Lifewave Links for Doctors

LifeWave Links for Doctors is a great research source for what has happened with LifeWave Testing.

Research Links for Doctors


LifeWave X39 PhotoTherapy Patch Raises Copper Peptide Levels (GHK Levels) in a statistically significant manner:

Clinical Studies pulled from Internet until Publication in May 2020.  Here’s a YouTube Link by David Schmidt, discussing X39:

https://www.youtube.com/watch?v=qh56ubopMIU&t=17s


GHK (Copper Peptide) and DNA: Resetting the Human Genome to Health: Dr Loren Pickart

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4180391/

Abstract

During human aging there is an increase in the activity of inflammatory, cancer promoting, and tissue destructive genes plus a decrease in the activity of regenerative and reparative genes. The human blood tripeptide GHK possesses many positive effects but declines with age. It improves wound healing and tissue regeneration (skin, hair follicles, stomach and intestinal linings, and boney tissue), increases collagen and glycosaminoglycans, stimulates synthesis of decorin, increases angiogenesis, and nerve outgrowth, possesses antioxidant and anti-inflammatory effects, and increases cellular stemness and the secretion of trophic factors by mesenchymal stem cells. Recently, GHK has been found to reset genes of diseased cells from patients with cancer or COPD to a more healthy state. Cancer cells reset their programmed cell death system while COPD patients' cells shut down tissue destructive genes and stimulate repair and remodeling activities. In this paper, we discuss GHK's effect on genes that suppress fibrinogen synthesis, the insulin/insulin-like system, and cancer growth plus activation of genes that increase the ubiquitin-proteasome system, DNA repair, antioxidant systems, and healing by the TGF beta superfamily. A variety of methods and dosages to effectively use GHK to reset genes to a healthier state are also discussed.

3. Discussion

Even though numerous and diverse beneficial effects of GHK have been known for decades, it was not clear how one simple molecule could accomplish so much. The use of gene expression data greatly extends our understanding of GHK's effects and its potential treatments of some of the diseases and biochemical changes associated with aging. As a potential therapeutic agent GHK has a clear advantage over many other active chemicals that may also show promising results in gene profiling experiments, its gene modulating effects correspond to findings from in vivo experiments. When GHK is administered internally to an animal, it induces actions throughout the body.

The treatment of rats, mice, and pigs with GHK was shown to effectively activate systemic healing throughout the animal. For example, if GHK is injected into the thigh muscles of rats, it induces accelerated healing in implanted Hunt-Schilling wound chambers. If the GHK is injected into the thigh muscles of mice, it accelerates the healing of an experimental full thickness surgical defect wound model on its back. If injected into thigh muscles of pigs, it induces accelerates healing of full thickness surgical defect wounds on its back [37]. If GHK is injected intraperitoneally into rats, it heals tubular bone fractures [38]. Wound healing requires activation of gene expression for numerous pathways and wound healing data confirms that GHK is able to activate gene expression in animals [3945].

There is still not enough information to translate gene profiling data into biological effects. However, based on the documented activity of GHK in vivo, we can predict the following beneficial actions from our gene profiling data.

3.1. Fibrinogen

Fibrinogen, the protein which is used to make blood clots, is also a strong predictor of mortality in cardiovascular patients. After vascular incidents, such as myocardial infarction, fibrinogen concentrations increase sharply. The free, unclotted fibrinogen protein increases the “stickiness” of red blood cells which stack together forming rouleaux. This increases the time of the “solid” blood state which decreases blood flow through the microcirculation where blood flows like a thixotropic fluid, switching between a solid phase and a liquid phase, somewhat like toothpaste. As a solid, it stops oxygen and nutrient flow to the tissues. This, in itself, can cause tissue damage.

The gene data on GHK's suppression of FGB (the fibrinogen beta chain) combined with its actions on lowering IL-6 secretion on fibroblasts and sebocytes appears to be sufficient to explain its lowering effect on fibrinogen.

3.2. Ubiquitin Proteasome System

The ubiquitin proteasome system (UPS) functions in the removal of damaged or misfolded proteins. Aging is a natural process that is characterized by a progressive accumulation of unfolded, misfolded, or aggregated proteins. In particular, the proteasome is responsible for the removal of normal as well as damaged or misfolded proteins. Recent work has demonstrated that proteasome activation by either genetic means or use of compounds retards aging [13, 14].

In our screening of UPS genes with a percent change of at least ±50%, GHK increased gene expression in 41 UPS genes while suppressing 1 UPS gene. Thus, it should have a positive effect on this system [13, 14, 46].

3.3. DNA Repair

It is estimated that normal metabolic activities and environmental factors such as UV light and radiation can cause DNA damage, resulting in somewhere between 1000 and as many as 1 million individual molecular lesions per cell per day. Lack of sufficient DNA repair is considered a cause of cell senescence, programmed cell death, and unregulated cell division, which can lead to the formation of a tumor that is cancerous [47–50].

GHK was stimulatory for DNA repair genes (47 stimulated, 5 suppressed) suggesting an increased DNA repair activity.

3.4. Antioxidant Defense

Free radicals and toxic end products of lipid peroxidation are linked to atherosclerosis, cancer, cataracts, diabetes, nephropathy, Alzheimer's disease, and other severe pathological conditions of aging. Reactive oxygen species (ROS) and reactive carbonyl species (RCS) are produced in cells in small quantities under physiological conditions and play an important role in cell signaling and immune defense. A robust antioxidant network maintains balance between free radical production and scavenging, ensuring that the overall damage from free radicals is low. However, in the course of aging and in pathological conditions such as inflammation, the balance may shift toward free radical accumulation that can lead to oxidative stress and eventually to cell death [51].

GHK increases gene expression of 14 antioxidant genes and suppresses the expression of 2 prooxidant genes. It increases the expression of the oxidative/inflammatory gene NF-κB2 103% but also increases the expression of two inhibitors of NF-κB, TLE1 by 762% and IL18BP by 295%; thus, it possibly inhibits the activity of the NF-κB protein.

GHK also possesses antioxidant activities in cell culture and in vivo.

In dermal wound healing in rats, GHK, attached to biotin to bind it to collagen pads covering wounds, produced a higher production of protein antioxidants in the wound tissue. Superoxide dismutase was increased 80% while catalase was increased 56% [52, 53]. GHK reduced gastric mucosal damage by 75% against lipid peroxidation by oxygen-derived free radicals induced by acute intragastric administration of ethanol [54].

Interleukin 1 beta can induce serious oxidative damage to cultured cells [55, 56]. GHK markedly reduced oxidative damage by interleukin 1-beta to cultured insulin secreting pancreatic cells [57].

In another study, GHK entirely blocked the extent of in vitro Cu(2+)-dependent oxidation of low density lipoproteins (LDL). Treatment of LDL with 5 microM Cu(2+) for 18 hours in phosphate buffered saline (PBS) resulted in extensive oxidation as determined by the content of thiobarbituric acid reactive substances. Oxidation was entirely blocked by GHK. In comparison, copper, zinc-superoxide dismutase provided only 20% protection [58].

Acrolein, a well-known carbonyl toxin, is produced by lipid peroxidation of polyunsaturated fatty acids. GHK directly blocks the formation of 4-hydroxynonenal and acrolein toxins created by carbonyl radicals that cause fatty acid decomposition [59, 60]. GHK also blocks lethal ultraviolet radiation damage to cultured skin keratinocytes by binding and inactivating reactive carbonyl species such as 4-hydroxynoneal, acrolein, malondialdehye, and glyoxal [61].

Iron has a direct role in the initiation of lipid peroxidation. An Fe(2+)/Fe(3+) complex can serve as an initiator of lipid oxidation. The major storage site for iron in serum and tissue is ferritin and the superoxide anion can promote the mobilization of iron from ferritin which can catalyze lipid peroxidation. GHK : Cu(2+) produced an 87% inhibition of iron release from ferritin by apparently blocking iron's exit channels from the protein [62].

3.5. Insulin and Insulin-Like Pathways

The insulin/IGF-1-like receptor pathway is a contributor to the biological aging process in many organisms. The gene expression data suggests that GHK suppresses this system as 6 of 9 of the affected insulin/IGF-1 genes are suppressed.

Insulin/IGF-1-like signaling is conserved from worms to humans. In vitro experiments show that mutations that reduce insulin/IGF-1 signaling have been shown to decelerate the degenerative aging process and extend lifespan in many organisms, including mice and possibly humans. Reduced IGF-1 signaling is also thought to contribute to the “antiaging” effects of calorie restriction [63].

3.6. COPD

COPD (chronic obstructive lung disease) is a leading cause of death in the world. It is a deadly and painful disease of the lungs that causes difficulty in breathing. In people with COPD, the tissues necessary to support the physical shape and function of the lungs are destroyed. COPD is most often caused by tobacco smoking and long-term exposure to air pollution but is also a component of normal aging. As the lungs get older, the elastic properties decrease, and the tensions that develop can result in areas of emphysema.

The most explored of GHK's actions is the repair of damaged tissues (skin, hair follicles, stomach and intestinal linings, and boney tissue) either by the use of copper-peptide containing creams or by induction of systemic healing. Campbell et al. found that GHK's resetting of gene expression of fibroblasts from COPD patients fits into this category of tissue repair via the TGF beta superfamily. Campbell et al. found that GHK directly increases TGF beta and other family members which activate the repair process [10].

Treatment of human fibroblasts with GHK recapitulated TGF beta-induced gene expression patterns, led to the organization of the actin cytoskeleton and elevated the expression of integrin beta1. Furthermore, addition of GHK or TGF beta restored collagen I contraction and remodeling by fibroblasts derived from COPD lungs compared to fibroblasts from former smokers without COPD.

On another note, persons with severe COPD use air inhalation systems that pump misty, water-filled air in and out of the lungs. Often steroids are added to the solution to suppress the lung inflammation, while this provides short-term help, it also inhibits lung repair. In theory, GHK could be infused into the blood stream of patients to repair the lung tissue, added to a misting solution or used in combination of a carrier like DMSO along with GHK (use a 1 : 1 molar ratio of GHK to DMSO). DMSO and GHK or GHK : Cu(2+) has always worked well together on wound healing. DMSO has been used in the past as a treatment for COPD, so there should be few safety issues.

Also, it may be possible to induce more extensive rebuilding of lung tissue. The mixture of GHK, transferrin, and somatostatin was sufficient to promote branching in the absence of serum in organ culture, all of which could be added to the misting solution [64].

3.7. Cancer

In 2010, Hong et al. identified 54 genes associated with aggressive, metastatic, human colon cancer [8]. The Broad Institute's Connectivity Map was used to find compounds that reverse the differential expressions of these genes. The results indicated that two wound healing and skin remodeling molecules, GHK at 1 micromolar and securinine at 18 micromolar, could significantly reverse the differential expression of these genes and suggested that they may have a therapeutic effect on the metastasis-prone patients.

Normal healthy cells have checkpoint systems to self-destruct if they are synthesizing DNA incorrectly through programmed cell death or the apoptosis system. Matalka et al. demonstrated that GHK, at 1 to 10 nanomolar, reactivated the apoptosis system, as measured by caspases 3 and 7, and inhibited the growth of human SH-SY5Y neuroblastoma cells, human U937 histiocytic lymphoma cells, and human breast cancer cells [9]. In contrast, the GHK accelerated the growth of healthy human NIH-3T3 fibroblasts.

Our analysis of GHK's actions found that it increased gene expression in 6 of the 12 human caspase genes that activate apoptosis. In 31 other genes, GHK altered the pattern of gene expression in a manner that would be expected to inhibit cancer growth. In DNA repair genes there was an increase (47 UP, 5 DOWN) [7]. These results support the idea that GHK may help slow or suppress cancer growth.

Linus Pauling's group once used a copper tripeptide, Gly-Gly-His : Cu(2+) and ascorbic acid as a cancer treatment method. In a recent paper, we used their basic method but with GHK : Cu(2+) and ascorbic acid, which strongly suppressed sarcoma 180 in mice without any evident distress to the animals [7]. GHK altered gene expression in 84 genes (caspases, cytokines, and DNA repair genes) in a manner that would be expected to suppress cell growth. On skin, GHK seems to act most strongly in the late stage of healing, called remodeling, where cellular migration into the wound area is stopped and cellular debris is removed. The anticancer actions of small copper peptides may be a side effect of this system.

The use of GHK : Cu(2+) and ascorbic acid should be investigated in more detail. The mice treated in this manner appeared to remain very healthy and active, in contrast to the toxicities of current cancer chemotherapy.

3.8. GHK as a Clinical Treatment

GHK, abundantly available at low cost in bulk quantities, is a potential treatment for a variety of disease conditions associated with aging. The molecule is very safe and no issues have ever arisen during its use as a skin cosmetic or in human wound healing studies.

GHK has a very high affinity for Cu(2+) (pK of association = 16.4) and can easily obtain copper from the blood's albumin bound Cu(2+) (pK of association = 16.2) [3]. Most of our key experiments used a 1 : 1 mixture of copper-free GHK and GHK : Cu(2+). In wound healing experiments, the addition of copper strongly enhanced healing. However, others often obtain effective results without added copper.

Cells within tissues are under the influence of many other regulatory molecules. Thus, GHK would be expected to influence the cells' gene expression to be more similar to that of a person of age 20–25, an age when the afflictions of aging are very rare. Based on our studies, in which GHK was injected intraperitoneally once daily to induce systemic wound healing throughout the body, we estimate about 100–200 mgs of GHK will produce therapeutic actions in humans. But even this may overestimate the necessary effective dosage of the molecule. Most cultured cells respond maximally to GHK at 1 nanoM. GHK has a half-life of about 0.5 to 1 hour in plasma and two subsequent tissue repair studies in rats found that injecting GHK intraperitoneally 10 times daily lowered the necessary dosage by approximately 100-fold in contrast to our earlier studies [38, 65].

The most likely effective dosage of GHK was given to rats for healing bone fractures. This mixture of small molecules included Gly-His-Lys (0.5 μg/kg), dalargin (1.2 μg/kg) (an opioid-like synthetic drug), and the biological peptide thymogen (0.5 μg/kg) (L-glutamyl-L-tryptophan) to heal bones. The total peptide dosage is about 2.2 μg/kg or, if scaled for the human body, about 140 μg per injection with 10 treatments per day [38, 65].

The use of portable continuous infusion pumps for a treatment might maintain an effective level in the plasma and extracellular fluid with the need for much less GHK. Possibly the peptide could be administered with a transdermal patch [66]. Another approach could be to use peptide-loaded liposomes as an oral delivery system for uptake into the intestinal wall without significant breakdown [67, 68].

4. Conclusion

Most current theories and therapies to treat disease tend to target only one biochemical reaction or pathway. But for human aging, our data suggests that we must think of simultaneously resetting hundreds to thousands of genes to protect at-risk tissues and organs. GHK may be a step towards this gene resetting goal.



Characterizing the Effect of the Energy Emitted

https://www.semanticscholar.org/paper/CHARACTERIZING-THE-EFFECT-OF-THE-ENERGY-EMITTED-BY-Rein/2932b96b03060bd695b3ac8b5ff30daf8944ea40

DISCUSSION 

The results in the three Tables indicate that under resonance conditions using certain excitation parameters (frequency and amplitude) the three LifeWave patches tested increase the electrical conductivity of human DNA. In order to reach this conclusion for the Aeon patch, two different statistical methods were used to analyze the raw data. This was necessary because of the relatively large standard deviation values obtained under these experimental conditions and the relatively few independent measurements (n=3). Based on delta values between experimental and control runs, we can conclude that the Aeon patch when excited at 39.8 kHz is the most effective at stimulating DNA. The EE patch and the SP6 patch were somewhat less effective and showed a similar response to each other. 

The fact that DNA stimulation only occurs at certain excitation frequencies (and their corresponding voltages) indicates that this frequency say, 35.5 kHz for the SP6 patch, is required for the transfer of information from the patch to the DNA. 

In these experiments, there are three different energies interacting with the DNA:

1. the geomagnetic field in the lab located in Ridgway, CO

2. the bio-energy emitted by the P8 acupoint

3. the energy emitted from the LifeWave patch 

In addition to these three energies, there is a fourth energy (an electric field) generated from the voltage spike (at a particular frequency) used to excite the DNA during each measurement. However, the only difference between the control and experimental conditions is the presence of the energy from the LifeWave patch. It is proposed here that information is transferred from the patch to the DNA, when excitation frequency matches the resonance frequency of the patch. If this hypothesis is correct than the following resonance frequencies may be assigned to the LifeWave patches. 

 Resonance Frequencies (kHz)

 Aeon Patch - 39.8 and 79.4

Energy Enhancer Patch – 1.78

SP6 Patch – 35.5

As explained in the introduction, increased electrical conductivity is associated with and in some cases controls the functional properties of DNA in the cell. Since measurements are made under resonance conditions, conductivity of electrons is believed to be occurring via a unistep super-exchange mechanism involving quantum tunneling. Therefore we can also conclude that this particular quantum property of DNA is enhanced by all three Lifewave patches. The ability of an energy field generated from the Lifewave patches to stimulate quantum processes at the biomolecular level is of fundamental importance. This conclusion is consistent with the known clinical efficacy of the Lifewave patches to promote a variety of healing processes in the body. 


Another LifeWave Links for Doctors


Report for Human Clinical Pilot Study

LifeWave Glutathione Patch

https://lifewave.com/Content/images/home/science/pdf/Research-HumanClinicalPilotStudy.pdf

Discussion 

Results of this pilot study demonstrate that the LifeWave GSH Patch increases blood GSH significantly in several of the subjects. Although there was variability in baseline GSH measurements, all of the averaged measurements after patch placement for each time point were above 264.6%, and more importantly, above the average baseline measurement benefit of LifeWave GSH patches. Furthermore, when comparing the lowest baseline value to post-patch values, the increase was as high as 454%. 

The GSH increases are substantial in subjects with a lower GSH baseline value, indicating that LifeWave GSH patches are more beneficial for individuals that are deficient in GSH. Another potential benefit for the LifeWave GSH Patches is that they do not overstimulate the GSH system, which could potentially cause harm. 

There were no appreciable changes in either GSH Reductase, or GSH S-Transferase, suggesting that these enzymes are not involved in the actions of LifeWave GSH Patches. 

There were some spikes in urine mercury levels in some of the subjects, indicating that a consequence of increased GSH levels is an enhanced detoxification. However, the changes in GSH and mercury were not tightly correlated, which does not demonstrate conclusively that LifeWave GSH Patch induced increases in GSH are related to changes in mercury. Further characterization of the amount of GSH needed to change mercury levels and the timing of increases in GSH and mercury are needed. However, it appears that the LifeWave Patches are altering mercury levels, which likely means they are contributing to detoxification of heavy metals., which would be an important benefit of LifeWave GSH Patches. Further investigation is need to determine if LifeWave Patches alter mercury levels and to characterize the effects on GSH production. 

References 

Shade, Christopher W., 2008, Automated simultaneous analysis of monomethyl and mercuric Hg in biotic samples by Hg-thiourea complex liquid chromatography following acidic thiourea leaching, Environmental Science & Technology, 42, 6604-6610. 

Shade, Christopher W. and Hudson, Robert J.M., 2005 Determination of MeHg in environmental sample matrices using Hg-Thiourea Complex Ion Chromatography with on-line cold vapor generation and atomic fluorescence spectrometric detection (HgTU/IC-CVAFS), Environmental Science & Technology, 39, 4974-4982 

Research Team 

Research was conducted by Lisa Tully, PhD, Andrew Lange, ND and Christopher Shade, PhD 



Nanoscale Glutathione Patches Improve Organ Function

https://www.researchgate.net/publication/289299383_Nanoscale_Glutathione_Patches_Improve_Organ_Function

Abstract - Glutathione, termed the “ultimate” or “master” antioxidant, is a vital intracellular tripeptide molecule and plays a central role in cellular physiologic functions. Currently the undeniable connection between glutathione and good health is very well established. 

Bioelectrical impedance data indicative of cellular physi- ologic organ function (status), using an Electro Interstitial Scanning (EIS) system, were acquired from two cohort volun- teers. Cohort 1 comprised of 10 subjects: 1 male and 9 females, 18-86 (mean 58) years of age while Cohort 2 were 20 subjects: 4 males and 16 females, 19-80 (mean 54) years of age. Cellular physiologic function in subjects were evaluated in 8 organs (pancreas, liver, gall bladder, intestines, left and right adrenal glands, hypothalamus and pituitary gland) while wearing the glutathione patch for a period of 4 weeks. Physiologic function testing was repeated each week. Cohort 1 wore the glutathione patch for 12 hours/day daily, while Cohort 2 wore the gluta- thione patch for 12 hours/day on weekdays. Cellular physiologic function baseline data were acquired from all subjects at the beginning of the study period before the glutathione patch was worn. Subjects were instructed to keep well hydrated during the study period. All subjects served as their own control. The hypothesis to be tested was: The glutathione patch worn 12 hours daily for 4 weeks significantly improves cellular physiolog- ic functional status in different organs. 

The overall data in Cohort 1 in this study demonstrated that glutathione patches worn 12 hours daily over a period of 4 weeks produced a highly significant improvement in physiolog- ic functional status of pancreas, liver, gall bladder, intestines, left and right adrenals, hypothalamus and pituitary gland and very significant improvement in pancreas with a statistical power of at least 72%. Stated differently all organs achieved significant cellular physiologic functional status improvement compared to baseline with a statistical power of at least 91%. 

Keywords— Nanotechnology, Glutathione patch, Cellular physiologic function measurements, Electro interstitial scan (EIS) system, LifeWave. 



The Effect of a Non-Transdermal Surface

https://lifewave.com/Content/images/home/science/pdf/Research-TheEffectOfANonTransdermalSurface.pdf

Results

Application of the LifeWaveTM Energy Enhancer patch produced a significant increase over placebo in maximum aerobic ATP, maximum ATP from fatty acid metabolism, resting ATP, and maximum aerobic work. There was no significant effect on resting ATP from fatty acid metabolism. There were no significant side effects from the patch.

Discussion

This study demonstrates a statistically significant improvement from the LifeWaveTM Energy Enhancer patch in responders in all metabolic markers except resting fatty acid metabolism. In some cases very dramatic improvements were noted. These results coincide with other performance related studies using the patch. The implications are that the patches would be valuable in a selected subset of individuals seeking improved metabolic performance and/or help with weight control.

However, it is important to note that not all subjects responded to the patch application. Specifically:

1. Maximum aerobic work improved in 50% of subjects.

2. Maximum aerobic from fatty acid metabolism improved in 36% of subjects.

3. Maximum aerobic ATP improved in 46% of subjects.

4. Resting ATP improved in 23% of subjects.

5. Resting ATP from fatty acid metabolism improved in 40% of subjects.

A possible explanation for a failure to improve in the non-responders may be patch location variability. It may be that there is a certain amount of individual variation in the locations of patch placement that will be effective.

Another reason may be that diet was not controlled for. The carbohydrate content of the diet during the 4-5 days before an CO2/O2 evaluation has been shown to skew the CO2/O2 ratio such that in a resting state glucose metabolism becomes greater than fatty acid metabolism. This latter fact may explain why there was no consistency found in the responders regarding resting fatty acid metabolism, while there was consistency in exertional fatty acid metabolism.



Silent Nights® Patch Improves Qualitative and Quantitative Measures of Sleep and Enhances Quantitative Markers of Organ Function

https://pdfs.semanticscholar.org/18e8/ea4d1035a4d8e628df3a9fd15ce164c91b93.pdf

Sherry Blake-Greenberg MA, HMD, Homer Nazeran PhD, CPEng (Biomed.)*Health Integration Therapy, Palos Verdes Estates, California 90274, USA*Electrical and Computer Engineering, University of Texas at El Paso, El Paso Texas 79968, USA

DISCUSSION AND CONCLUSION

Actigraphic data analysis demonstrated that compared to baseline on average there was 29% reduction in activity level during sleep, 22% reduction in total awake time, 28% increase in ratio of time in bed over awake time, and 28% reduction in restlessness after wearing the Silent Nights Patch nightly 1 hour before sleep for 2 weeks. The analysis of the Leeds sleep evaluation scores over the study period revealed that there was a very significant (p < 0.01) improvement in sleep attributes indicating that after wearing the Silent Nights Patch 2 weeks, overall: it was easier and quicker than usual for subjects to get to sleep; the subjects felt calmer with less wakeful periods than usual during sleep (better sleep quality); it was easier and requiring less time to wake up than usual in the mornings; and the subjects felt more alert than usual, experiencing less disrupted balance and coordination upon awakening.

The sleep diary data on average also confirmed considerable qualitative improvements at the end of the study period in different sleep attributes. Overall the subjects felt that compared to usual it was easier to fall to sleep, woke up less number of times during the night with less time during each waking period, waking up later in the mornings, feeling more refreshed requiring less naps with shorter duration during the day.

Statistical analysis of the EIS data revealed that there were significant improvements in cellular physiologic functional status of the brain (frontal lobe, temporal lobe, hippocampus, hypothalamus), cardiac ventricles, adrenals, and thyroid gland at the end of the study period with respect to the corresponding baseline data. The results showed a highly significant (p < 0.001) improvement in the physiologic functional status of the temporal lobe, hippocampus, hypothalamus (average statistical power = 100%) and adrenal glands (statistical power = 96%) with a very significant improvement (p <0.01) in the functioning of the frontal lobe (statistical power = 75%). There was a significant (p < 0.05) improvement with an average statistical power of at least 72% in the functional status of the thyroid gland and cardiac ventricles. The liver, kidneys, and intestines did not achieve statistical significance over this period.

In summary, the overall data in this pilot investigation demonstrated that the Silent Nights Patch worn on the right temple nightly 1 hour before sleep for 2 weeks produced considerable improvements in the objective and subjective measures of sleep and caused an impressive improvement in the physiologic functional status of different parts of the brain and adrenal glands with significant enhancement on the functioning of the cardiac ventricles and thyroid glands. Therefore, the hypothesis was accepted as true.

In future studies double-blind placebo-controlled protocols will be used to further investigate the efficacy of these nanoscale devices on improvement of sleep.

REFERENCES

1. http://www.healthcare.philips.com/main/homehealth/sleep/actiwatch/default.wpd. Retrieved June 2011. 2. http://www.lifewave.com/silentnights.asp. Retrieved June 2011.

3. Ancoli-Israel S, Cole R, Alessi C, Chambers M, et al (2003). The Role of Actigraphy in the Study of Sleep and Circadian Rhythms. Sleep. 26 (3): 342-390.

4. http://www.bmedical.com.au/shop/actiwatch-2-minimitter-philips.html. Retrieved June 2011.

5. Van De Water JM, Miller TW, Vogel RL, et al (2003). Impedance cardiography: the next vital signtechnology? Chest.123:2028-33.

6. Critchley LAH (1998). Impedance cardiography. The impact of new technology. Anaesthesia. 53:677-84.

7. Cotter G, Schachner A, Sasson L, et al (2006). Impedance cardiography revisited. Physiol Meas. 27:817-27.

8. http://www.fda.gov/cdrh/pdf/p970033.html.

9. Fricke H, Morse S (1926). The electric capacity of tumors of the breast. J Cancer Res. 16:310 - 376.

10. Morimoto T, Kinouchi Y, Iritani T, Kimura S et al (1990). Measurement of the electrical bio- impedance of breast tumors. Eur Surg Res. 22:86-92.

11. http://nibblesoftware.com/health/category/services/eis-scan-–-electro-interstitial-scan/. Retrieved June 2011.

12. Parrott AC, Hindmarch I (1980). The Leeds Sleep Evaluation Questionnaire in psychopharmacological investigations - a review. Psychopharmacology (Berl). 71(2): 173-9.


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