Obesity and Overweight Conditions

Paul L. Reller L.Ac. / Last Updated: August 03, 2017

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Information Resources / Additional Information and Links to Scientific Studies

  1. A 2010 study at Yale University Medical School showed that the rise in the percentage of the population in the United States that are obese correlates with the use of non-caloric artificial sweeteners, such as aspartame and sucralose, and outlines how these chemicals are more problematic in the cycle of addiction than sugars themselves, creating the food cravings but not satisfying the reward mechanism: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2892765/
  2. A 2009 statement from the American Heart Association Committee of the Council on Nutrition stated that it is now clear that increased intake of sugars in the diet is a major cause of both the alarming rise in obesity and the failure to decrease cardiovascular disease and mortality in the United States. This study clearly outlines how various sugars in a variety of processed foods, but especially in sugary drinks, whether cane sugar, high fructose corn syrup, or other sugar substitutes are used, contribute greatly to addictions, obesity, Metabolic Syndrome and cardiovascular disease: http://circ.ahajournals.org/content/120/11/1011.full
  3. A 2016 study by experts at the University of California Los Angeles, led by the director the Dieting, Stress and Health Laboratory (DISH) at UCLA, found that there is no universal and direct relationship between the oversimplified measure of obesity today, the BMI, and actual ill health, but that many tens of millions of Americans are being diagnosed as obese, treated in a too simplified manner, discriminated at work, and having their health insurance premiums raised dramatically and unfairly. This study, published in the International Journal of Obesity, shows that a real and objective measure of health is needed for overweight individuals, not a continued labeling and discrimination against those who have a problem with weight loss. These findings focus on recent employment and insurance discrimination, but actually say a lot about the approach to obesity in standard medicine, not focusing on the actual health, but just on the BMI and weight loss: http://www.nature.com/ijo/journal/vaop/naam/abs/ijo201617a.html
  4. A July, 2010 article by CNN outlines the current state of affairs with pharmaceuticals that treat obesity, and the newest combo drug seeking FDA approval, a combination of two older drugs with poor reputations, Topamax (topiramate) and part of the banned Phen-Fen. The benchmark for success with long-term use is only a 5% weight loss: http://www.cnn.com/2010/HEALTH/07/14/new.diet.drugs/index.html
  5. A review of Topiramate, or Topomax, the new drug touted in treatment of obesity is conservatively presented on Drugs.com, and the number of adverse physical effects from long-term use is alarming: http://www.drugs.com/pro/topiramate.html
  6. As far back as 2004, the FDA issued warnings about common side effects that occurred either acutely or after chronic use of Topiramate, the new drug touted for obesity, including the prevalence of systemic metabolic acidosis, which has many serious potential consequences over time: http://findarticles.com/p/articles/mi_hb4345/is_2_32/ai_n29074942/
  7. Studies at prestigious U.S. Universities have found that metabolic acidosis has serious chronic consequences, including the development of insulin resistance and metabolic syndrome, which is also one of the chief causes of obesity: http://www.nature.com/ajgsup/journal/v1/n1/full/ajgsup20125a.html
  8. A 2009 New York Times article reveals research that finds a low-acid diet with reduction of meat and simple starches and high consumption of alkaline fresh vegetables to significantly prevent and reverse osteoporosis: http://www.nytimes.com/2009/11/24/health/24brod.html
  9. A 2011 study at the University of Eastern Finland showed that a diet that combined fatty fish, bilberries and wholegrain products may improve intestinal endothelial dysfunction and inflammation in overweight and obese individuals to help prevent diabetes onset, Metabolic Syndrome and cardiovascular disease: http://www.ncbi.nlm.nih.gov/pubmed/21870174
  10. A 2013 review of a Harvard Medical School and Massachusetts General Hospital study of the physiological effects of gastric banding showed that at least 20 percent of the weight loss could be attributed to changes in the microbiota, or normal symbiotic bacterial colony of the intestines. Such study points to the importance of Complementary Medicine and restoration of the body's homeostasis, with professional probiotics along with other symbiotic treatments, in the healthy treatment of obesity: http://news.harvard.edu/gazette/story/2013/03/major-weight-loss-tied-to-microbes/
  11. A study in 2012 at the Mayo Clinic, University of Colorado, and Cedars-Sinai found that energy regulation and obesity is closely tied to gut microbiota: http://www.nature.com/ajgsup/journal/v1/n1/full/ajgsup20125a.html
  12. A study in 2013, at New York University School of Medicine, found that antibiotic exposure in the first 6 months of human infancy is associated with increase weight gain, and could by associated with future consequences, such as Metabolic Syndrome, diabetes, and obesity. Prior studies by one of the researchers, Dr. Martin J. Blaser, showed that laboratory mice that were induced to obesity with a high carbohydrate high calorie diet, that were given antibiotics, ballooned with almost twice the fatty weight gain as the mice that were not given antibiotics: http://www.ncbi.nlm.nih.gov/pubmed/22907693
  13. A talk during a conference on obesity, by Dr. Martin Blaser M.D., chair of the department of medicine at New York University, in 2012, describes the connection between antibiotic overuse and obesity in children: http://www.hcplive.com/hcplive-tv/Dr-Martin-Blaser-on-Antibiotics-and-Obesity
  14. A 2014 meta-analysis of all published studies of the link between duration of breastfeeding and development of childhood obesity showed that this is a significant factor in obesity risk. A 2016 study in the U.S. showed that pregnant mothers with the lowest levels of folates, some of which are derived from folic acid in the diet, showed a 45 percent increased risk of their children developing obesity as well: http://bmcpublichealth.biomedcentral.com/articles/10.1186/1471-2458-14-1267
  15. A 2015 study at the University of California in La Jolla, U.S.A. showed that a significant percentage of children diagnosed with obesity have markers of chronic kidney disease or dysfunction, showing that the problem of obesity is more complex than the simple explanation we have had for decades, and thus may be more difficult to reverse. Since the kidney regulates much or our metabolism, this creates a problem bigger than weight loss. A more holistic approach to reversing obesity is needed: http://www.ncbi.nlm.nih.gov/pubmed/25322907
  16. In 2010, experts at Case Western Reserve University School of Medicine, in Cleveland, Ohio, explored common markers of early kidney disease, and found that a metabolic maker of lysosome activity related to complex sugar and protein molecules, NAG (n-acetyl-beta D-glucosaminidase) correlated with a marker of kidney dysfunction, the albumin excretion rate, and with advanced glycation endproducts (AGEs), but that when AGEs were adjusted with NAG the correlation between kidney dysfunction and AGEs dissappeared. What is not discussed is the apparent correlation between AGEs and NAG, showing that accumulation of AGEs in the body, from both diet and metabolic dysfunction, is a significant problem with obesity and related disorders: http://www.ncbi.nlm.nih.gov/pubmed/20138413
  17. A 2015 study at the Icahn School of Medicine at Mt. Sinai, in New York, U.S.A. and the Oxford University School of Medicine, in the UK, shows that AGEs (advanced glycation endproducts) are a strong modifiable risk factor for obesity, Metabolic Syndrome, diabetes and cardiovascular disease, and thus serum AGE levels may be a significant marker for distinguishing dangerous types of obesity syndromes from benign obesity :http://www.ncbi.nlm.nih.gov/pubmed/25695886
  18. A study at Washington University in St. Louis, Missouri, published in the September 5, 2013 issue of the journal Nature, describes how biota from a lean person may cure obesity when introduced into an obese person: http://www.nature.com/news/bacteria-from-lean-mice-prevents-obesity-in-peers-1.13693
  19. A 2009 meta-review of study of the relationship between gut microbiota and the pathology of obesity, by the Catholic University of Louvrain, in Brussels, Belgium, concluded that there was evidence that the gut biota is different between lean and obese children, and healthy adults and those with Metabolic Syndrome or diabetes type 2. Moreover, the mechanisms of obesity tied to a chronic high-fat diet, with inflammation and insulin resistance, are linked to bacterial lipopolysaccharides and immune response, including those with excess free fatty acids and toll-like receptors, as well as the obvious ties to energy absorption from nutrients tied to microbiotic functions, and the production of nutrient molecules tied to the biota that aid energy homeostasis, or hurt it: http://www.ncbi.nlm.nih.gov/pubmed/19442172
  20. A 2011 meta-review of the evidence linking the gut microbiota with the pathological mechanisms of obesity, by the University of Louisville School of Medicine, Louisville, Kentucky, U.S.A. also noted that models of obesity caused by high fat and/or high fructose diets include the hallmarks of an unhealthy biota, namely gut permeability, low-grade endotoxemia, and fatty liver disease, and that animal and human studies show that prebiotics and probiotics appear to alter both obesity and fatty liver disease. It appears to these experts that the gut biota may function as a metabolic organ, and the ill health or dysfunction of this biotic organ could be the key to obesity: http://www.ncbi.nlm.nih.gov/pubmed/21807932
  21. A 2006 study at the Genetics and Genomonica Research Institute of the Imperial College London, and the University of Oxford, in the United Kingdom, outlined the key mechanisms by which an unhealthy gut microbiota alters nutrient energy metabolism and contributes greatly to fatty liver disease, the hallmark of obesity, as liver glycogen stores reach capacity and energy homeostasis is tilted toward obesity. These researchers noted that unhealthy dietary changes stress the superorganism of the microbiota and human genome and epigenome, creating metabolic disease. The principle mechanisms appeared to be low phosphatidylcholine, high choline metabolites such as methylamines, which leads to liver toxicity, fatty liver disease, impaired glucose homeostasis, poor regulation of fat storage, and suppression of health inflammatory responses: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1567909/
  22. A more thorough review of scientific study of the gut microbiota, largely composed of symbiotic bacteria, and its relationship to obesity and disease, is found here in a 2011 article from experts at Wageningen University, and the University of Helsinki, in The Netherlands and Finland: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3145058/
  23. A 2015 study at Kyung Hee University and the Korean Institute of Science and Technology, in Seoul, South Korea, found that a simple combination of the Chinese herbs Shan zha (Crataegus pinnatifida) and Wenzhou migan (Citrus unshui or mandarin orange peel) could help prevent obesity and reduce body fat by decreasing fat cell expressions of PPAR-gamma and C/EBP-alpha, pro-inflammatory and leptin hormone promoting mediators: http://www.ncbi.nlm.nih.gov/pubmed/26016552
  24. A 2012 study at the Korea Food Research Institute, in Seongnam, South Korea, found that the alcohol extract of the Chinese herb Gao liang jiang (Alpinia officinarum), of the wild ginger family, inhibits obesity and fat cell growth via regulation of adipogenesis and lipogenesis at the level of genetic expression: http://www.ncbi.nlm.nih.gov/pubmed/23126661
  25. A 2012 study at the Korea Food Research Institute, in Seongnam, South Korea, found that the alcohol extract of the Chinese herb Hu jiao, or Zanthoxylum Piperitum negrum DC, inhibits fat accumulation in fat cells by downregulating expression of PPAR-gamma, SREBP-1 and 3T3L 1, inhibiting adipogenesis: http://www.ncbi.nlm.nih.gov/pubmed/23419397
  26. A meta-review of all published scientific studies of herbal and dietary polyphenols, such as green tea catechins, EPG (epigallococatechin gallate), resveratrol and curcumin, by experts at Texas Tech University, in Lubbock, Texas, U.S.A. found that animal studies showed profound benefits on preventing or reducing obesity via a number of chemical and genetic pathways, but that small human clinical trials have produced inconsistent outcomes. These experts, in reviewing the studies, concluded that the study designs and improper chemical forms of these polyphenols likely led to this discrepancy, as well as the effects of other weight-reducing agents affecting the study findings: http://www.ncbi.nlm.nih.gov/pubmed/24314860
  27. A 2013 meta-review of all published scientific studies of herbal and nutrient flavonoids, by the University of Utah College of Health, in Salt Lake City, Utah, U.S.A. found that abundant evidence exists to support the use of herbal flavonoids in the holistic treatment of diabetes and obesity, with evidence of target signaling modulation of a number of biochemical pathways, affecting pancreatic and liver cells, as well as fat cells, enhancing insulin secretion, reducing insulin resistance, promoting growth of pancreatic beta-cells, and reducing inflammatory and oxidative stress in organ and fat cells: http://www.ncbi.nlm.nih.gov/pubmed/24029069
  28. A concise review of the complexity of insulin resistance is presented on this website, entitled News Medical: http://www.news-medical.net/health/Insulin-Resistance-Pathophysiology.aspx
  29. A 2010 study at the University of Milan found that subclinical hypothyroid dysfunction was correlated wtih obesity and mainly influenced by insulin resistance: http://www.ncbi.nlm.nih.gov/pubmed/20339314
  30. A 1976 study of the effects of synthesized glutamates, such as monosodium glutamate, of which there are now hundreds of variations disguised with names such as umami, yeast extract, and natural flavoring, found that laboratory animals could have a state of obesity induced in 90 percent of subjects with these glutamates ingested in childhood or infancy, and that this glutamate-induced obesity did not involve excess appetite or dramatic increase in body weight: http://www.ncbi.nlm.nih.gov/pubmed/1106764
  31. A 2014 study at the University Hospital of Getafe, in Madrid, Spain, found that about 30 percent of children who were overweight could be diagnosed with an obesity syndrome, with about 20 percent having measurable fatty liver disease (hepatic steatosis), involving elevation of the liver enzyme glutamic pyruvate transaminase (GPT), and correlated with excess accumulation of mercury toxin (HGNA): http://www.ncbi.nlm.nih.gov/pubmed/24768200
  32. A 2014 study at the Zabolotny Institute of Microbiology and Virology, in Kyiv, Ukraine, found that glutamates such as MSG presented to infant laboratory animals caused obesity later in life, but periodic administration of probiotics in infancy and childhood often resulted in recovery of healthy lipid metabolism and prevention of obesity development: http://www.ncbi.nlm.nih.gov/pubmed/24410812
  33. A 2007 study at Pamukkale University in Turkey also found that thyroid stimulating hormone (TSH), secreted by the hypothalamus/pituitary, was positively correlated with the degree of obesity independent of clinical thyroid disease. Poor function of the regulatory hypothalamus is suspect: http://www.ncbi.nlm.nih.gov/pubmed/17705106
  34. A 2010 study at Duke University Medical Center correlated the degree of severity of hyperparathyroidism with obesity, with larger tumors, higher parathyroid hormone levels, and a higher frequency of the related symptoms of depression, gastroesophageal reflux, musculoskeletal symptoms of pain and weakness, etc. These findings were independent of the Vitamin D3 hormonal levels that are associated with primary hyperparathyridism: http://www.ncbi.nlm.nih.gov/pubmed/20685860
  35. A 2008 review of scientific studies of environmental chemicals contributing to obesity by hormonal disruption, conducted at the University of Alabama, concluded that an array of common environmental chemicals may contribute to obesity mechanisms at low dose, including BPA, DES, PBDE, DDT, chemical solvents, flame-retardant chemicals, phthalates, dioxins, PCBs and butylltins: http://www.medicinenet.com/script/main/art.asp?articlekey=56339&page=2
  36. A typical standard warning of the increasingly alarming findings of the number of pharmaceutical drugs that cause or contribute to obesity is found on MedicineNet.com: http://www.medicinenet.com/script/main/art.asp?articlekey=56339&page=2
  37. Another typical website that explores more clearly the array of medications that cause obesity is found at the women's health organization Green Mountain: http://www.fitwoman.com/fitbriefings/medications-weight-gain-2.shtml
  38. A 2007 report by the Federal government AHRQ reported that there was insufficient evidence to justify the off-label uses of many atypical antipsychotic pharmaceuticals, and that a high incidence of weight gain offset the very modest benefits, especially with Olanzapine/Zyprexa: http://www.ahrq.gov/news/press/pr2007/antipsypr.htm
  39. A 2006 study of over 20,000 patients at Universities in Norway found that common antidepressants and antianxiety medications, SSRIs (selective serotonin reuptake inhibitors), were associated with obesity, metabolic syndrome, and an unhealthy lipid profile: http://cat.inist.fr/?aModele=afficheN&cpsidt=18367468
  40. A 2009 review of Bisphenol A, a chemical in many plastic products, by the Dartmouth Journal of Science, reveals how research found that BPA could contribute to obesity by inhibiting adiponectin and contributing to Metabolic Syndrome and insulin resistance - a 2010 President's Council on Obesity confirmed this warning: http://dujs.dartmouth.edu/fall-2009/bisphenol-a-unfit-for-consumption
  41. A 2005 review of the fat cell hormone adiponectin, whose deficiency is highly correlated with obesity and insulin resistance, is note here, from experts at Sumitomo Hospital in Japan: http://www.sciencedirect.com/science
  42. A 2014 multicenter study of the proven relationship between hormone Vitamin D deficiency and obesity, at the University of Oulu Oulu Institute of Biomedicine in Finland, The University of South Adelaide in Australia, University College London in the UK, and the Imperial College London in the UK, found that a higher BMI was causally related to lower cholecalciferol (D(25(OH)D), but that no immediate effect was achieved with cholecalciferol supplementation. The Vitamin D3 hormone receptor was central to many metabolic effects associated with obesity, though, and that active D3, or calcitriol, was produced by the fat cells, and was integral to regulation of the inflammatory mediators in the fat cells. Therefore, these studies showed clearly that deficient modulation of fat cell inflammatory processes contributed heavily to increased growth of fat cells, and this was directly linked to hormone Vitamin D deficiency, but that these effects were non-linear and dependent on a large array of other molecules. The fat cells are now known to produce over 260 protein or peptide hormones and chemokines, which may interact with the hormone Vitamin D, and excess growth of fat cells may be a reason for decreased production of the hormone D3 as well. Once again, large scientific studies show the need to take a comprehensive and holistic approach to correction of these problems, and that simple allopathic approaches, such as prescribing large dosage of Vitamin D, will not work: http://www.ncbi.nlm.nih.gov/pubmed/25009502
  43. A 2012 study at Nanjing University of Traditional Chinese Medicine, in Nanjing, China, found that electroacupuncture stimulation 3 times per week for 4 weeks on laboratory animals with induced obesity and metabolic syndrome led to a decrease in plasma leptin, an increase in leptin receptor expression at the hypothalamus, and a reduction in body weight, elucidating one pathway that could explain the efficacy of acupuncture in weight reduction: http://www.ncbi.nlm.nih.gov/pubmed/22745067
  44. A 2013 study at Nanjing University of Chinese Medicine, in Nanjing, China, found that electroacupuncture at ST36 and ST44 on the left side and ST25 bilaterally effectively reduced body weight, body fat, serum leptin, resistin, TNF-alpha, and neuropeptide Y, while increasing serum adiponectin and cholecystokinin-8, perhaps by affecting the function of glucose-inhibited regulatory neurons in the hypothalamus. This broad set of benefits shows the potential for electroacupuncture in the holistic treatment protocol for obesity: http://www.ncbi.nlm.nih.gov/pubmed/25206728
  45. A 2014 randomized controlled study at Nanjing University of Chinese Medicine showed that electroacupuncture stimulation at just 2 points, ST36 and ST44, stimulated conversion of white adipose tissues (WAT) associated with obesity and inflammatory hormonal dysfunction to brown adipose tissues, and modulated inflammatory cytokines and chemokines in white adipose tissues that would help with reversing obesity: http://www.ncbi.nlm.nih.gov/pubmed/25514854
  46. A 2015 randomized controlled study at the Nanjing University of Chinese Medicine, in Nanjing, China, found that electroacupuncture can attenuate a high-fat diet induced condition of fatty liver accumulation, and that this effect is mediated through AMPK signaling pathways associated with inflammatory regulation. Electroacupuncture treatment for 12 weeks led to a reduction in body, liver and abdominal fat accumulation for study animals, showing the homeostatic benefits of adding this treatment to a broader protocol: http://www.ncbi.nlm.nih.gov/pubmed/26619891
  47. A 2015 randomized controlled study of electroacupuncture stimulation at the points ST36 and ST25 as part of an acupuncture treatment protocol, by experts at the Federal University of Rio Grande do Sul, in Porto Alegro, Brazil, found that this protocol resulted in lowered body fat, improved metabolism with cholesterol lipids, triglycerides and blood sugar, and improved behavioral parameters with study animals with induced obesity from a high fat, high sugar, high calorie diet. The point of such studies is to prove that such treatment works as part of a more holistic protocol in resolving health problems seen in obese patients: http://www.ncbi.nlm.nih.gov/pubmed/26314894
  48. A randomized controlled human clinical trial of electroacupuncture at Mashad University of Medical Sciences, in Mashad, Iran, found that this therapy lowered plasma leptin levels in obese patients significantly more than sham acupuncture controls, as well as decreasing body fat mass overall: http://www.ncbi.nlm.nih.gov/pubmed/23594450
  49. A 2012 study at the Ankara Physical Medicine and Rehabilitation Training and Research Hospital, in Ankara, Turkey, that was randomized with placebo control, showed that acupuncture stimulation for 5 weeks (at the points LI4, H7, ST36, ST44, SP6) resulted in lowered leptin and insulin, weight loss, decreased BMI, and increases in ghrelin and CCK, demonstrating the remarkable benefits holistically that account for resolution of obesity: http://www.ncbi.nlm.nih.gov/pubmed/22729015
  50. A 2015 randomized controlled study in China with electroacupuncture at the points ST36 and Ren12 in the treatment of obesity showed that this protocol achieved measurable improvements in body weight, leptin levels, Lee's index, and liver expression of p-JAK2 and p-STAT 3, tyrosine kinase enzymes that are important in regulation of growth and proliferation of fat cells: http://www.ncbi.nlm.nih.gov/pubmed/25845212
  51. A randomized controlled human clinical trial of acupuncture in obesity, at Qingdao University Medical School, in Qingdao, China, found that acupuncture significantly restored nesfatin-1 levels in obese adults, resulting in a 7 percent reduction in weight after a 45 day treatment period with acupuncture and dietary changes compared to dietary changes alone. It is believed that a rise in deficient nesfatin-1 would result in long-term benefits: http://www.ncbi.nlm.nih.gov/pubmed/24813558
  52. A 2014 study at the National Research Center of Cairo University, in Cairo, Egypt, found that nesfatin-1, a protein hormone that controls eating behaviors and glucose homeostasis, is consistently lower in obese patients, and even in obese children is correlated both with appetite controls and the pathogenesis of insulin resistance in obesity: http://www.ncbi.nlm.nih.gov/pubmed/24333832
  53. A 2009 placebo-controlled randomized study at the National Yang-Ming University Institute of Traditional Medicine, in Taipei, Taiwan, found that ear acupuncture alone for 6 weeks resulted in significant increase in ghrelin and decrease in leptin, key aspects in resolution of obesity. While the immediate effects of this ear acupuncture alone did not reduce weight, the protocol may be added to a comprehensive treatment protocol in TCM which includes meridian acupuncture, herbal and nutrient medicine, and changes in diet and lifestyle. A prior study in 2005 at this University showed that electroacupuncture stimulation produced significant weight loss, reduction in BMI, and waist circumference (PMID: 15989416): http://www.ncbi.nlm.nih.gov/pubmed/19445642
  54. A 2010 study at the University of Ulm, Germany, found that a chemical constituent of Chinese herbs, resveratrol, countered insulin resistance and inflammatory cytokines (IL6 and IL8) associated with the pathophysiology of insulin resistance in fat cells. The conclusion was that resveratrol could be a novel addition to the treatment of obesity-associated hormonal and metabolic dysfunction: http://www.ncbi.nlm.nih.gov/pubmed/20463039
  55. A 2010 study at the Karolinka University Hospital in Stockholm, Sweden, found that a Chinese herb, Gymnostemma pentaphyllum, or Jiao gu lan, significantly decreased insulin resistance and A1C index with 12 weeks of use, in a modulatory fashion that had no adverse effects and did not affect glucagon levels, cortisol levels, lipid profiles, or blood pressure: http://www.ncbi.nlm.nih.gov/pubmed/20213586
  56. A 2012 study at Kyunpook National University in South Korea found that the Chinese herb Gynostemma pentaphyllum (Jiao gu lan), in alcohol extracts, lessened obesity by activating protein kinase metabolic pathways, significantly stimulating fat oxidation and glucose uptake, decreasing body weight and fatty liver, and normalizing circulating cholesterols: http://www.ncbi.nlm.nih.gov/pubmed/22576281
  57. A 2012 study at the Seoul National University, Institute of Molecular Biology and Genetics, found that a standardized extract of Glabridin, a constituent of the Chinese herb Gan cao (Glycyrrizha, or Licorice root), exerted significant effects on weight loss and obesity, by promoting fatty acid oxidation, and also aided normalization of fatty liver and high triglycerides. This product is available as VFM-100, a Kaneka Glavanoid extract, and should be prescribed by a professional herbalist or naturopath: http://www.ncbi.nlm.nih.gov/pubmed/22493094
  58. A 2009 study at the Chungman University Colege of Pharmacy in Daejeon, Korea, found that the Chinese herb Moutan, or Mu dan pi, paeonia suffruticosa, significantly stimulated glucose uptake and glycogen synthesis in insulin resistant liver cells: http://www.ncbi.nlm.nih.gov/pubmed/19716700
  59. A 2015 study at the Daegu Haany University School of Medicine, in Daegu, South Korea, found that an active chemical in the Chinese herb Radix Bupleuri (Chai hu), a saikosaponin (SSNa), could inhibit the inflammatory expressions of fat cells that are linked to the pathology of obesity:http://www.ncbi.nlm.nih.gov/pubmed/25672367
  60. A 2010 study at Tajen University in Taiwn found that the Chinese herb Abelmoschus maschatus (Ye or Shan you ma / Huang kui / muskmallow) significantly increased post-receptor insulin signaling in skeletal muscle, making this herb a useful adjunct therapy for patients with insulin resistance: http://www.ncbi.nlm.nih.gov/pubmed/19610024
  61. A 2009 study at the University of Hong Kong found that chemicals in the Chinese herb Astragalus (Huang qi) improved insulin resistance by elevating adiponectins in circulation, and were thus potentially useful in the treatment of obesity as part of the treatment protocol: http://www.ncbi.nlm.nih.gov/pubmed/18927219
  62. A 2014 study at the University of Prince Edward Island, in Charlottetown, PE, Canada, proved that the common Chinese Herbal Formula, Liu Wei di Huang, restored adiponectin levels, increased antioxidant SOD, and decreased inflammatory markers related to obesity, CRP, TNF-alpha and IL-6, with a 9 week course of treatment: http://www.ncbi.nlm.nih.gov/pubmed/25292344
  63. A second 2014 study by the National Research Council of Canada, in Charlottestown, PE, Canada, found that an alcohol extract of the Chinese Herbal Formula Liu Wei di Huang exerted lipid-based hormonal effects that significantly reduced weight gain and visceral fat in laboratory animals with induced obesity: http://www.ncbi.nlm.nih.gov/pubmed/24603076
  64. A September 7, 2010 article in the New York Times Health reviews the evidence linking excessive weight gain and obesity in pregnancy with passing of epigenetic traits of obesity to children, with small metabolic changes likely to be compounded over time if health corrections are not made: http://www.nytimes.com/2010/09/07/health/07brody.html?src=me
  65. A February 8, 2011 article in the New York Times describes a Harvard Medical School public health study called Project Viva that showed that infants not breast fed till the fourth month, but fed infant formula, and that were introduced to solid baby food by age 4 months, were 6 times more likely to develop obesity by age 3: http://well.blogs.nytimes.com/2011/02/08/timing-of-baby-food-tied-to-obesity-risk/