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Due to the nature of fat loss, there is an absolute need for a comprehensive approach. This includes the reduction of body fat by boosting fatty acid oxidation while concurrently increasing energy expenditure. This approach also preserves the loss of unwanted body fat- by overcoming homeostatic mechanisms that attempt to maintain bodyweight by stimulating appetite and therefore food consumption.

The need for increased energy expenditure- and not just fatty acid oxidation- to trim down fat started to come to light unexpectedly well over a decade ago, with the discovery of the AMP-activated protein kinase (AMPK) signaling pathway.1 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 appears that enhanced fatty acid oxidation alone does not actually reduce adiposity.2 This is likely because, while activated AMPK increases fatty acid oxidation, it does not increase energy expenditure. In fact, fatty acid oxidation without energy expenditure actually increases energy production in the form of ATP. Therefore, the combination of increased energy production (ATP) 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 fat,3 ultimately resulting in no net loss of body fat.

Because of this fact, it became pretty clear that boosting energy expenditure was vital 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. This is done by uncoupling the normally linked process of fat burning with cellular energy (ATP) production instead converting this energy into heat, which effectively increases energy expenditure. Importantly, there has been an abundance of scientific evidence demonstrating that thermogenesis increases energy expenditure while decreasing body fat levels in adult humans.4-6 Furthermore, additional research has discovered many naturally occurring compounds that potently enhance thermogenic-induced fat loss, many of which can be found in the newly released cutting-edge product Thermo-Heat.

Unfortunately, while increased fat loss and energy expenditure are two key elements in the battle against body fat, their enhancement will likely initiate homeostatic mechanisms that conserve bodyweight by triggering hunger, resulting in increased food consumption. This will not only be counterproductive in achieving further fat loss, but may also contribute significantly to regaining some or most of the lost weight. Consequently, the mitigation of cravings and increased appetite must also be addressed to fully support decreased body fat for extended periods of time.

Fortunately, Thermo-Heat has an exclusive blend of compounds that attack body fat by increasing thermogenic-driven fat loss and energy expenditure while also potently alleviating appetite, resulting in suppressed cravings for food, which enhances the capacity to lose body fat and keep it off for good.

Capsaicin and Capsaicinoids Burn Fat and Reduce Hunger

Interventions aimed to improve weight loss and weight maintenance have rapidly embraced the use of several naturally occurring compounds that burn fat while also decreasing appetite. A few potent representatives include capsaicin and capsaicinoids, which are naturally found in chili peppers where they contribute to the hot and spicy flavor of the chili pepper. Several studies have shown both capsaicin and capsaicinoids increase fat-burning thermogenesis in humans through activation of the TRPV1 receptor found in the oral cavity and gastrointestinal tract. Activation of TRPV1 stimulates the sympathetic nervous system, which releases noradrenaline driving thermogenesis and fat loss.7-9 Furthermore, additional studies have shown the power of capsaicin and capsaicinoids to10-12 reduce food intake while another study demonstrated that capsaicin also significantly reduced the desire to eat more food.11

Although an influence on appetite has been observed in several trials, the mechanism of action is not fully understood. It may be that the release of noradrenaline triggered by capsaicin minimizes appetite, as the stimulation of the noradrenaline receptors in the brain has been shown to produce feelings of satiety.13 In addition, the consumption of capsaicin has also been shown to cause an increase in gut-derived hormone GLP-1, which regulates regions of the brain that regulate food intake resulting in reduced hunger.14
Taken together, there is ample evidence that capsaicin and capsaicinoids, which are abundantly found in Thermo-Heat, potently stimulate and preserve fat loss, as recent evidence clearly shows their comprehensive ability to increase energy expenditure and fat oxidation while also reducing appetite.

Piperine Decreases Appetite

Another fat-burning compound found in Thermo-heat is piperine, which is normally responsible for the pungency of black pepper. Piperine has been reported to activate the TRPV1 receptor, triggering thermogenic energy expenditure in a similar fashion to capsaicin and capsaicinoids.15 In addition, piperine has been shown to decrease appetite, putting it in similar category with capsaicin and capsaicinoids as compounds that effectively trigger long-term fat loss by increasing energy expenditure and decreasing appetite.16-17

The control of food intake by the brain relies upon the detection and integration of signals reflecting the storage and flux of energy within the body. Insulin provides one of these signals to the brain by representing an abundance of both circulating energy as glucose and stored energy in the form of body fat. Altogether, insulin signaling tells the brain to reduce appetite and food intake.

Piperine suppresses appetite by modulating insulin signaling. It does this by inhibiting a receptor in the liver known as the liver X receptor alpha (LXR alpha), which normally turns on fat-promoting target genes such as the fatty acid synthase that catalyzes the production of fatty acids. The inhibition of fatty acid synthase by piperine reduces the accumulation of fat within the liver, which increases whole-body insulin sensitivity- ultimately enhancing insulin signaling activity in the brain and reducing appetite.

Mucuna Pruriens Suppresses Cravings and Binge Eating

In addition to energy stores and energy flux functioning as signals of satiation, changes in the level of the brain neurotransmitter dopamine, which controls incentive and reward within the central nervous system, also influences the sensation of hunger. In fact, reduction in dopamine within certain regions of the brain increases hunger. This is based on evidence that showed obese people have an underactive dopamine response to food intake, causing them to eat more until they feel fully rewarded and satiated.18 Consequently, increasing dopamine levels should reduce hunger.

The tropical plant mucuna pruriens found in Thermo-Heat, which is loaded with the dopamine precursor L-dopa, has been shown to increase the diminished dopamine levels found in patients with Parkinson's disease.19-20 The ability of mucuna pruriens to boost dopamine makes it a terrific choice for diminishing cravings and sustaining permanent fat loss.

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.


1. Steinberg, G.R., and Kemp, B.E. (2009). AMPK in Health and Disease. Physiol Rev 89, 1025-1078.
2. Hoehn, K.L., Turner, N., Swarbrick, M.M., Wilks, D., Preston, E., Phua, Y., Joshi, H., Furler, S.M., Larance, M., Hegarty, B.D., Leslie, S.J., Pickford, R., Hoy, A.J., Kraegen, E.W., James, D.E., and Cooney, G.J. (2010). Acute or chronic upregulation of mitochondrial fatty acid oxidation has no net effect on whole-body energy expenditure or adiposity. Cell Metab 11, 70-76.
3. Randle, P.J., Garland, P.B., Hales, C.N., and Newsholme, E.A. (1963). The glucose fatty-acid cycle. Its role in insulin sensitivity and the metabolic disturbances of diabetes mellitus. Lancet 1, 785-789.
4. Nedergaard, J., Bengtsson, T., and Cannon, B. (2007). Unexpected evidence for active brown adipose tissue in adult humans. Am J Physiol Endocrinol Metab 293, E444-452.
5. Saito, M., Okamatsu-Ogura, Y., Matsushita, M., Watanabe, K., Yoneshiro, T., Nio-Kobayashi, J., Iwanaga, T., Miyagawa, M., Kameya, T., Nakada, K., Kawai, Y., and Tsujisaki, M. (2009). High incidence of metabolically active brown adipose tissue in healthy adult humans: effects of cold exposure and adiposity. Diabetes 58, 1526-1531.
6. van Marken Lichtenbelt, W.D., Vanhommerig, J.W., Smulders, N.M., Drossaerts, J.M., Kemerink, G.J., Bouvy, N.D., Schrauwen, P., and Teule, G.J. (2009). Cold-activated brown adipose tissue in healthy men. N Engl J Med 360, 1500-1508.
7. Ludy, M.J., Moore, G.E., and Mattes, R.D. (2012). The effects of capsaicin and capsiate on energy balance: critical review and meta-analyses of studies in humans. Chem Senses 37, 103-121.
8. Snitker, S., Fujishima, Y., Shen, H., Ott, S., Pi-Sunyer, X., Furuhata, Y., Sato, H., and Takahashi, M. (2009). Effects of novel capsinoid treatment on fatness and energy metabolism in humans: possible pharmacogenetic implications. Am J Clin Nutr 89, 45-50.
9. Whiting, S., Derbyshire, E., and Tiwari, B.K. (2012). Capsaicinoids and capsinoids. A potential role for weight management? A systematic review of the evidence. Appetite 59, 341-348.
10. Yoshioka, M., St-Pierre, S., Drapeau, V., Dionne, I., Doucet, E., Suzuki, M., and Tremblay, A. (1999). Effects of red pepper on appetite and energy intake. Br J Nutr 82, 115-123.
11. Yoshioka, M., Imanaga, M., Ueyama, H., Yamane, M., Kubo, Y., Boivin, A., St-Amand, J., Tanaka, H., and Kiyonaga, A. (2004). Maximum tolerable dose of red pepper decreases fat intake independently of spicy sensation in the mouth. Br J Nutr 91, 991-995.
12. Westerterp-Plantenga, M.S., Smeets, A., and Lejeune, M.P. (2005). Sensory and gastrointestinal satiety effects of capsaicin on food intake. Int J Obes (Lond) 29, 682-688.
13. Wellman, P.J. (2000). Norepinephrine and the control of food intake. Nutrition 16, 837-842.
14. Smeets, A.J., and Westerterp-Plantenga, M.S. (2009). The acute effects of a lunch containing capsaicin on energy and substrate utilisation, hormones, and satiety. Eur J Nutr 48, 229-234.
15. McNamara, F.N., Randall, A., and Gunthorpe, M.J. (2005). Effects of piperine, the pungent component of black pepper, at the human vanilloid receptor (TRPV1). Br J Pharmacol 144, 781-790.
16. Jwa, H., Choi, Y., Park, U.H., Um, S.J., Yoon, S.K., and Park, T. (2012). Piperine, an LXRalpha antagonist, protects against hepatic steatosis and improves insulin signaling in mice fed a high-fat diet. Biochem Pharmacol 84, 1501-1510.
17. Woods, S.C., Lutz, T.A., Geary, N., and Langhans, W. (2006). Pancreatic signals controlling food intake; insulin, glucagon and amylin. Philos Trans R Soc Lond B Biol Sci 361, 1219-1235.
18. Stice, E., Spoor, S., Bohon, C., and Small, D.M. (2008). Relation between obesity and blunted striatal response to food is moderated by TaqIA A1 allele. Science 322, 449-452.
19. Tharakan, B., Dhanasekaran, M., Mize-Berge, J., and Manyam, B.V. (2007). Anti-Parkinson botanical Mucuna pruriens prevents levodopa induced plasmid and genomic DNA damage. Phytother Res 21, 1124-1126.
20. Katzenschlager, R., Evans, A., Manson, A., Patsalos, P.N., Ratnaraj, N., Watt, H., Timmermann, L., Van der Giessen, R., and Lees, A.J. (2004). Mucuna pruriens in Parkinson's disease: a double blind clinical and pharmacological study. J Neurol Neurosurg Psychiatry 75, 1672-1677.