Overnutrition

Overnutrition induces adipocytes to secrete chemokines such as monocyte chemoattractin-1 protein (MCP-1), leukotriene B4 (LTB4), and others, creating a chemotactic gradient that attracts monocytes into adipose tissue, where they undergo activation.

From: Mechanisms and Manifestations of Obesity in Lung Disease, 2019

Chapters and Articles

Throat pain

In The Treatment of Pain with Chinese Herbs and Acupuncture (Second Edition), 2011

Bad diet

Overeating of very cold food and drinking too many cold drinks may damage the Yang of the Spleen and Stomach, leading to the formation of Cold and Damp. Overeating of pungent, sweet or fatty food, as well as drinking too much alcohol, may cause the formation of Damp and Heat. Irregular food intake, whether in quantity or time, may disturb the transportation and transformation in the Spleen and Stomach, and Damp-Phlegm forms. When Damp-Phlegm accumulates in the throat, it blocks the Qi and Blood circulation in the body as well as in the throat, causing throat pain.

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Nutritional Support

Daniel H. Teitelbaum, Arnold G. Coran, in Pediatric Surgery (Sixth Edition), 2006

Complications from Overfeeding

Overfeeding can lead to a number of adverse consequences. The administration of excessive dextrose may lead to osmotic diuresis and subsequent dehydration due to serum glucose levels exceeding the renal tubular reabsorption threshold. Immunologic suppression has also been associated with overfeeding and is believed to be due to an inactivation of the complement system, as well as depression of natural killer activation. Overfeeding may also adversely affect the liver, because excessive glucose that is not oxidized is converted into fat (lipogenesis). These changes may lead to elevated serum triglyceride levels and hepatic steatosis. Additionally, overfeeding from carbohydrates associated with lipogenesis leads to high carbon dioxide production, as reflected by an elevated respiratory quotient.230 Any respiratory quotient value exceeding 1.0 represents overfeeding; this high level may exacerbate ventilatory impairment in a critically ill child because it represents excessive carbon dioxide production. Avoidance of overfeeding may be difficult, emphasizing the importance of estimating nutritional needs in the intensive care unit setting. Caloric needs are best assessed using indirect calorimetry. Overfeeding critically ill patients may also lead to fluid retention, which may further compromise respiratory function.

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DNA Methylation and Endocrinology

Michel Neidhart, in DNA Methylation and Complex Human Disease, 2016

Overnutrition can affect DNA methylation of specific promoters, leading to insulin resistance, type 2 diabetes, and obesity. Glucocorticoids cause local DNA demethylation of the tyrosine aminotransferase gene. Similarly, stimulation of estrogen receptors and parathyroid hormone leads to demethylation of the PS2 and CYP27B1 genes, respectively. This occurs independently from DNA replication and involves demethylases. Differential methylation of estrogen receptors leads to masculinization or feminization of the neonatal brain. Furthermore, stress has a profound effect on the methylation of glucocorticoid receptors in the hippocampus. This disrupts the feedback loop of increased cortisol and allows an enhanced response to stress. In addition, differential methylation of the PTX1 binding site in the proopiomelanocortin gene promoter influences food intake and body weight, and can be responsible for obesity. The epigenetic control of metabolic regulators, particularly those involved in lipid metabolism (e.g., PPARα), is altered in malnutrition and overfeeding. These new observations shed a new light on the importance of epigenetic modification in the response of target tissues to hormones and the development of obesity.

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Obesity/Perinatal Origins of Obesity

T’ng Chang Kwok, ... Michael E. Symonds, in Maternal-Fetal and Neonatal Endocrinology, 2020

50.6.1.2 Maternal Overnutrition

Overnutrition is becoming a major public health issue globally with the increasing prevalence of obesity, including obesity rates in pregnant women. Many human epidemiological studies have found that infants who are born to women who have raised BMI, especially in the first trimester, are at an increased risk of obesity and metabolic disorders in adulthood.66 Interestingly, offspring born to mothers who underwent bariatric surgery have a lower risk of obesity than offspring born before the surgery. However, human studies have their own limitations, as obesity is a lifelong condition that may precede pregnancy. Hence it is difficult to differentiate between gestational obesity and preconception obesity in women. Besides, it is difficult to eliminate all the confounding factors, as offspring may be exposed to the same adverse, obesity-predisposing environment postpartum that their mothers were exposed to during pregnancy.

Animal models of maternal overnutrition, especially in rodents, where a high-fat low carbohydrate maternal diet is given during pregnancy and lactation, is associated with an increased risk of obesity and metabolic disorder in the offspring,31,36 without any change in birth weight. The neuronal axon projection of the anorexigenic and orexigenic neurons in the arcuate nucleus to the PVN is impaired in the offspring of maternal rodents fed the high-fat diet.76 An increase in the proliferation of the orexigenic neuropeptide expressing neurons and a reduction in that of the anorexigenic neuropeptides are noted in the offspring of rodents with maternal overnutrition.31 This subsequently alters the appetite regulatory pathway in the hypothalamus, leading to increased appetite and predisposing the offspring to obesity, which persists into adulthood.

The impact of maternal overnutrition on gene expression of orexigenic and anorexigenic neuropeptides in the hypothalamus is diverse. Various studies have produced conflicting results,36 making it hard to interpret as compared with that of maternal undernutrition. Some of the changes seen in the neuropeptide levels in the offspring may be a compensatory mechanism for maternal overnutrition, which may change later on in life. Hence further research in this field is needed to provide further clarity on the impact of maternal overnutrition on the expression of these neuropeptides.

Maternal overnutrition in rodents was also found to cause central leptin resistance in the offspring.31 This leads to an increase in the activity of the orexigenic pathway and a decrease in the activation of the sympathetic nervous system. As a result, the long-term body weight set point is altered, leading to obesity.

Interestingly, obese mothers who lose weight during gestation can increase the risk of intrauterine growth (IUGR) restriction in their offspring, predisposing them to obesity in adulthood.77 The increased risk of IUGR may be due to a few reasons, including ketosis from the maternal mobilization of WAT; increased maternal cortisol level from weight lost, which inhibits fetal protein synthesis; or reduced fetal nutrient supply as a result of the increased utilization of nutrients by maternal tissue and the reduced uteroplacental blood flow.66

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Models for the Study of Stroke

Thiruma V. Arumugam, Mark P. Mattson, in Handbook of Models for Human Aging, 2006

Lifestyle

Overeating, a sedentary lifestyle, smoking, and diets high in saturated and trans-fats and cholesterol and low in whole grains and vegetables increase the risk of stroke (www.strokeassociation.org). Conversely, diets low in calories and “bad” fats and high in vegetables and whole grains, regular exercise, and abstinence from smoking reduce the risk of stroke. These factors may promote or inhibit the pathological processes involved in atherosclerosis. In addition, dietary restriction and physical exercise may protect neurons against ischemic damage, enhance neurogenesis, and improve functional outcome by stimulating the production of neurotrophic factors in brain cells (Mattson et al., 2002).

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Obesity and Hypertension: Pathophysiology and Treatment

Michael E. Hall, ... John E. Hall, in Hypertension (Fourth Edition), 2024

Activation of Neurohormonal Mechanisms in Obesity Hypertension

Overfeeding rapidly activates the sympathetic nervous system (SNS) and RAAS, even before major increases in body weight or adiposity occur.17 Conversely, large reductions in caloric intake rapidly decrease SNS and RAAS activity as well as BP prior to significant decreases in VAT or other fat depots.18,19 Although SNS and RAAS activation in obesity is modest, it elicits increased renal sodium reabsorption and expansion of extracellular fluid volume accompanied by increases in renal blood flow and glomerular filtration rate (GFR) (see Fig. 37.1).16 Blood flows in other tissues also increase in obesity, likely due to higher metabolic rate, leading to greater venous return and elevated cardiac output.16

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Disorders of Growth

ADDA GRIMBERG, DIVA D. DE LEÓN, in Pediatric Endocrinology, 2005

Obesity

Overnutrition during childhood typically accelerates growth slightly and advances skeletal maturation in a manner comparable with height age. This association is so characteristic that the linear growth pattern is the single most important “test” in the evaluation of children with obesity. Those with exogenous (nutritional) obesity maintain robust linear growth, whereas those with short stature or linear growth fall-off should be evaluated for an underlying pathological condition. IGF-I levels are normal in the presence of low GH levels. The mechanisms involved in the overgrowth of children with obesity include the effects of elevated insulin levels (due to obesity-induced insulin resistance) cross-reacting with IGF-1R. Early activation of adrenarche and pubarche is common. Increased aromatization of adrenal androgens by fat tissue causes advancement of bone maturation and, as a result, adult height is normal.

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The Human Hypothalamus

Dongsheng Cai, Sinan Khor, in Handbook of Clinical Neurology, 2021

Hypothalamic Microinflammation: A Basis for Hypertension

Overnutrition leading to central leptin and insulin resistance is known as a critical factor in the central mechanism of hypertension (Simonds et al., 2014). The underlying changes have been shown to be a number of factors contributing to hypothalamic microinflammatory activation through overactivity of NF-κB signaling (Zhang et al., 2008). NF-κB activation alone leading to hypothalamic microinflammation can drive increases in BP in an obesity-independent manner (Arruda et al., 2011; Purkayastha et al., 2011a, b; Cardinale et al., 2012). Short-term HFD feeding leads to body weight increase, but chronically this is dissociable from its effects on BP (Purkayastha et al., 2011a), suggesting that while NF-κB-driven microinflammatory changes are a root cause of metabolic dysregulation, they do not necessarily follow the same time course or signaling pattern. One appealing mechanism is through increased activation of the renin–angiotensin system (RAS), and this effect can be abrogated by bilateral NF-κB inhibition within the paraventricular nucleus (PVN) of the hypothalamus (Cardinale et al., 2012). PVN neurons regulate BP at multiple physiologic levels, including through activation of the sympathetic nervous system (SNS) and RAS, as well as control over release of adrenocorticotropic hormone (Schiltz and Sawchenko, 2003; Felder, 2010).

Likely dependently of NF-κB activation, increased hypothalamic inflammatory cytokine expression and hypothalamic oxidative stress have also been shown to induce RAS-mediated hypertension, implicating various mechanisms as stimuli for inducing BP increase in the inflammatory microenvironment (Qi et al., 2013; Su et al., 2014). Among cytokines, TNF-α and IL-1β have more often been shown to induce pressor effects within the hypothalamus. Notably, brain excess of leptin via central leptin administration can increase hypothalamic TNF-α expression, leading to increased SNS activation and BP increase (Han et al., 2016). These pressor effects can be exacerbated in dietary obesity conditions, whereby leptin and TNF-α concertedly stimulate glutamatergic and melanocortinergic neurons leading to hypertensive effects (Yu and Cai, 2017). In parallel with their direct effects on hypothalamic neuronal signaling, TNF-α and IL-1β also increase BBB permeability, partially through disrupting endothelial tight junctions, which may also allow for peripheral circulating cytokines as well as angiotensin to penetrate through the BBB in leaky or damaged areas, which could further exacerbate the central inflammatory action in inducing hypertension (Labus et al., 2014; Rochfort et al., 2014). In summary, these studies have presented strong evidence supporting the role of hypothalamic microinflammation for BP increase and hypertension in obesity. Changes in signaling at multiple levels through NF-κB-driven effects augment sympathetic and angiotensin signaling, leading to an hypertensive outcome in these etiological conditions.

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Traditional nutritional and health practices to tackle the lifestyle diseases

Kirti Aggarwal, ... Maryam Sarwat, in Herbal Medicines, 2022

11.5 Lifestyle affecting pregnancy and lactation

Over nutrition and lifestyle disorders begins early, even at intrauterine developmental stage. An example is the misconception that “an expectant mother has to eat for two” herself and the baby. The truth is a balanced diet of about 3000 calories per day is sufficient for her.

Excessive nutrition intake may result in enormous weight gain, greater risk of labor induction, cesarean section, higher birth weight and other complications during pregnancy and/or delivery. Higher calorie intake develops poor dietary habits and perhaps even metabolic characteristics that can have lifelong consequences. Also, poor lifestyle practices can cause mentally retarded or still born baby.

Lactating women must consume high amount of vitamin A, C, E, and certain B. Meat is considered to be the major source for saturated fat and cholesterol, it is also the most common source for easily ingestible pathogens and a rich supply of arachidonic acid, a pioneer of the immunosuppressive agent eicosanoid PGE2 [12]. In order to prevent neural tube defects, it is necessary to intake folates in required quantities prior to conception [13]. The amount of folate in vegetarian diet is quite high in comparison to a diet consisting of fast food [14]. To fight against lifestyle diseases, the expecting mother should take diet rich in calcium, phosphorus, magnesium, iron, zinc, potassium, selenium, copper, chromium, manganese, and molybdenum, etc. [15]. Prenatal vitamin-mineral formulas are advised in to meet their requirement.

There are different nutritional requirements throughout the life cycle. Over nutrition is the predominant problem in the developed countries, it has led to obesity and various chronic lifestyle diseases. Secondly, renewed focus on vegetables, fruits, whole grain, and legumes can help prevent weight gain problems and chronic illnesses, including cardiovascular diseases. National Academy of Sciences has proposed dietary reference intake (DRI) that are specific for various stages of life. Such guidelines are not meant for people who are ill or chronically ill or those who are at high risk of diseases due to age, genetic or lifestyle factors.

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Volume 2

Robert Kachko ND, LAc, Pina LoGiudice ND, LAc, in Textbook of Natural Medicine (Fifth Edition), 2020

Calorie Restriction

Overeating is a major modifiable risk factor for several age-related diseases, including PD. Calorie restriction (CR) is usually defined as 10% to 25% less caloric intake than the average Western diet. Throughout history, the majority of the world’s population has struggled to obtain food. The ability to overeat is a relatively new phenomenon, and accordingly, the amount of food one should eat has only recently become a subject of study. In a primate model of PD, a CR diet (30% reduced) decreased the progression of PD. Animals that had been fed the reduced-intake diet had more dopamine in their brains and more glial-cell-line–derived neurotrophic factor (GDNF), a small protein that promotes the survival of neurons. GDNF’s most prominent feature is its ability to support the survival of dopaminergic and motoneurons. The results suggest that CR extends the life span and increases the resistance of the brain to insults that involve metabolic compromise and excitotoxicity.69 As opposed to the attempts at augmenting antioxidant levels using exogenously supplied antioxidants, which have been largely unsuccessful, one of the proposed mechanisms of CR is enhanced production of antioxidants via intrinsic pathways.70 Given what is known about PD and CR, this theory is highly plausible and warrants further investigation.

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