Understanding Obesity

Compiled by John G. Connor, M.Ac., L.Ac., edited by Barbara  Connor, M.Ac., L.Ac.

Table of Contents

Introduction

Globally, one in three of the world’s adults are overweight and one in 10 is obese. By 2015, the World Health Organization (WHO) estimates the number of overweight adults will balloon to 2.3 billion — equal to the combined populations of China, Europe and the United States. (Roh et al 2012)

The global increase in body mass is an escalating societal concern. Concomitant environmental factors such as poor dietary habits, sedentary lifestyle, socioeconomic influences; and less frequently, genetic disorders that impact on hormone secretion and metabolism, result in weight gain. The WHO projects that by 2015, more than 700 million adults will be obese. (McArdle et al 2013) 

Obesity is a state of chronic low-grade systemic inflammation. This chronic inflammation is deeply involved in insulin resistance, which is the underlying condition of type 2 diabetes and metabolic syndrome. (Ota T 2013) 

Obesity has reached pandemic proportions and is rapidly surpassing smoking as the number one killer in the industrialized world, as well as costing an estimated $117 billion annually in related illnesses and loss of productivity. (Yarnell et al 2013)

This poses major economic and public health issues as some of the leading causes of mortality (ie, cardiovascular diseases and cancer) are strongly associated with obesity. Obesity also leads to a reduced lifespan and accelerates cellular processes similar to aging such as oxidative stress and disturbance in homeostatic pathways. (Carter et al 2013)

Several studies have reported that obesity, generally defined as a body mass index (BMI) >30, increases the risk of disease and all-cause mortality and reduces life expectancy. Obesity has not only been linked to reduced life expectancy but also to accelerated aging, as demonstrated by obese women having telomeres that were 240?bp shorter compared to lean women of similar age. (Businaro et al 2012)

The maximum years of life lost for white men aged 20 to 30 years with a severe level of obesity (BMI >45) is 13 and is 8 for white women. For men, this could represent a 22% reduction in expected remaining life span. Among black men and black women older than 60 years, overweight and moderate obesity were generally not associated with an increased years of life lost and only severe obesity resulted in years of life lost. However, blacks at younger ages with severe levels of obesity had a maximum years of life lost of 20 for men and 5 for women. (Fontaine et al 2003)

Obesity and associated chronic inflammation initiate a state of insulin resistance (IR). The secretion of chemoattractants such as MCP-1 and MIF and of cytokines IL-6, TNF-a, and IL-1ß, draw immune cells including dendritic cells, T cells, and macrophages into adipose tissue (AT). Dysfunctional AT lipid metabolism leads to increased circulating free fatty acids, initiating inflammatory signaling cascades in the population of infiltrating cells. A feedback loop of pro-inflammatory cytokines exacerbates this pathological state, driving further immune cell infiltration and cytokine secretion and disrupts the insulin signaling cascade. Disruption of normal AT function is causative of defects in hepatic and skeletal muscle glucose homeostasis, resulting in systemic IR and ultimately the development of type 2 diabetes. (McArdle et al 2013)

High Fructose Corn Syrup and Obesity

Excessive fructose intake from high-fructose corn syrup (HFCS) and sucrose has been implicated as a driving force behind the increasing prevalence of obesity and its downstream cardiometabolic complications including hypertension, gout, dyslidpidemia, metabolic syndrome, diabetes, and non-alcoholic fatty liver disease (NAFLD). Most of the evidence to support these relationships draws heavily on ecological studies, animal models, and select human trials of fructose overfeeding. (Ha et al 2013)

  1. The meta-analysis articles found that consumption of high fructose corn syrup (HFCS) beverages can contribute to childhood obesity, and limitation of sweetened beverages may help decrease obesity in children. (Morgan RE 2013)
  2. The fast food diet which includes fructose and fats produces a gene expression signature of increased hepatic fibrosis, inflammation, endoplasmic reticulum stress and lipoapoptosis. (Basaranoglu et al 2013)
  3. Excess fructose intake causes hypertriglyceridemia and hepatic insulin resistance in sedentary humans. Since exercise improves insulin sensitivity in insulin-resistant patients, we hypothesized that it would also prevent fructose-induced hypertriglyceridemia. This study was therefore designed to evaluate the effects of exercise on circulating lipids in healthy subjects fed a weight-maintenance, high-fructose diet.The data from this study indicate that exercise prevents the dyslipidemia induced by high fructose intake independently of energy balance. (Egli et al 2013)
  4. Adverse effects of hypercaloric, high-fructose diets on insulin sensitivity and lipids in human subjects have been shown repeatedly. The implications of fructose in amounts close to usual daily consumption, however, have not been well studied. This study assessed the effect of moderate amounts of fructose and sucrose compared with glucose on glucose and lipid metabolism. This study clearly shows that moderate amounts of fructose and sucrose significantly alter hepatic insulin sensitivity and lipid metabolism compared with similar amounts of glucose. (Aeberli et al 2013)
  5. In addition to the malnutrition of a sedentary lifestyle, high calorie intake leads to obesity with many negative health consequences. Macrophages infiltrate adipose tissue and induce chronic inflammation by secreting pro-inflammatory cytokines, including COX-2 and iNOS, among other mediators of inflammation. Free fatty acids mediate adipose tissue signalling through toll-like receptor 4 and the expression of these pro-inflammatory mediators via NF-?B or JNK. PPAR ? activators can inhibit the activation of NF-?B, down-regulating the expression of pro-inflammatory cytokines. (Jungbauer & Medjakovic 2012)
  6. This experiment tested whether consuming ‘free’ fructose (high fructose corn syrup) had a greater impact on body weight and metabolic abnormalities than when consumed ‘bound’ within the disaccharide sucrose. Animals with access to sugar beverages consumed 20% more calories, but did not show greater weight gain than controls. Nevertheless, they developed larger abdominal fat pads, higher triglyceride levels and exhibited impaired insulin/glucose homeostasis. Comparison of the two sugars revealed increased fasting glycaemia in the FructoseGlucose group, but not in the Sucrose group, whereas the Sucrose group was more active in an open field. A metabolic profile indicating increased risk of diabetes mellitus and cardiovascular disease was observed in animals given access to sugar-sweetened beverages. Notably, ‘free’ fructose disrupted glucose homeostasis more than did ‘bound’ fructose, thus posing a greater risk of progression to type 2 diabetes. (Sheludiakova et al 2012)
  7. Higher intake of added sugars is associated with higher energy intake and lower diet quality, which can increase the risk for obesity, prediabetes, type 2 diabetes, and cardiovascular disease. (Fitch et al 2012)
  8. Consumption of added sugars among US adolescents is positively associated with multiple measures known to increase cardiovascular disease risk. (Welsh et al 2011)
  9. In humans, fructose has long been known to increase plasma triglyceride concentrations. In addition, when ingested in large amounts as part of a hypercaloric diet, it can cause hepatic insulin resistance, increased total and visceral fat mass, and accumulation of ectopic fat in the liver and skeletal muscle. Several effects of a high-fructose diet in humans can be observed with high-fat or high-glucose diets as well, suggesting that an excess caloric intake may be the main factor involved in the development of the metabolic syndrome. Consumption of sweetened beverages is however clearly associated with excess calorie intake, and an increased risk of diabetes and cardiovascular diseases through an increase in body weight. This has led to the recommendation to limit the daily intake of sugar calories. (Tappy et al 2010)
  10. Fructose acutely increases thermogenesis, triglycerides and lipogenesis as well as blood pressure, but has a smaller effect on leptin and insulin release than comparable amounts of glucose. In controlled feeding studies, changes in body weight, fat storage and triglycerides are observed as well as an increase in inflammatory markers. The present review concludes on the basis of the data assembled here that in the amounts currently consumed, fructose is hazardous to the cardiometabolic health of many children, adolescents and adults. (Bray GA 2010)
  11. Metabolic syndrome is a cluster of common pathologies, including abdominal obesity linked to an excess of visceral fat, fatty liver, insulin resistance, hyperinsulinemia, dyslipidemia, and hypertension. Trends in all of these alterations are related to the consumption of dietary fructose and the introduction of high-fructose corn syrup (HFCS) as a sweetener in soft drinks and other foods. Experimental and clinical evidence suggests a progressive association between HFCS consumption, obesity, and the other injury processes. However, experimental HFCS consumption seems to produce some of the changes associated with metabolic syndrome even without increasing the body weight. Metabolic damage associated with HFCS probably is not limited to obesity-pathway mechanisms. (Ferder et al 2010)
  12. Compared with glucose-sweetened beverages, consumption of fructose-sweetened beverages with meals elevates postprandial plasma triglycerides (TG) and lowers 24-h insulin and leptin profiles in normal-weight women. The effects of fructose, compared with glucose, ingestion on metabolic profiles in obese subjects has not been studied. In obese subjects, consumption of fructose-sweetened beverages with meals was associated with less insulin secretion, blunted diurnal leptin profiles, and increased postprandial TG concentrations compared with glucose consumption. Increases of TGs were augmented in obese subjects with insulin resistance, suggesting that fructose consumption may exacerbate an already adverse metabolic profile present in many obese subjects. (Teff et al 2009)
  13. Consumption of fructose-sweetened beverages increased postprandial triacycleglyceride and fasting apoB concentrations, and the present results suggest that long-term consumption of diets high in fructose could lead to an increased risk of cardiovascular disease. (Swarbrick et al 2008)
  14. There is also considerable evidence that fructose, rather than glucose, is the more damaging sugar component in terms of cardiovascular risk. (Brown et al 2008)
  15. In terms of fructose and hormonal regulators of energy, fructose tends to blunt insulin responses compared with glucose; these findings are very consistent. (Melanson et al 2008)
  16. The present study extends results from prior studies that reported that a greater intake of soft drinks is associated with increased prevalence of metabolic syndrome, higher risk of obesity, high blood pressure, and diabetes mellitus. The similar metabolic hazard posed by both regular and diet soft drinks is noteworthy given the lack of calories in the latter; however, other studies have also reported associations of diet soft drinks with weight gain in boys and with hypertension in adult women. (Dhingra et al 2007)
  17. Diets high in sugars have been associated with various health problems, including dental caries, dyslipidemias, obesity, bone loss and fractures, and poor diet quality. (Johnson & Frary 2001)

Food Addiction

Food addiction may play a role in the obesity epidemic.  While food addiction certainly does not explain all cases of obesity, the increased number of persons with interest in eating above that which is required for the basic energetic needs of survival, suggests that food intake is no longer simply for survival purposes. It has been demonstrated that rats overeating sugar solution developed many behavioral and brain changes resembling the effects of drugs of abuse. Also similar to drug addictions, the reward circuitry of the brain, especially the dopaminergic system, was found to be involved in animals overfed highly palatable foods (Yarnell et al 2013)

Not all foods are currently implicated in the development of food addictions. Foods that are thought to be addictive tend to be highly palatable and are rich in fats, sugars, salt, and are calorie dense. Further, these foods often are comprised of synthetic combinations of ingredients that may make them more potentially addictive than traditional foods. Beyond this, research has recently demonstrated that each of these nutrient elements affects specific neurotransmitter systems in the brain. Genetics may play a role in the underlying addictive feeding. (Yarnell et al 2013)

A number of excellent reviews have been written outlining the endogenous neurotransmitter involvement in food addicts, including papers on opiates , neuropeptide Y and leptin, cannabinoids, and dopamine. (Yarnell et al 2013)

The neuropsychiatric evidence integrated here suggests that salted food acts like an, albeit mild, opiate agonist which drives overeating and weight gain. The opiate dependent group studied developed a 6.6% increase in weight during opiate withdrawal. Salted Food may be an addictive substance that stimulates opiate and dopamine receptors in the brain’s reward and pleasure center more than it is “tasty”, while salted food preference, urge, craving and hunger may be manifestations of opiate withdrawal. Salted food and opiate withdrawal stimulate appetite, increases calorie consumption, augments the incidence of overeating, overweight, obesity and related illnesses. Obesity and related illnesses may be symptoms of Salted Food Addiction. (Cocores & Gold 2009)

Sugar, as common as it is, nonetheless meets the criteria for a substance of abuse and may be “addictive” for some individuals when consumed in a “binge-like” manner. This conclusion is reinforced by the changes in limbic system neurochemistry that are similar for the drugs and for sugar. The effects we observe in this animal study are smaller in magnitude than those produced by drug of abuse such as cocaine or morphine; however, the fact that these behaviors and neurochemical changes can be elicited with a natural reinforcer is interesting. (Avena et al 2008)

Leptin Resistance and Insulin Resistance in Obesity

An important common feature of obesity and aging is the development of resistance to certain hormones such as insulin and leptin, which triggers metabolic dysregulations such as type 2 diabetes and failure to regulate food intake as well as fat distribution. Since obese patients will make up an important proportion of the elderly population in the near future, it is important to determine the causes and effects of leptin resistance in age-related diseases. (Carter et al 2013)

* Leptin is a hormone that plays a key role in regulating energy intake and expenditure, including appetite and hunger. Leptin signals the brain that the body has had enough to eat, producing a feeling of satiety. (wikipedia.org)

* Leptin acts as a major adipostat: it suppresses food intake and activates catabolic pathways associated with increased energy production. It improves the peripheral insulin sensitivity and affects beta-cell function. Ghrelin, a circulating orexigenic hormone, stimulates food intake. (Koleva et al 2013)

Insulin resistance is associated with obesity and is a central component of type 2 diabetes, leading to altered glucose and lipid metabolism in adipose tissue, liver, and skeletal muscles. Insulin resistance is characterized by a decrease in insulin signaling mainly in the Insulin Receptor Substrate (IRS)/PI-3-kinase/PKB axis that is responsible for most of the metabolic actions of the hormone. It is now recognized that a chronic low-grade systemic and local inflammation that develops during obesity could connect obesity to the development of insulin resistance. (Tanti et al 2012)

Once established, leptin resistance increases adipose tissue inflammation through preadipocytes activation and seems to negatively impact cognitive function. When comparing the effects of leptin resistance to the metabolic dysfunctions observed in aging, leptin resistance appears to be an early contributor to the development of metabolic abnormalities in old age. Studies on leptin show that this hormone is central to the dysregulations observed in aging and obesity. Exercise could be a large-scale and affordable manner of maintaining leptin signaling. (Carter et al 2013)

Leptin is known as a key appetite-regulating hormone, which effects on appetite, energy expenditure, behavior, and glucose metabolism. Much evidence suggests that insulin and leptin act in the brain as adiposity negative feedback signals. Indeed, recent studies revealed that leptin has the effect to normalize hyperglycemia and hyperinsulinemia and to increase insulin sensitivity. (Amitani et al 2013)Hyperleptinemia, which either manifests gradually in association with age-related obesity or is produced rapidly by the consumption of energy-enriched diets, is associated with decreased brain leptin concentrations in rodents and humans. (Amitani et al 2013)

  1. In obese subjects, consumption of fructose-sweetened beverages with meals was associated with less insulin secretion, blunted diurnal leptin profiles, and increased postprandial triglyceride (TG) concentrations compared with glucose consumption. Increases of TGs were augmented in obese subjects with insulin resistance, suggesting that fructose consumption may exacerbate an already adverse metabolic profile present in many obese subjects. (Teff et al 2009)
  2. The increased use of high fructose corn syrup (HFCS) in the United States mirrors the rapid increase in obesity. The digestion, absorption, and metabolism of fructose differ from those of glucose. Hepatic metabolism of fructose favors de novo lipogenesis. In addition, unlike glucose, fructose does not stimulate insulin secretion or enhance leptin production. Because insulin and leptin act as key afferent signals in the regulation of food intake and body weight, this suggests that dietary fructose may contribute to increased energy intake and weight gain. Furthermore, calorically sweetened beverages may enhance caloric overconsumption. Thus, the increase in consumption of HFCS has a temporal relation to the epidemic of obesity, and the overconsumption of HFCS in calorically sweetened beverages may play a role in the epidemic of obesity. (Bray et al 2004)
  3. Consumption of high fructose meals produced a rapid and prolonged elevation of plasma triglycerides compared with the high glucose day. Because insulin and leptin, and possibly ghrelin, function as key signals to the central nervous system in the long-term regulation of energy balance, decreases of circulating insulin and leptin and increased ghrelin concentrations, as demonstrated in this study, could lead to increased caloric intake and ultimately contribute to weight gain and obesity during chronic consumption of diets high in fructose. (Teff et al 2004)

Sugar, Diabetes, Obesity and Cancer

  1. Although there is inconsistency among the clinical studies, it seems that overweight and obesity are related to a modestly increased thyroid cancer risk. (Pappa & Alevizaki 2013)
  2. Epidemiological and clinical data have clearly demonstrated that non-alcoholic steatohepatitis (NASH) predisposes risk to the development of hepatocellular carcinoma. NASH is the liver manifestation of metabolic syndrome, which constellates obesity, insulin resistance and dyslipidemia. (Yu et al 2013)
  3. A positive association between obesity and the risk of incident postmenopausal breast cancer has been consistently observed in epidemiologic studies. Although most studies of premenopausal women have not found a similar relationship between breast cancer and obesity, the prognosis for both pre- and postmenopausal breast cancer is substantially worse among obese than normal-weight individuals. (Ligibel & Strickler 2013)
  4. The worldwide epidemic of obesity is associated with increasing rates of the metabolic syndrome and type 2 diabetes. Epidemiological studies have reported that these conditions are linked to increased rates of cancer incidence and mortality. (Ferguson et al 2013)
  5. Epidemiology studies have shown that obesity increases risk for colorectal cancer (CRC). (Flores et al 2012)
  6. Cancer cell metabolism is characterized by high rates of glucose uptake and anaerobic glycolysis. Sugar consumption has increased dramatically in the industrialized world, with refined fructose intake skyrocketing upwards in the USA over the past 30 years. Fructose intake is associated with increased risk of pancreatic and small intestinal cancers, and possibly others. Whereas glucose favors overall growth kinetics, fructose enhances protein synthesis and appears to promote a more aggressive cancer phenotype. Fructose has become ubiquitous in our food supply, with the highest consumers being teens and young adults. (Port et al 2012)
  7. The majority of human tumors express mutant forms of p53 at high levels, promoting gain of oncogenic functions and correlating with disease progression, resistance to therapy and unfavorable prognosis. p53 mutant accumulation in tumors is attributed to the ability to evade degradation by the proteasome, the only currently recognized machinery for p53 disruption. We report here that glucose restriction (GR) induces p53 mutant deacetylation, routing it for degradation via autophagy. Depletion of p53 leads, in turn, to robust autophagic activation and to cell death, while expression of degradation-defective mutant p53 blocks autophagy and enables survival to GR. Furthermore, we found that a carbohydrate-free dietetic regimen that lowers the fasting glucose levels blunts p53 mutant expression and oncogenic activity relative to a normal diet in several animal model systems. These findings indicate that the stability of mutant forms of p53 is influenced by the levels of glucose and by dietetic habits. They also unravel the existence of an inhibitory loop between autophagy and mutant p53 that can be exploited therapeutically. (Rodriguez et al 2012)
  8. Apoptosis is one of the most potent defenses against cancer since this process eliminates potentially deleterious, mutated cells. (Davis et al 2010)  However, glucose stimulates anti-apoptotic signaling pathways.  It is well documented that increased glucose metabolism is characteristic of cancer cells and cells stimulated by growth factors.  Glucose metabolism can act as a direct survival mechanism in highly proliferating cells, such as cancer cells and activated lymphocytes. Highly proliferative cells such as growth-factor stimulated or cancerous cells often have high rates of glucose metabolism and are resistant to cell death. (Zhao et al 2008)
  9. In this study whereas only 1 mouse on the Western diet achieved a normal life span, due to cancer-associated deaths, more than 50% of the mice on the low carbohydrate diet reached or exceeded the normal life span. Taken together, our findings offer a compelling preclinical illustration of the ability of a low carbohydrate diet in not only restricting weight gain but also cancer development and progression. (Ho et al 2011)
  10. The results of this study suggest that high glucose promotes pancreatic cancer cell proliferation via the induction of EGF expression and transactivation of EGFR. (Han et al 2011)
  11. Diabetes as indicated by elevated fasting blood glucose was independently associated with a significantly higher risk of all-cause mortality in patients with non-small cell lung cancer (NSCLC), indicating that diabetes or hyperglycemia effectively controlled may present an opportunity for improving prognosis in NSCLS patients with abnormal glucose level. (Luo et al 2011)
  12. Overall, studies indicate that diabetes risk increases twofold for liver, pancreatic, and endometrial cancer and 1.2- to 1.5-fold for colorectal, breast, and bladder cancer, but is associated with decreased risk for prostate cancer. Diabetes is an independent risk factor for liver cancer. Cancer patients with diabetes relapse, and die, sooner than those without the disease, and diabetics at the time of their cancer diagnosis have a 41% higher relative risk of death than nondiabetics. Diabetes is characterized by high levels of both insulin and blood sugar, and both promote cancer cell proliferation in preclinical models, according to Geoffrey Kabat, Ph.D., senior epidemiologist at the Albert Einstein College of Medicine in New York. (Brower V 2012)
  13. Excess weight has been associated with increased mortality from all cancers combined and for cancers of several specific sites. Obesity-related dysregulation of adipokines has the ability to contribute to tumorigenesis and tumor invasion via metastatic potential. (Fair & Montgomery 2009)
  14. Restriction of calories by 10 to 40% has been shown to decrease cell proliferation, increasing apoptosis through anti-angiogenic processes. (Fair & Montgomery 2009)

Obesity and Cardiovascular Disease

  1. Although population ageing is regarded as an important contributor to the atrial fibrillation epidemic, obesity and its associated cardiometabolic comorbidities may represent the principal driving factor behind the current and projected atrial fibrillation epidemic. Obesity-related risk factors, such as hypertension, vascular disease, obstructive sleep apnea and pericardial fat, are thought to result in atrial electro-structural dysfunction. (Abed & Wittert 2013)
  2. Obesity affects the development of hypertension and other metabolic risk factors. And the mechanism of development hypertension has been investigated from adipocyte standpoints. Recently, physiology or pathophysiology functions of adipocyte including TNF-alpha or leptin have been elucidated. Leptin makes sympathetic nerve activity by effects of the central nerve system. TNF-alpha induces insulin resistance. These effects cause hypertension. (Saitoh S 2013)
  3. Obesity is one of the more common vascular risk factor for heart failure (HF) and is found in >40% of HF patients. Obesity in HF and cardiovascular disease populations is associated with numerous adverse outcomes, including increased mortality risk, reduced quality of life, poor emotional and physical well-being, and increased depressive symptomatology. (Alosco et al 2012) 
  4. Abdominal obesity is independently associated with hypertension after adjusting for body mass index (BMI). After adjusting for covariables and parameterizing BMI categories and abdominal obesity the new variable showed a progressive increase in the odds of hypertension. Both BMI and waist circumference should be included in models assessing hypertension risks. (Ostechega et al 2012)
  5. Chinese adults over age 40 years with obesity have a significantly higher risk of hypertension and type 2 diabetes. (He et al 2009)

Obesity and Cognitive Impairment

  1. Central obesity was significantly associated with the risk of cognitive impairment in Shanghai rural elderly population. (Cui et al 2013) 
  2. We demonstrate for the first time that diet-induced obesity (DIO) induces higher levels of reactive oxygen species (ROS) in the brain and promotes cognitive impairment. Importantly, we also demonstrate for the first time in these studies that both body weight and adiposity are tightly correlated with the level of ROS. Interestingly, ROS were not correlated with cognitive decline in this model. Alterations in the antioxidant/detoxification Nrf2 pathway, superoxide dismutase, and catalase activity levels were not significantly altered in response to DIO. However, a significant impairment in glutathione peroxidase was observed in response to DIO. Taken together, these data demonstrate for the first time that DIO increases the levels of total and individual ROS in the brain and highlight a direct relationship between the amount of adiposity and the level of oxidative stress within the brain. (Freeman et al 2013)
  3. This study shows that as the body mass index increased, subjects had a higher probability of dementia; additionally, it suggests that abdominal obesity could be related to a higher probability of dementia. (Chang et al 2012)
  4. The conditions of chronic obesity and overweight status are risk factors for lower cognitive performance, cognitive decline, cognitive deficit, and dementia. But lower cognitive performance early in life itself may be a risk factor for an increase in body weight over time. (Elias et al 2012)
  5. Obesity is associated with increased risk of Alzheimer’s Disease as well as cognitive dysfunction and neuroimaging abnormalities independent of neurological and cardiovascular disease. (Alosco et al 2012)
  6. There is growing evidence that obesity represents a risk for enhanced gray matter density changes comparable to those demonstrated for mild cognitive impairment in the elderly. (Mueller et al 2012)
  7. There is a general consensus that the aberrant inflammatory response underlying the metabolic syndrome may arise from a deregulation of the endocrine homeostasis of adipose tissue. Hence, it might be assumed that the subclinical inflammation of adipose tissue may interact with the impaired central inflammatory response, leading to neurodegeneration. (Misiak et al 2012)
  8. A bulk of studies has provided evidence to support the role of obesity as a risk factor for Alzheimer’s Disease development and the possible role of psychosocial factors (e.g., professional achievements, stimulant mental activities, social engagement, and physical activity) as protective factors. (Businaro et al 2012)
  9. In middle aged or aged residents, glucose tolerance status, obesity, and especially central obesity may be the important contributors to cognitive impairment. (Lu et al 2012)
  10. Recent findings suggest obesity is associated with reduced memory performance in older adults. The present study examined whether similar deficits also exist in younger adults. Results showed obese individuals had poorer memory performance when comparing persons across the adult lifespan (age 21-82 yr), but also when examining only younger and middle-aged adults (age 21-50 yr). (Gunstad et al 2006)

Benefits of Botanicals and Nutrients in Obesity

  1. Ginseng (the root of Panax ginseng C. A. MEYER), which contains protopanaxadiols and protopanaxatriols as its main constituents, has been used for many disorders, such as cancer, diabetes, inflammation, and hyperlipidemia. Of these ginsenosides, protopanaxadiol ginsenoside Rh2 alone is reported to inhibit adipogenesis in 3T3-L1 in vitro. Based on this study, ginsenoside Rh1 may ameliorate obesity, by inhibiting adipocyte differentiation and inflammation. (Gu et al 2013)
  2. Taken together, germinated brown rice (GBR) administration suppressed body weight gain and lipid accumulation in the liver and epididymal adipocytes, and improved serum lipid profiles, in part, by controlling adipogenesis through a reduction in transcriptional factors. These results suggest that GBR is a potential agent against obesity. (Ho et al 2012)
  3. Supplementation with omega-3 long-chain polyunsaturated fatty acids (n-3 LC-PUFAs) might improve some obesity-associated metabolic syndrome features such as insulin resistance, hypertension and dyslipidemia by decreasing plasma triglycerides. Moreover, the blood pressure-lowering and anti-inflammatory properties of these fatty acids and their benefits in vascular function might confer cardioprotection. (Lorente-Cebrian et al 2013)
  4. Epididymal adipose tissue and liver weights were significantly decreased in mice fed high-fat diet (HFD) plus 2% green tomato extract (GTE) compared to those in HFD. Serum total cholesterol and low-density lipoprotein cholesterol levels in mice fed GTE were modestly reduced, and liver total cholesterol level was strongly decreased in HFD plus GTE-fed mice compared to that in HFD-fed mice. Adenosine-monophosphate-activated protein kinase (AMPK) and acetyl-CoA carboxylase phosphorylation in liver from HFD plus GTE-fed mice was significantly elevated, and HMG-CoA reductase expression was also significantly decreased. GTE strongly decreased the expression of peroxisome proliferator-activated receptor gamma, CCAAT/enhancer-binding protein alpha and perilipin in the adipose tissue of mice fed HFD plus GTE. Our results indicate that the antiobesity effects of GTE may be associated with activation of the AMPK pathway. (Choi et al 2013)
  5. Tests of hematological, cardiovascular, liver, and kidney function following berberine treatment showed no detrimental side effects to this natural compound. Collectively, this study demonstrates that berberine is a potent lipid-lowering compound with a moderate weight loss effect, and may have a possible potential role in osteoporosis treatment/prevention. (Hu et al 2012)
  6. Administration of garlic significantly reduced high-fat diet (HFD)-induced body weight, epididymal fat accumulation, hyperlipidemia and hypercholesterolemia. Consequently, the atherogenic indexes were reduced by 83% and 91%, respectively, in 2% and 4% garlic supplemented group. Liver steatosis induced by HFD was ameliorated by garlic supplementation. Furthermore, garlic affected the down regulation of expression patterns of epididymal adipose tissue genes such as peroxisome proliferator-activated receptor gamma (PPAR gamma), acetyl CoA carboxylase (ACC), adipose specific fatty acid binding protein (aP2), and glycerol-3-phosphate dehydrogenase (GPDH). These results suggest that garlic may have a potential benefit in preventing obesity. (Kim & Kim 2011)
  7. Resveratrol decreased adipogenesis and viability in maturing preadipocytes; these effects were mediated not only through down-regulating adipocyte specific transcription factors and enzymes but also by genes that modulate mitochondrial function. Additionally, resveratrol increased lipolysis and reduced lipogenesis in mature adipocytes. In addition, combining resveratrol with other natural products produced synergistic activities from actions on multiple molecular targets in the adipocyte life cycle. Treatment of mice with resveratrol alone was shown to improve resistance to weight gain caused by a high-fat diet. (Baile et al 2011)
  8. High fat diet (HFD) induced obesity associated with a disturbed lipid profile, defective antioxidant stability, and high values of insulin resistance parameters; this may have implications for the progress of obesity related problems. Treatment with L-carnitine, or HMF (consisting of T. chebula, Senae, rhubarb, black cumin, aniseed, fennel and licorice) extract improved obesity and its associated metabolic problems in different degrees. Also HMF has antioxidant, hypolipidaemic insulin sensitizing effects. Moreover HMF might be a safe combination on the organs whose functions were examined, as a way to surmount the obesity state; and it has a distinct anti-obesity effect. (Amin & Nagy 2009)
  9. These results suggest that the perilla leaf extract supplement suppressed body weight gain and improved the blood lipid profiling, in part by down-regulating adipogenic transcription factor and other specific target genes. (Kim & Kim 2009)
  10. Tart cherry intake was associated with reduced hyperlipidemia, percentage fat mass, abdominal fat (retroperitoneal) weight, retroperitoneal interleukin-6 (IL-6) and tumor necrosis factor-alpha (TNF-alpha) expression, and plasma IL-6 and TNF-alpha. Tart cherry diet also increased retroperitoneal fat PPAR-alpha and PPAR-gamma mRNA (P = .12), decreased IL-6 and TNF-alpha mRNA, and decreased nuclear factor kappaB activity. In conclusion, in at-risk obese rats fed a high fat diet, physiologically relevant tart cherry consumption reduced several phenotypes of metabolic syndrome and reduced both systemic and local inflammation. Tart cherries may reduce the degree or trajectory of metabolic syndrome, thereby reducing risk for the development of type 2 diabetes and heart disease. (Seymour et al 2009)
  11. Berberine from rhizoma coptidis is an oral hypoglycemic agent. It also has anti-obesity and anti-dyslipidemia activities. The action mechanism is related to inhibition of mitochondrial function, stimulation of glycolysis, activation of AMPK pathway, suppression of adipogenesis and induction of low-density lipoprotein (LDL) receptor expression. (Yin et al 2008)
  12. Bitter melon or bitter gourd (Momordica charantia) – The present study demonstrated that MC caused dose-dependent reductions in body weight and serum cholesterol concentration in male Sprague-Dawley rats. MC may, therefore, be useful in controlling body weight increase in individuals of growing age as well as be a potential agent in the management of overweight and obesity. (Yama et al 2010)
  13. Bitter melon or bitter gourd (Momordica charantia) is able to reduce blood glucose and lipids in both normal and diabetic animals. It may also protect beta cells, enhance insulin sensitivity and reduce oxidative stress. (Yin et al 2008)
  14. Considering all the evidence relating to diet and inflammation, the best diet for protecting against the metabolic derangements associated with obesity and metabolic syndrome would be high in fibre-rich cereals, fruit, vegetables, fish, virgin olive oil and nuts; moderate in wine; and low in meat, processed meat foods and trans-fatty acids. (Bullo et al 2007)
  15. After 12 days of treatment with ginseng berry extract (150 mg/kg body wt.), overall glucose exposure improved significantly, and the AUC decreased 31.0% (P < 0.01). In addition, we observed that body weight did not change significantly after ginseng root extract (150 mg/kg body wt.) treatment, but the same concentration of ginseng berry extract significantly decreased body weight (P < 0.01). These data suggest that, compared to ginseng root, ginseng berry exhibits more potent anti-hyperglycemic activity, and only ginseng berry shows marked anti-obesity effects in ob/ob mice. (Dey et al 2003)

Benefits of Exercise in Weight and Fat Loss

The current physical activity guideline for adults of 30 minutes of moderate intensity activity daily, preferably all days of the week, is of importance for limiting health risks for a number of chronic diseases including coronary heart disease and diabetes. However for preventing weight gain or regain this guideline is likely to be insufficient for many individuals in the current environment. There is compelling evidence that prevention of weight regain in formerly obese individuals requires 60-90 minutes of moderate intensity activity or lesser amounts of vigorous intensity activity. Although definitive data are lacking, it seems likely that moderate intensity activity of approximately 45 to 60 minutes per day, or 1.7 Physical Activity Level is required to prevent the transition to overweight or obesity. For children, even more activity time is recommended. (Saris et al 2003)

  1. Based on the small number of short-term trials currently available on overweight children, both diet-only and diet plus exercise interventions resulted in weight loss and metabolic profile improvement. However, the addition of exercise to dietary intervention led to greater improvements in levels of high-density lipoprotein cholesterol (3.86 mg/dL; 95% CI, 2.70 to 4.63), fasting glucose (-2.16 mg/dL; 95% CI, -3.78 to -0.72), and fasting insulin (-2.75 µIU/mL; 95% CI, -4.50 to -1.00) over 6 months. The diet-only intervention caused greater reductions in levels of triglycerides (at the end of active intervention) and low-density lipoprotein cholesterol (at subsequent follow-up). (Ho et al 2013)
  2. This study demonstrates the positive impact of a strength training physical exercise program on reduction of body fat, metabolic syndrome and cardiovascular risk factors. This study supports the use of exercise as a treatment for obesity and its comorbidities in schoolchildren. (Vasquez et al 2013)
  3. Aerobic training is the most prescribed exercise modality for the management of pediatric obesity. There is strong evidence that it decreases waist circumference, percent body fat and visceral fat, increases cardiorespiratory fitness, and decreases blood pressure in obese adolescents. (Alberga et al 2013)
  4. One proposed mechanism linking obesity to chronic diseases is an alteration in adipose-derived adiponectin and leptin levels. We investigated the effects of 12-month reduced calorie, weight loss and exercise interventions on adiponectin and leptin concentrations. The reduced calorie diet had a 10% weight-loss goal. The exercise intervention consisted of 45 min of moderate-to-vigorous aerobic activity 5 days per week. Adiponectin increased by 9.5% in the diet group and 6.6% in the diet + exercise group (both P = 0.0001 vs. control). Compared with controls, leptin decreased with all interventions. Weight loss through diet or diet + exercise increased adiponectin concentrations. Leptin concentrations decreased in all of the intervention groups, but the greatest reduction occurred with diet + exercise. (Abbenhardt et al 2013)

Plasma adiponectin levels have also been reported to be reduced in obese humans, particularly those with visceral obesity, and to correlate inversely with insulin resistance. Prospective and longitudinal studies have shown that lower adiponectin levels are associated with a higher incidence of diabetes. Reduced plasma adiponectin levels are also commonly observed in a variety of states frequently associated with insulin resistance, such as cardiovascular disease and hypertension. (Kadowaki et al 2006)

Leptin is a mediator of long-term regulation of energy balance, suppressing food intake and thereby inducing weight loss. (Klok et al 2007) <ol >

  • Minority breast cancer survivors were recruited and retained in a weight loss study. Six months of the Curves program resulted in moderate weight loss, but weight loss was not maintained postintervention. (Greenlee et al 2013)
  • In many interventions that are based on an exercise program intended to induce weight loss, the mean weight loss observed is modest and sometimes far less than the individual expected. The individual responses are also widely variable, with some individuals losing a substantial amount of weight, others maintaining weight, and a few actually gaining weight. The media have focused on the sub-population that loses little weight, contributing to a public perception that exercise has limited utility to cause weight loss. The purpose of the symposium was to present recent, novel data that help explain how compensatory behaviors contribute to a wide discrepancy in exercise-induced weight loss. The presentations provide evidence that some individuals adopt compensatory behaviors, i.e. increased energy intake and/or reduced activity, that offset the exercise energy expenditure and limit weight loss. (Melanson et al 2013)
  • In frail, obese older adults, lifestyle interventions associated with weight loss improve insulin sensitivity and other cardiometabolic risk factors, but continued improvement in insulin sensitivity is only achieved when exercise training is added to weight loss. (Bouchonville et al 2013)
  • We evaluated the individual and combined effects of a reduced-calorie weight loss diet and exercise on serum sex hormones in overweight and obese postmenopausal women. Compared with controls, estrone decreased 9.6% with diet, 5.5%  with exercise, and 11.1% with diet + exercise. Estradiol decreased 16.2% with diet, 4.9% with exercise, and 20.3%  with diet + exercise. SHBG increased 22.4% with diet and 25.8% with diet + exercise. Free estradiol decreased 21.4% with diet and 26.0% with diet + exercise. Free testosterone decreased 10.0% with diet and 15.6% with diet + exercise. Greater weight loss produced stronger effects on estrogens and SHBG. Weight loss significantly lowered serum estrogens and free testosterone, supporting weight loss for risk reduction through lowering exposure to breast cancer biomarkers. (Campbell et al 2012)
  • Recent guidelines on exercise for weight loss and weight maintenance include resistance training as part of the exercise prescription. Yet few studies have compared the effects of similar amounts of aerobic and resistance training on body mass and fat mass in overweight adults. Balancing time commitments against health benefits, it appears that aerobic training is the optimal mode of exercise for reducing fat mass and body mass, while a program including resistance training is needed for increasing lean mass in middle-aged, overweight/obese individuals. (Willis et al 2012)
  • One of the basic effects of exercise training is augmenting oxidative capacity of skeletal muscles, which results in an improvement in the rate of whole body fat oxidation. Exercise also activates AMP kinase, which stimulates fatty acid oxidation, glucose uptake, and mitochondrial biogenesis. (Golbidi et al 2012)
  • Low intensity (40% of V’O(2)max) physical activity favors fat oxidation and it seems advisable to encourage obese adolescents to perform low intensity physical activity which is more feasible and acceptable than intense exercise. (Lazzer et al 2011)
  • Total fat oxidized was significantly higher during the low-intensity than during high-intensity exercise in obese adolescents. However, the equicaloric exercise intensity did not influence energy expenditure, fat and carbohydrate oxidation rate during the recovery period. (Lazzer et al 2010)
  • There is strong evidence that weight loss in overweight and obese individuals improves risk factors for diabetes and CVD. Additional evidence indicates that weight loss and the associated diuresis reduce blood pressure in both overweight hypertensive and nonhypertensive individuals, reduce serum TG levels, increase high-density lipoprotein cholesterol levels, and may produce some reduction in low-density lipoprotein cholesterol concentrations. Of interest, even if weight loss is minimal, obese individuals showing a good level of cardiorespiratory fitness are at reduced risk for cardiovascular mortality than lean but poorly fit subjects. (Poirier & Despres 2001)

Benefits of Acupuncture in Obesity

  1. Electroacupuncture (EA) stimulation of ST 36-SP 6 can reduce body weight in rats with simple obesity, and the effect of higher intensity of EA is apparently better. Accordingly, EA intervention induces down-regulation of SOCS-3 and PPAR-gamma mRNA expression in the epididymis adipose tissue. (Gao et al 2013)
  2. Combination of different forms of acupuncture with diet and exercise seems to be necessary for achieving and maintaining weight loss.  Further prospective clinical trials are needed to establish the effectiveness of this complementary method for obesity treatment. (Belivani et al 2013)
  3. Chinese herbal medicine and acupuncture were more effective than placebo or lifestyle modification in reducing body weight. They had a similar efficacy as the Western anti-obesity drugs but with fewer reported adverse effects. However, these conclusions were limited by small sample size and low quality of methodologies. (Sui et al 2012)
  4. Acupuncture therapy can significantly decrease BMI and delay the digesting time and control the appetite in obesity patients, which may contribute to its effect in body weight reduction. (Yao et al 2012)
  5. Acupuncture intervention has a significant effect on reducing abdominal obesity in abdominal obesity patients. (Liang et al 2012)
  6. The results suggest that acupuncture reduced body weight in the obese women, and the weight loss occurred earlier in the treatment process for simple obesity than perimenopausal obesity. (Wang et al 2012)
  7. Auricular acupuncture in combination with diet restriction was effective for weight loss and dyslipidemia. (Abdi et al 2012)
  8. Acupuncture combined with dietary adjustments and aerobic exercise can reduce the body weight, BMI and serum leptin level, which is better than dietary adjustments plus aerobic exercise. (Yang et al 2010)
  9. To compare the therapeutic effects of acupuncture combined with diet adjustment and aerobic exercise and simple diet adjustment combined with aerobic exercise for treatment of simple obesity, in order to scientifically evaluate the therapeutic effect of acupuncture combined with diet adjustment and aerobic exercise for simple obesity. Both two treatments can decrease the body weight and waist-hip ratio (WHR) of patients with simple obesity, while the effect of acupuncture combined with diet adjustment and aerobic exercise is more obvious in the early stage of the treatment for body weight and WHR. (Yang et al 2010)

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Compassionate Acupuncture and Healing Arts, providing craniosacral acupuncture, herbal and nutritional medicine in Durham, North Carolina. Phone number 919-309-7753.

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