Resetting Fat Loss Hormones
by Rebecca Berzow, N.D.
It’s January. That time of year when many people turn their attention to eating better and losing weight. One likely reason for this annual reassessment is the fact that modern lifestyles have caused many patients to forget the fundamentals of healthy living—eat moderately, exercise regularly, get enough sleep and stay hydrated.
Mixed into this formula are seven little-known hormones that play a large role in weight gain and loss. In fact, these “fat loss” hormones—ghrelin, leptin, cholecystikinin (CCK), insulin, irisin, CRP and adiponectin—have become the focus of researchers. Each of these hormones is a hopeful target in the search to cure obesity.
Sadly, living a less than optimal lifestyle can alter the fat loss regulatory hormones, causing you to be more prone to obesity and fat storage. Fortunately, this is not a permanent state of affairs. Through diet, lifestyle and medical intervention, fat loss hormones can be reset to guide the body more toward a lean state.
While it is made in the gut, primarily by the stomach, ghrelin is actually described as an appetite-stimulatory signal that acts on the brain.1 Studies have also suggested that ghrelin regulates the release of growth hormone from the pituitary.2
Ghrelin has been found to increase food intake and body weight. To this point, a recent study demonstrated increased ghrelin levels in subjects when they simply observed pictures of food.3
A review article looking at ghrelin’s role in the body identified ghrelin as an important regulator of growth and metabolism. It has a role in obesity, cachexia (physical wasting and malnutrition) and eating disorders. It also potentially suppresses anti-inflammatory molecules, blocks insulin secretion and is known to be fast-acting.4-6
Unlike ghrelin, leptin is more important for long-term regulation of energy balance and is involved in the reduction of appetite and cravings.6 Even more important, leptin levels have been found to be increased in obese individuals.
Recently it has been determined that obesity leads to a leptin-resistant state, much like insulin-resistance develops under the same circumstances.6 Increased levels of leptin have been associated with an increase in pro-inflammatory chemicals such as cytokines, suggesting a possible relationship between leptin, immunity and inflammation-related conditions related to obesity, including cardiovascular disease.7
Cholecystokinin (CCK) is a hormone secreted by the small intestine. It is involved in the regulation of both satiety and digestion.8 Leptin resistance in rats led to a reduction of sensitivity to CCK, thus reducing the satiety effect.9 This inter-relationship between leptin and CCK is important for understanding one possible cause of obesity.
Other studies show that CCK plays a significant role in obesity-induced insulin resistance,10 and that eating an obesity-promoting diet can reduce CCK sensitivity, thereby allowing for overconsumption of food leading to more weight gain.11
Insulin is a peptide produced in the pancreas. It helps to burn glucose for fuel by aiding in the transport of glucose into the cells. Insulin also halts the process of burning fat for energy by inhibiting the release of glucagon. Therefore, overproduction of insulin can prevent fat-burning and lead to more fat storage.
Insulin resistance often happens in obesity due to the over-consumption of calories, which leads to prolonged elevated levels of glucose and therefore insulin. This long-term insulin exposure causes the insulin receptors to lose sensitivity, which leads to elevated insulin levels, along with elevated blood glucose. Maintaining proper glucose/insulin balance is crucial for weight management and healthy aging.12
Irisin is induced with exercise and acts on white adipose (fat) cells to stimulate brown fat development. Brown fat is more metabolically active, contains more mitochondria and is thermogenic, meaning it can boost metabolism and promote fat-burning. Irisin causes increased energy expenditure in mice and leads to improvements in obesity and blood sugar control.13
The key takeaway when it comes to irisin is that exercise is critical when it comes to healthy weight maintenance.
C-Reactive Protein and Adiponectin
High-sensitivity C-reactive protein (CRP) is a known risk factor for coronary artery disease. Additionally, higher levels are seen in obese individuals. Specifically, CRP is a known marker for inflammation and gives further credence to the belief that inflammation and obesity are interrelated.
Adiponectin, an antiatherogenic plasma protein, is inversely correlated to body fat percentage in adults, which in turn is correlated with insulin resistance.14 However, another study suggested that there was a closer relationship between adiponectin levels and insulin resistance than to obesity alone.15 CRP has shown an inverse correlation to adiponectin levels, suggesting a mechanism for the higher risk of obese individuals for developing coronary artery disease.16
Resetting Fat Loss Hormones
Any of the fat loss hormones mentioned above can be regulated by both lifestyle and dietary measures. Dietary fiber is important in the regulation of healthy leptin and ghrelin levels. Sleep, hydration and stress management are also paramount to reaching and maintaining a healthy weight and balancing levels of fat loss hormones.17
It is important to note that, given the links we have discussed above, anti-inflammatory herbs and supplements can also be helpful in managing the conditions associated with imbalanced fat loss hormones.
While some studies have suggested that acute exercise has no effect on ghrelin levels,18 other long-term studies have shown ghrelin to increase progressively with increased activity and weight loss.19 Even so, the benefits of exercise likely outweigh the slight increase in ghrelin.
Additionally, the Wisconsin sleep cohort study showed that sleeping less than eight hours is correlated with increased BMI, increased circulating ghrelin and decreased leptin.17
Increasing dietary fiber is another strategy for balancing ghrelin. Studies have shown that intake of beta-glucan (ranging from 4-6 grams) appears to decrease appetite.20 Numerous other studies have suggested that the feeling of fullness in the stomach after fiber consumption helps to modulate ghrelin, and a diet high in fiber helps to accomplish this while minimizing caloric intake. One study concluded, “Although the mechanism is not precisely known, the data suggest that the fiber intake may inhibit high-fat diet induced leptin secretion and gastric ghrelin gene expression.”21
Modulating Leptin and Other Fat Loss Hormones
High viscosity polysaccharides and esterified fatty acids have been shown to balance leptin and adiponectin. A placebo-controlled, double-blind study that combined high viscosity polysaccharides and esterified fatty acids supplementation with calorie restriction and cardiovascular exercise showed that the treatment group displayed significant reductions in body weight, body fat percentage, leptin and insulin. Adiponectin levels also increased.22
Studies have also shown a correlation between EGCG administration (from green tea) and reduced food intake, body weight and serum leptin levels, along with other benefits, after just four weeks.23
Conjugated linoleic acid (CLA) also is beneficial for weight management and leptin balancing. CLA reduced abdominal weight in obese men with signs of metabolic syndrome after four weeks at a dose of 4.2g/CLA/day.24 Furthermore, 3.2 grams of CLA/day for six months showed reduced body fat and appeared to prevent holiday weight gain.25 Similarly, a meta-analysis determined that at a dose of 3.2g/day CLA produces a modest loss of body fat in humans.26
Finally, in another study, 20 obese women were given 1.8 grams/day CLA for eight weeks. At the end of the study period, researchers saw significant decreases in triglyceride levels, total cholesterol, LDL cholesterol and leptin levels.27
Increasing chlorophyll consumption appears to increase CCK. A study in mice suggests that increased ingestion of chloroplast membranes called thlyakoids resulted in suppressed food intake, body weight gain and body fat compared to the control mice. Levels of glucose, triglyceride and free-fatty acids were also reduced in the thylakoid-fed animals.28
According to a study using beans as a source of dietary fiber (11 grams/meal), cholecystokinin levels were increased.29 This study suggests adding fiber content to meals increases satiety and may lead to reduced caloric intake and weight reduction.
Curbing Insulin/Blood Glucose
Two good options for balancing insulin and glucose levels are cinnamon and bitter melon. Cinnamon has shown in clinical trials to reduce serum fasting glucose, triglycerides and LDL cholesterol at dosages of 1-6 grams/daily.30
When it comes to bitter melon, a study comparing this nutrient to the drug metformin showed a significant hypoglycemic effect at 2,000 mg/day. However, the effect was less than the drug metformin administered at 1,000 mg/day.31 Bitter melon has also shown ACE inhibitory and nitric oxide generation effects in addition to its glucose-lowering properties.32
As discussed earlier, exercise appears to be the best way to increase irisin and convert white adipose into more metabolically active brown fat.33
Reducing CRP and Adiponectin
High viscosity polysaccharides increase adiponectin.22 This includes thick, syrupy starches like beta-glucan and glucomannan. Given what we know about the inverse correlation between adiponectin and CRP,16 it is possible CRP may also be reduced.
There are many anti-inflammatory herbs that can also be used concurrently with the supplements mentioned above to balance levels of fat hormones. These herbs include turmeric, ginger and boswellia, among others to aid in fighting the inflammatory component of obesity.
Reset Your Fat Hormones
Today’s modern lifestyle has caused a disruption in fat loss hormones. Fortunately, implementing certain lifestyle changes and consuming key nutrients can help reset fat loss hormones while guarding against obesity. Use the following regimen to balance levels of ghrelin, leptin, cholecystikinin (CCK), insulin, irisin, CRP and adiponectin.
- Eat high-fiber, low calorie meals; sleep eight hours per night and drink 64 ounces of water every day.
- Get at least 30 minutes of exercise daily.
- 1-6 grams of cinnamon a day can lower glucose, triglycerides and LDL.
- 2,800 mg of beta-glucan a day can reduce body weight, body fat percentage, leptin and insulin while also increasing adiponectin levels.
- Bitter melon has a hypoglycemic effect at 2,000 mg/day.
- CLA at a dosage of 3.2 grams/day can help lower lipids, leptin and body weight.
- To fight the inflammatory component of obesity, use anti-inflammatory herbs such as:
- Turmeric: 500 – 1,000 mg
- Ginger: 400 mg per day
- Boswellia: 120 mg
- Green tea (EGCG): 120 mg
- Asakawa A, et al. Gut. 2005;54:18-24.
- Kojima M, et al. Nature. 1999 Dec 9;402(6762):656-60.
- Schussler P, et al. Obesity (Silver Spring). 2012 Jun;20(6):1212-7.
- Wu JT, Kral JG. Ann Surg. 2004;239:464-74.
- Verhulst PJ, Depoortere I. World J Gastroenterol. 2012 July 7;18(25):3183-95.
- Klok MD, et al. Obes Rev. 2007 Jan;8(1):21-34.
- Loffreda S, et al. FASEB J. 1998 Jan;12(1):57-65.
- Little TJ, et al. Obes Rev. 2005 Nov;6(4):297-306.
- deLartigue G, et al. PLoS One. 2012;7(3):e32967.
- Lavine J, et al. Endocrinology. 2010 August;151(8):3577-88.
- Daly D, et al. J Physiol. 2011 June 1;589(pt 11):2857-70.
- Preuss HG. J Am Coll Nutr. 1997 Oct;16(5):397-403.
- Bostrom P, et al. Nature. 2012 January 11;481(7382):463-8.
- Ukkola O, et al. J Mol Med. 2002 Nov;80(11):696-702.
- Putz DM, et al. Metabolism. 2004 Nov;53(11):1454-61.
- Ouchi N, et al. Circulation. 2003 Feb 11;107(5):671-4.
- Taheri S, et al. PLoS Med. 2004 Dec 7;1(3):e62.
- Schmidt A, et al. Horm Metab Res. 2004 Mar;36(3):174-7.
- Foster-Schubert KE, et al. J Clin Endocrinol Metab. 2005 Feb;90(2):820-5.
- Malkki Y, et al. Lebensmittel-Wissenchaft Technologie. 2001;34(6):337-47.
- Wang Z, et al. Metabolism. 2007 Dec;56(12):1635-42.
- Fragala MS, et al. Eur J Appl Physiol 2009 Mar;105(5):665-72.
- Kao YH, et al. Endocrinology 2000 Mar;141(3):980-7.
- Riserus U, et al. Int J Obes Relat Metab Disord. 2001 Aug;25(8):1129-35.
- Watras AC, et al. Int J Obes (Lond). 2007 Mar;31(3):481-7. Epub 2006 Aug 22.
- Whigham LD, et al. Am J Clin Nutr. 2007 May;85(5):1203-11.
- Sahin H, et al. Pakistan J of Nutr., 2008;7(4):546-9.
- Kohnke R, et al. Phytother Res. 2009 Dec;23(12):1778-83.
- Bourdon, I, et al. J Nutr. May 1, 2001;131(5):1485-90.
- Khan A, et al. Diabetes Care. 2003 Dec;26(12):3215-8.
- Fuangchan A, et al. J Ethnopharmacol. 2011 Mar 24;134(2):422-8.
- Clouatre DL, et al. J Med Food. 2011 Dec;14(12):1496-504.
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