My Cart

Close

science nutrition blog

science nutrition <strong>blog</strong>

Weight-loss programs typically involve caloric restriction combined with rigorous exercise to generate an energy deficit, causing the body to burn fat in order to replenish this energy deficiency. Although this approach seems pretty straightforward and should work well, it has been pretty ineffective at achieving fat loss— as demonstrated by the continuous increase of obesity in the United States.1 On top of that, fat-burning regimens usually require extensive cardiovascular exercise, which mitigates muscle growth— making them a less effective choice for those trying to lose fat and increase muscle size. What's more, if dieting does actually lead to weight loss, it has been shown that in response to reduced food intake and weight loss there is an accompanying reduction in energy expenditure triggered within the body to maintain energy homeostasis. These energy-sparing mechanisms are not only counterproductive in achieving further fat loss, but also contribute significantly to regaining some or most of the lost weight. 

The Search for Fat-Loss Supplements That Burn Fat and Keep It Off

An understanding of the fundamental limitations of dieting and exercise on fat loss has fueled the search for innovative nutraceuticals that not only increase fatty acid oxidation, but also energy expenditure— in order to burn fat and keep it off by dampening the compensatory mechanisms that reduce energy expenditure. 

A turning point in the search for potential fat-burning compounds occurred well over a decade ago with the discovery of the AMP-activated protein kinase (AMPK) signaling pathway.2 Activation of AMPK conveys many of the beneficial effects associated with exercise, including increased fatty acid oxidation. So it was initially believed that AMPK-activating compounds boosting fatty acid oxidation would reduce body fat. Yet surprisingly, it seems that enhanced fatty acid oxidation does not actually reduce adiposity, as the upregulation of fatty acid oxidation has been shown to have no apparent effect on adiposity.3 This is likely because, while activated AMPK increases fatty acid oxidation, it does not increase energy expenditure. As a matter of fact, fatty acid oxidation actually increases energy production (in the form of ATP). Thus, the combination of increased energy production from burning fat without greater energy expenditure generates an overall energy surplus that supports the reestablishment of body fat levels, primarily by converting glucose into fat4, likely resulting in no net loss of body fat.

Thermogenic Breakthrough

In view of the above research, it became pretty clear that boosting energy expenditure is also required to promote leanness. This led to considerable interest in a process known as thermogenesis, because of its unique capacity to simultaneously drive fatty acid oxidation while also increasing energy expenditure. While thermogenesis occurs in most tissue types, brown adipose tissue (BAT) is the most influential thermogenic tissue for fat loss. BAT normally generates thermogenic-derived heat within the body in response to cold temperature exposure, to maintain normal body temperature. This is done by uncoupling the normally linked process of fat burning with cellular energy (ATP) production instead of creating heat, which effectively increases energy expenditure. Supporting the role of BAT in fat loss, there has been an abundance of scientific evidence demonstrating that BAT increases energy expenditure while decreasing body fat levels in adult humans.5-7 Furthermore, additional research has discovered numerous naturally occurring compounds that potently enhance BAT-induced fat loss— many of which can be found in the recently released fat-incinerating product Thermo-Heat that is taking the nutritional supplement world by storm!

Superior Thermogenic Effect of Protein Over Carbs and Fat

In addition to BAT-driven thermogenesis, another key thermogenic inducer is the diet— where one major aspect of diet-induced thermogenesis involves the energy cost associated with metabolizing nutrients.8 A commonly used estimate of this type of thermogenic effect of food is roughly 10 percent of one's caloric intake, although the effect varies substantially for each macronutrient with proteins burning approximately 23 percent, carbohydrates 6 percent and fat 3 percent.9,10 Therefore, the superior thermogenic response to protein intake relative to carbohydrates and fat makes isocaloric diets higher in protein the optimal choice for thermogenic fat loss.

In addition to consuming more protein to trigger thermogenesis, altering the protein source can also be an effective way to trigger fat loss as certain protein types boost thermogenesis more effectively. This was shown in a recent study comparing the thermogenic effects of isocaloric high-protein meals containing either casein, whey or soy protein, where it was reported that the whey protein diet elicited a greater thermogenic response and higher fat oxidation than either casein or soy protein.11 The authors of this study proposed that since whey increases protein synthesis more than casein or soy12,13 and that increased protein synthesis is one of the postulated mechanisms that induces thermogenesis, perhaps the difference in thermogenesis from whey protein consumption observed in this study is due to heightened protein synthesis. 

The Best Thermogenic Fats

Fatty acids are carboxylic acids attached to chains of carbon atoms that vary in length, with long-chain fatty acids having lengths of 12 carbons or more, and medium-chain fatty acids with carbon lengths typically between six and 10 carbon atoms. They also deviate in their saturation level, appearing in three main forms: saturated, monounsaturated and polyunsaturated. Saturated fatty acids contain no double bonds within the carbon chain, while both monounsaturated and polyunsaturated fatty acids contain either one or more double bonds, respectively, which significantly alters their chemical structure. 

The diversity in fatty acid structure due to the differences in chain length and degree of saturation influences their metabolic fate by directing them to separate metabolic pathways that have a different level of impact on thermogenesis. In fact, there are several studies showing that the thermogenic effect of meals rich in medium-chain fatty acids is greater than meals rich in long-chain fatty acids. Other studies demonstrate that diets high in polyunsaturated or monounsaturated fatty acids are more thermogenic than diets high in saturated fatty acids14-16, with no differences between meals rich in polyunsaturated versus monounsaturated fatty acids on thermogenesis.17,18

In addition to fatty acids directly influencing thermogenesis, certain sources of dietary fat contain additional compounds that also drive thermogenesis. One of the more potent ones being oleuropein, a polyphenolic found in extra-virgin olive oil (also found in Thermo-Heat). Oleuropein stimulates the sympathetic nervous system to secrete noradrenaline, which increases production of UCP-1, the protein that uncouples fat oxidation with ATP production in BAT- stimulating energy expenditure via thermogenesis.19

Temporary Fasting Drives Permanent Thermogenesis

Intermittent fasting has increased in popularity recently as a unique way to bolster weight loss.20 This approach typically involves the consumption of approximately 600 calories per day for one or two days per week. Although consuming only 600 calories a day may seem unusual, especially if you want to pack on muscle mass, recent findings indicate that intermittent fasting may be effective for weight loss without affecting lean body mass.21,22

Although the exact mechanisms remain unclear, the fat-lowering capability of intermittent fasting appears to be caused, in part, by the ability to boost levels of the thermogenic molecule fibroblast growth factor 21.23 While FGF21 is upregulated in liver during fasting and switches peripheral tissues toward oxidative metabolism, increasing fatty acid oxidation, it also plays an important role in enhancing the thermogenic capacity of white adipose tissue (WAT) by increasing expression of UCP-1. In fact, mice deficient in FGF21 display an impaired ability to adapt to chronic cold exposure due to diminished WAT-driven thermogenic heat production24, suggesting that FGF21 activates the thermogenic machinery as a defense against hypothermia and may be a novel way to drive thermogenic fat loss.

In conclusion, sustainable fat loss requires greater fatty acid oxidation combined with increased energy expenditure. Thermogenesis represents an innovative way to potently accomplish both of these processes. While there are many ways to induce thermogenesis, the most effective combination consists of a high-protein diet infused with unsaturated fatty acids, while supplementing with the potently thermogenic product Thermo-Heat for maximal thermogenesis that not only burns body fat but keeps if off.

For most of Michael Rudolph's career he has been engrossed in the exercise world as either an athlete (he played college football at Hofstra University), personal trainer or as a Research Scientist (he earned a B.Sc. in Exercise Science at Hofstra University and a Ph.D. in Biochemistry and Molecular Biology from Stony Brook University). After earning his Ph.D., Michael investigated the molecular biology of exercise as a fellow at Harvard Medical School and Columbia University for over eight years. That research contributed seminally to understanding the function of the incredibly important cellular energy sensor AMPK— leading to numerous publications in peer-reviewed journals including the journal Nature. Michael is currently a scientist working at the New York Structural Biology Center doing contract work for the Department of Defense on a project involving national security.

References:

1. Haslam, D. Obesity: a medical history. Obes Rev 2007;8 Suppl 1, 31-36.
2. Steinberg GR and Kemp BE. AMPK in Health and Disease. Physiol Rev 2009;89, 1025-1078.
3. Hoehn KL, Turner N, et al. Acute or chronic upregulation of mitochondrial fatty acid oxidation has no net effect on whole-body energy expenditure or adiposity. Cell Metab 2010;11, 70-76.
4. Randle PJ, Garland PB, et al. The glucose fatty-acid cycle. Its role in insulin sensitivity and the metabolic disturbances of diabetes mellitus. Lancet 1963; 1, 785-789.
5. Nedergaard J, Bengtsson T and Cannon B. Unexpected evidence for active brown adipose tissue in adult humans. Am J Physiol Endocrinol Metab 2007; 293, E444-452.
6. Saito M, Okamatsu-Ogura Y, et al. High incidence of metabolically active brown adipose tissue in healthy adult humans: effects of cold exposure and adiposity. Diabetes 2009;58, 1526-1531.
7. van Marken Lichtenbelt WD, Vanhommerig JW, et al. Cold-activated brown adipose tissue in healthy men. N Engl J Med 2009;360, 1500-1508.
8. Westerterp, K.R. Diet induced thermogenesis. Nutr Metab 2004 (Lond); 1, 5.
9. Tappy L, Jequier E and Acheson K. Thermic effect of infused amino acids in healthy humans and in subjects with insulin resistance. Am J Clin Nutr 1993;57, 912-916.
10. Acheson KJ, Ravussin E, et al. Thermic effect of glucose in man. Obligatory and facultative thermogenesis. J Clin Invest 1984;74, 1572-1580.
11. Acheson KJ, Blondel-Lubrano A, et al. Protein choices targeting thermogenesis and metabolism. Am J Clin Nutr 2011;93, 525-534.
12. Boirie Y, Dangin M, et al. Slow and fast dietary proteins differently modulate postprandial protein accretion. Proc Natl Acad Sci USA 1997;94, 14930-14935.
13. Tipton KD, Elliott TA, et al. Ingestion of casein and whey proteins result in muscle anabolism after resistance exercise. Med Sci Sports Exerc 2004;36, 2073-2081.
14. St-Onge MP and Jones PJ. Physiological effects of medium-chain triglycerides: potential agents in the prevention of obesity. J Nutr 2002;132, 329-332.
15. Piers LS, Walker KZ, et al. The influence of the type of dietary fat on postprandial fat oxidation rates: monounsaturated (olive oil) vs saturated fat (cream). Int J Obes Relat Metab Disord 2002;26, 814-821.
16. Jones PJ, Jew S and AbuMweis S. The effect of dietary oleic, linoleic, and linolenic acids on fat oxidation and energy expenditure in healthy men. Metabolism 2008;57, 1198-1203.
17. Casas-Agustench P, Lopez-Uriarte P, et al. Acute effects of three high-fat meals with different fat saturations on energy expenditure, substrate oxidation and satiety. Clin Nutr 2009;28, 39-45.
18. Flint A, Helt B, et al. Effects of different dietary fat types on postprandial appetite and energy expenditure. Obes Res 2003;11, 1449-1455.
19. Oi-Kano Y, Kawada T, et al. Oleuropein, a phenolic compound in extra virgin olive oil, increases uncoupling protein 1 content in brown adipose tissue and enhances noradrenaline and adrenaline secretions in rats. J Nutr Sci Vitaminol (Tokyo) 2008;54, 363-370.
20. Mattson MP and Wan R. Beneficial effects of intermittent fasting and caloric restriction on the cardiovascular and cerebrovascular systems. J Nutr Biochem 2005;16, 129-137.
21. Harvie MN, Pegington M, et al. The effects of intermittent or continuous energy restriction on weight loss and metabolic disease risk markers: a randomized trial in young overweight women. Int J Obes (Lond) 2011;35, 714-727.
22. Williams KV, Mullen ML, et al. The effect of short periods of caloric restriction on weight loss and glycemic control in type 2 diabetes. Diabetes Care 1998;21, 2-8.
23. Bass J. Forever (FGF) 21. Nat Med 2013;19, 1090-1092.
24. Fisher FM, Kleiner S, et al. FGF21 regulates PGC-1alpha and browning of white adipose tissues in adaptive thermogenesis. Genes Dev 2011;26, 271-281.