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eISSN: 2374-6947

Diabetes, Metabolic Disorders & Control

Research Article Volume 9 Issue 1

Balancing hormones improves Type 2 diabetes 

Xanya Sofra

Department of Research, New School for Social Research, New York, USA

Correspondence: Xanya Sofra, Department of Research, New School for Social Research, New York, USA, Tel +85293405069

Received: August 03, 2022 | Published: August 17, 2022

Citation: Sofra X. Balancing hormones improves Type 2 diabetes. J Diab Metab Disorder. 2022;9(1):16-25. DOI: 10.15406/jdmdc.2022.09.00232

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Abstract

Treating physicians have consistently recommended exercise to either prevent diabetes or de-escalate symptomatology. Diabetic complications render physical activity undesirable or unattainable. Diabetes has been often associated with hypothyroidism, weight gain, fatigue, accumulation of white adipose tissue, and inadequate supply of brown fat to generate energy. Accumulated toxicity results in hormonal imbalance, increased hunger, chronic pain, and wounds on extremities associated with diabetic neuropathy. Recent research with an effortless exercise method has demonstrated enhanced fitness and T3 increase, juxtaposed by decreased inflammation, an optimal relationship between leptin and ghrelin that control appetite, and a significant decrease of visceral fat along with VLDL, the very low-density lipoprotein that carries triglycerides to the tissues. This clinical trial measured triglycerides, metabolic efficiency as reflected by T3, inflammation level and fasting / postprandial glucose and insulin of 21 diabetics and 20 prediabetics respectively, pre and post twenty treatments. There was a statistically significant decrease in both fasting and postprandial glucose and insulin for all subjects who exhibited increased skeletal muscle mass, normalized T3 levels, decreased visceral and overall fat, and reduced CRP, advocating diminished inflammation. Dyslipidaemia appeared to subside as indicated by suppressed triglyceride levels contrasted by elevated HDL.

Keywords: diabetes mellitus, metabolism, visceral fat, insulin, cholesterol, glucose, muscle mass, inflammation, dyslipidaemia, T3 increase

Abbreviations

VLDL, very low density lipoprotein; CRP, C-reactive protein; HDL, high-density lipoprotein

Diabetes definition

Diabetes encompasses a variety of metabolic disorders primarily related to either an insulin deficit which defines the primary cause of Type 1 diabetes (T1D) or an insulin resistance commonly found in Type 2 diabetes (T2D).1 Autoimmune diabetes falls under the T1D category. T1D ordinarily emanates out of defective immunity characterized by an insufficient amount of B-cells whose primary function is to develop antibodies against invasive antigens. T1D is distinguished by usually normal weight. It is primarily diagnosed in children, adolescents, and young adults who exhibit symptomatology such as polyuria, polydipsia and fatigue.2

T2D is a cluster of diseases associated with both hyperglycaemia and the metabolic syndrome that is typically represented by obesity, with excessive visceral fat deposits, low-grade inflammation and increased mortality rates. T2D is associated with an inverse relationship between triglycerides and high-density lipoproteins (HDL), where increased levels of triglycerides are accompanied by abnormally low HDL. It is also linked to hypertension, which often leads to an enhanced risk of coronary heart disease (CRD) or strokes. The severity of T2D progresses over a dimension that ranges from reduced insulin secretion to persisting insulin resistance induced by deficient insulin production.3

Diabetes has been connected to several other disorders that include Cushing Syndrome, defined by hypercortisolism;4 pancreatitis, propagated by pancreatic inflammation;5 acromegaly, distinguishable by an enlargement on the hands and feet due to an excess of growth hormone (GH);6 cystic fibrosis that affects the lungs, liver, kidneys and intestine and is expressed in difficulty breathing or coughing;7 hemochromatosis delineated by an iron overload;8 and pheochromocytoma that involves a benign tumour in the adrenal gland. There is clinical evidence that diabetes may develop as a result of pharmaceutical treatments with atypical neuroleptics.10 often prescribed to treat schizophrenia, glucocorticoids,11 or alpha-interferons.12

T3 Levels, diabetes and hypothyroidism

Experimental evidence links T1D with hypothyroidism by showing that subclinical hypothyroid adolescents demonstrate a higher incidence of hypoglycaemic symptomatology.13 A study on 1112 diabetics found a connection between T2D and hypothyroidism, especially in individuals over 65.14 An earlier investigation of the records of 922 T2D patients unveiled a high correlation between T2D and hypothyroidism, with a prevalence in white subjects.15 Diabetes is associated with a defective ability of thyroxine (T4) to generate sufficient levels of Triiodothyronine (T3). T4 is the 4-iodine atoms hormone produced in the thyroid gland.16,17

Diabetes, VLDL, Triglycerides, LDL and HDL

The very low-density protein (VLDL) that is normally composed in the liver, transports triglycerides (esters comprised of glycerol and three fatty acids), which represent the main source of energy storage in tissues, otherwise known as overall body fat. Increased levels of triglycerides carried by VLDL are the hallmark of dyslipidaemia that is commonly accompanied by inhibited levels of the high-density lipoprotein (HDL). HDL absorbs both low-density and very low-density lipoproteins transferring them back to the liver, thus relieving the arteries of potential plaque build-ups, and reducing the risk of both atherosclerosis and heart disease. Dyslipidaemia is intrinsically linked both to insulin resistance and T2D.18 Liu et al.19 demonstrated that ischemic strokes and heart disease are directly related to a high ratio of triglycerides reciprocated by low HDL. These investigators examined the health status of 30,378 individuals over a period of fifteen years. They confirmed the strong connection between a pathological lipid profile of high triglycerides predicting coronary heart disease, and low HDL associated with ischemic stroke, with a high prevalence of Diabetes and high low-density lipoproteins (LDL) being present in patients with coronary heart disease.19

Recent studies have associated T2D Neuropathy with dyslipidaemia defined by abnormally high triglycerides / low HDL profile.20 Diabetic neuropathy is characterized by chronic pain, anomalous sensations and malfunctioning nerve conduction velocities (NVCs) underlaid by deficient sural nerve myelinated fibre densities (MFDs). Wiggin et al.21 followed patients with high triglycerides and abnormalities in motor nerve conducting velocities for one year. Their study unveiled a significant correlation between dyslipidaemia and deficient motor nerve conduction velocities that are the foundation of diabetic neuropathy.

Increased oxidative stress and inflammation associated with diabetes

Hyperglycaemia disrupts both insulin signalling and insulin secretion by pancreatic B cells, provoking an inevitable deterioration of the diabetic condition.22 Clinical research has demonstrated that increased hyperglycaemia elevates oxidative stress and suppresses antioxidant production that could potentially donate electrons to reinstate symmetry in the otherwise disequilibrium state of the radical oxygen species (ROS). In vitro studies on the mitochondria of obese type-2 diabetics have evidenced a significant increase in ROS.23

For the average individual, the absence of exercise renders detoxification insufficient and therefore, unable to establish the necessary balance between production and elimination of free radical species, routinely formed by normal aerobic metabolism via oxygen. Toxicity erodes the boundaries between health and illness, being exacerbated by the growing immune limitations during ageing. Inadequate detoxification results in accumulated oxidative damage that adversely affects the diabetic condition instigating glucotoxicity, lipotoxicity, and cardiac dysfunction. Exercise and antioxidants are routinely recommended for both T1D and T2D.24 The American Diabetes Association has disclosed clinical evidence of reducing the prevalence of T2D by 58% as a result of an active lifestyle.25-27

Oxidative stress has been intricately related to C-Reactive protein, the hepatic origin inflammation marker that is linked to proinflammatory cytokines, and which has been consistently associated with both diabetes and cardiac dysfunction.28-30 An experimental study on 529 subjects established a statistically significant correlation between CRP and mononuclear cells’ oxidative stress, as well as demonstrating that ROS in polymorphonuclear leucocytes and mononuclear cells were prevalent in both diabetes and hypertension.31

Diabetes and exercise

A literature search on the multidimensional spectrum of diabetic treatments usually reiterates the same recommendation, pertaining to lifestyle changes and exercise.32-34 Nevertheless, there are concerns associated with certain types of exercise, which increase blood glucose levels and, in certain subjects, result in abnormal hypoglycaemia.35 Clinical studies on dynamic exercise have demonstrated hyperglycaemia and hyperinsulinemia in diabetics, persisting for at least one hour after physical training.36 Additional research has delineated a disproportionate increase of seven- to eightfold glucose production as a result of intensified catecholamine signalling, accompanied by a deficient glucose utilization, limited to only three- to fourfold.37,38 Sedentary lifestyles increase the incidence of diabetes and coronary heart disease by 30-50%. Exercise spends glucose-derived energy that could theoretically help diabetic hyperglycaemia, however, the long-term effects of exercise on diabetes’ dysregulated metabolic profile remain inconclusive.39 A 2006 survey revealed that exercise was recommended to 73% of diabetes patients as opposed to only 31% of non-diabetic adults, however, very few of these patients increased their physical activity.40 Exercise appears to decrease diabetic symptomatology, hence being beneficial to those with both T1D and T2D who can use exercise as a protective, therapeutic method against further deterioration. However, patients with advanced diabetes complicated by obesity or neuropathic pain will be obviously less willing or capable of exercising.41,42 A number of clinical studies on a novel effortless fitness technology from London University have delineated a reduction in both visceral and overall fat, demonstrating improved hormonal regulation, and a reversal of the diabetic status into either the realm of prediabetes or normalcy.43-48 A more recent clinical study on diabetics with hyperphagia reports hunger suppression as a result of an optimal inverse relationship between leptin increase and ghrelin decrease.49

The current research examined levels of pre-and-post T3 and C-reactive Protein (CRP), as well as pre and post-fasting and postprandial (PP) insulin and glucose levels in the blood samples of forty-one diabetic and prediabetic subjects. The study also looked at visceral fat reduction and measured the potential of the treatment attaining an optimal inverse relationship between triglycerides and HDL. The goal of the study was to offer diabetics the benefit of enhanced fitness and weight control while overcoming the general resistance to exercise.

Methodology

We utilized an apparatus originally built in London University 2008 by Gerald Pollock, an electronics engineer who was also involved in the invention of the first pacemaker in the UK, based on his combined research with Donald Gilbert, a molecular biology London University professor. Patents of four out of the eight hand-made boards were obtained during the early 80s when the empirical studies commenced. The voltage driven apparatus consists of multiple connections between the eight boards that are made by hand to synthesize and regulate the unlimited resolution complex waveforms that are composed out of four thousand frequencies, each having a specific resultant frequency that ranges from 55Hz to 888Hz. At a resistance of 500 Ω the maximum voltage is 15V, increasing to 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 directly measured. The technology is classified as IEC class I according to the IEC60601-1 standard, and it is used with 3-pin din and 4-pin din IEC 60601-1 compliant cables and silver threaded self-adhesive pads that have been awarded their own FDA clearance. The technology 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 general design of this technology has had no known side effects, in the past 20 years that it has been used in clinical practice by over 5,430 physicians, aesthetic practitioners and private users. The only contraindication, according to the FDA, is having an implanted device like a pacemaker. The main caution is pregnancy. All major medical and mental disorders require clearance by the patient’s physician. Adverse reactions are limited to temporary skin redness from the gel pads, that occurs sporadically and usually dissipates within a few hours. Earlier versions of this technology based on the same electronic design have FDA clearance numbers K132158 and K132179.

Measuring instruments included: 1) a blood test that measured Free T3, CRP, triglycerides, HDL, fasting and PP glucose and insulin levels; 2) a conductance scale that calculated BMI, overall fat, visceral fat, and skeletal muscle mass (SMM). 3) Before and after treatments fatty liver results on the sonography reports of 11 diabetic subjects.

Procedure

A total of twenty-one Diabetic and 20 Prediabetic obese individuals, 15-82 years of age, with an average BMI of 36.9 consented to release their records. These included eleven diabetic females, ten diabetic males, ten prediabetic females and ten diabetic males. Eleven diabetic subjects, nine females and two males were also diagnosed with fatty liver on their sonography reports. All subjects had completed 20 treatments with the London University technology before the study commenced. Since the study was based on the chart results of all participants, there was no subject attrition. The current research project fulfils the double blind standards, since neither the subjects nor the operators of the technology knew at the time of the treatments’ administration that these results were going to be used in a clinical trial. The subjects were made aware of this clinical research only after they had competed all 20 treatments and were asked to sign a consent form. Subjects were randomly selected out of four different clinics on the basis of the following inclusion and exclusion criteria:

Inclusion Criteria: 1) Overweight or obese; 2) BMI > 29; 3) Age above 12 years old; 4) At least three months after a surgery procedure; 5) At least three months after childbirth; 6) Diabetes; 7) Prediabetes; 8) Had completed 20 treatments with the London University Technology; 9) Had received the treatment at least twice or three times weekly.

Exclusion Criteria: 1) Pregnancy or trying to get pregnant; 2) An implanted device like a cardiac pacemaker; 3) Severe medical condition other than Diabetes or Prediabetes; 4) Hepatic cirrhosis; 6) Renal failure; 7) Surgery or childbirth less than three months prior to treatment; 8) Cancer; 9) Hernia; 10) Other severe medical or mental condition; 11) Had not received any additional treatments with lasers, radiofrequency, any other slimming devices or any technologies similar to the London University Technology.

Inclusion and exclusion criteria were verified by a certified physician in each of the four clinics. As part of each clinic’s general policy, a physician was routinely available during the entire duration of the twenty treatment packages, to ensure the comfort and safety of the participants. All subjects reportedly underwent the treatment with no adverse reactions or side effects.

Subjects were not in a dependent relationship with the technology operators, the lab and measurement technicians, or the authors. The subjects were given some general diet instructions like increasing their vegetables, lean protein, and fruit intake while reducing sugar and oily foods. However, there was no structured measure of calculating daily caloric intake or the veracity of their statements regarding their eating habits. Subjects were instructed to continue taking their prescribed medications and follow the guidance and recommendations of the physician in charge of their medical status. Subjects were specifically told that the treatment they were receiving was intended as a weight loss/ fitness enhancement to potentially jump-start a healthier lifestyle, and it was not meant to replace exercise or treat their diabetic condition. None of the subjects had a history of exercising or an active lifestyle or was engaged in a regular exercise regimen.

Four independent labs with no personal interest in the direction of the results, one from each of the four participating clinics, were assigned to take blood samples before and after the completion of twenty one-hour treatments that took place two to three times weekly, for a total of seven to eight weeks. Subjects were asked to fast for twelve hours prior to their blood tests. The conductance scale measurements were performed by technicians who obtained a printout of the results that were included in the chart and were subsequently used in the study. Eleven subjects offered their sonography results before and after the twenty treatments, but without releasing the full sonography report. Only 27 out of the 41 subjects had measurements from the same conductance scale for BMI, Overall Fat, Visceral Adipose Tissue (VAT) and Skeletal Muscle Mass (SMM). Only twenty of the subjects offered measurements on their Free T3 and CRP levels, ten of which subjects were diabetics and 10 prediabetics.

Following blood tests and measurements, each subject went to a private treatment room and lay on a massage table, where the self-adhesive silver-threaded gel pads and silver plated microphone cables from the 16 channels of the electronic apparatus were attached to his / her body by the operator. The cables from ten of the channels were attached to the gel pads of the buttocks and the abdomen, and the cables from the six remaining channels were attached to the gel pads placed along the lymphatic system pathways of the legs and arms. The operators were present throughout the procedure on every procedure and they made sure that all subjects were comfortable during the treatment.

Ethical consideration: 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 discontinue treatment at any time. The procedure was in accordance with the ethical standards and principles for medical research involving human subjects and it was deemed safe and comfortable by the ethical boards of the different clinics who volunteered the results of their patients for this clinical study.

Results

Statistical analysis was based on a repeated measures design where subjects’ results after the twenty treatments were compared to their baseline. Table 1 displays the results of the twenty- -one diabetic subjects on pre and post-treatment fasting glucose and postprandial (PP) blood glucose levels. Both fasting and postprandial glucose levels decreased in 100% of the subjects in an average percentage that reached -38.44% decrease for fasting glucose, and -39.1% for postprandial glucose.

No

Gender

Age

Medical
Diagnosis

Blood Glucose Fasting mg./dL
Pre

Blood Glucose Fasting mg/dL
Post

Blood Glucose
Normal <100 mg/dL

Blood Glucose PP
mg/dL
Pre

Blood Glucose PP
mg/dL
Post

Blood Glucose PP Normal < 140 mg/dL

1

Female

45y

Diabetes
Fatty liver

178

104

Prediabetic

260

185

Prediabetic

2

Male

69y

Diabetes

209

108

Prediabetic

230

125

Normal

3

Male

46y

Diabetes

131.7

99.15

Normal

290

183.2

Prediabetic

4

Female

50y

Diabetes

177

106

Prediabetic

221

176

Prediabetic

5

Female

49y

Diabetes
Fatty Liver

192

102

Prediabetic

248

175

Prediabetic

6

Female

48y

Diabetes
Fatty Liver

189

115

Prediabetic

224

163

Prediabetic

7

Male

44y

Diabetes
Fatty Liver

178

109

Prediabetic

196

162

Prediabetic

8

Female

45y

Diabetes
Fatty Liver

186

117

Prediabetic

197

126

Normal

9

Female

47y

Diabetes
Fatty Liver

169

102

Prediabetic

243

178

Prediabetic

10

Male

45y

Diabetes

135

92

Normal

218

156

Prediabetic

11

Male

82y

Diabetes

136

87

Normal

191

142

Prediabetic

12

Male

46y

Diabetes

134

97

Normal

216.3

139

Normal

13

Male

59y

Diabetes

106.8

82

Normal

199.9

133

Normal

14

Female

45y

Diabetes
Fatty Liver

186

117

Prediabetic

207.5

123

Normal

15

Male

59y

Diabetes

188

119

Prediabetic

202

133

Prediabetic

16

Male

49y

Diabetes

141

99

Normal

125.6

144

Prediabetic

17

Female

69y

Diabetes
Fatty Liver

136

87

Normal

231.4

131

Normal

18

Female

53y

Diabetes

190

108.5

Prediabetic

212

118

Normal

19

Female

68y

Diabetes
Fatty Liver

176

92

Normal

209.8

98

Normal

20

Female

61y

Diabetes
Fatty Liver

157.5

98.5

Normal

204

103

Normal

21

Male

55y

Diabetes
Fatty Liver

194

107

Prediabetic

231

138

Normal

 

 

TOTAL

3490

2148..15

 

4557.5

3031.2

 

AVERAGE

166.19

102.29

NORMAL

237.02

144.34

NORMAL

PERCENTAGE OF BLOOD GLUCOSE DECREASE

FASTING
BLOOD GLUCOSE
% DECREASE

 

-38.44%

 

PP
BLOOD GLUCOSE
% DECREASE

 

-39.1%

 

Table 1 Type 2 diabetics
Pre and post treatment results on blood glucose (Fasting and PP)
Fasting blood glucose: Normal <100 mg/dL; Prediabetes = 100 - 125 mg/dL; Diabetes >126 mg/dL
Blood glucose postglandial (PP): Normal < 140 mg/dL; Prediabetes = 140 - 199 mg/dL; Diabetes > 199 mg/dL

Table 2 displays the results of the twenty prediabetic subjects on pre and post treatment fasting insulin and postprandial (PP) insulin levels. Both fasting and postprandial insulin levels decreased in 100% of the subject in an average percentage decrease that reached -54.53% for fasting insulin, and -44.7% for postprandial insulin.

No

Gender

Age

Medical
Diagnosis

Insulin Fasting mIU/ml
Pre

Insulin Fasting mIU/ml
Post

Insulin Fasting Normal
< 25 mIU/ml

Insulin PP
mIU/ml

Pre

Insulin PP mIU/ml
Post

Insulin PP Normal <75 mIU/ml

1

Female

43y

Prediabetes

72

15.7

Normal

174.3

73.9

Normal

2

Female

27y

Prediabetes

25.8

8.7

Normal

136

74

Normal

3

Female

63y

Prediabetes

105

12.27

Normal

150

76.2

Normal

4

Female

24y

Prediabetes

34

21

Normal

139.9

71.8

Normal

5

Female

30y

Prediabetes

27.4

18.5

Normal

241

24.6

Normal

6

Male

15y

Prediabetes

29

10.9

Normal

136.6

74.8

Normal

7

Male

58y

Prediabetes

50.4

24

Normal

246

68.4

Normal

8

Male

46y

Prediabetes

25.56

12.56

Normal

68.8

23.5

Normal

9

Female

39y

Prediabetes

48

24.9

Normal

69.7

72

Normal

10

Male

40y

Prediabetes

22.2

11.8

Normal

127.2

73.4

Normal

11

Male

53y

Prediabetes

23.8

14.6

Normal

102.8

96.8

Prediabetes

12

Male

39y

Prediabetes

19.5

14.6

Normal

103.9

68.8

Normal

13

Male

31y

Prediabetes

43.5

22.8

Normal

116.3

73.4

Normal

14

Female

33

Prediabetes

41.9

18.6

Normal

109.3

68.4

Normal

15

Male

49y

Prediabetes

53.7

24.8

Normal

126.4

73.8

Normal

16

Male

69y

Prediabetes

35.8

27.4

Prediabetic

112.4

83.74

Prediabetic

17

Male

53y

Prediabetes

42.7

23.12

Normal

93.4

71.6

Normal

18

Female

68y

Prediabetes

53.6

28.9

Prediabetic

77.2

70.65

Normal

19

Female

49y

Prediabetes

42.8

23.4

Normal

81.4

72.5

Normal

20

Female

52y

Prediabetes

39.8

21.7

Normal

76.8

64.3

Normal

TOTAL

836.46

380.25

 

2489.4

1376.59

 

AVERAGE

41.823

19.02

NORMAL

124.47

68.83

NORMAL

PERCENTAGE OF INSULIN DECREASE

FASTING INSULIN % DECREASE

 

-54.52%

 

PP INSULIN % DECREASE

 

-44.7%

 

Table 2 Prediabetics
Pre and Post Treatment Results on Insulin (Fasting and PP)
Insulin Fasting: Normal < 25 mIU/ml Insulin Postprandial (PP): Normal <75

Table 3 offers the results of pre and post sonography reports on the eleven diabetic subjects’ fatty liver that indicates no fatty liver after the 20 treatments. Additionally, table 3 displays the results on the triglycerides and HDL levels of all twenty one diabetic subjects. All diabetic subjects (100% of diabetics) evidenced an average of -28.56% decrease in triglycerides and an average of +49.12% increase in HDL. Table 4 depicts the results on the triglycerides and HDL levels of the twenty prediabetic subjects. All prediabetic subjects’ triglycerides (100% of the prediabetics) indicated a reduction in triglycerides at an average of -22.88% from what it used to be previously, and an average increase of +30.34% in blood plasma HDL.

No

Gender

Age

Medical
Diagnosis
Pre Treatment

Fatty Liver
Post on Sonography Reports

Triglycerides
mg/dL
Pre

Triglycerides
mg/dL
Post

Triglycerides
mg/dL
decrease

HDL
mg/dL
Pre

HDL
mg/dL
Post

(HDL) mg/d
Increase

1

Female

45y

Diabetes
Fatty liver

No fatty liver

203

158

Improved
(abnormal)

32

39

Improved
at risk

2

Female

46y

Diabetes
Fatty Liver

No fatty liver

287

176

Improved
(abnormal)

32

39

Improved
at risk

3

Female

48y

Diabetes
Fatty Liver

No fatty liver

266

147

Normal

29

41

Improved
at risk

4

Male

44y

Diabetes
Fatty Liver

No fatty liver

283

189

Improved
(abnormal)

30

35

Improved
at risk

5

Female

45y

Diabetes
Fatty Liver

No fatty liver

225

179

I Improved
(abnormal)

33

40

Improved
at risk

6

Female

47y

Diabetes
Fatty Liver

No fatty liver

237

188

Improved
(abnormal)

31

41

Improved
at risk

7

Female

45y

Diabetes
Fatty Liver

No fatty liver

228

134

Normal

34

58

Normal

8

Female

45y

Diabetes
Fatty Liver

No fatty liver

214

138

Normal

28

51

Normal

9

Female

68y

Diabetes
Fatty Liver

No fatty liver

198

122

Normal

31

59

Normal

10

Female

61y

Diabetes
Fatty Liver

No fatty liver

219

112

Normal

28

52

Normal

11

Male

55y

Diabetes
Fatty Liver

No fatty liver

223

106

Normal

24

66

Normal

 

12

Male

69y

Diabetes

 

215

158

Normal

35

47

Improved
at risk

13

Male

46y

Diabetes

230

176

Improved
(abnormal)

28

37

Improved
at risk

14

Female

52y

Diabetes

196.7

147

Normal

47.6

53

Normal

15

Female

49y

Diabetes

193

189

Normal

34.5

38

Improved
at risk

16

Male

45y

Diabetes

212

179

Normal

41

45

Improved
at risk

17

Male

72y

Diabetes

197

188

Normal

26

38

Improved
at risk

18

Male

59y

Diabetes

202

134

Normal

31

62

Normal

19

Male

49y

Diabetes

197

138

Normal

44

71

Normal

20

Male

57y

Diabetes

192

122

Normal

37

61

Normal

21

Male

55y

Diabetes

199

112

Normal

42

68

Normal

TOTAL

4616.7

3298

 

698.1

1041

 


AVERAGE

219.84
HIGH

157.04
Improved

Improved

33.24
LOW

49.57
Improved

Improved

Table 3 TYPE 2 DIABETICS
Triglycerides, High-Density Protein (HDL),
Triglycerides, High-Density Protein (HDL),
High-Density Lipoprotein (HDL) At Risk: Men: < 40 mg/dL; Women < 50 mg/dL
Triglycerides Normal Range: > 150 mg/dL;
High-Density Lipoprotein (HDL) Normal Range: Men >60 mg/dL; Women >60 mg/dL

Table 4 gives the results of the pre and post blood levels of Free T3 and C Reactive Protein of ten diabetic and 10 prediabetic subjects. All diabetic and prediabetic subjects (100% of diabetics and 100% of prediabetics) demonstrated an average increase of 40.78% in Free T3 levels, and an average decrease of -37.88% in blood CRP. Table 6 gives the results on the pre and post BMI, overall fat, visceral fat and skeletal muscle mass (SMM) of twenty seven out of the 41 subjects that were measured with the same conductance scale.

Subject NO from
Table 1
DIABETES

Gender

Age

Medical Condition

Free T3 PRE
pg/mL

Free T3 POST
pg/mL

Free T3 Normal Range
pg/mL

CRP PRE
mg/dL

CRP 
POST

mg/dL

Normal
Range
mg/dL

12

Male

46y

Diabetes

1.99

2.69

2.30-4.20

1.45

1.05

<1.00

13

Male

59y

Diabetes

1.92

2.78

2.30-4.20

1.29

1.08

<1.00

14

Female

45y

Diabetes
Fatty Liver

2.12

2.55

2.30-4.20

2.51

1.25

<1.00

15

Male

59y

Diabetes

1.97

2.62

2.30-4.20

1.83

0.96

<1.00

16

Male

49y

Diabetes

1.18

2.29

2.30-4.20

1.13

0.91

<1.00

17

Female

69y

Diabetes
Fatty Liver

1.43

2.42

2.30-4.20

1.67

1.01

<1.00

18

Female

53y

Diabetes

1.63

2.15

2.30-4.20

1.09

0.86

<1.00

19

Female

68y

Diabetes
Fatty Liver

1.93

2.88

2.30-4.20

1.18

0.84

<1.00

20

Female

61y

Diabetes
Fatty Liver

2.23

2.37

2.30-4.20

1.94

0.95

<1.00

21

Male

55y

Diabetes

1.47

2.26

2.30-4.20

2.23

1.03

<1.00

Subject NO from
Table 2
PREDIABETES

 

14

Female

33

Prediabetes

2.25

2.77

2.30-4.20

1.09

0.76

<1.00

15

Male

49y

Prediabetes

2.22

2.58

2.30-4.20

1.59

1.05

<1.00

16

Male

69y

Prediabetes

1.68

2.51

2.30-4.20

1.19

1.02

<1.00

17

Male

53y

Prediabetes

1.99

2.89

2.30-4.20

2.42

1.25

<1.00

18

Female

68y

Prediabetes

1.28

2.25

2.30-4.20

1.98

0.99

<1.00

19

Female

49y

Prediabetes

1.43

2.36

2.30-4.20

1.52

1.14

<1.00

20

Female

52y

Prediabetes

1.53

2.14

2.30-4.20

1.75

1.03

<1.00

14

Female

33

Prediabetes

1.97

2.78

2.30-4.20

1.08

0.89

<1.00

 

 

 

 

32.22

45.29

 

28.94

18.07

 

Average Free T3 Pre & Post

1.79
BELOW Normal

2.52
Normal

Average CRP Pre & Post

1.61
BELOW Normal

1.00
Improved

 

Free T3 Percentage Increase


+40.78%

Average CRP Percentage Decrease


-37.88%

Table 4 Free T3 (triiodothyronine) and CRP (C-Reactive Protein)
Free T3 Normal Range: 2:30-4.20 pg/mL. CRP Normal Range <1 mg/dL

Table 5 shows the pre and post-treatment results on BMI, overall Fat, visceral fat, and skeletal muscle mass.

S #

Gender

Age

MEDICAL
CONDITION

BMI
Pre

BMI
Post

Overall Fat
Pre

Overall Fat
Post

Visceral
Fat

Pre

Visceral
Fat
Post

SMM
Pre

SMM
Post

1

Female

46

Diabetes
Fatty Liver

39.2

36.2

44.6

36.8

35

24.8

22.1

29.4

2

Female

48

Diabetes
Fatty Liver

41.2

38.5

42.9

33.5

33

29

23.8

29.7

3

Male

44

Diabetes
Fatty Liver

42.6

38.2

34.9

24.6

29

26

34.5

47.3

4

Female

48

Diabetes
Fatty Liver

32.0

30.1

42.9

33.5

29

24

23.8

31.8

5

Female

45

Diabetes
Fatty Liver

29.1

25.1

34

28.7

31

27

20.7

26.3

6

Female

24

Prediabetes

29.3

25.0

34.7

33

9.5

5

21.8

24.2

7

Male

40

Prediabetes

33.7

25.1

33.0

13.4

21

13.4

28.8

31.2

8

Male

39

Prediabetes

36.2

32.0

41.1

37.4

18

14.5

36

38.9

9

Male

31

Prediabetes

43.8

39.1

37.6

34.6

30

25

25.2

27.4

10

Male

46

Diabetes

39.2

24.6

42.3

25.6

24.7

10.8

28.9

39.4

11

Male

59

Diabetes

36.5

28.9

37.9

31.6

32.3

16.4

26

41

12

Female

45

Diabetes
Fatty Liver

41.3

27.4

43.8

22.7

39.5

19.4

23.8

38.5

13

Male

59

Diabetes

34.2

24.8

36.9

25.8

35.4

22.8

28.9

41.2

14

Male

49

Diabetes

37.4

29.5

41.3

22.5

29.3

18.3

35.7

42.6

15

Female

69

Diabetes
Fatty Liver

42.6

36.8

44.2

37.9

34.6

31.7

27.9

33.2

16

Female

53

Diabetes

33.5

25.1

30.1

25.7

38.2

30.1

32.4

39.9

17

Female

68

Diabetes
Fatty Liver

40.7

36.1

42.3

39.8

37.4

33.8

30.2

39.7

18

Female

61

Diabetes
Fatty Liver

34.2

25.3

36.7

33.2

38

36.1

23.8

28.6

19

Male

55

Diabetes

36.7

26.4

38.7

29.6

33.5

23.2

27.9

39.4

20

Female

33

Prediabetes

36.8

22.5

39.2

21.3

25.3

9.4

32.5

43.2

21

Male

49

Prediabetes

35.9

24.6

39.4

18.4

24.3

8.5

35.4

48.3

22

Male

69

Prediabetes

38.2

33.7

39.6

31.5

28.3

24.6

31.4

37.8

23

Male

53

Prediabetes

37.2

30.3

40.2

29.3

36.2

30.6

29.3

36.7

24

Female

68

Prediabetes

35.7

29.4

33.6

31.4

37.3

32.9

30.8

34.2

25

Female

49

Prediabetes

35.3

25.4

37.4

21.5

27.6

10.8

38.9

47.2

26

Female

52

Prediabetes

36.1

29.6

36.5

28.3

29.7

25.3

37.5

41.3

27

Female

37

Prediabetes

39.2

23.9

47.3

24.1

28.4

12.3

24.6

42.8

TOTAL

997.8

793.6

1013.5

775.7

815.5

585.7

782.6

1001.2

MEAN AVERAGE

36.9

29.4

38.9

28.73

30.20

21.69

28.98

37.1



MEAN OVERALL BMI DECREASE:
-7.5   

MEAN AVERAGE OVERALL FAT DECREASE %    
-26.14%

MEAN VISCERAL FAT DECREASE %
-28.17%

 

MEAN SMM % INCREASE +28.02%

Table 5 Pre and Post Treatment Results on BMI, Overall Fat, Visceral Fat, and Skeletal Muscle Mass (SMM)

Table 6 gives the results of t tests on all variables. The pre and post comparison of all variables demonstrated a highly significant statistical difference at the p<0.00001 (one in one hundred thousand shall not entertain such result) level, except for the fasting insulin of prediabetics that was significant at the 0<0.0001 (one in ten thousand) lever, and the PP insulin of prediabetics that was significant at the p<0.001 (one in one thousand level).

 

MEAN

SS⁄df 

T-VALUE

P-VALUE

Significance
level

Blood Glucose Fasting mg./dL Diabetics
Decrease

-63.9

414.64

 -14.38

P < 0.00001

P < 0.00001

Blood Glucose PP
mg/dL Diabetics
Decrease

-72.68

 

891.07

-11.16


P < 0.00001


P < 0.00001

Insulin Fasting mIU/ml
Prediabetis
Decrease

-22.8

390.6

-5.16

P < 0.0003

P < 0.0001

Insulin PP
mIU/ml
Prediabetics
Decrease

-55.64

3071.35

 -4.49

P< 0.00013

P< 0.001

Triglycerides
mg/dL
Diabetics
Decrease

 -67.84

1056.27

-9.57

P < 0.00001

P < 0.00001

HDL
mg/dL
Diabetics
Increase

16.33

120.72

6.81

P < 0.00001

P < 0.00001

Triglycerides
mg/dL
Prediabetics
Decrease

-40.29

630.05

 -7.18

P < 0.00001

P < 0.00001

HDL
mg/dL
Prediabetics Increase

13.24

 57.92

7.78

P < 0.00001

P < 0.00001

Free T3 Increase

0.73

0.07

12.06

P < 0.00001

P < 0.00001

CRP Decrease

-0.6

0.15

-6.64

P < 0.00001

P < 0.00001

BMI Decrease

-7.56

 14.72

-10.24

P < 0.00001

P < 0.00001

Overall Fat Decrease

 -10.27

43.89

 -8.06

P < 0.00001

P < 0.00001

Overall Visceral Fat Decrease

-8.51

30.14

-8.06

P < 0.00001

P < 0.00001

Skeletal Muscle Mass Increase

8.1

18.66

9.74

P< 0.00001

P< 0.00001

Table 6 T-test Statistical Significance

Discussion

Several physicians treating diabetics recommend exercise and physical activity to either prevent the diabetic condition or avoid further complications via enhancing health and fitness. These recommendations are based on a large body of research. There are numerous problems with this notion, however. a/ Obesity makes physical training cumbersome; b/ Diabetic neuropathy increases fragility and resistance to movement; c/ Clinical studies have demonstrated that certain modes of exercise may induce temporary hyperglycaemia and hyperinsulinemia in diabetics. There is a novel method from London University that offers an effortless exercise solution that can improve the balance of the diabetic metabolic equilibrium and jump-start a more active lifestyle. The most central active metabolic hormone is T3. As previously stated the mechanism of converting T4 (the inactive part of the thyroid hormonal system) into T3 (the active part of the metabolic process) is defective in diabetics.19

T3 partly reversed the artificially precipitated diabetic condition caused experimentally by streptozotocin injections, in an animal study. T3 prevented cellular apoptosis and protected B cells by reportedly activating the PI3K-Akt (Ak strain transforming) signalling pathway that promotes cellular survival and growth. The beneficial effects of T3 on cellular integrity are significant in light of the connection between hyperglycaemia and the defective proliferation, or extensive apoptosis of B cells. Hyperglycaemia is considered the cornerstone of both T1D and T2D. T3 injections appear to act as an “anti-diabetic” intervention counteracting the diabetic deterioration following streptozotocin injections, illustrated by a documented reinstatement of insulin responsiveness as well as the euglycemic range of serum glucose levels.50-54 The results of our research achieved external validity of all variables by confirming previous findings.56-61 We demonstrated a statistically significant improvement in T3 levels for all subjects (100%). T3 was elevated to the normal range in 14 out of 20 subjects, indicating that 70% of subjects reached normalcy after 20 treatments.

In Liu et al.’s research.18 diabetes was associated with a pathological lipid profile of high triglycerides and low HDL that predicted coronary heart disease and ischemic stroke. Research has demonstrated that diabetic neuropathy with dyslipidaemia is characterized by abnormally high triglycerides accompanied by a low HDL profile.20 High triglycerides are highly correlated with abnormalities in motor nerve conducting velocities which are the foundation of diabetic neuropathy.21 In our study triglycerides decreased in all 21 diabetic subjects (100%) juxtaposed by a consistent elevation in HDL. Despite the statistically significant improvement, the decrease and increase of Triglycerides and HDL respectively did not reach normalcy for all subjects. Fifteen out of the 21 diabetics with abnormal triglycerides levels displayed normal levels of triglycerides after twenty treatments (71.4%). Only nine of these diabetic subjects (42.9%) indicated HDL levels that were within the normal range. Eighteen prediabetic subjects (90%) manifested normal triglycerides levels and 85% of prediabetics demonstrated HDL levels within the normal range.

Diabetes is aggravated by obesity which is defined by low-grade inflammation and an excess of CRP, identified in the white adipose tissue (WAT). WAT is primarily used for energy storage, in contrast to the brown adipose tissue (BAT) that is predominantly involved in energy production.55 Overall, visceral adipose tissue (VAT) is associated with diabetic hyperinsulinemia, glucose intolerance, hypertriglyceridemia, and dyslipidaemia, defined as a combination of high triglycerides and inhibited HDL, oxidative stress and inflammation as marked by CRP.56-58 This clinical trial revealed a statistically significant decrease of CRP in 100% of the subjects, implying a notable reduction in low-grade inflammation. Despite the prominent improvement evidenced in all subjects, only eight out of the 20 subjects with previously abnormally high CRP attained normalcy after 20 treatments (40% of the subjects). All subjects indicated an overall and visceral fat reduction at an average of 26.14% and 28.17% respectively. The visceral fat reduction was substantiated by the sonography reports of eleven diabetic subjects that showed no fatty liver after the twenty treatments. Skeletal muscle mass increased by an average of 28.2% in all subjects.

The abnormally high fasting and postprandial (PP) glucose recorded before the 20 treatments significantly decreased in all 21 diabetic subjects (100%) post treatments. Nine of the diabetic subjects (42.85%) manifested normal fasting glucose levels after 20 treatments, while the fasting glucose of the remaining twelve diabetic subjects (57.2%) dropped down to the prediabetic level. Ten of the diabetic subjects (47.6%) manifested normal PP glucose levels, while the PP glucose of the remaining eleven diabetic subjects (52.38%) dropped to the prediabetic level after the 20 treatments. Prediabetics had more robust results as expected by their average younger age and baseline healthier status. Eighteen prediabetics (90%) manifested both normal fasting and PP insulin levels after the 20 treatments, while the fasting and PP insulin of the remaining two subjects (10%) remained within the prediabetic level.

Overall, results indicated a remarkable improvement in the diabetic/prediabetic condition. This improvement was predicted by a large body of literature documenting that enhancing T3 and fitness results in a decrease in dyslipidaemia. The deleterious effects of inflammation, marked by abnormally high CRP levels, are also counteracted by exercise and or an active lifestyle. This new method of effortless, simulated exercise has repeatedly demonstrated a CRP reduction.45-50 These and other studies mentioned earlier that have used either regular or effortless exercise have demonstrated a significant decrease in visceral fat, and both fasting and PP glucose and insulin. The advantage of this effortless method is that it can jumpstart an active lifestyle while bypassing the resistance to exercising that is clinically observed in overweight individuals with a diabetic or a prediabetic condition.

Conclusion

The findings of this clinical study support and validate the results of previous studies that some mode of exercise, regular or simulated/effortless is necessary to enhance the health status of the diabetic and prediabetic status. The scope of this research was to offer an intermediate solution that can potentially commence a healthier lifestyle, but without implying or proposing that this novel method is a medical intervention or a conclusive treatment for diabetes. All subjects included in the study were instructed to continue taking their medications and remain under their physicians’ care. Upon thorough examination of the results, it became apparent that the resistance to attaining normalcy appeared to be contingent on disease severity and age. A higher percentage of prediabetics when compared to diabetics reached normalcy in all variables. Most diabetics had a substantial improvement in all variables but without reaching the optimal level of health. This suggested the necessity of continuing with a lifestyle that includes fitness attained either by regular or effortless exercise, in conjunction with the medical treatments recommended. To speed up weight loss, a structured nutritional plan may be useful. The sonograph reports evidencing no fatty liver after 20 treatments validated the results obtained on visceral fat reduction. We are involved in conducting more studies that examine visceral fat deposits and fatty liver by using sonography or magnetic resonance imaging diagnostic methods.

Acknowledgments

The authors would like to thank all the patients who gave consent to release their records for this clinical trial. Special thanks to the eleven subjects who volunteered to offer the results of their sonography reports on their fatty liver condition.

Conflicts of interest

The authors declare no conflict of interest. All treatments were performed by operators without the direct presence or hands-on supervision by any of the authors.

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