from 7 to 18 years. In both fitness studies,17,21 unfit-overweight and unfit-obese groups had higher type 2 diabetes risks, but unfit-normalweight groups did not differ from their respective reference groups. Type 2 diabetes risks were significantly higher for unfit participants who were obese, had a low or high waist circumference, and a low or high percentage body fat compared with their respective fit and normal reference groups. In both physical activity studies,34,35 more extreme differences in relative risks were observed for low-activity groups when comparing normal-weight with obese categories (1. As to our second question on the relative importance of poor fitness, inactivity, and obesity as predictors of morbidity and mortality, the findings were less uniform. In the studies that used fitness as the exposure, obesity appeared to have less predictive power among fit individuals. On the contrary, the combination of being unfit and obese was associated with higher health risks, especially for type 2 diabetes, compared with being unfit and of normal weight. Whether poor fitness or inactivity is more important as a risk factor is difficult to ascertain. Future studies on fitness, fatness, and health outcomes with simultaneous, objective measures of physical activity and fitness are needed to directly address this important question. In contrast, less is known about how obesity, poor fitness, and an inactive lifestyle coalesce into a risk cluster that is greater than the sum of their parts. For example, leptin has been shown to increase fatty acid oxidation in skeletal muscle from lean but not obese human subjects,45 and in an intervention study46 of 316 older overweight or obese men and women, concentrations of inflammatory markers were reduced with diet-induced weight loss but not exercise. While this may partially explain the independent cardiometabolic risk of obesity, the relationship between inflammatory cytokine secretion from adipose tissue and insulin resistance is not well understood. Compared with men in the upper third of fitness, nonalcoholic fatty liver disease was 10 times more prevalent among men in the lower third of fitness. Therefore, interactions among fitness, physical activity, adiposity, and risk factors are complicated by the responsiveness of ectopic and visceral fat stores to changes in fitness and physical activity. Similarly, intervention trials aimed at evaluating the effect of exercise in improving insulin sensitivity are particularly insightful. In a study52 of 110 obese women with impaired glucose tolerance from the Indian Diabetes Prevention Program, diabetes incidence was reduced by 29% in the exercise group without significant weight loss. In another study of eight obese and inactive but otherwise healthy men, insulin sensitivity improved after 4 weeks of endurance training without a significant change in body weight or percentage body fat (measured by skinfolds). In this regard, avoiding Several mechanisms have been proposed in an attempt to explain how an increase in fitness or physical activity might ameliorate the health hazards of obesity. Physical activity, fitness and fatness: Relations to mortality, morbidity and disease risk factors. Relationship between low cardiorespiratory fitness and mortality in normal-weight, overweight, and obese men. Associations of cardiorespiratory fitness and obesity with risks of impaired fasting glucose and type 2 diabetes in men. Fitness and fatness as predictors of mortality from all causes and from cardiovascular disease in men and women in the lipid research clinics study. Associations of fitness and fatness with mortality in Russian and American men in the lipids research clinics study. A prospective study of cardiorespiratory fitness and risk of type 2 diabetes in women. Exercise capacity and body mass as predictors of mortality among male veterans with type 2 diabetes. Physical activity questionnaires for adults: A systematic review of measurement properties. The effects of physical activity and body mass index on cardiovascular, cancer and all-cause mortality among 47 212 middle-aged Finnish men and women. Combined effects of obesity and physical activity in predicting mortality among men.

By the mid-1930s, its efforts were scaled back considerably, "confined to meetings in which the pineapple transactions of its members are clarified. In 1929, the Ho`olehua homesteaders tried a different version of the cooperative business model when they launched the Ho`olehua Mercantile Company. A year in, it incorporated as the Ho`olehua Company with more than 80 homesteaders investing in the venture. The company built a store and stocked it with nearly everything the Ho`olehua homesteaders might need. The Moloka`i Trading Company (discussed below) eventually took over operations but the store later closed after running into financial difficulties. In 1931, 23 homesteaders executed a five-year hauling agreement with the trucking contractor for Libby, McNeill & Libby, one of the big pineapple corporations on Moloka`i. At the close of the trial period in 1926, the Hawaiian homesteading program was judged a success and made permanent. The commission received the go-ahead to establish homesteading communities elsewhere on the 200,000-plus acres the Hawaiian Homes Commission Act had carved out as "available" for homesteading. The next group of homesteads went up for lease in 1930 in Nnkuli on O`ahu, followed by Waimea on Hawai`i Island six years later. The Homes Commission broke ground in Papaklea, Kewalo, and Waimnalo on O`ahu between 1937 and 1940. Kaua`i received its first homestead sites in Anahola in 1957 and Maui at Paukkalo in 1963. Except for the ranchlands in Waimea, the newer homestead communities lacked the agrarian culture and infrastructure of the first Moloka`i settlements. The remaining 1,667 beneficiaries of the program hold leases on houselots, an indication that the overwhelming emphasis of the program has been the development of urban and suburban housing, rather than agricultural homesteads. If economic self-sufficiency occupied the attention of the first homesteaders on Moloka`i, then the orderliness and safety of the neighborhood and the comfort of its residents became priorities in their own right as dwellings grew to outnumber farms. Hawaiian Homestead Associations When each new site opened up, the formation of an association typically followed so that by the 1950s, every homestead community could claim a homestead association of its own. There were three on Moloka`i: Ho`olehua Community Association, Kalama`ula Community Association, and One Ali`i Community Association. In a 1936 assessment of the homesteading program, the researcher Keesing noted "the growth of benevolent associations" as being a "characteristic feature of modern Hawaiian life" in Moloka`i. These associations provided important services for its dues-paying members, he explained; namely, ensuring that they received "sick benefits and a suitable funeral at death[. This prompted some homesteaders to look at alternative offerings and business models. Six farmers from Ho`olehua resurrected the cooperative model in 1972, organizing themselves as Na Hua Ai Farms. Expecting an uptick in need for equipment and provisions from farmers forced to transition to other crops, Hikiola began as a supply and marketing cooperative in 1976. Today, it is primarily a supply cooperative and continues to offer its farmer-members affordable fertilizers, fuel, and other goods on cheap credit. A 2012 agricultural needs assessment for Moloka`i reported that, as a group, the homestead farmers "rely on each other to share farming techniques, information on new equipment, and promote their produce together. In 1994, Hui Mlama O Mo`omomi received a license from the commission to manage 338 acres of Hawaiian home lands in North Moloka`i. The group designated it the Mo`omomi Recreational and Cultural Park and assumed management over facilities and stewardship of a coastal shoreline that features Mo`omomi Bay.

Indeed, the extent of the metabolic dysfunction is compounded by a postnatal hypercaloric diet, that is, an environment that presents a greater degree of mismatch. As adults, these offspring became hypertensive and dyslipidemic and demonstrated impaired glucose tolerance. Livers of the offspring were characterized by hypomethylation Fetal and Early Postnatal Life Determinants of Adiposity 131 of the Nr3c1 and Ppara promoters, together with increased expression of the gene products and histone modifications at the Nr3c1 promoter that favor its transcription. As these observations were made in a healthy population in which pregnancies were uneventful, this shows that the developmental induction of metabolic risk, and the associated epigenotype, can occur under outwardly normal conditions and apply to virtually every pregnancy. First, and arguably the most likely factor to have the greatest impact in terms of sizes of populations affected, is the economic advancement occurring in many developing countries, including the urbanization of rural areas. This advancement is accompanied by a rapid nutritional transition wherein food is more plentiful and its composition more akin to that of the so-called Western diet-high in calories, glycemic index, and sugar. Second, abrupt nutritional transition may be experienced by those who were undernourished in utero but who then relocate to a more prosperous, nutrient-dense region or country. Such scenarios may eventuate from sociological factors such as internal migration from rural areas to cities and voluntary emigration or refugee displacement to more developed countries. There is evidence pointing toward increased rates of obesity and other metabolic diseases among migrants compared to their counterparts in their original region or country of inhabitance. The processes of maternal constraint, whereby maternal factors restrain fetal growth in part by limiting nutrient availability to the fetus,56 operate in all pregnancies to varying degrees. A consequence of maternal constraint is a bias toward predictions of undernutrition. Maternal constraint affects firstborns to a greater extent than their siblings, possibly because vasodilation of the blood vessels supplying the uterus is less efficient in primigravidae and perhaps because, in evolutionary terms, the firstborn was likely to have been conceived while the mother herself was still growing, pelvic size not being maximal until about 4 years after menarche. Accordingly, firstborns tend to be about 100 g lighter at birth than their later-born siblings, and in line with the predictive model, recent studies have found that they have increased adiposity, higher blood pressure, and a poorer metabolic risk profile in early adulthood compared to those who are second or subsequent children. There is a greater extent of maternal constraint in teenage mothers in whom maximal pelvic dimensions have not yet been reached, as well as in mothers of short stature. Uterine size has been found to be smaller in women who were born small for gestational age60; maternal constraint in turn results in female offspring with a smaller uterus with the same propensity to produce smaller children. Another factor that greatly increases maternal constraint is twinning, for which a later start to motherhood-an increasingly prevalent occurrence in many countries-is a risk factor. The age-related decline in fertility has led to increased use of assisted reproductive technologies, which also are associated with a higher risk of twinning and higher-order multiple pregnancies. Studies in sheep have uncovered similar epigenetic alterations in key hypothalamic metabolic regulators from fetuses that were twins or moderately undernourished singletons, compared to control singletons. Indeed, infants of diabetic mothers show relative adiposity from about age 4 years, with the differential showing marked increases after 6 years of age. Moderately increased insulin production induced by mild fetal hyperglycemia has growthand adiposity-promoting effects that probably enhance fitness, at least in infancy. In fact, humans hold the distinction of having the highest proportion of body fat at birth among mammals, possibly for thermogenesis and to buffer the large brain from nutritional depletion. As is observed in humans,64 maternal obesity is associated with offspring obesity in animal experiments:72 altered growth and metabolic sequelae are seen in offspring, which display features such as obesity, insulin and leptin resistance, hypertension, dyslipidemia, and impaired glucose tolerance. Studies in rats have suggested that a high-fructose maternal diet may compromise endocrinological integrity in female offspring. For example, rats that received high-fat nutrition in utero showed hypomethylation at the hepatic cyclin-dependent kinase inhibitor 1a (Cdkn1a) gene, which suggests hepatic dysfunction that is consistent with a fatty liver phenotype. In addition to the heightened risk of obstetric complications in these women, the adverse impact on offspring health means that the maternal phenotype is in danger of becoming perpetuated through the generations in a vicious cycle of "diabesity. Postnatal nutrition, received indirectly through the maternal lactational diet or directly through infant feeding, can modulate the risk of obesity later in life. It is notable that the fatty acid content of human milk has changed dramatically over the past two decades, presumably reflecting maternal dietary changes. In addition to the obvious public health implications for fathers-to-be, these studies have significant ramifications for our understanding of the transgenerational transmission of obesity and other disease risk. Several indirect pathways of non-Mendelian mechanisms of disease risk inheritance have been defined, including maternal effects, grandmaternal effects, and maternal care (reviewed in Ref.

Other downstream effects of metabolic sensing are activation/repression of gene transcription and release of neurotransmitters or neuropeptides. Key neural systems responsible are the hippocampal complex and associated cortical areas involved in spatial orientation and explicit memory functions, the striatum, which is primarily involved in habit and skills learning, and the amygdala, which is involved in emotional learning (Figures 14. Although humans have the ability to make conscious, voluntary decisions and choices, many of our actions have a subconscious component that escapes voluntary control. The right prefrontal cortex appears to play a critical role in behavioral restraint and moral self-control by keeping reward-generating mechanisms in check. Representations of experience with a particular food (food memories) take into account (1) exteroceptive cues including taste, available before ingestion of significant amounts; (2) postingestive consequences elicited by ingesting the food (digestion, absorption, and metabolism); and (3) the prevailing deprivation state for the particular nutrient at the time of replenishment. The hypothalamic metabolic sensor may be involved in generating a general hunger signal (incentive), and the corticolimbic, reward-based decision-making circuitry may confer the behavioral specificity for the selection process. Successful dieters who have significantly higher levels of dietary restraint than nondieters show increased neural activity in the right dorsolateral prefrontal cortex in response to food consumption. With projections from the ventral tegmental area to the nucleus accumbens and prefrontal cortex, the mesolimbic dopamine system is the most crucial component of the implicit or subconscious "wanting" system. Rewarding aspects of food-related experiences are processed by a complex neural system that includes the nucleus accumbens and ventral pallidum in the ventral striatum, the midbrain ventral tegmental area whose dopamine neurons project back to the nucleus accumbens and prefrontal cortex, the hippocampus, and amygdala (Figure 14. Besides neural circuits in the hindbrain, the nucleus accumbens and ventral pallidum in the limbic forebrain are key components of the distributed neural network mediating "liking" of palatable foods where 14. That food deprivation or restriction increases the reinforcement value of a food reward has been known since the discovery of hypothalamic self-stimulation by the late Bart Hoebel,49 but the mechanisms for such bottom-up 168 Handbook of Obesity modulation were missing. The process of fasting-induced heightening of motivation has been termed "incentive salience attribution. The recent obesity epidemic makes clear that metabolic homeostatic regulatory processes can be overridden by other influences. Despite this, the animals overeat and become obese suggesting that the rewarding properties of the diet can easily override the neurons involved in metabolic regulation to produce hyperphagia and obesity. Second, the prominent projections from cortex, amygdala, and hippocampus to the hypothalamus61 (see Dhillon et al. First, in lower animals and many humans, obesity is associated with increased blood levels of both insulin and leptin. Normally, this would feedback to inhibit further intake and increase energy expenditure. However, in some individuals, a state of central "resistance" to the catabolic effects of leptin and insulin occurs. While there is some dispute about the use of this term, the fact is that, despite very high plasma levels, the inhibitory effects of leptin and insulin are markedly attenuated in many obese individuals. The obesity-prone/obesity-resistant rat model has proven invaluable for demonstrating that both prenatal and postnatal maternal diet, obesity, and diabetes can all play a major role in altering the development of obesity in offspring dependent on genetic predisposition. For example, obesity-resistant rats can be made obese as adults if they are fostered to obese, obesity-prone dams at birth. This phenotypic switch may result from the highly abnormal milk of the obese dam that contains low polyunsaturated and monounsaturated fatty acid and high insulin levels. This produces a series of metabolic and physiological adaptations during caloric restriction that provide powerful metabolic and motivational drives that contribute to the high recidivism rate in the treatment of obesity. During short-term caloric deficits seen with fasting, plasma leptin and insulin levels fall precipitously to levels that are no longer representative of adipose stores. While the inhibitory effects on intake and stimulation of expenditure caused by increased plasma leptin and insulin levels associated with increased adiposity do provide a homeostatic feedback in many individuals, this system takes days to effectively regulate body weight. It is insensitive in some individuals to a slow accretion of excess calories and adipose tissue. More importantly, these negative feedback signals are easily overridden or subverted by the highly rewarding effects of palatable diets and to various social and environmental conditions. To assure survival, the brain has developed a highly redundant set of neural systems that serve as backup systems when primary ones are damaged or deleted by genetic manipulations or naturally occurring mutations. Defense of differing body weight setpoints in diet-induced obese and resistant rats.

Juice: If you serve juice, make it 100% juice and only provide to children older than 12 months. Instead, offer milk to provide calcium and Vitamin D which are essential for bone growth. Lownutrition, high fat, high calorie foods: Offer sparingly and provide healthy suggestions to parents for special events. Serve food in common bowls and pitchers to pass around so children can serve themselves. Incorporate movement (stretching, dancing, marching, jumping, crawling) into all aspects of the curriculum, including transition times. Even young children are widely exposed to screen media-television, video, video games, computers, phones-every day. Encourage active games, listening and moving to music, and creative play to foster interaction and help brain development. Healthy child development depends on eating nutritious food and being physically active every day. This is especially important during the preschool years when children are rapidly building their brains and bodies. The care environment greatly influences what children eat and do, and can play a key role in preventing childhood obesity. Policies for nutrition, physical activity, screen media, and training for child care providers are important tools for getting children on track for good health. Many young children have little opportunity for sustained physical activity during child care and are fed high calorie, low nutrient foods. A large national study found that the type of child care in the year before kindergarten is linked to obesity. Children cared for by a parent or in licensed child care centers are less likely to start kindergarten obese than children in child care offered by extended family, friends, and neighbors. Guidelines that encourage healthy behaviors for children in child care can also benefit their families. Well fed, healthy children are better prepared to focus and learn in the classroom. Quality child care across all settings would help reduce differences in early learning experiences that can lead to gaps in school readiness. Support for this project was provided by a grant from the Robert Wood Johnson Foundation. Review with parents how to properly store and label milk for child care program use. Provide a comfortable place for mothers to nurse their babies or pump (express milk). Develop a feeding plan with the parents that is regularly updated and posted in the infant room. Keep a list of community resources related to breastfeeding and infant nutrition in child care and contact them for educational opportunities. Display posters and provide brochures for new mothers and parents of breastfeeding babies to show that your child care supports breastfeeding and best practice. Get feedback about your breastfeeding support by including a related question on your parent surveys. Promoting, Protecting and Supporting Breastfeeding: A North Carolina Blueprint for Action. Planning for playtime, field trips, or weather safety is part of the daily routine. The changes in weather require the child care provider to monitor the health and safety of children. Clothe children to maintain a comfortable body temperature (warmer months - lightweight cotton, colder months - wear layers of clothing).