Posts Tagged ‘adipokines’

Cancer and Obesity Explored

November 3rd, 2011

The Institute of Medicine’s National Cancer Policy Forum this week convened a two-day workshop, “The Role of Obesity in Cancer Survival and Recurrance.” So this is a good opportunity to re-visit the relationship between these two deadly diseases. Susan Gapstur of the American Cancer Society noted the growing list of cancers associated with obesity. For men, these include cancers of the colon, esophagus, kidney, colorectum, pancreas, gallbladder and liver. Women are affected by the same cancers as well as of the endometrium and postmenopausal breast cancer. Evidence is accumulating for an association with non-Hodgkin’s lymphoma, ovarian cancer in women and aggressive prostate in men. Obesity, she pointed out, is not the second (to tobacco) leading risk factor of cancer. Ominously, she pointed out we do not know what the health effects will be for the children now obesity who will obese for a lifetime.

Pamela J. Goodwin of the University of Toronto explored potential mechanisms in the progression to cancer including inflammation, adipokines, hyperinsulinemia, diabetes/diabetes drugs and sex steroids. She pointed to studies showing reductions in cancer risk with intentional weight loss of 20 pounds or more. Intentional weight loss and in… [Int J Obes Relat Metab Disord. 2003] – PubMed – NCBI and reduction in the relative risks of death and of cancer following bariatric surgery. Metabolic surgery and cancer: protective effects of b… [Cancer. 2011] – PubMed – NCBI.  Specifically, she showed the positive effect of intentional weight loss on breast cancer risk   Does intentional weight loss reduce canc… [Diabetes Obes Metab. 2011] – PubMed – NCBI and the impact of physical activity on improvements in insulin in breast cancer survivors Impact of a mixed strength and endurance exerci… [J Clin Oncol. 2008] – PubMed – NCBI.

Bruce Wolfe of the Oregon and Science University and a bariatric surgeon reminded the participants that the Swedish Obesity Study found the reduction in mortality after bariatric surgery was greater for cancer than for cardiovascular events Effects of bariatric surgery on mortality in Sw… [N Engl J Med. 2007] – PubMed – NCBI. In a Utah study, bariatric surgery reduced deaths from cancer by 60% compared to a 48% reduction in cardiovascular events. Long-term mortality after gastric bypass surgery. [N Engl J Med. 2007] – PubMed – NCBI

Rachel Ballard-Barbash of the National Cancer Institute, who has been a leader in exploring the obesity-cancer connection for many years, moved the discussion to look at the co-morbid conditions of obesity and their relationship to cancer mortality, including renal disease, congestive heart failure, cerebrovascular disease, citing A refined comorbidity measurement algorithm fo… [Ann Epidemiol. 2007] – PubMed – NCBI

Patricia Ganz of the UCLA Schools of Medicine picked up the point and explained that about half of all deaths of breast cancer survivors are due to causes other than breast cancer. She recommended prevention of weight gain and/or weight loss in those breast cancer survivors who are obese. 

Thomas Wadden described the non-surgical approaches to weight loss used in the Diabetes Prevention Program and the LOOK Ahead study and the contribution of intensive behavioral counseling to reduction in comorbid conditions associated with obesity

Some of the workshop’s presentations are on-line at Workshop on the Role of Obesity in Cancer Survival and Recurrence – Institute of Medicine. Watch that site for future information on a publication from the workshop.

Downey Fact Sheet 1 – About Obesity

September 27th, 2009

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Obesity is a global epidemic and a major health concern because of its premature mortality and extensive comorbidities. Obesity is a common, complex, multifactorial disease with a high degree of heritability. Between 25 and 40% of person with obesity have a parent who is obese. There are several significant facts to bear in mind when discussing obesity:

By Julie Snider for the Downey Obesity Report

By Julie Snider for the Downey Obesity Report

Every individual inherits a certain number of fat cells or adipose tissue. Obesity requires (a) a large number of fat cells or (b) a large volume in each fat cell or (c) both. Adipose tissue continues throughout the lifespan. Weight loss, including surgically-induced weight loss, does not remove fat cells. This is why weight regain is so common. Individuals with obesity have significantly more fat cells than the non-obese, 23-65 billion compared to 37-237 billion for persons with obesity . Early onset obesity is associated with increase adipose cell number while adult obesity is associated with normal cell number. There are two phases of life in which growth of adipose cells are likely to develop: very early, within the first few years of life and between the ages of 9-13 years of age. Those who become very obese early in life are the ones who have nearly normal cell size but have the greatest increase in cell number; whereas those with onset of obesity between 9-13 have more change in cell size than cell number. Salans LB, Cushman SW, Weisman RE, Studies of human adipose tissue. Adipose cell size and number in non0bese and obese patients. J. Clin Invest. 1973 Apr’ 52(4): 929-41)

Extremely obese individuals may have four times the number of fat cells as lean counterparts. http://www.jpp.krakow.pl/journal/archive/1205_s6/pdf/5_1205_s6_article.pdf

Human food intake and energy expenditure are controlled by complex, redundant and distributed neural systems that reflect fundamental biological reaction to food supply and energy balance. The hypothalamus and caudal brainstem play a critical role. The limbic system is important for processing information regarding previous experience with food, reward and emotion. The predisposition to store considerable amounts of energy as fat for later use is now a major health risk. Brain, appetite and obesity – PubMed Results

Extensive research over the past 10 years has shown that appetite is regulated by a complex system of central and peripheral signals which interact in order to modulate the individual response to nutrient ingestion. Satiety signals include cholecystokinin, glucagon-like peptide and peptide YY which originate from the gastrointestinal tract during a meal and through the vagus nerve reach the caudal brainstem. Here the signals move to the arcuate nucleus where satiety signals are integrated with adiposity signals, namely leptin and insulin, and with several other inputs create a neural circuit which controls the individual’s response to a meal, i.e. keep eating or stop. Neuro-hormonal control of food intake: basic mecha…[J Physiol Pharmacol. 2005] – PubMed Result

Adipose tissue, rather than some inert, jello-like, substance is an active hormonal tissue, secreting many hormones which are involved in creating signals from the gut to the brain, indicating hunger or satiety. These hormones include insulin, leptin, ghrelin, PYY-33-6, adiponctin, resistin and visfatin as well as cytokines and chemokines, such as tumor necrosis factor-alpha, interleukin-6 and others. These can lead to a chronic sub-inflammatory state which plays a critical role in the development of insulin resistance, type 2 diabetes, increased risk of cardiovascular disease associated with obesity. Adipokines: the missing link between insulin resis…[Diabetes Metab. 2008] – PubMed Result