Fast weight loss gimmicks

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Everyone want to lose weight fast, for various reasons, and many use the modern electrotherapy ways that promise to get you there in no time. If you use such procedures, my suggestion is to go to a qualified nutritionist who knows how to counteract the metabolic effects of sudden weight loss. To understand why I’m making this recommendation, please read this article in full before you trash down your metabolism.


1. Metabolic effects of weight loss thermotherapy

The basic concept behind the apparent efficacy of weight loss thermotherapy is the physiological adaptation to either cold or heat. So implicitly, weight loss thermotherapy contains procedures that expose the body to abrupt temperature changes.

Besides the apparent fast weight loss, this type of procedures have the following side effects:

1.1. Appetite hormones deregulation

From the neurophysiological point of view, the first problem is that the nervous centers responsible for thermic regulation are located in the hypothalamus, very close to the nervous centers of hunger and satiety.

Cold is perceived near the hunger centre, and  heat next to the satiety one.

For this reason, people who still behave physiologically (such as small children, adults who are not on a diet or people who do not eat compulsively) have a natural tendency to eat more in the winter and less in the summer.

But this natural tendency can be intensified by the abrupt temperature changes induced by weight loss thermotherapy procedures. Thus, even if it theoretically stimulates brown fat tissue, “cold” thermotherapy ( and the many exotically-weird types of wrapping) indirectly stimulates NPY and AgRP secretory neurons in the arcuate nucleus of the hypothalamus – thus increasing the perception of hunger.

Such procedures do not increase metabolism because heat generation in adults is generated by muscle contraction, not by mitochondrial activity in brown adipocytes (1).

On the other hand, “hot” thermotherapy (classical sauna or various new types of sauna “in the weight loss capsule”) indirectly stimulates POMC and CART secreting neurons from the same hypothalamic nucleus, generating satiety and lowering metabolism in order not to produces even more heat through muscle contraction.

However, these indirect stimuli – either for the hunger or for the satiety nervous centres – generate sensations that may not coincide with the blood glucose levels, thus these fakery hunger or satiety are associated with a disturbed appetite (2).

This paves the foundation for leptin resistance (3,4). Thus, by regularly practicing weight loss thermotherapy procedures you risk perceiving less and less satiety, while becoming quasi-continuously hungry (5).

1.2. Metabolic decrease

The second problem, apart from the disturbed appetite, is that the weight loss generated by these procedures is only apparent, the decrease in total weight being obtained either by dehydration or by muscle catabolism (6).

The easy to maintain long-term weight loss involves lowering the percentage of fat, not dehydration or the decreasing of the percentage of active striated muscle mass.

Thermotherapy procedures can lead to some detoxification through sweat or some muscle contraction through tremor, not to fat loss.

Replacing regular physical exercise and proper nutrition with weight loss thermotherapy and crash diets leads to dyslipidemia and insulin resistance, not to fat loss:

  • dyslipidemia aggravates leptin resistance (7),
  • leptin stimulates insulin secretion
  • and hyperinsulinism decreases the percentage of active muscle mass by blocking glucose entrance through these muscles’ membrane – which is gradually manifested by gaining weight while eating less and less (8).

1.3. Insulin resistance

The third problem – besides disturbed appetite and metabolic decrease though dehydration and muscle catabolism – is the potential under-eating that a person who wants to lose weight quickly can get while on weight loss thermotherapy.

In the case of cold thermotherapy, the feeling of hunger increases due to the indirect stimulation of the cold perception center, amplifying the physical hunger generated throughout the day by the physiological blood glucose decrease.

If starvation is part of the prescribed diet, and the person who does the weight loss thermotherapy does not eat, despite the perception of gastric hunger (9), lipolysis is initiated in the adipose tissue with the delivery of fatty acids to the muscle tissue for energy.

But if this person does not practice regular sports, the percentage of active muscle mass will be low and the amount of glycogen stored within these sedentary cells will be low as well. This is physiologically aggravated as the person is more sedentary and older  and it is called sarcopenic obesity (10).

Thus, theAcetyl-Co derived from the beta-oxidation of the fat delivered to these muscles cannot be introduced into the Krebs cycle due to the fact that these cells contain insufficient oxaloacetate.

Consequently, either muscle protein catabolism occurs to make the oxaloacetate , or dyslipidemia occurs with elevated blood LDL-cholesterol levels and triglycerides, eventually doubled by depositing some of these triglycerides inside the liver or inside the muscle cell (similar to that of an Argentinian beef steak) (11).

In order to obtain long-term fat loss, we have to practice sports regularly to avoid leptin resistance, insulin resistance and dyslipidemia and to avoid excessive or inadequate carbohydrate intake.

And in the case of hot electrotherapy procedures applied without proper nutrition, all that can be lost is water ± your metabolism down the toilet (12).

Lipolysis is not activated because it is too hot, but vasodilatation will lead to dehydration by increased water loss. Dehydration can overstimulate the satiety nervous centre (13).

As with dietary starvation in people who practice cold thermotherapy procedures, people who practice hot thermotherapy procedures can involuntarily eat too little because of the over-stimulated satiety centre.

Insulin resistance does not occur only when overeating,  but also when undereating – being a protective mechanism meant to keep the internal organs and the brain alive when nutrients availability is too low.

And, just as with hot thermotherapy procedures, fat loss stops due to insulin resistance, together with a gradual increase in fat deposition inside muscle, blood, liver, and even kidneys (14).

Of course, dehydration has an absolutely immediate weight loss effect by lowering the total body weight.

Just that the weight loss obtained through thermotherapy is associated with metabolic decrease, while that obtained through regular physical exercises (especially anaerobic) and proper nutrition is associated with an improved metabolism (15).


2. Metabolic effects of weight loss electrotherapy

Unlike weight loss thermotherapy, there is a little more science behind the combination of electrotherapy and fat loss. It’s just that electrotherapy is aimed at physical therapy for people with disabilities, not for weight loss. And even in these people, electrotherapy is just an adjuvant to the overall recovery treatment, the basis being medical physical exercise.

2.1. Metabolic effects of cavitation by ultrasound

One of the most expensive passive-non-invasive weight loss procedures is ultrasound cavitation.

Ultrasounds are extremely powerful waves – very useful in physical therapy – that are able to break adipocytes and eliminate the triglycerides stored whithin them.

But as with dyslipidemia obtained as a consequence of thermotherapy, moving fat from the fat tissue into the blood generates leptin resistance (generating decreased satiety and increased food cravings) and insulin resistance (generating decreased metabolism that will get you fattened while eating less and less ).

The difference is that in the case of cavitation dyslipidemia is much more pronounced, and leptin disorder can have serious health implications long-term.

Thus, since leptin does not only regulate satiety but also immunity, fertility, osteogenesis, cellular apoptosis and memory, the regular occurrence of massive dyslipidemia produced by repeated cavitation procedures increases the risk of:

  • Weight gain (16)
  • Polycystic ovary and anovulatory infertility (17)
  • Osteoporosis (18)
  • Cancer (especially estrogenic ones) (19)
  • Alzheimer (20)

And, of course, because of the increased amount of fat that floods the striated muscle cells, insulin resistance also occurs alongside the consequent metabolic decline, adding liver or kidney steatosis (21, 22), cardiovascular disease (23), and type 2 diabetes (24) to the picture of the risks of such abrupt dyslipidemia as the one caused by cavitation.

Unfortunately for your long-term health and body image, on the outside of your body the short term effect is sudden weight loss, and the long term side effects are not immediately visible.

2. 2. Metabolic effects of muscle electrostimulation

A cheaper and less harmful form of weight loss electrotherapy is muscle stimulation.

Also coming from physical therapy, electrostimulation is a passive form of muscle contraction, designed to help atrophic or paralysed muscles gain back their former functions. Muscle electrostimulation mimics resistance exercise, generating an anaerobic metabolic adaptation.

Just that, if 0 represents the force of a paralyzed muscle and 5 represents the force of a healthy muscle, electrotherapy without physical therapy cannot increase muscle force over 2 (a force that is not enough to perform anti-gravitational movements) (25).

Muscle electrostimulation is just an adjuvant to physical therapy, medical physical exercise being the basis. So even people with disabilities have to move or to be moved in order to increase strength and muscle tone.

Moreover, anabolism generates nutrient anabolism, not nutrient catabolism.

Anaerobic sports may increase the percentage of active striated muscle mass, increasing metabolism (mainly by increasing the energy consumed per 24 hours for tonic muscle contraction) (26).

Fat loss is achieved by practicing aerobic exercise (cardio type) with a sufficiently high intensity (or interval training – HIIT – the most effective form of physical exercise for weight loss) (27).

So, if in the weight loss equation (= healthy eating + cardio + anaerobic) we replace only the anaerobic exercise part with muscle electrostimulation, healthy eating and proper cardio should still be done regularly to actually lose fat (28).

Weight loss electrostimulation per se – either in the absence of aerobic exercise, either in the presence of starvation diets or in the presence of continuously mindless eating, leads to fat gain, not to fat loss even while the total body weight temporarily decreases (29,30).



Healthy weight loss is fat loss, optimally paralleled with increased active muscle mass that will help you easily maintain your hard earned results long-term.

Fast weight loss gimmicks are fattening in the long run.


Quoted studies

(1) Ravussin, Yann et al. “Effect of intermittent cold exposure on brown fat activation, obesity, and energy homeostasis in mice.” PloS one 9.1 (2014): e85876.

(2) Eccles, R. et al. “Cold pleasure. Why we like ice drinks, ice-lollies and ice cream.” Appetite 71 (2013): 357-360.

(3) Crujeiras, Ana B. et al. “Weight regain after a diet-induced loss is predicted by higher baseline leptin and lower ghrelin plasma levels.” Journal of Clinical Endocrinology & Metabolism 95.11 (2010): 5037-5044.

(4) Schwartz, Michael W. et al. “Specificity of leptin action on elevated blood glucose levels and hypothalamic neuropeptide Y gene expression in ob/ob mice.” Diabetes 45.4 (1996): 531-535.

(5) Münzberg, H. et al. “Leptin receptor action and mechanisms of leptin resistance.” Cellular and Molecular Life Sciences 62.6 (2005): 642-652.

(6) Steen, Suzanne Nelson, Robert A. Oppliger, and Kelly D. Brownell. “Metabolic effects of repeated weight loss and regain in adolescent wrestlers.” Jama 260.1 (1988): 47-50.

(7) Kaur, Kawaljit, Sharda Sidhu, and Gurcharan Kaur. “Association between leptin and lipid profile among women.” Annual Review & Research in Biology 4.5 (2014).

(8) Yoshino, Jun, et al. “Diurnal Variation in Insulin Sensitivity of Glucose Metabolism Is Associated With Diurnal Variations in Whole-Body and Cellular Fatty Acid Metabolism in Metabolically Normal Women.” The Journal of Clinical Endocrinology & Metabolism (2014).

(9) Ciampolini, Mario et al. “Sustained self-regulation of energy intake: Initial hunger is associated with low pre-meal blood glucose and prevents energy accumulation.” Manuscript submitted for publication March 2009 (2008).

(10) Roubenoff, Ronenn. “Sarcopenic obesity: the confluence of two epidemics.” Obesity research 12.6 (2004): 887-888.

(11) Pan, D.A. et al. Skeletal muscle triglyceride levels are inversely related to insulin action. Diabetes, 1997, 46.6: 983-988.

(12) Cheuvront, Samuel N. et al. Water-deficit equation: systematic analysis and improvement. The American journal of clinical nutrition, 2013, 97.1: 79-85.

(13) Hamilton, C.L. Interactions of food intake and temperature regulation in the rat. Journal of comparative and physiological psychology, 1963, 56.3: 476.

(14) Montani, Jean-Pierre et al. “Ectopic fat storage in heart, blood vessels and kidneys in the pathogenesis of cardiovascular diseases.” International Journal of Obesity 28 (2004): S58-S65.

(15) Holloszy, John O. Exercise-induced increase in muscle insulin sensitivity. Journal of Applied Physiology, 2005, 99.1: 338-343.

(16) Torres‐Andrade, Rodrigo et al. “The increase in body weight induced by lack of methyl CpG binding protein‐2 is associated with altered leptin signalling in the hypothalamus.” Experimental physiology (2014).

(17) Messinis, Ioannis E. et al. “Polycystic ovaries and obesity.” Best Practice & Research Clinical Obstetrics & Gynaecology (2014).

(18) Upadhyay, Jagriti, Olivia M. Farr, and Christos S. Mantzoros. “The role of leptin in regulating bone metabolism.” Metabolism (2014).

(19) Pan, Haitao, Jiao Guo, and Zhengquan Su. “Advances in understanding the interrelations between leptin resistance and obesity.” Physiology & behavior 130 (2014): 157-169.

(20) Bonda, David J. et al. “Dysregulation of leptin signaling in Alzheimer disease: evidence for neuronal leptin resistance.” Journal of neurochemistry 128.1 (2014): 162-172.

(21) Birkenfeld, Andreas L., and Gerald I. Shulman. “Nonalcoholic fatty liver disease, hepatic insulin resistance, and type 2 diabetes.” Hepatology 59.2 (2014): 713-723.

(22) de Vries, Aiko PJ et al. “Fatty kidney: emerging role of ectopic lipid in obesity-related renal disease.” The Lancet Diabetes & Endocrinology 2.5 (2014): 417-426.

(23) Shulman, Gerald I. “Ectopic Fat in Insulin Resistance, Dyslipidemia, and Cardiometabolic Disease.” New England Journal of Medicine 371.12 (2014): 1131-1141.

(24) Gastaldelli, Amalia. Role of beta-cell dysfunction, ectopic fat accumulation and insulin resistance in the pathogenesis of type 2 diabetes mellitus. Diabetes research and clinical practice 93 (2011): S60-S65.

(25) Doucet, Barbara M., Lam, Amy, Griffin, Lisa. Neuromuscular electrical stimulation for skeletal muscle function. The Yale journal of biology and medicine, 2012, 85.2: 201.

(26) Hunter, Gary R. et al. Resistance training increases total energy expenditure and free-living physical activity in older adults. Journal of Applied Physiology 89.3 (2000): 977-984.

(27) Shiraev, Tim, and Gabriella Barclay. Evidence based exercise: Clinical benefits of high intensity interval training. Australian family physician 41.12 (2012): 960.

(28) Watanabe, Kohei, Yoshiki Taniguchi, and Toshio Moritani. Metabolic and cardiovascular responses during voluntary pedaling exercise with electrical muscle stimulation. European journal of applied physiology (2014): 1-7.

(29) Carpenter, Catherine L. et al. Body Fat and Body-Mass Index among a Multiethnic Sample of College-Age Men and Women. Journal of obesity, 2013, 2013.

(30) Mauriège, P. et al. Weight loss and regain in obese individuals: A link with adipose tissue metabolism indices?. Journal of physiology and biochemistry, 2013, 1-9.

About the Author

Diana Artene

Sunt Nutritionist-Dietetician, Master in Nutritie si Doctor in Nutritie Oncologica, Nutritionist Sportiv acreditat de Societatea Internationala de Nutritie Sportiva si membru al American Society for Nutrition și al European Society of Medical Oncology.