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Stress research studies for holistic treatments

Around the world over thousands of years, patients have received root-cause holistic treatment for their diseases with personalized
treatment, diet and lifestyle modification recommendations. Read the inspiring true stories of practitioners who heal people and who recovered
from their problems after stress treatment at their clinics. Many have been generous to share their knowledge and experience for the benefit
of other holistic experts and patients alike. Many practitioners share their Case Studies and the healing powers of stress and related therapies
as they heal people who benefited from our expertise.

/ title=”Resveratrol interacts with estrogen receptor-? to inhibit cell replicative growth and enhance stress resistance by upregulating mitochondrial superoxide dismutase.”>
Resveratrol interacts with estrogen receptor-? to inhibit cell replicative growth and enhance stress resistance by upregulating mitochondrial superoxide dismutase.

January 2008

trans-Resveratrol (RES) is one of a number of dietary polyphenols that have been reported to beneficially affect human physiology. Although numerous studies have attributed this to direct interactions between RES and histone deacetylases, recently the reliability of these results has been questioned. We have shown that the mitochondrial superoxide dismutase (MnSOD) is substantially upregulated in RES-treated cells. Here we explore the mechanisms underlying this, showing that two of RES’s more interesting effects, inhibition of replication and enhancement of stress resistance, are mediated by MnSOD upregulation in three cell lines: MRC5 human lung fibroblasts, C2C12 mouse myoblasts, and SHSY5Y human neuroblastoma cells. When small interfering RNA was used to prevent induction of MnSOD expression, the effects of RES on population doubling time of cells in culture, and resistance to cell death after exposure to hydrogen peroxide or paraquat, were abolished. Interestingly, the RES-induced upregulation of MnSOD levels could be prevented by the estrogen receptor antagonist ICI 182780. RES’s effects also could be reproduced using estradiol or the estrogen receptor-? agonist diarylpropionitrile, but not using the estrogen receptor-? agonist propylpyrazole triol. Thus, we suggest that RES interacts with estrogen receptor-? to induce the upregulation of MnSOD, which affects cell cycle progression and stress resistance. These results have important implications for our understanding of RES’s biological activities and potential applications to human health.

/ onclick=”MoreLine(‘10856’, ‘Resveratrol interacts with estrogen receptor-? to inhibit cell replicative growth and enhance stress resistance by upregulating mitochondrial superoxide dismutase.’)”>
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/ title=”Association between fatty acid supplementation and prenatal stress in African Americans: a randomized controlled trial.”>
Association between fatty acid supplementation and prenatal stress in African Americans: a randomized controlled trial.

November 2014

OBJECTIVE:
To test the association between docosahexaenoic acid (DHA) supplementation and perceived stress and cortisol response to a stressor during pregnancy in a sample of African American women living in low-income environments.
METHODS:
Sixty-four African American women were enrolled at 16-21 weeks of gestation. Power calculations were computed using published standard deviations for the Perceived Stress Scale and the Trier Social Stress Test. Participants were randomized to either 450 mg per day of DHA (n=43) or placebo (n=21). At baseline and at 24 and 30 weeks of gestation, perceived stress was assessed by self-report. Cortisol response to a controlled stressor, the Trier Social Stress Test was measured from saliva samples collected upon arrival to the laboratory and after the completion of the Trier Social Stress Test.
Results:
Women in the DHA supplementation group reported lower levels of perceived stress at 30 weeks of gestation, controlling for depression and negative life events (mean 27.4 compared with 29.5, F [3, 47] 5.06, P=.029, Cohen’s d=0.65). Women in the DHA supplementation had lower cortisol output in response to arriving to the laboratory and a more modulated response to the stressor (F [1.78, 83.85] 6.24, P=.004, Cohen’s d=0.76).
Conclusion:
Pregnant women living in urban low-income environments who received DHA reported reduced perceived stress and lower levels of stress hormones in the third trimester. Docosahexaenoic acid supplementation may be a method for attenuating the effects of maternal stress during late pregnancy and improving the uterine environment with regard to fetal exposure to glucocorticoids. CLINICAL TRIAL REGISTRATION: ClinicalTrials.gov, www.clinicaltrials.gov, NCT01158976.

/ onclick=”MoreLine(‘10833’, ‘Association between fatty acid supplementation and prenatal stress in African Americans: a randomized controlled trial.’)”>
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/ title=”Modified apolipoprotein (apo) A-I by artificial sweetener causes severe premature cellular senescence and atherosclerosis with impairment of functional and structural properties of apoA-I in lipid-free and lipid-bound state.”>
Modified apolipoprotein (apo) A-I by artificial sweetener causes severe premature cellular senescence and atherosclerosis with impairment of functional and structural properties of apoA-I in lipid-free and lipid-bound state.

May 2011

Long-term consumption of artificial sweeteners (AS) has been the recent focus of safety concerns. However, the potential risk of the AS in cardiovascular and lipoprotein metabolism has not been investigated sufficiently. We compared the influence of AS (aspartame, acesulfame K, and saccharin) and fructose in terms of functional and structural correlations of apolipoprotein (apo) A-I and high-density lipoproteins (HDL), which have atheroprotective effects. Long-term treatment of apoA-I with the sweetener at physiological concentration (3 mM for 168 h) resulted in loss of antioxidant and phospholipid binding activities with modification of secondary structure. The AS treated apoA-I exhibited proteolytic cleavage to produce 26 kDa-fragment. They showed pro-atherogenic properties in acetylated LDL phagocytosis of macrophages. Each sweetener alone or sweetener-treated apoA-I caused accelerated senescence in human dermal fibroblasts. These results suggest that long-term consumption of AS might accelerate atherosclerosis and senescence via impairment of function and structure of apoA-I and HDL.

/ onclick=”MoreLine(‘9152’, ‘Modified apolipoprotein (apo) A-I by artificial sweetener causes severe premature cellular senescence and atherosclerosis with impairment of functional and structural properties of apoA-I in lipid-free and lipid-bound state.’)”>
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/ title=”Vitamin D modifies the associations between circulating betatrophin and cardiometabolic risk factors among youths at risk for metabolic syndrome.”>
Vitamin D modifies the associations between circulating betatrophin and cardiometabolic risk factors among youths at risk for metabolic syndrome.

October 2016

Background:
Betatrophin has been recently reported to play a role in glucose homeostasis by inducing beta-cell proliferation in mice. However, studies in human are inconsistent. As a diet therapyally-regulated liver-enriched factor, we hypothesize that betatrophin might be regulated by vitamin D, and ignorance of vitamin D status may explain the discrepancy in previous human studies. The aims of this study were to assess the association between circulating betatrophin and glucose homeostasis as well as other cardiometabolic variables in a cohort of youths at risk for metabolic syndrome and test the possible influence of vitamin D status on the association.
METHODS:
559 subjects aged 14-28 years were recruited from Beijing children and adolescents metabolic syndrome study. All underwent a 2 h-oral glucose tolerance test. Serum levels of betatrophin, 25-hydroxy-vitamin D as well as adipokines including adiponectin and fibroblast growth factor 21 (FGF21) were measured by immunoassays. The relationships between betatrophin and insulin resistance, beta-cell function, other cardiometabolic variables and vitamin D status were evaluated.
Results:
Participants in the highest quartile of betatrophin levels had the highest levels of total cholesterol (P < 0.001), triglyceride (P < 0.001) and low-density lipoprotein cholesterol (P < 0.001) and the lowest levels of vitamin D (P = 0.003). After stratification by vitamin D status, betatrophin in subjects with vitamin D deficiency were positively correlated with unfavorable metabolic profiles including high blood pressures, dyslipidemia and hyperglycemia, whereas betatrophin inthose with higher vitamin D levels only showed negative association with fasting insulin, 2 h-insulin, and insulin resistance. In addition, adiponectin and FGF21 demonstrated the expected associations with metabolic parameters. CONCLUSIONS: Elevated betatrophin levels were associated with cardiometabolic risk factors in this young population, but the association was largely dependent on vitamin D status. These findings may provide valuable insights in the regulation of betatrophin and help explain the observed discrepancies in literature.

/ onclick=”MoreLine(‘9062’, ‘Vitamin D modifies the associations between circulating betatrophin and cardiometabolic risk factors among youths at risk for metabolic syndrome.’)”>
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/ title=”Effects of yogurt containing Lactobacillus plantarum HOKKAIDO on immune function and stress markers.”>
Effects of yogurt containing Lactobacillus plantarum HOKKAIDO on immune function and stress markers.

June 2016

Lactobacillus plantarum HOKKAIDO (HOKKAIDO strain) was isolated from well-pickled vegetables in Hokkaido, Japan. We report a randomized, double-blind, placebo-controlled study evaluating the effects of L. plantarum HOKKAIDO on immune function and stress markers in 171 adult subjects. Subjects were divided into three groups: the L. plantarum HOKKAIDO yogurt group, the placebo-1 group who ingested yogurt without the HOKKAIDO strain, and the placebo-2 group who ingested a yogurt-like dessert withoutthe HOKKAIDO strain. Hematological tests and body composition measurements were performed before and after 4 and 8 weeks of blinded ingestion. Although no significant differences in natural killer cell activity were observed, it was found that neutrophil ratio significantly decreased and lymphocytestended to increase in the HOKKAIDO strain yogurt group compared with the yogurt-like dessert group. In addition, the neutrophil-to-lymphocyte ratio, a stress marker, tended to improve in the HOKKAIDO strain yogurt group compared with the yogurt-like dessert group. These results suggest that the ingestion of HOKKAIDO strain yogurt tends to improve immune activity and decrease stress markers.

/ onclick=”MoreLine(‘8184’, ‘Effects of yogurt containing Lactobacillus plantarum HOKKAIDO on immune function and stress markers.’)”>
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/ title=”Caffeic acid phenethyl ester enhances TRAIL-mediated apoptosis via CHOP-induced death receptor 5 upregulation in hepatocarcinoma Hep3B cells.”>
Caffeic acid phenethyl ester enhances TRAIL-mediated apoptosis via CHOP-induced death receptor 5 upregulation in hepatocarcinoma Hep3B cells.

June 2016

Caffeic acid phenethyl ester (CAPE) exhibits various pharmaceutical properties, including anti-bacterial, anti-inflammatory, anti-viral, anti-cancer, and anti-oxidative activity. Tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) has been a promising anti-cancer agent that preferentially induces cancer cell apoptosis with negligible cytotoxicity toward normal cells. Therefore, the present study investigated whether CAPE promotes TRAIL-mediated cytotoxicity in hepatocarcinoma Hep3B cells. The present study demonstrated that CAPE sensitized TRAIL-mediated cell death in Hep3B carcinoma cells. The percentages of the apoptotic cells and annexin-V(+) cells significantly increased in combined treatment with CAPE and TRAIL (CAPE/TRAIL). Treatment with pancaspase inhibitor, z-VAD-fmk, attenuated CAPE/TRAIL-induced apoptosis, suggesting that the combined treatment triggers caspase-dependent apoptosis. Additionally, we found that CAPE stimulated the expression of death receptor 5 (DR5) and treatment with DR5/Fc chimera protein significantly blocked CAPE/TRAIL-induced apoptosis, which indicates that CAPE/TRAIL stimulated apoptosis through the binding of TRAIL to DR5. Moreover, expression of transcription factor C/EBP homologous protein (CHOP) markedly increased in response to CAPE and transient knockdown of CHOP abolished CAPE/TRAIL-mediated apoptosis. These results suggest that CHOP is a key regulator in CAPE/TRAIL-mediated apoptosis. Taken together, the present study found that CAPE significantly enhanced TRAIL-mediated apoptosis in Hep3B carcinoma cells and suggested that CAPE has promising potential in chemoprevention of hepatocellular carcinomas.

/ onclick=”MoreLine(‘8137’, ‘Caffeic acid phenethyl ester enhances TRAIL-mediated apoptosis via CHOP-induced death receptor 5 upregulation in hepatocarcinoma Hep3B cells.’)”>
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