06 Apr The Weight switch
The way to treat obesity, which is an important risk factor for heart disease, diabetes, liver disease and many forms of cancer, has been reinforced with the discovery of the “switch”, which regulates how much fat a person burns after eating.
The complex process is controlled by a switch-like mechanism in the brain, which “turns on” and “off”, something that alternatively leads to either storage or burning of fat.
In obese people, this switch is constantly “on” so that the body does not “burn” fat.
In their case, the body does not expend excess energy, resulting in weight gain.
Leptin is the hormone-switch that regulates our body weight and manages fat burning, that is, whether the amounts of fat will be stored or used directly for energy production, while at the same time regulates the feeling of hunger. The two hormones that work together in order to manage the energy stores (in fat burning) in the human body are insulin and leptin.
The message that leptin sends to the brain is that fat stores are full, energy reserves are adequate and the body does not need any other food.
But, when someone continues eating beyond this point, although leptin production increases, the brain slowly ceases to respond to this stimulus. The feeling of satiety is lost and weight begins to increase.
For the last fifteen years we have been able to control the operation of the “switch”, so that people can better control the way their bodies “handle” fat.
Thus, we have the ability to measure this “switch” and in combination with the measurement of other metabolic indicators, to have a representation of the cell’s metabolic pathways. A treatment containing the appropriate vitamins, micro- and macro-nutrients will gradually restore the imbalanced metabolic pathways and the cells biochemistry.
The goal of such an evidence-based therapeutic process is to provide the human body with all those biomolecules that will enable fat-burning, balance of blood sugar levels, optimal synthesis of hormones and the re-activation of the hormone “switch”.
Dr. Nikoleta Koini, M.D.
Doctor of Functional, Preventive, Anti-ageing and Restorative Medicine.
Diplomate and Board Certified in Anti-aging, Preventive, Functional and Regenerative Medicine from A4M (American Academy in Antiaging Medicine).
- Bouret S, Levin BE, Ozanne SE (January 2015). “Gene-environment interactions controlling energy and glucose homeostasis and the developmental origins of obesity”. Physiological Reviews. 95 (1): 47–82. doi:10.1152/physrev.00007.2014. PMC 4281588. PMID 25540138.
- Pan H, Guo J, Su Z (May 2014). “Advances in understanding the interrelations between leptin resistance and obesity”. Physiology & Behavior. 130: 157–69. doi:10.1016/j.physbeh.2014.04.003. PMID 24726399. S2CID 12502104.
- Wang MY, Chen L, Clark GO, Lee Y, Stevens RD, Ilkayeva OR, Wenner BR, Bain JR, Charron MJ, Newgard CB, Unger RH (March 2010). “Leptin therapy in insulin-deficient type I diabetes”. Proc. Natl. Acad. Sci. USA. 107 (11): 4813–19. Bibcode:2010PNAS..107.4813W. doi:10.1073/pnas.0909422107. PMC 2841945. PMID 20194735. Lay summary – medicinenet.com.
- Elmquist JK, Elias CF, Saper CB (Feb 1999). “From lesions to leptin: hypothalamic control of food intake and body weight”. Neuron. 22 (2): 221–32. doi:10.1016/S0896-6273(00)81084-3. PMID 10069329. S2CID 1712670.
- Perrier S, Caldefie-Chézet F, Vasson MP (January 2009). “IL-1 family in breast cancer: potential interplay with leptin and other adipocytokines”. FEBS Lett. 583 (2): 259–65. doi:10.1016/j.febslet.2008.12.030. PMID 19111549. S2CID 30801028.
- Caro JF, Sinha MK, Kolaczynski JW, Zhang PL, Considine RV (November 1996). “Leptin: the tale of an obesity gene”. Diabetes. 45 (11): 1455–62. doi:10.2337/diab.45.11.1455. PMID 8866547. S2CID 5142768.
- Frodermann, Vanessa; Rohde, David; Courties, Gabriel; Severe, Nicolas; Schloss, Maximilian J.; Amatullah, Hajera; McAlpine, Cameron S.; Cremer, Sebastian; Hoyer, Friedrich F.; Ji, Fei; van Koeverden, Ian D. (2019-11-07). “Exercise reduces inflammatory cell production and cardiovascular inflammation via instruction of hematopoietic progenitor cells”. Nature Medicine. 25 (11): 1761–1771. doi:10.1038/s41591-019-0633-x. ISSN 1078-8956. PMC 6858591. PMID 31700184.
- Green ED, Maffei M, Braden VV, Proenca R, DeSilva U, Zhang Y, Chua SC, Leibel RL, Weissenbach J, Friedman JM (August 1995). “The human obese (OB) gene: RNA expression pattern and mapping on the physical, cytogenetic, and genetic maps of chromosome 7”. Genome Res. 5 (1): 5–12. doi:10.1101/gr.5.1.5. PMID 8717050.
- Farooqi, I. Sadaf; Keogh, Julia M.; Kamath, Sri; Jones, Sarah; Gibson, William T.; Trussell, Rebecca; Jebb, Susan A.; Lip, Gregory Y. H.; O’Rahilly, Stephen (November 1, 2001). “Partial leptin deficiency and human adiposity”. Nature. 414 (6859): 34–35. Bibcode:2001Natur.414…34F. doi:10.1038/35102112. ISSN 0028-0836. PMID 11689931. S2CID 4344492.
- Paracchini V, Pedotti P, Taioli E (2005). “Genetics of leptin and obesity: a HuGE review”. Am. J. Epidemiol. 162 (2): 101–14. doi:10.1093/aje/kwi174. PMID 15972940.
- Ahima RS, Prabakaran D, Mantzoros C, Qu D, Lowell B, Maratos-Flier E, Flier JS (July 1996). “Role of leptin in the neuroendocrine response to fasting”. Nature. 382 (6588): 250–52. Bibcode:1996Natur.382..250A. doi:10.1038/382250a0. PMID 8717038. S2CID 4331304.
- Hickey MS, Considine RV, Israel RG, Mahar TL, McCammon MR, Tyndall GL, Houmard JA, Caro JF (November 1996). “Leptin is related to body fat content in male distance runners”. Am. J. Physiol. 271 (5 Pt 1): E938–40. doi:10.1152/ajpendo.1996.271.5.E938. PMID 8944684.