Effects of Dietary Composition on Energy Expenditure During Weight-Loss Maintenance
Is a Calorie a Calorie in Our Body?
The Journal of the American Medical Association published an important study today further assessing the “calorie is a calorie” dictum of the dieting world. As there are three main controversies in this world: politics, religion, and calories in=calories out, the authors must be congratulated for taking on such a controversial task. The study is only a preliminary report, but the findings are exciting.
In this study, Dr. Ebbeling and her group took 21 participants and placed them on 3 different isocaloric diets with different macronutrients1. They initially underwent a 7-month run-in diet for weight loss. They then were placed on a 4-week conventional low-fat, low–glycemic index, or very low-carbohydrate diet along with undergoing a variety of tests. What separates this study from the masses is their measurement of resting energy expenditure and total energy expenditure in the participants.
They also assessed leptin, thyroid stimulating hormone (TSH), triiodothyronine (T3), urinary cortisol), insulin sensitivity high-density lipoprotein (HDL) cholesterol, total cholesterol, triglycerides, plasminogen activator inhibitor 1 activity, C-reactive protein (CRP), and ratings of hunger and well-being.
The results were interesting, though not surprising to many low-carb advocates. During the run-in phase of the study, the participants lost an average of around 30 pounds, which corresponded to 13.6% of their baseline body weight. Body fat percentage decreased from 33.6% to 29.1% and daily energy intake during the test diet phase was 2626 calories.
However, the meat of this paper (pun intended) was the resting energy expenditure findings. Resting energy expenditures represents the amount of calories required by the body during a day of non-activity. The higher the energy expenditure, the more the body burns throughout a day. Therefore, in terms of achieving weight loss or maintaining decreased amounts of adipose tissue, the higher the resting energy the better.
Resting and Total Energy Expenditure:
All diets showed a decrease in resting energy with weight loss, but the difference between the diets was statistically significant. The decrease in resting energy was least in the low-carb diet and greatest in the low-fat diet. Values were -205 (calories per day) for the low-fat diet, -166 for the low-GI diet, and -138 for the low-carb diet. Those of us that have switched to a low-carb lifestyle have all experienced this firsthand, especially those of us that have tried calorie restriction and felt our energy levels plummet to nonexistence.
Total energy expenditure revealed similar results, decreasing by 423 calories per day for the low-fat diet, 297 for the low-GI diet, and only 97 calories per day for the low-carb diet. Basically, these results show us that weight loss on a low-carb diet leaves the dieter with a body that continues to burn more calories than other diets. In other words, a low-carb diet leaves the body more metabolically demanding than the other diets – i.e. it leaves the body with a metabolic advantage.
Other Variables Observed:
- Leptin: a hormone that controls appetite and is associated with inflammation and cancer2-6 was found to be significantly lower in the low-carb dieters.
- Insulin sensitivity: another major risk factor for cancer induction and recurrence7-11 was highest in the low-carb dieters.
- Cortisol: a glucocorticoid hormone that counteracts insulin and the body uses to raise blood sugar when it is low via stimulation of gluconeogenesis (conversion of fat to glucose) predictably rose in the low-carbers.
- Serum TSH and T3: these thyroid values were the lowest for the low-carb diet, which is expected and has been shown previously.
- Serum HDL: “good” cholesterol was significantly higher in the low-carbohydrate diet versus the others.
- Serum triglycerides, which are associated with cardiovascular disease, stroke, and cancer12-15 were significantly lower in the low-carb group versus the other two.
- Plasminogen activator inhibitor 1: it has been found to be increased in cancer and even predicts for cancer metastases16, obesity, inflammation, and the metabolic syndrome17-19, and was reduced in the low-carb group.
- CRP: C-reactive protein is a marker of inflammation and has been correlated with poorer outcomes in cancer, stroke, depression, and cardiovascular disease20,21 and was increased in the low-carb group.
- Hunger and well-being: did not differ between the trials.
No study is perfect, and as is often the case in dietary studies, this one had its fair share of issues. The study was short term, with each diet consumed for only 4 weeks. This plagues many dietary studies, but due to the inherent cost of these clinical trials, we often encounter such issues. Also, physical activity was measured with accelerometry, which is imperfect. The other typical dietary trial criticisms (measuring methods, etc.) apply here as well.
The inflammatory serum marker C-reactive protein (CRP) was increased in the low-carb group, and unfortunately this has made the headlines in many reports. This finding has been shown before over the short term, and longer-term studies have shown a low-carb diet to reduce inflammation, as previously discussed. Also, leptin and plasminogen activator inhibitor 1, which are also associated with inflammation were significantly elevated in the other diets versus the low-carb, so from this data it is difficult to decipher which is the most inflammatory short term. Once again, I will defer to the long-term data. Conversely, all markers of metabolic syndrome were improved in the low-carb diet, which is consistent with the ever-expanding literature22-28.
Directly comparing a low-carbohydrate versus a conventional low-fat diet, though short term, showed that the low-carb diet resulted in a resting energy expenditure that was 67 calories per day higher and a total energy expenditure that was 300 calories per day higher, even though physical activity did not change during the study. Therefore, the low-carb dieters appeared to simply burn more calories per day than the other two dieters. This parallels other reports on the “metabolic advantage” of low-carbohydrate diets29-31 that lead to so much controversy in the field of nutrition. However, for those of us who have been following this diet for years, we have witnessed this first hand, often with effortless weight loss. The exact cause for this is unknown, but is likely interplay between hormones and our body’s inherent storage versus burning capabilities and mechanisms, which cause it to view fats and carbohydrates as different sources of fuel.
It is well established that weight loss results in a decrease in resting energy expenditure, i.e. as you lose weight, your body burns less fuel (calories, fat, etc.) and this is often the reason why as patients lose weight, it becomes more difficult to continue a diet. This is also why telling a patient to markedly reduce their calories while increasing their activity is so difficult to adhere to32,33, rarely works, and merely sets them up for emotional and physical failure. This also is why telling a patient to eat less and exercise more (especially when based on a low-fat diet) is not a dietary strategy, but rather torture.
Keep eating like a caveman, keep curbing those carbs, and keep watching the studies pour in to support this lifestyle.
1. Ebbeling Cb SJFFHA, et al. EFfects of dietary composition on energy expenditure during weight-loss maintenance. JAMA: The Journal of the American Medical Association. 2012;307(24):2627-2634.http://dx.doi.org/10.1001/jama.2012.6607
2. Cirillo D, Rachiglio AM, la Montagna R, Giordano A, Normanno N. Leptin signaling in breast cancer: an overview. J Cell Biochem. Nov 1 2008;105(4):956-964.http://www.ncbi.nlm.nih.gov/pubmed/18821585
3. Fantuzzi G, Faggioni R. Leptin in the regulation of immunity, inflammation, and hematopoiesis. J Leukoc Biol. Oct 2000;68(4):437-446.http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=11037963
4. Friedman JM, Halaas JL. Leptin and the regulation of body weight in mammals. Nature. 1998;395(6704):763-770.http://dx.doi.org/10.1038/27376
5. Garofalo C, Surmacz E. Leptin and cancer. J Cell Physiol. Apr 2006;207(1):12-22.http://www.ncbi.nlm.nih.gov/pubmed/16110483
6. Hekerman P, Zeidler J, Korfmacher S, et al. Leptin induces inflammation-related genes in RINm5F insulinoma cells. BMC Molecular Biology. 2007;8(1):41.http://www.biomedcentral.com/1471-2199/8/41
7. Goodwin PJ, Ennis M, Pritchard KI, et al. Fasting insulin and outcome in early-stage breast cancer: results of a prospective cohort study. J Clin Oncol. Jan 1 2002;20(1):42-51.http://www.ncbi.nlm.nih.gov/pubmed/11773152
8. Jaggers JR, Sui X, Hooker SP, et al. Metabolic syndrome and risk of cancer mortality in men. Eur J Cancer. 2009;45(10):1831-1838.http://www.sciencedirect.com/science/article/pii/S0959804909000574
9. Kanety H, Madjar Y, Dagan Y, et al. Serum insulin-like growth factor-binding protein-2 (IGFBP-2) is increased and IGFBP-3 is decreased in patients with prostate cancer: correlation with serum prostate-specific antigen. Journal of Clinical Endocrinology & Metabolism. July 1, 1993 1993;77(1):229-233.http://jcem.endojournals.org/content/77/1/229.abstract
10. Pollak M. Insulin, insulin-like growth factors and neoplasia. Best Pract Res Clin Endocrinol Metab. Aug 2008;22(4):625-638.http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=18971123
11. Sachdev D, Yee D. The IGF system and breast cancer. Endocr Relat Cancer. Sep 2001;8(3):197-209.http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=11566611
12. Cabin HS, Roberts WC. Relation of serum total cholesterol and triglyceride levels to the amount and extent of coronary arterial narrowing by atherosclerotic plaque in coronary heart disease. Quantitative analysis of 2,037 five mm segments of 160 major epicardial coronary arteries in 40 necropsy patients. The American journal of medicine. Aug 1982;73(2):227-234.http://www.ncbi.nlm.nih.gov/pubmed/7114080
13. Freiberg JJ, Tybjærg-Hansen A, Jensen JS, Nordestgaard BG. Nonfasting Triglycerides and Risk of Ischemic Stroke in the General Population. JAMA: The Journal of the American Medical Association. November 12, 2008 2008;300(18):2142-2152.http://jama.ama-assn.org/content/300/18/2142.abstract
14. Goodwin PJ, Boyd NF, Hanna W, et al. Elevated levels of plasma triglycerides are associated with histologically defined premenopausal breast cancer risk. Nutr Cancer. 1997;27(3):284-292.http://www.ncbi.nlm.nih.gov/pubmed/9101559
15. Hokanson JE, Austin MA. Plasma triglyceride level is a risk factor for cardiovascular disease independent of high-density lipoprotein cholesterol level: a meta-analysis of population-based prospective studies. Journal of cardiovascular risk. Apr 1996;3(2):213-219.http://www.ncbi.nlm.nih.gov/pubmed/8836866
16. Foekens JA, Schmitt M, van Putten WL, et al. Plasminogen activator inhibitor-1 and prognosis in primary breast cancer. Journal of Clinical Oncology. August 1, 1994 1994;12(8):1648-1658.http://jco.ascopubs.org/content/12/8/1648.abstract
17. Landin K, Stigendal L, Eriksson E, et al. Abdominal obesity is associated with an impaired fibrinolytic activity and elevated plasminogen activator inhibitor-1. Metabolism. 1990;39(10):1044-1048.http://www.sciencedirect.com/science/article/pii/0026049590901648
18. Alessi M-C, Juhan-Vague I. PAI-1 and the Metabolic Syndrome. Arteriosclerosis, Thrombosis, and Vascular Biology. October 1, 2006 2006;26(10):2200-2207.http://atvb.ahajournals.org/content/26/10/2200.abstract
19. Mertens I, Verrijken A, Michiels JJ, Van der Planken M, Ruige JB, Van Gaal LF. Among inflammation and coagulation markers, PAI-1 is a true component of the metabolic syndrome. Int J Obes. 2006;30(8):1308-1314.http://dx.doi.org/10.1038/sj.ijo.0803189
20. Kuo HK, Yen CJ, Chang CH, Kuo CK, Chen JH, Sorond F. Relation of C-reactive protein to stroke, cognitive disorders, and depression in the general population: systematic review and meta-analysis. Lancet neurology. Jun 2005;4(6):371-380.http://www.ncbi.nlm.nih.gov/pubmed/15907742
21. Pierce BL, Ballard-Barbash R, Bernstein L, et al. Elevated Biomarkers of Inflammation Are Associated With Reduced Survival Among Breast Cancer Patients. Journal of Clinical Oncology. July 20, 2009 2009;27(21):3437-3444.file:/content/27/21/3437.abstract
22. Forsythe C, Phinney S, Feinman R, et al. Limited Effect of Dietary Saturated Fat on Plasma Saturated Fat in the Context of a Low Carbohydrate Diet. Lipids. 2010;45(10):947-962.http://dx.doi.org/10.1007/s11745-010-3467-3
23. Forsythe C, Phinney S, Fernandez M, et al. Comparison of Low Fat and Low Carbohydrate Diets on Circulating Fatty Acid Composition and Markers of Inflammation. Lipids. 2008;43(1):65-77.http://dx.doi.org/10.1007/s11745-007-3132-7
24. Volek J, Phinney S, Forsythe C, et al. Carbohydrate Restriction has a More Favorable Impact on the Metabolic Syndrome than a Low Fat Diet. Lipids. 2009;44(4):297-309.http://dx.doi.org/10.1007/s11745-008-3274-2
25. Brehm BJ, Seeley RJ, Daniels SR, D’Alessio DA. A randomized trial comparing a very low carbohydrate diet and a calorie-restricted low fat diet on body weight and cardiovascular risk factors in healthy women. J Clin Endocrinol Metab. Apr 2003;88(4):1617-1623.http://www.ncbi.nlm.nih.gov/pubmed/12679447
26. Gardner CD, Kiazand A, Alhassan S, et al. Comparison of the Atkins, Zone, Ornish, and LEARN diets for change in weight and related risk factors among overweight premenopausal women: the A TO Z Weight Loss Study: a randomized trial. Jama. Mar 7 2007;297(9):969-977.http://www.ncbi.nlm.nih.gov/pubmed/17341711
27. Hession M, Rolland C, Kulkarni U, Wise A, Broom J. Systematic review of randomized controlled trials of low-carbohydrate vs. low-fat/low-calorie diets in the management of obesity and its comorbidities. Obesity Reviews. 2009;10(1):36-50.http://dx.doi.org/10.1111/j.1467-789X.2008.00518.x
28. Hite AH, Berkowitz VG, Berkowitz K. Low-carbohydrate diet review: shifting the paradigm. Nutrition in clinical practice : official publication of the American Society for Parenteral and Enteral Nutrition. Jun 2011;26(3):300-308.http://www.ncbi.nlm.nih.gov/pubmed/21586415
29. Browning JD, Baker JA, Rogers T, Davis J, Satapati S, Burgess SC. Short-term weight loss and hepatic triglyceride reduction: evidence of a metabolic advantage with dietary carbohydrate restriction. The American Journal of Clinical Nutrition. May 1, 2011 2011;93(5):1048-1052.http://www.ajcn.org/content/93/5/1048.abstract
30. Feinman RD, Fine EJ. “A calorie is a calorie” violates the second law of thermodynamics. Nutr J. Jul 28 2004;3:9.http://www.ncbi.nlm.nih.gov/pubmed/15282028
31. Fine EJ, Feinman RD. Thermodynamics of weight loss diets. Nutr Metab (Lond). Dec 8 2004;1(1):15.http://www.ncbi.nlm.nih.gov/pubmed/15588283
32. Bautista-Castano I, Molina-Cabrillana J, Montoya-Alonso JA, Serra-Majem L. Variables predictive of adherence to diet and physical activity recommendations in the treatment of obesity and overweight, in a group of Spanish subjects. Int J Obes Relat Metab Disord. 2004;28(5):697-705.http://dx.doi.org/10.1038/sj.ijo.0802602
33. Burke LE, Dunbar-Jacob J. Adherence to medication, diet, and activity recommendations: from assessment to maintenance. The Journal of cardiovascular nursing. 1995;9(2):62-79.http://ukpmc.ac.uk/abstract/MED/9197995
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