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).

Conclusion

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.

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From a metabolic point a view, being pregnant means decreased muscle insulin sensitivity to redirect glucose to feed the fetus. This physiological pregnancy insulin resistance is the reason weight gain during pregnancy seems to happen even after drinking water, as its direct effect is a decreased metabolism for the mother. As you might know, metabolism it is not something that we can increase by drinking tea. Any tea. Metabolism is the energy required by the internal organs and brain, plus the energy needed for thermoregulation, plus the energy needed for digesting food, plus the energy needed by the contracting skeletal muscle cell to maintain tonus. The only metabolic factor that can be increased or decreased without pathology is this number of skeletal muscle cells that contract 24/7.

Pregnancy does not equal gaining body fat, but gaining body weight. This is true up to about 9 kg gestational weight increase, above which we start to talk about fat gain. At first, pregnant women do not gain weight by eating too much but by physiological metabolic decrease due to insulin resistance, which can healthily generate a gestational weight gain of about 9 to 15 kg. Above this value, we stop talking about a healthy gestational weight gain, and the “unhealthy” reverse refers to the fetus, not to the mother. Sadly, many mothers gain far too much weight during pregnancy, way above the recommended gestational weight gain range, risking both to remain overweight after birth, and to increase the child’s risk of developing a bucket full of diseases among which obesity is the less dangerous one. The child of a mother who gained too much during pregnancy has an increased risk of metabolic syndrome, (8) obesity, (9) and eating disorders (10) because the fetus develops insulin resistance while in the womb. (11)

In many maternities, newborns are fed on a schedule. Once home, the new mom must decide two things: if she will breastfeed her baby, and if she will demand feed him (or her) or feed him on a schedule. The first decision is widely debated and most mothers do their best to breastfeed their newborns. Yet, from a public health point of view, we mostly do not address the second decision even though demand feeding children of mothers who gained too much weight during pregnancy can balance their metabolic adaptations to the mother’s gestational eating behavior. (12)

When a pregnant woman overeats the fetus overeats, increasing the adipose cells number and decreasing the muscle mitochondria number he will be born with. (13) The thrifty genes hypothesis can be explained as a fetal insulin resistance’s side effect. Because of the reactive increased fetal insulinemia – reactive to the huge amount of nutrients the fetus receives due to the mother’s increased insulin resistance – glucose cannot enter through skeletal muscles’ GLUT4 membrane transporters and it’s redirected either towards the fetal adipose tissue causing macrosomia, (14) either towards the liver where it is transformed into fatty acids that can potentially clog placental vessels causing the child to be born with a weight below his gestational age. (15) So, it is not the birth weight of the newborn, but the gestational weight gain that can tell us something about the newborn’s metabolism. An insulin resistant fetus will genetically adapt by coding thrifty genes that will help his starving muscular cells survive his mother’s overeating. Scientists knew this survival mechanism from children of diabetic mothers, but studies on infantile obesity etiology link the thrifty genes hypothesis to children of mothers who gained too much weight during pregnancy also. (16) Scientists hypothesize that these children are born with a normal number of skeletal muscle cells, but with fewer mitochondria, and with a higher number of adipose fat cells = an innate low metabolism. This innate low metabolism can be aggravated by feeding the newborn regardless of his hunger, on a tight meal schedule, and it can be balanced by demand feeding. (17)

We know that adipose hyperplasia mostly happens up to one year of age if newborns are overfed, regardless of their hunger and satiation, increasing their obesity risk for life. (18) Such a behavior is also more prevalent in overweight, obese or eating disorder affected parents, which further increase the child obesity risk. However, eating without hunger or past satiation – either when we are talking about fetuses, newborns, adolescents or grandparents – has more risks than just gaining weight, due to the satiety hormone, leptin. Leptin is secreted by the fat tissue, and it inhibits the hunger neurons within the arcuate nucleus from the hypothalamus. It is responsible for the lack of hunger we experience during night sleep (based on an insulin – melatonin interaction), and for the long term control of satiety. More fat tissue, means more leptin, but – and this is a huge but – the hypothalamus’s becomes leptin resistance exactly as the muscle cell become insulin resistance. And during pregnancy even the placenta secrete leptin, so a fetus of a mother who overeats during pregnancy will be born both insulin resistant and with a degree of leptin insensitivity. Insulin resistance means increased obesity risk, and leptin resistance means a huge number of other risks.

Now, besides leptin, there are other satiety hormones of which I want to mention two: CCK (colecistokinin), and PYY (polypeptide Y). CCK is secreted when special cells within the small intestine’s lining come in contact with lipids, and it generates short term satiety. For meals constituted of “milk” only, replacing natural, whole fat milk with degreased types of milk or with low fat vegetal versions of “milk” can deregulate CCK secretion, causing infant hyperphagia. (19) PYY is secreted when other special cells within ileum and colon lining come into contact with digestion products, and it generates satiety between meals. Snacking can deregulate PYY and cause an insulin secretion spike if it happens too soon after a full meal. (20) It is true that there are no black and white solutions when it comes to preventing or treating children’s obesity, but snacking can potentially do more harm than good for a child born insulin resistant, and with a higher body fat percentage that will secrete a higher amount of leptin. (21) And this higher amount of leptin will not translate in higher satiety, but in lesser as the arcuate nucleus of the hypothalamus adapts to the leptin flood by becoming leptin resistant.

The fetus’ hypothalamus can become leptin resistant during pregnancy if the mother overeats to the point of highly increasing her body fat percentage, while decreasing her insulin and leptin sensitivity. (22) The newborn of an insulin and leptin resistant mother can also become leptin resistant during his first year of life – “eating well” enough to sooth parents and grandparents worries – if he is fed regardless of his hunger and satiation. He will mostly grow well, but what if he’ll grow too “well?” The World Health Organization scientists predict that 30 million children more than today will become overweight or obese in the next 10 years, and the children born insulin and leptin resistant fed regardless of their hunger and/ or satiation will be a huge part of them. Moreover, leptin – the main satiety hormone – does not regulate only satiety. It regulates cellular replication, differentiation and apoptosis – potentially linking obesity with the cancer risk. (23) It stimulates the release of gonadotropin hormones (GNRH), which will command the release of the lutein hormone (LH) – linking leptin resistance with PCOS and infertility. (24) Optimal leptin secretion, along with STH and GNRH secretions, is also essential for puberty onset when the body is ready, and not before. (25) The same leptin is essential for fetal brain development, learning capacity and memory. (26) And the same leptin is crucial for innate and acquired immunity, fetal leptin resistance being linked with thyme atrophy or with a decreased function of the macrophage cells. (27) So, when the pregnant mother overeats and gain too much weight during pregnancy and/ or when she feeds her children regardless of their hunger and satiation, she unknowingly risk to disturb all this leptin regulated systems, obesity being the smaller risk of all. (28)

It is true that a meal schedule is easier to apply and more emotionally comfortable than demand feeding newborns. But a meal schedule can only regulate ghrelin, (29) while the other hormones involved in regulating appetite are more sensitive to blood sugar than to the emptiness of the stomach – which can coincide or not with a blood sugar decreased enough to stimulate the hunger center. (30) The energy needs of different bodies are different from day to day, but the newborn bodies’ needs differ far more than others as a newborn almost triples his weight in the first year of life. Predicting his food needs based on other newborn needs, without considering his unique metabolism, can undernourish or overnourish this particular child generating or aggravating insulin and leptin resistance. (31) And then we see he’s fat, and/ or that he has a low immunity, and/ or that his gonads are not properly developed, and/ or that he’s brain abilities are not what we’ve expected, and/ or that he has a cancer risk – all in the name of the soothing feeling we have as parents when we know a child “ate well.”

Feeding any child regardless of his hunger and satiation puts him at these risks, but a child born from a mother who overate during pregnancy is much more at risk for developing metabolic complications than the children born by mothers who stayed within the recommended gestational weight gain range. Demand feeding can balance their innate low metabolism and increase their leptin sensitivity, (32) being the best chance we got to reverse this increasing infantile obesity trend that we, almost hopelessly, witness today.

By Diana Artene, PT, ND, MSN.

References

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