The Challenges of Weight Loss, Part 2
As we explored in part 1, diet and exercise remains a key factor in weight loss. But what happens when these are not enough? When what has worked in the past is no longer working? There could be other factors involved that could be hindering your ability to lose weight.
Do you have a slow metabolism or fast metabolism? Your thyroid gland plays a role in your metabolism. If it is low or hypofunctioning, this could lower your overall metabolic rate leading to weight gain. A blood test can determine your thyroid functioning.
Sugar metabolism plays a large role in energy expenditure and fat storage. However, not all sugars act the same in our bodies. Glucose stimulates insulin secretion that then promotes the cells to take up glucose for use as energy or to store as glycogen. The presence of insulin inhibits fat breakdown for energy (because now the body is using sugar) and promotes fat cells to not only take in fat, but also to produce fat (typically in the form of triglycerides). Therefore in the presence of circulating insulin, the body is going to make and store fat. This is why insulin resistance is associated with weight gain.
Fructose on the other hand, does not stimulate insulin production. It is metabolized in the liver and stored as glycogen or fat (in the form of triglycerides). Therefore, if we are inactive and not using our glycogen store in our muscles, we will convert fructose directly to fat. This is why fructose sweetened beverages and excessive consumption of fructose may be a possible health problem and could be contributing to the obesity epidemic. 1,2,3 Glucose, insulin, and triglyceride blood tests can be performed to determine your metabolic status.
Chronic inflammation can also lead to weight gain. Most commonly inflammation is thought of as painful or swollen joints, but chronic inflammation can brew in the body as a response to diet and environment. Inflammation may have an affect on a hormone called leptin.4,5 Leptin, mostly produced in fat cells, sends signals to the brain to decrease appetite and increase energy expenditure. Since leptin is produced in the fat cells, it circulates in our bodies proportionally to the total number of fat cells. This makes sense since leptin decreases appetite and the more fat cells there are, the less need there would be to eat. However, inflammation and too much leptin leads to leptin resistance, causing a decreased ability for leptin to decrease appetite. One way to reduce inflammation is to investigate any food allergies that could be causing chronic inflammation. I have seen success with patients who follow a personalized hypoallergenic diet according to their food allergy results and successfully lose weight. Having a personalized diet plan is often more successful than trying a diet that is marketed to the masses for weight loss.
Dietary fructose reduces circulating insulin and leptin, attenuates postprandial suppression of ghrelin, and increases triglycerides in women
J Clin Endocrinol Metab. 2004 Jun;89(6):2963-72.
Teff KL, Elliott SS, Tschöp M, Kieffer TJ, Rader D, Heiman M, Townsend RR, Keim NL, D’Alessio D, Havel PJ.Monell, Chemical Senses Center, University of Pennsylvania, Philadelphia 19104, USA
Fructose and metabolic diseases: new findings, new questions
Nutrition 2010 Nov-Dec;26(11-12):1044-9. Epub 2010 May 14.
Tappy L, Lê KA, Tran C, Paquot N. Department of Physiology, University of Lausanne, Lausanne, Switzerland
Consumption of high-fructose corn syrup in beverages may play a role in the epidemic of obesity
Am J Clin Nutr. 2004 Apr;79(4):537-43.
Bray GA, Nielsen SJ, Popkin BM. Pennington Biomedical Research Center, Louisiana State University, Baton Rouge, LA 70808, USA
Leptin in immunology
J Immunol. 2005 Mar 15;174(6):3137-42.
Matarese G, Moschos S, Mantzoros CS. Gruppo di ImmunoEndocrinologia, Istituto di Endocrinologia e Oncologia Sperimenttale, Consiglio Nazionale delle Ricerche, Naples, Italy
Leptin resistance: a possible interface of inflammation and metabolism in obesity-related cardiovascular disease
J Am Coll Cardiol. 2008 Oct 7;52(15):1201-10.
Martin SS, Qasim A, Reilly MP. Department of Medicine, Cardiovascular Institute, University of Pennsylvania School of Medicine, Philadelphia, Pennsylvania 19104-6160, USA
