The weight-regulating hormone leptin is the antagonist of ghrelin, the orexigenic hormone that stimulates appetite. Research has shown that ghrelin-producing cells seem to be more abundant in morbidly obese patients (Abdemur et al, 2014). Ghrelin is secreted in the stomach and is inhibited by the satiety effects of leptin that functions as a feedback signalling mechanism mediated by the hypothalamus (Yildiz et al, 2004). From an intuitive point of view, decreasing ghrelin and increasing leptin may be the apparent target of weight loss methods. However, there is a fine line between altering leptin/ghrelin concentrations and unsettling the hormonal balance that usually precipitates weight gain. Unwarrantable ghrelin decrease and leptin increase may also impose a health risk. Ghrelin is expressed in human T cells and monocytes to inhibit the expression of pro-inflammatory anorectic inflammatory cytokines, such as IL-1β and IL-6, which are implicated in chronic low-grade inflammation and aging (Hart, 1988; Ershler and Keller, 2000; Dixit et al, 2004). Regulation of inflammatory cytokines by normal levels of ghrelin may be crucial in preventing inflammation. Health is hormonal balance-contingent. Therefore, optimal levels of ghrelin are necessary to regulate persistent inflammation leading to ageing and disease. Symptom-targeted weight loss that imbalances hormones and increases oxidative damage, toxicity and inflammation is not only a health risk, but pointless, since inflammation and hormonal imbalance will negate all attained benefits, leading to weight gain rebound. Weight loss-targeting interventions, either for health or aesthetic purposes, cannot be merely based on the restricted perspective of symptom elimination. Practitioners should adopt an enriched frame of reference centred on overall physical health.
Principally, obesity, oxidative damage and inflammation are inherent in most pathological conditions, including diabetes, cardiovascular disease (CVC) and even COVID-19. Furthermore, reports suggest that a high percentage of the population who will contract COVID-19 will also have a BMI of 25 and over, and more than 73.4% of COVID-19 patients in intensive care are classified as overweight (Davenport and Nainggolan, 2020; Osborne, 2020). The common denominators of inflammation-compromised health are adiposity, excess very-low-density lipoprotein (VLDL) and triglycerides, metabolic dysfunction and dysregulation of appetite-controlling hormones, leptin and ghrelin, reinforcing excess food consumption. Inflammation is at the core of susceptibility to illness and increased mortality. Recent research reports that patients with viral infections, including COVID-19, do not develop a high ‘viral load’ but a ‘cytokine storm’ syndrome, an immune reaction in which the body releases too many cytokines into the blood, resulting in hyperinflammation that turns out to be lethal for the patient. During this inflammatory state, interferons trigger cascades of antiviral activity; however, in the process, they shut down host protein synthesis, inducing cell death (Tanaka et al, 2014; Ruan et al, 2020). Systemic balance and moderation, including hormonal levels within the normal range, appear to be an essential requirement for optimal health.
The study included 10 healthy adults and took place in three different private aesthetic clinics in separate countries
So, what is the solution for those that have already accumulated excess visceral adiposity, along with its inherent inflammatory toxicity and hormonal imbalance? Very few clinical trials use lasers for visceral fat reduction. In one trial, low-level laser therapy (LLLT) was offered to women aged 20–40 years old with BMI ≥30 kg/m2. LLLT was delivered for 16 minutes after subjects completed 1 hour of aerobic and resistance exercises. The combination of LLLT and physical training was offered three times weekly for 16 weeks. Results revealed a statistically significant reduction in neck and waist circumferences, which, however, do not represent the main sites of visceral adipose tissue (VAT) concentrations. These investigators report visceral fat decrease based on a conductance instrument, as well as leptin decrease after the 16 combined treatments (Duarte et al, 2015). The inclusion of a placebo group increases the study's validity; however, there was no experimental group using LLLT alone. Therefore, it is not clear whether the VAT outcome was the result of the LLLT treatment or the exercise. Moreover, there was no substantial evidence confirming that these subjects were leptin-resistant to justify the observed leptin suppression, or whether the decrease of the weight-regulating hormone was the result of increased energy expenditure due to exercise, triggering the need for more food consumption. A similar clinical trial was conducted with women 20–40 years old and with BMIs of 30–40 kg/m2, who were treated with a combination of LLLT and exercise three times a week for 4 months, and reportedly yielded a reduction in interleukin 6 (IL-6) and an increase in WNT5 signalling. However, no differences in visceral fat, lean mass, VLDL, LDL, and triglycerides were demonstrated between the experimental and control groups (da Silveira Campos et al, 2018).
Radiofrequency studies on VAT reduction are sparse and present methodological limitations. The Cairo University clinical trial published in the Bulletin of Cairo University (Sabbour et al, 2009) used cavitation ultrasound therapy (CUT) on 50 perimenopausal women aged between 37–39 years with a BMI of 31.5–40.04 kg/m2. The experimental group that received CUT treatments plus a low-calorie diet for 3 months was compared to a control group that was only given the low-calorie diet for the same period. They report significant differences in both of the groups' weight, waist and hips circumferences, BMI, triglycerides, low-density lipoprotein (LDL) and high-density lipoprotein (HDL), with the CUT group showing an advantage in overall body fat loss, as well as a decrease in triglycerides and LDL. These investigators report a decrease of VAT based on the CUT group's advantage of overall fat reduction. However, they present no proof that these subjects lost visceral rather than subcutaneous fat. Additionally, visceral fat is more prominent in the lower abdominal area and not the waist and hip circumferences that were the main measurement targets of this clinical study.
Randomised placebo-controlled data indicates that exercise reduces visceral adipose tissue and liver fat. Liver fat spectroscopy and magnetic resonance imaging of visceral adipose tissue were adopted to evaluate physique before and after three different modes of exercise performed by inactive, overweight adults, over a period of 8 weeks. This well-designed study using highly reliable measures found no significant differences between dose or intensity of exercise. There was a small reduction in visceral adipose tissue and fatty liver without a clinically significant weight loss (Keating et al, 2015). Another well-designed study on 160 healthy Korean adults (38 men and 122 women) explored the results of exercise on visceral adiposity and C-reactive protein (CRP), one of the most prominent markers of inflammation. The abdominal fat area was measured by computed tomographic scanning. They also looked at blood levels of glucose, lipids, CRP and leptin, among other variables. Visceral fat was the best predictor of inflammation, as measured by CRP, along with insulin resistance and endothelial dysfunction-related factors. Exercise participants had significantly lower visceral fat. However, no significant difference in BMI or physical fitness was found. These investigators interpreted their findings as evidence that even in the absence of visible results, exercise can still act as a protective measure in safeguarding health (Kim et al, 2008).
Exercise is beneficial in moderation. However, excessive physical activity is perceived by the body as a form of stress, stimulating the release of cortisol that can be deleterious to older individuals already burdened by age-related cortisol increase. Excess cortisol may cause tissue breakdown or result in stress-eating behaviours that can compromise the benefits of exercise (George et al, 2010). Cortisol is involved in the conversion of protein to glucose, potentially predisposing older individuals to type 2 diabetes (Chiodini et al, 2007). Moreover, strenuous exercise, which is necessary to reduce visceral adipose tissue, is associated with a negative relationship between cortisol and testosterone. As cortisol increases, testosterone decreases, resulting in weight gain and other complications that inevitably offset the benefits of exercise (Hill et al, 2008; Skoluda et al, 2012). Importantly, during overtraining, muscle-derived IL-6 is released into the circulation in high amounts, resulting in increased inflammation (Klarlund Pederson et al, 2001). Prolonged exercise decreases leptin concentrations by 32% and increases free fatty acids, as expected by the understanding that free fatty acids act as an energy replenishment mechanism after energy expenditure (Landt et al, 1997). Leptin reduction will reinforce increased food consumption after exercise, again undermining the weight loss benefits.
In search of solutions that can proactively protect and enhance health, the research focuses on levels of visceral adipose tissue, skeletal muscle mass, basal metabolic rate (BMR) and weight in kilograms, as well as plasma levels of IGF-1, VLDL, triglycerides, leptin, ghrelin, Free T3, testosterone and cortisol, which have been identified as the common denominators of obesity, inflammation, toxicity and oxidative damage. The author adopted a technology recently used in two clinical trials (Sofra, 2020a; 2020b) that reported a statistically significant reduction in visceral adipose tissue, overall fat mass, a decrease in triglycerides and VLDL, accompanied by an increase of skeletal muscle mass (SMM) and Free T3. Goldspink et al (1991) used an earlier modified version of this type of technology exploring gene expression in muscle fibre phenotypes. They reported a rapid hypertrophy of adult skeletal muscle after stimulation, signifying an increase of up to 250% in ribonucleic acid (RNA) content primarily involving the activation of the slow skeletal muscle genes. They concluded that their results have implications for rehabilitation and athletic training.
Methodology
The technology used was completed in 2008 by Gerald Pollock and Donald Gilbert. The technology was originally built at the University of London for muscle-wasting conditions and multiple sclerosis, and was then revised with upgraded electronics at the European Union-funded Business Innovation Centre, London.
The technology offers 24 distinct voltage-driven complex square waveforms, each synthesised by 4000 sine frequencies with a resultant frequency that ranges from 55 Hz to 888 Hz. The two waveform control knobs are manually combined to form 144 combinations, inducing 1000 full body musculature contractions, each sustained for 8 seconds, with 2 seconds rest time, including deep slow motion contractions and significantly faster ones that involuntarily twist and shake the body.
The technology has 16 channels isolated by separate transformers, reaching the skin via 16 silver-plated tour grade microphone cables connected to gel pads that are attached to the body. It has a maximum voltage of 15V at 500 Ω, 25V at 2000 Ω and 50V at 10K Ω. Any current generated by the voltage based on Ohm's law is minuscule and cannot be measured. The leakage is 0.007µa (µa = 10−6A). It is classified as IEC Class I according to IEC60601-1 standard and it is used with three-pin din and four-pin din IEC 60601-1 compliant cables. It has a CE marketing directive of Class I with electromagnetic compatibility regulations applied standards EN50081-1 and EN50082-1. It complies with the EEC UK directive of electrical equipment safety applied standard EN 60601-1. The technology has had no known side effects in the past 20 years that it has been used in clinical practice by over 5430 physicians and aesthetic practitioners. The only contraindication, according to the US Food and Drug Administration (FDA), is having an implanted device like a pacemaker. The main caution is pregnancy. Adverse reactions are limited to temporary skin redness from the pads, which occurs sporadically and usually dissipates within an hour. Earlier versions of this technology based on the same electronic design have FDA clearance numbers K123158 and K132179.
Measuring instruments included: a blood test that examined levels of VLDL, triglycerides, free T3, IGF-1, testosterone, cortisol, leptin and ghrelin; a conductance scale that calculated weight, BMR, VAT and SMM; and structured interviews designed with open questions that explored subjective experiences of the treatment; treatment effectiveness; results maintenance; and eating habits or cravings after treatments.
Procedure
Ten overweight, healthy adults (five males and five females, 39–48 years of age with an average BMI of 27.8) participated and completed the clinical trial that took place in three different private aesthetic clinics in separate countries. Each clinic offered a list of 4–5 eligible candidates without names or other information. The author randomly chose 10 out of 15 eligible candidates. The main exclusion criteria were pregnancy, an implanted device (such as a cardiac pacemaker) and medical and mental disorders that were assessed by a comprehensive health questionnaire completed by all subjects. Every precaution was taken to protect the subjects' privacy and the confidentiality of their personal information. Subjects were informed that they had the right to refuse participation at any time. All subjects were presented with the consent form, which they had to read thoroughly and sign, after confirming that they had clearly understood its contents. Subjects were not in a dependent relationship with the technology operators, the lab and measurement technicians or the author. The subjects did not receive a specific diet or instructions regarding changes in their lifestyles.
The three individuals that were randomly selected as technology operators (one in each clinic) were given basic training on how to operate the technology without disclosing the experimental hypotheses or the goals of the treatment. None of them had any known bias or any personal interest in the direction of the results.
Three independent labs (one from each private clinic that provided the subjects) were assigned to take blood samples before and 10 days after the completion of 12 1-hour treatments that took place three times a week, for 4 weeks. Subjects were asked to fast for 12 hours before going to the lab for their blood tests.
A physician was available in each of the three clinics during the entire course of this trial to make sure that none of the subjects had any adverse reactions.
The conductance scale measurements were performed in a separate room by an independent technician with no prior knowledge of the technology or conflicts of interest.
Following blood tests and measurements, each subject went to a private treatment room and lay on a massage table while the gel pads and the cables from the 16 channels of the device onto their body. The cables from 10 of the channels were attached onto the gel pads of the waist and upper and lower abdomen, and the cables from the six remaining channels were attached onto the gel pads placed along the lymphatic system pathways of the legs and arms to enhance lymphatic drainage during treatment.
Ten days later and then a month after the last treatment, all subjects gave a detailed report of their subjective experience during the procedures. The subjects' responses were recorded by the technology operators based on four open-ended questions:
- How would you describe your experience during your treatment?
- How effective was your treatment?
- How long did the results last?
- Did you notice any changes in your eating habits or sweet cravings after treatment?
The procedure was in accordance with the ethical standards and principles for medical research involving human subjects.
Results
The data was analysed for repeated measures and T-tests for two dependent means where subjects' baselines were compared against their post-treatment results. There was an inverse testosterone/cortisol relationship where testosterone increased while cortisol decreased within the normal range. Testosterone increase reflected a p-value of p=0.00157. For cortisol decrease, the p-value was p=0.00041. The findings contradicted the results of strenuous exercise where cortisol increase is accompanied by testosterone decrease. Upon further examination, it became evident that testosterone increased by 90.04% in females, while males demonstrated a 35.36% testosterone rise. Since testosterone elevations did not spike outside the normal range in both genders, this substantial difference between males and females may be an artefact of the inherently lower female testosterone levels.
Table 1 reveals that IGF-1 increased by 25.8% after the 12 treatments. As expected, SMM also increased significantly by an average percentage of 36.45%.
Table 1. Blood test subjects' results on IGF-1 and scale results on skeletal muscle mass (SMM)
| Gender | IGF-1 before (nmol/L) | IGF-1 after (nmol/L) | Normal range (nmol/L) | IFG-1 percentage increase | SMM before | SMM after | SMM percentage increase |
|---|---|---|---|---|---|---|---|
| Male | 25.97 | 30.35 | 15.08–32.5 | 16.86% | 36.40 | 43.80 | 20.3% |
| Male | 23.98 | 31.12 | 15.08–32.5 | 29.77% | 30.30 | 38.60 | 27.39% |
| Female | 16.33 | 20.75 | 11.25–28.8 | 27.06% | 18.40 | 27.00 | 46.79% |
| Female | 15.14 | 19.21 | 11.25–28.8 | 26.88% | 17.00 | 26.80 | 57.64% |
| Male | 22.27 | 28.11 | 15.08–32.5 | 26.22% | 37.80 | 44.80 | 18.5% |
| Male | 26.98 | 30.52 | 15.08–32.5 | 11.80% | 29.40 | 38.30 | 30.27% |
| Female | 15.86 | 21.08 | 11.25–28.8 | 32.91% | 17.20 | 26.80 | 55.81% |
| Female | 18.55 | 23.50 | 11.25–28.8 | 26.68% | 19.80 | 28.80 | 45.45% |
| Male | 24.56 | 31.34 | 15.08–32.5 | 27.60% | 29.80 | 37.22 | 25.89% |
| Female | 19.34 | 25.66 | 11.25–28.8 | 32.67% | 17.95 | 26.63 | 48.35% |
Note: The mean average percentage increase of IGF-1 was 25.85%. IGF-1 remained within the normal range. The mean average percentage increase for SMM was 36.45%.
Table 2 displays a 30.34% average decrease in visceral adipose tissue. After the 12 treatments, free T3 was elevated towards the peak of the normal range with an average percentage increase of 30%.
Table 2. Scale results on visceral adipose tissue and blood test results on free T3 for each subject
| Gender | Visceral fat before | Visceral fat after | Percentage decrease | Free T3 before (nmol/L) | Free T3 after (nmol/L) | Normal range (nmol/L) | Percentage increase |
|---|---|---|---|---|---|---|---|
| Male | 139.30 | 93.80 | 32.66% | 2.98 | 4.22 | 2.63–5.7 | 41% |
| Male | 102.20 | 69.30 | 32.19% | 3.69 | 4.98 | 2.63–5.7 | 34.95% |
| Female | 93.50 | 58.30 | 37.64% | 4.77 | 5.37 | 2.63–5.7 | 12.5% |
| Female | 85.50 | 61.40 | 28.30% | 4.56 | 5.31 | 2.63–5.7 | 16.44% |
| Male | 76.40 | 48.80 | 36.12% | 4.15 | 5.47 | 2.63–5.7 | 31.80% |
| Male | 118.60 | 89.30 | 24.70% | 3.29 | 4.86 | 2.63–5.7 | 47.7% |
| Female | 98.80 | 70.60 | 28.54% | 4.36 | 5.64 | 2.63–5.7 | 29.35% |
| Female | 102.70 | 77.30 | 24.73% | 3.66 | 4.79 | 2.63–5.7 | 30.87% |
| Male | 145.30 | 104.34 | 28.18% | 3.19 | 4.12 | 2.63–5.7 | 29.15% |
| Female | 109.80 | 74.67 | 31.99% | 4.09 | 5.12 | 2.63–5.7 | 25.18% |
Note: The average percentage decrease of visceral adipose tissue was 30.5% and average percentage decrease of free T3 was 30%
Table 3 depicts a 6% average leptin increase and an average -8.75% decrease in ghrelin. BMR showed a consistent increase after the 12 treatments. The average weight loss was 6.32 kg (Table 4).
Table 3. Blood test results on leptin and ghrelin for each subject
| Gender Leptin | before (ng/mL) | Leptin after (ng/mL) | Normal range (ng/mL) | Percentage increase | Ghrelin before (pg/mL) | Ghrelin after (pg/mL) | Normal range (pg/mL) | Percentage decrease |
|---|---|---|---|---|---|---|---|---|
| Male | 7.38 | 7.84 | 1.2–9.5 | 6.2% | 683 | 614 | 520–700 | 10.1% |
| Male | 6.25 | 7.03 | 1.2–9.5 | 12.48% | 588 | 576 | 520–700 | 2% |
| Female | 12.43 | 13.22 | 4.1–25.0 | 6.35% | 612 | 584 | 520–700 | 4.5% |
| Female | 11.98 | 12.09 | 4.1–25.0 | 0.9% | 599 | 543 | 520–700 | 9.34% |
| Male | 5.53 | 5.94 | 1.2–9.5 | 7.41% | 599 | 553 | 520–700 | 8.13% |
| Male | 6.42 | 6.97 | 1.2–9.5 | 8.56% | 603 | 576 | 520–700 | 4.47% |
| Female | 10.87 | 11.84 | 4.1–25.0 | 8.92% | 687 | 612 | 520–700 | 10.9% |
| Female | 9.89 | 10.54 | 4.1–25.0 | 3.53% | 623 | 565 | 520–700 | 9.30% |
| Male | 5.47 | 6.01 | 1.2–9.5 | 4.1% | 589 | 532 | 520–700 | 9.71% |
| Female | 9.99 | 10.83 | 4.1–25.0 | 6.4% | 634 | 513 | 520–700 | 19.08% |
Note: There was an optimal inverse relationship between leptin and ghrelin where leptin increased and ghrelin decreased. Mean average percentage leptin increase was 6% and ghrelin decrease was -8.75%. All subjects' leptin and ghrelin fluctuations were within the normal range
Table 4. Results on BMR increase and weight loss in KG
| Gender | BMR before | BMR after | Percentage increase | Weight before (Kg) | Weight after (Kg) | Kg decrease |
|---|---|---|---|---|---|---|
| Male | 1505 | 1585 | 80% | 93.4 | 88.3 | 5.1 |
| Male | 1854 | 1969 | 115% | 86.7 | 80.4 | 6.3 |
| Female | 1210 | 1386 | 176% | 63.4 | 58.9 | 4.5 |
| Female | 1414 | 1626 | 212% | 59.5 | 53.6 | 5.9 |
| Male | 1821 | 1933 | 112% | 97.2 | 86.5 | 10.7 |
| Male | 1743 | 1784 | 41% | 89.6 | 83.7 | 5.9 |
| Female | 1266 | 1316 | 50% | 61.3 | 58.2 | 3.1 |
| Female | 1195 | 1243 | 48% | 67.8 | 62.3 | 5.5 |
| Male | 1894 | 1937 | 43% | 98.4 | 88.9 | 9.5 |
| Female | 1237 | 1276 | 39% | 59.3 | 52.6 | 6.7 |
Note: BMR showed a consistent increase after the 12 treatments. The average weight loss was 6.32 kg
All other variables' highly statistical significance values are displayed in Table 5. Importantly, all hormonal increases and decreases remained within the normal range.
Table 5. T-tests statistical significance results on blood tests and measurement variables
| Mean | S2 =SS/df | S2M = S2/N | SM= √S2M | T value | p value | Probability | |
|---|---|---|---|---|---|---|---|
| VLDL | -0.77 | 0.09 | 0.01 | 0.1 | -7.95 | <0.00001 | P <0.00001 |
| Triglycerides | -0.67 | 0.26 | 0.03 | 0.26 | -4.2 | 0.00115 | P<0.01 |
| Free T3 | 1.11 | 0.08 | 0.01 | 0.09 | 12.1 | <0.00001 | P<0.00001 |
| Leptin | 0.61 | 0.06 | 0.001 | 0.08 | 7.69 | 0.00002 | P<0.0001 |
| Ghrelin | -55 | 929.29 | 92.93 | 9.64 | -5.73 | 0.00003 | P<0.0001 |
| Cortisol | -12.2 | 59.96 | 6.0 | 2.45 | -4.98 | 0.00028 | P<0.001 |
| Testosterone | 2.46 | 6.14 | 0.61 | 0.78 | 3.14 | 0.006 | P<0.01 |
| VAT | -32.43 | 47.62 | 4.76 | 2.18 | -14.86 | <0.00001 | P<0.00001 |
| SMM | 8.47 | 0.89 | 0.09 | 0.3 | 28.39 | <0.00001 | P<0.00001 |
| IGF-1 | 5.27 | 1.47 | 0.15 | 0.38 | 13.72 | <0.00001 | P<0.00001 |
| Weight (Kg) | -6.52 | 5.69 | 0.57 | 0.75 | 8.78 | <0.00001 | P<0.00001 |
| BMR | 91.6 | 3782.04 | 378.2 | 19.45 | 4.71 | 0.00055 | P<0.001 |
IGF-1 increased by 25.8% after the 12 treatments. As expected, SMM also increased significantly by an average percentage of 36.45%.
Subjects reported that they experienced a large variety of 8-second long vigorous contractions, some of them resembling resistance exercises, while others subjectively perceived them as body twists or fast-paced aerobics. Contractions were painless, intense and involuntary, and involved the entire body's musculature contracting in a coordinated fashion.
In both of the interviews (10 days and a month after their last treatment), the subjects consistently reported a sustainable weight reduction, enhanced fitness and an inhibition of cravings for sweets and fatty foods.
» Cortisol, ghrelin and leptin fluctuations within the normal range are crucial in maintaining the results, since leptin/ghrelin regulate appetite and relatively low cortisol levels will reduce stress-eating behaviours «
Discussion
Results of this randomised, double-blind pilot study consistently validated the experimental hypothesis by signifying a reduction of visceral adipose tissue, VLDL and triglycerides, contrasted by an increase in skeletal muscle mass, IGF-1, testosterone, and free T3 that peaked towards the upper end of the normal range. Subjects lost an average of 6.32 kg, displayed enhanced fitness and an increase in basal metabolic rate (BMR) after 12 treatments that were completed within 1 month. The findings are juxtaposed against research on short-term exercise that has produced modest results in BMI and weight loss reduction with minimal gains in physical appearance (Kim et al, 2008). The inverse relationship of testosterone increase and cortisol decrease within the normal range demonstrated in this clinical trial was the opposite of the negative cortisol/testosterone correlation observed after strenuous exercise that may undermine weight loss by increasing food consumption (Landt et al, 1997; Khlarlund Pederson, 2001; Hill et al, 2008; Skoluda et al, 2012). Our subjects reported reduced cravings for sweets and fatty foods, as well as regular appetite, possibly indicating a combination of optimal levels of ghrelin, leptin and cortisol, along with decreased systemic toxins. Cortisol, ghrelin and leptin fluctuations within the normal range are crucial in maintaining the results, since leptin/ghrelin regulate appetite and relatively low cortisol levels will reduce stress-eating behaviours. Importantly, hormonal fluctuations within the normal range suggested that the intervention did not adversely affect the body's feedback mechanisms, which cease hormonal secretion when an optimum level is reached to sustain hormonal balance.
The primary study limitation was assuming decreased toxicity and inflammation based on circumstantial evidence of a reduction in VAT, VLDL and triglycerides, but without directly measuring systemic oxidative damage or inflammation. Additional research measuring ROS levels, CRP or IL-6 is necessary to substantiate our results. Moreover, visceral fat and skeletal muscle mass measurements were based on a conductance scale, rather than more conclusive diagnostic instruments such as magnetic resonance imaging or sonography to explore the possible improvement of liver steatosis. Other methodological limitations included a small sample size and the lack of a control group receiving equivalent regular exercise sessions as the experimental group. Overall, the results of this study validated the results of previous studies. However, the study's shortcomings suggest a need for further exploration of this method with more subjects, a control group, imaging techniques and inspection of inflammation and oxidative damage markers.
Conclusion
Different methods of reducing visceral adipose tissue were explored, including laser combined with resistance and aerobics training, radiofrequency and exercise alone. Physical activity was reliable in reducing visceral fat; however, short-term exercise produced negligible gains in weight loss and physical appearance. Furthermore, overtraining evidenced negative effects, including increased inflammation, leptin suppression and an inverse negative cortisol/testosterone incongruity bound to negate the benefits of exercise by increasing food consumption. In the trial, the blood samples of 10 healthy adults demonstrated a significant increase in BMR and SMM, contrasted by a decrease in VAT, VLDL, and triglycerides. Free T3, IGF-1, leptin and testosterone were elevated towards the top of the normal range, while cortisol and ghrelin gravitated towards the low end of the normal range. These results have important implications for weight loss, plus speedy fitness, that balances hormones and safeguards health. Limitations of the design methodology included a small sample size, the absence of imaging techniques and further exploration of inflammatory and oxidative damage markers.
Key points
- Fat reduction alone may lead to weight gain rebound due to hormonal imbalances inducing hunger
- The use of lasers and radiofrequency in visceral fat reduction has produced modest or controversial results
- Strenuous exercise results in a negative cortisol/testosterone relationship provoking caloric consumption
- A health-centred perspective focuses on fitness, metabolism and appetite control
- An exercise alternative method evidenced cortisol, lipids and visceral fat decrease, optimal ghrelin suppression and an upsurge of testosterone, leptin, IGF-1 and Free T3 towards the peak of the normal range.