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Measles Outbreak, Fake News, Mass Hysteria

Which is Greater Threat, Measles or Measles Vaccine ?

WaPo Says that Anti-Vaxxers are Dangerous and Should Be Arrested

Aluminum in Vaccines Causes Autism

Financial Kickbacks to Pediatricians Harms Children

Jeffrey Dach MD

7450 Griffin Road Suite 180/190

Davie, Florida 33021

Published on September 1st, 2019 by
Jeffrey Dach MD

The post Protecting Public Health With Mandatory Vaccination appeared first on Jeffrey Dach MD.

Childrens Health Defense Robert F Kennedy Jr

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Published on September 01, 2019 07:08

June 30, 2019

July Fourth Medical Freedom Day

[image error]July 4 Medical Freedom Day by Jeffrey Dach MD

On this Fourth of July we celebrate our Independence and Freedom from oppression. The Statue of Liberty is a stirring reminder of the price our founders paid so we could live in freedom. However, our right to medical freedom is in danger, not from an outside enemy, but from one inside our own country, a form of “organized crime” , our very own drug industry (Big-Pharma).

Eliminating Vaccine Exemptions Strips Away Your Constitutional Right to Medical Freedom.

Your medical freedoms are being stripped away by “Pharma-Driven” legislation which eliminates vaccine exemptions. By eliminating vaccine exemptions we remove the individual right to make medical decisions for ourselves and our families. These rights are protected by the constitution, yet they are stripped away in states like California and New York where a corrupt political process is bought and paid for by the pharmaceutical industry that manufactures a liability free vaccine product, with safety testing that omits inert placebo. How is this possible without the consent of the people? This is made possible by silence. It is time to raise your voices, stand up and be counted as a force for freedom against medical tyranny. Above image of Stature of Liberty, Courtesy of Wikimedia commons.

The New York State has just eliminated the vaccine religious exemption. California State eliminated their religious exemption a few years ago, and is now going after the remaining medical exemption. California and New York are heavily liberal democrat states which have legislative bodies packed with liberal democrats. After receiving legal bribes in the form of massive campaign funding from the pharmaceutical industry, these corrupt politicians are working hand in glove with the drug industry.

Republican States are Pushing Back

In Republican states, on the other hand, Republican dominated legislative bodies are standing up and opposing the drug industries’ attempts to pass legislation which strips away medical freedom, protecting rather than eliminating your constitutional rights and medical freedoms.

Defend Your Rights: – Informed Father Luke Smith-Anderson

Join the medical freedom movement at:

Del Bigtree and the HighWire

ICAN Informed consent Action Network

Barbara Loe Fisher the Vaccine Reaction

Articles with Related Topics:

Washington Post Says Unvaccinated Are Dangerous

Measles Outbreak Fake News

GMO Food and Forced Vaccination Its a Great Country

Aluminum in Vaccines Cause Autism

Which is Greater threat Measles or Measles Vaccine?

Measles and Somalis in Minnesota

Financial Kickbacks to Pediatricians is Illegal and Harms Children

HPV Vaccine the Greatest Scandal of Our Time

Italy Overturns Mandatory Vaccination

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Published on June 30th, 2019 by
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Endometriosis Natural Treatments Part One

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Published on June 30, 2019 06:27

May 19, 2019

Fenofibrate for Endometriosis, Part Two

[image error] Fenofibrate for Endometriosis, Part Two

by Jeffrey Dach MD

A 29 year old real estate agent arrived in my office and told me her story. She had been suffering with pelvic pain, recurrent urinary tract infections and severe PMS for many years now. Her many previous doctors could do little to help. Finally, she underwent an exploratory laparoscopic procedure which showed extensive endometriosis. The examining doctor found scattered endometrial implants throughout the peritoneal cavity which in retrospect had been causing all the pain. Although the symptoms improved from the laparoscopic surgery which removed most of the implants, the patient still had considerable abdominal discomfort and pain around the monthly menstrual cycles. Above image : Endometriosis in lymph node courtesy of wikimedia commons.

This article is part two. For part one, Click here.

Endometriosis, What is It?

Endometriosis is implantation of endometrial tissue outside the uterine cavity in the peritoneal space. In part on of this series, we discussed how these peritoneal implants originate from retrograde flow of endometrial cells out of the fallopian tubes. Although they are not cancerous, these endometrial implants may share many features common to cancer cells , such as activation of inflammatory pathways (NF-kB Nuclear Factor Kappa-B, and IL-6), with stimulation of angiogenesis, upregulation of VEG-F , (Vascular Endothelial Growth Factor), and PDGF (platelet derived growth factor). In addition, the implants stimulate neuro-genesis, the growth of new nerve fibers accounting for increased pain sensations.

Dr Bedaiwy summarizes new treatments in 2017:(1-3)

“The current treatments are surgical and hormonal but have limitations….New treatments include gonadotropin-releasing hormone analogues, selective progesterone (or estrogen) receptor modulators, aromatase inhibitors, immunomodulators, and anti-angiogenic agents.”(1-3)

Angiogeneisis Inhibitors as Novel Treatment for Endometriosis

Blocking NF-KB Activation with HCG

Since NFKB activation is a key feature of endometriosis, one might think that blocking this activation might be useful in treating the disease. That is exactly what Dr. Huber found using HCG (human chorionic gonadotropin) in a series of studies from 2004 and 2007. In a 2004 clinical study, Dr Huber found that weekly injections of HCG was effective for reducing endometriosis pain.(5) Further studies show HCG is anti-inflammatory with blockade of Nuclear factor K-B activation.(6-7)

“HCG suppressed TNF-alpha- or IL-1beta-induced NF-kappaB DNA-binding activity” (7)

The HCG Protocol developed by Dr Wright includes nightly melatonin and gluten free diet.(4)

Statin Drugs Block NF-KB Activation

The statin drugs are another class of drugs with potent blockage of Nuclear factor Kappa Beta Activation.(9) In the first study of its kind, in 2013, Dr Fariba Almassinokiani used simvastatin 20 mg daily to successfully treat endometriosis pain after laparoscopic surgery.(10) Sixty women were treated with either simvastatin or a Gonadotropin Inhibitor (Decapeptyl which blocks secretion of LH,FSH) for 16 weeks, finding both groups had equal and highly significant reduction in pain symptoms.

Statin drugs are potent inhibitors of NFKB activation, and have even been suggested as repurposed anti-cancer drugs.

Fenofibrate Novel Treatment for Endometrisosis

Fenofibrate is an old drug used to control lipids which has been repurposed as an anti-cancer drug. Fenobrate down regulates both NFK-B and VEGF, both key targets for endometriosis treatment.(20) Based on our concept that endometriosis has “cancer-like” biological properties, repurposed anti-cancer-agdrugs such as fenofibrate might be useful. As one might expect, Fenofibrate was effective for regression of endometrial implants in an animal model. in a 2009 study, Dr Onalan found “Fenofibrate causes regression of endometriotic implants: a mouse model” in a dose dependent manner.(18)

Notes: Rapamycin and Itraconazole, Dipyridimole Inhibits Platelet Derived growth factor

Articles with Related Interest:

Jeffrey Dach MD

7450 Griffin Road Suite 180/190

Davie, Fl 33314

954-792-4663

Links and references:

1) free pdf Bedaiwy, Mohamed A., et al. “New developments in the medical treatment of endometriosis.” Fertility and sterility 107.3 (2017): 555-565.

Endometriosis affects 1 in 10 women of reproductive-age. The current treatments are surgical and hormonal but have limitations, including the risk of recurrence, side effects, contraceptive action for women who desire pregnancy, and cost. New treatments include gonadotropin-releasing hormone analogues, selective progesterone (or estrogen) receptor modulators, aromatase inhibitors, immunomodulators, and antiangiogenic agents. Further research is needed into central sensitization, local neurogenesis, and the genetics of endometriosis to identify additional treatment targets. A wider range of medical options allows for the possibility of precision health and a more personalized treatment approach for women with endometriosis.

Aromatase Inhibitorsmfor endometriosis

2) Agarwal, Sanjay K., and Warren G. Foster. “Reduction in Endometrioma Size with Three Months of Aromatase Inhibition and Progestin Add-Back.” BioMed Research International 2015 (2015).

The purpose of this study was to assess the impact of 3 months of aromatase inhibition together with progestin add-back on ovarian endometrioma size. This prospective cohort study was performed at University Medical Center (UC San Diego). Women trying to conceive were excluded. After informed consent, all women were treated with the aromatase inhibitor letrozole (5 mg/d) with norethindrone acetate (5 mg/d) add-back for 3 months. Pre- and posttreatment assessments of endometrioma sizes were performed by ultrasound. The impact of treatment on pain was determined using the patient assessed endpoints of the Biberoglu and Behrman scale. These included assessing dysmenorrhea, dyspareunia, and nonmenstrual pelvic pain each on a scale from 0 to 3. The primary endpoint of this study was the change in ultrasound documented endometrioma size. Fourteen endometriomas in 8 consecutive women were treated for 3 m. Mean endometrioma diameter decreased 50% from 4.6 ± 1.6 cm to 2.3 ± 1.6 cm (mean ± SD). This represents a 75% decrease in endometrioma volume. Endometriosis symptoms of dysmenorrhea, dyspareunia, and nonmenstrual pelvic pain also improved with treatment. In conclusion, a 3-month course of high dose aromatase inhibition with progestin add-back significantly reduces ovarian endometrioma size and warrants further investigation.

Pathogenesis

3) Suardika, Anom, and Tjokorda Gede Astawa Pemayun. “New insights on the pathogenesis of endometriosis and novel non-surgical therapies.” Journal of the Turkish German Gynecological Association 19.3 (2018): 158.

Dienogest (DNG) is an oral progestin that has been recognized as single-drug therapy for endometriosis in Europe, Japan, Australia and Singapore (26,27). DNG is a 19-nortestosterone derivative with the advantage of short plasma half-life, strong progestin effect on endometrium, high bioavailability, anti-androgenic activity, and moderate gonadotropin secretion inhibition

The most important factor in the pathophysiology of endometriosis is the estrogen hormonal dysregulation and progesterone resistance.

DNG 2 mg/day has been shown to significantly inhibit the expression of genes and proteins associated with aromatase and cyclooxygenase (COX)-2, as well as prostaglandin E2 (PGE2) production (30,31).

Provision of long-term DNG has been proven to be effective, safe, tolerable, as well as low incidence of adverse events and drop-out rates (26,33). DNG administration, when compared to GnRH agonists, provides a similar improvement in the intensity of complaints, but lower decrease in estrogen level or negative impact on bone mass (26). DNG can be tolerated in long-term administration due to negligible antiestrogenic, glucocorticoid, and mineralocorticoids effects (26,29). The most frequent side effects are breast pain (4.2%), nausea (3.0%), and irritability (2,4%) (27,34).

AIs when combined with progestogen, COC, or GnRH agonist significantly decrease endometriotic pain intensity, thereby improving patient’s quality of life. AI is superior in preventing postoperative recurrence when compared to GnRH or Danazol, within 6 months period (40,41).

The recommended daily dose is 1 mg for anastrozole, 2.5 mg for letrozole and 25 mg for exemestane, with the lowest decrease in E2 levels caused by exemestane (52-72%) (39).

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Gluten Free !!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!

Going gluten-free significantly slashed endometriosis pain!

HCG- 1 to 2 intramuscular injections of 1500 to 5000 IU HCG per week for a period of 3-12 months.

4) The Hidden HCG breakthrough — totally eliminate or control excruciating endometriosis! Oct 13, 2014 | Dr. Jonathan V. Wright’s Articles

5) Wien Klin Wochenschr. 2004 Dec 30;116(24):839-43.

Systemic HCG treatment in patients with endometriosis: a new perspective for a painful disease. Huber AV1, Huber JC, Kolbus A, Imhof M, Nagele F, Loizou D, Kaufmann U, Singer CF.

Endometriosis is characterized by the presence of endometrium-like tissue outside the uterus. This condition causes painful periods, chronic pelvic pain, subfertility and a profound reduction in quality of life, especially during women’s reproductive years. Currently available medical therapies offer comparatively little therapeutic benefit and are often burdened by considerable side effects. However, since clinical evidence shows that pregnancy leads to alleviation of endometriotic symptoms, we have for the first time examined the effect of human chorionic gonadotrophin (HCG) injections on symptoms such as dysmenorrhea and pelvic pain.

PATIENTS AND METHODS:Thirty-one patients with histologically verified endometriosis refractory to therapy received 1 to 2 intramuscular injections of 1500 to 5000 IU HCG per week for a period of 3-12 months. A QoL questionnaire and the visual analog pain intensity scale (VAS) were used to evaluate quality of life and pain intensity, respectively, before and after three months of treatment.

RESULTS:Three months of HCG therapy led to a highly significant reduction of endometriosis-related pain (p

CONCLUSIONS:HCG injections lead to significant and clinically relevant reduction in pain intensity and to greatly improved quality of life in women with therapy-refractory endometriosis. The remarkable clinical effect of parenteral HCG in our study will have to be confirmed in additional trials but clearly indicates an extremely promising new perspective in the treatment of endometriosis.

6) Fertil Steril. 2007 Oct;88(4 Suppl):1232-9. Epub 2007 Jun 11.

Effect of highly purified human chorionic gonadotropin preparations on the gene expression signature of stromal cells derived from endometriotic lesions: potential mechanisms for the therapeutic effect of human chorionic gonadotropin in vivo.

Huber A1, Hudelist G, Knöfler M, Saleh L, Huber JC, Singer CF.

To investigate alterations in the overall gene expression profile of endometriosis-derived stroma with increasing concentrations of hCG by using the Affymetrix GeneChip U133 Set.

DESIGN:In vitro study.

SETTING:Academic research institution.

PATIENT(S):Women undergoing diagnostic laparoscopic surgery for endometriosis.

INTERVENTION(S):Increasing concentrations of hCG, added to fibroblast monocultures from endometriotic lesions.

RESULT(S):We have found that hCG concentrations of 0.1 U/mL and higher lead to a dose-dependent increase in the expression of 68 genes. Most of the up-regulated genes encoded proteins that are involved in cell adhesion, intercellular communication, extracellular matrix (ECM) remodeling, apoptosis, and inflammation. We then incubated stromal monocultures from nine patients treated with and without 50 U/mL of hCG and performed reverse transcriptase-polymerase chain reaction (RT-PCR) for selected, highly up-regulated genes to validate our DNA array findings and to confirm that the alterations in the gene expression signature are exemplary of patients with endometriosis.

CONCLUSION(S):We have shown that hCG induces dose-dependent alterations in the gene expression profile of stromal cells obtained from endometriotic lesions and have, for the first time, identified potential mechanisms by which hCG might exert its therapeutic effect on endometriotic lesions.

7) free pdf

Huber, A. V., et al. “Human chorionic gonadotrophin attenuates NF-κ B activation and cytokine expression of endometriotic stromal cells.” MHR: Basic science of reproductive medicine 13.8 (2007): 595-604.

Recently, a clinical study provided evidence that treatment of endometriotic women with human chorionic gonadotrophin (hCG) alleviates disease-related pain and sleeplessness suggesting therapeutic effects of the hormone. Since endometriosis is associated with aberrant concentrations of inflammatory mediators in the peritoneal fluid, we investigated whether hCG may affect cytokine-dependent activation of the key-regulatory transcription factor NF-kappaB and expression of two nuclear factor kappa B (NF-kappaB)-inducible genes, tumour necrosing factor (TNF-alpha) and interleukin (IL)-1beta, in stromal cells isolated from ectopic endometriotic tissues. Electrophoretic mobility shift assay revealed that treatment of these cultures with the urinary preparation hCG-A suppressed TNF-alpha- or IL-1beta-induced NF-kappaB DNA-binding activity, whereas another urinary hCG preparation (hCG-B) was less effective. Recombinant alpha-hCG or epidermal growth factor (EGF), a contaminant of some urinary hCG preparations, did not alter cytokine-dependent NF-kappaB activation. Immunofluorescene of its p65 subunit revealed that pre-incubation with hCG-A strongly decreased TNF-alpha-dependent nuclear expression of NF-kappaB. Accordingly, hCG-A diminished IL-1beta-induced TNF-alpha transcript levels and protein release measured by quantitative real-time PCR and enzyme-linked immunosorbent assay. The hormone also attenuated TNF-alpha-dependent mRNA expression of IL-1beta. Western blot analyses revealed that hCG-A impaired TNF-alpha-mediated phosphorylation and degradation of the inhibitor I kappa B alpha suggesting that the hormone may reduce nuclear import of NF-kappaB by stabilizing its inhibitor. The data suggest that hCG attenuates inflammation-dependent NF-kappaB activation and cytokine expression that could provide one explanation for the beneficial role of the hormone in endometriotic patients.

8) Rahman, Nafis A., and C. V. Rao. “Recent progress in luteinizing hormone/human chorionic gonadotrophin hormone research.” Molecular human reproduction 15.11 (2009): 703-711. Recent progress in luteinizing hormone human chorionic gonadotrophin Rahman Nafis Hum Mol Repro 2009

statins for endometriosis

9) Biol Reprod. 2006 Jul;75(1):107-11. Epub 2006 Mar 29.

Statins inhibit growth of human endometrial stromal cells independently of cholesterol availability. Piotrowski PC1, Kwintkiewicz J, Rzepczynska IJ, Seval Y, Cakmak H, Arici A, Duleba AJ.

Endometriosis is characterized by ectopic growth of endometrial tissues. Statins, inhibitors of 3-hydroxy-3methylglutaryl-coenzyme A reductase (HMGCR), have been shown to decrease proliferation of several mesenchymal tissues. Actions of statins may be related to decreased availability of cholesterol as well as intermediate metabolites of the mevalonate pathway downstream of HMGCR. This study was designed to evaluate effects of statins on growth of endometrial stromal cells and to investigate mechanisms of these effects. Human endometrial stromal cells were cultured in the absence and in the presence of serum and with or without mevastatin and simvastatin. DNA synthesis and viable cell numbers were determined. Effects of statins were also evaluated in the presence of mevalonate and squalene. Furthermore, effects on phosphorylation of mitogen-activated protein kinase 3/1 (MAPK3/1) (also known as extracellular signal-regulated kinase [ERK1/2]) were determined. Mevastatin and simvastatin induced a concentration-dependent inhibition of DNA synthesis and viable cell count in chemically defined media and in the presence of serum. Mevalonate, but not squalene, abrogated inhibitory effects of statins on cell proliferation. Statins inhibited MAPK3/1 phosphorylation. This is the first study demonstrating that statins inhibit growth of endometrial stromal cells. This effect is also demonstrable in the presence of a supply of cholesterol and may be related to decreased activation of MAPK3/1. The present observations may be relevant to potential therapeutic use of statins in conditions such as endometriosis.

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this study is that it is the first to evaluate use of simvastatin to relieve endometriotic pains.

10) Almassinokiani, Fariba, et al. “Effects of simvastatin in prevention of pain recurrences after surgery for endometriosis.” Medical science monitor: international medical journal of experimental and clinical research 19 (2013): 534.

prescribed simvastatin (film-coated tablet simvaHEXAL, 20 mg daily for 4 months)

Statin affects the growth of endometriotic tissues by inhibiting angiogenesis [8,16]. The severity of dyspareunia, dysmenorrhea, and pelvic pain before and after treatment were not significantly different between the 2 groups (Table 4). However, after treatment, the severity of dyspareunia, dysmenorrhea, and pelvic pain in the 2 groups was significantly reduced and the difference between before and after treatment in 3 parameters in each group was significant (Table 5). None of the patients showed adverse effects of simvastatin and all continued medical treatment for 4 months. Three of the patients in the simvastatin group became pregnant 4 months after surgery. All of them had mild endometriosis. To compare efficacy of simvastatin with GnRHa (Decapeptyl 3.75 mg) on endometriosis-related pains following surgery for endometriosis.

Material/Methods: Sixty women with pelvic endometriosis, after laparoscopic diagnosis and conservative laparoscopic surgery, were treated with either simvastatin (n=30) for 16 weeks or Decapeptyl (n=30) every 4 weeks for 4 doses.

Results: Using VAS, the score of dyspareunia, dysmenorrhea, and pelvic pain 6 months after laparoscopic surgery declined significantly in both groups (p=0.001), but the difference between results of the 2 groups was not significant (p>0.05).

Conclusions: Both treatment modalities showed comparable effectiveness in the treatment of pains related to endometriosis.

11) Nasu, Kaei, et al. “Simvastatin inhibits the proliferation and the contractility of human endometriotic stromal cells: a promising agent for the treatment of endometriosis.” Fertility and sterility 92.6 (2009): 2097-2099.

12) Yilmaz, Bulent, et al. “Atorvastatin causes regression of endometriotic implants in a rat model.” Reproductive biomedicine online 20.2 (2010): 291-299.

13) Gynecol Endocrinol. 2017 Dec;33(12):923-927. Efficacy comparison of oral rosuvastatin versus oral progesterone and bevacizumab on regression of surgically endometriotic implants in rats.

Kebapcilar AG1, Ilhan TT1, Dursunoglu D2, Kebapcilar L3, Ipekci SH3, Baldane S3, Ucar MG1, Kirac CO3, Kurt K1, Celik C1.

This study hypothesizes that oral rosuvastatin, oral dienogest and intraperitoneal bevacizumab might improve endometriosis in randomly selected female Wistar albino rats with surgically endometriotic implants. Thirty female Wistar albino rats with surgically endometriotic implants were randomized into three treatment groups: oral rosuvastatin (20 mg kg/day; oral rosuvastatin group 1; n = 10), oral progesterone (dienogest group 2; n = 10) and intraperitoneal bevacizumab (2.5 mg/kg of single intraperitoneal injection of bevacizumab; bevacizumab group 3; n = 10), for 10 days. Post-treatment variables were compared. The oral rosuvastatin group showed higher reduction for the glandular epithelium and uterine vessels of histopathological scores values than the oral progesterone group (both, p 0.017). Endometrial thickness values and uterine volume values were more significantly reduced in the oral rosuvastatin group than the oral progesterone group (both, p 0.017). In conclusion, oral rosuvastatin and intraperitoneal injection of bevacizumab may cause more significant regression of surgically endometriotic implants in rats than oral progesterone medications.

14) Patel, Tushar R., and Siobhan A. Corbett. “Simvastatin suppresses LPS-induced Akt-phosphorylation in the human monocyte cell line THP-1.” Journal of Surgical Research 116.1 (2004): 116-120.

15) Hölschermann, Hans, et al. “Statins prevent NF-κB transactivation independently of the IKK-pathway in human endothelial cells.” Atherosclerosis 185.2 (2006): 240-245

16) Ahn, Kwang Seok, Gautam Sethi, and Bharat B. Aggarwal. “Simvastatin potentiates TNF-α-induced apoptosis through the down-regulation of NF-κB-dependent antiapoptotic gene products: role of IκBα kinase and TGF-β-activated kinase-1.” The Journal of Immunology 178.4 (2007): 2507-2516.

17) Chae, Young Kwang, et al. “Statins as anti-cancer therapy; Can we translate preclinical and epidemiologic data into clinical benefit?.” Discovery medicine 20.112 (2015): 413-427.

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Fenofibrate

18) Fertil Steril. 2009 Dec;92(6):2100-2. Fenofibrate causes regression of endometriotic implants: a rat model. Onalan G1, Zeyneloglu HB, Bayraktar N.

Fenofibrate -a peroxisome proliferator-activated receptor-a agonist- is an angiostatic agent that is commonly used in human liver diseases, therefore it may interfere with the angiogenetic process required for endometriosis. In a rat endometriosis model, we demonstrated that peritoneal implant areas and vascular endothelial growth factor levels in the peritoneal fluid were significantly decreased in high dose or low dose finofibrate and luprolide acetate treated groups compared to control.

19) Herington, Jennifer L., et al. “Development and Prevention of Postsurgical Adhesions in a Chimeric Mouse Model of Experimental Endometriosis.” Fertility and sterility 95.4 (2011): 1295.

To examine the impact of a recent surgery on development of endometriosis-related adhesions in a chimeric model and to determine the therapeutic efficacy of pioglitazone (PIO).

Design Human endometrial biopsies were maintained in estradiol (E) with or without PIO for 24 hrs prior to intraperitoneal injection into immunocompromised mice at multiple timepoints following peritoneal surgery. The presence and extent of adhesions was examined in animals relative to the initial establishment of experimental endometriosis.

Endometrial biopsies for experimental studies described herein were provided by normally cycling women without a medical history indicative of endometriosis or adhesions.

Examination of the development of endometriosis-related adhesions in an experimental model.

Results Without therapeutic intervention, injection of E-treated human endometrial tissue into mice near the time of peritoneal surgery resulted in multiple adhesions and extensive endometriotic-like disease. In contrast, PIO treatment reduced adhesive disease and experimental endometriosis related to surgical injury.

Conclusions The presence of human endometrial tissue fragments in the peritoneal cavity of mice with a recent surgical injury promoted development of both adhesive disease and experimental endometriosis. Targeting inflammation and angiogenesis with PIO therapy limited the development of postsurgical adhesions associated with ectopic endometrial growth.

20) Koltai, Tomas. “Fenofibrate in cancer: mechanisms involved in anticancer activity.” F1000 Research 4 (2015).

The main mechanisms of anti-cancer activity:

1) A nti-angiogenesis through down-regulation of Vascular Endothelial Growth Factor (VEGF), Vascular Endothelial Growth Factor Receptor (VEGFR) and Hypoxia Inducible factor-1 a (HIF-1a),

2) inhibition of endothelial cell migration

Apoptosis and cell cycle arrest mechanism include:

1) down-regulation of Nuclear Factor Kappa B (NF-kB) and Protein kinase B (Akt)

2) Decrease of cellular energy by impairing mitochondrial function

3) Growth impairment from down-regulation of Phospho-Inositol 3 Kinase (PI3K)/Akt axis and down-regulation of the p38 map kinase (MAPK) cascade.

Anti-metastatic activities of Fenofibrate:

1) Down-regulation of MCP-1 (monocyte chemotactic protein-1),

2) decreased Metalloprotease-9 (MMP-9) production,

3) weak down-regulation of adhesion molecules like E selectin, intercellular adhesion molecules (ICAM) and Vascular Endothelial Adhesion Molecules (VCAM)

4) decreased secretion of chemokines like Interleukin-6 (IL-6), and down-regulation of cyclin D-1.

21) video Kirk hamilton – Endometriosis…HCG, Melatonin and Gluten-Free Diet Help!

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22) https://www.ncbi.nlm.nih.gov/pubmed/2...

Eur J Obstet Gynecol Reprod Biol. 2017 Feb;209:61-66. doi: 10.1016/j.ejogrb.2016.05.032. Epub 2016 May 27.

Hormonal therapy for endometriosis: from molecular research to bedside.

Tosti C1, Biscione A1, Morgante G1, Bifulco G2, Luisi S1, Petraglia F3.

Author information

Abstract

Endometriotic lesions are associated with hormonal imbalance, including increased estrogen synthesis, metabolism and progesterone resistance. These hormonal changes cause increased proliferation, inflammation, pain and infertility. Hormonal imbalances are targets for treatment. Therapeutic strategies and innovations of hormonal drugs for endometriosis are increasing. Acting on estrogen receptors are hormonal drugs decreasing systemic and local estrogen synthesis (GnRH analogs, GnRH antagonists, Aromatase inhibitors) or estrogen activity (selective estrogen receptor modulators). The progesterone resistance is counteracted by progestins (Medroxyprogesterone acetate, Dienogest, Danazol, Levonorgestrel) or by Selective progesterone receptor modulators, a class of drugs under development. The future trend will be to define new drugs to use for prolonged period of time and with poor side effects considering endometriosis a chronic disease.

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23) Br J Pharmacol. 2006 Sep; 149(2): 137–144.

Rapamycin induces regression of endometriotic lesions by inhibiting neovascularization and cell proliferation M W Laschke,1,* A Elitzsch,1 C Scheuer,1 J H Holstein,1 B Vollmar,2 and M D Menger1

Rapamycin is a widely used drug with antifungal, immunosuppressant and antiangiogenic effects. Herein, we studied whether immunosuppressive doses of rapamycin are capable of influencing endometriotic lesions.

Experimental approach: We tested in vitro the potential of rapamycin to inhibit endothelial cell sprouting using the aortic ring assay and we further studied its effect on the expression of proliferating cell nuclear antigen (PCNA), apoptotic cell death-associated activated caspase-3 and vascular endothelial growth factor (VEGF) in cultured endometrial tissue fragments. In addition, we analyzed the drug in vivo after induction of endometriotic lesions by transplanting isolated endometrial fragments into the dorsal skinfold chamber of Syrian golden hamsters. Using intravital fluorescence microscopy, we repetitively analyzed angiogenesis, neovascularization and microcirculatory parameters over a time period of 14 days in rapamycin-treated animals and DMSO-treated controls.

24) Head, Sarah A., et al. “Antifungal drug itraconazole targets VDAC1 to modulate the AMPK/mTOR signaling axis in endothelial cells.” Proceedings of the National Academy of Sciences 112.52 (2015): E7276-E7285.

Itraconazole, a clinically used antifungal drug, was found to possess potent antiangiogenic and anticancer activity that is unique among the azole antifungals. Previous mechanistic studies have shown that itraconazole inhibits the mechanistic target of rapamycin (mTOR) signaling pathway, which is known to be a critical regulator of endothelial cell function and angiogenesis. However, the molecular target of itraconazole that mediates this activity has remained unknown. Here we identify the major target of itraconazole in endothelial cells as the mitochondrial protein voltage-dependent anion channel 1 (VDAC1), which regulates mitochondrial metabolism by controlling the passage of ions and small metabolites through the outer mitochondrial membrane. VDAC1 knockdown profoundly inhibits mTOR activity and cell proliferation in human umbilical vein cells (HUVEC), uncovering a previously unknown connection between VDAC1 and mTOR. Inhibition of VDAC1 by itraconazole disrupts mitochondrial metabolism, leading to an increase in the cellular AMP:ATP ratio and activation of the AMP-activated protein kinase (AMPK), an upstream regulator of mTOR. VDAC1-knockout cells are resistant to AMPK activation and mTOR inhibition by itraconazole, demonstrating that VDAC1 is the mediator of this activity. In addition, another known VDAC-targeting compound, erastin, also activates AMPK and inhibits mTOR and proliferation in HUVEC. VDAC1 thus represents a novel upstream regulator of mTOR signaling in endothelial cells and a promising target for the development of angiogenesis inhibitors.

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pioglitazone (PIO

https://www.ncbi.nlm.nih.gov/pmc/arti...

Herington, Jennifer L., et al. “Development and Prevention of Postsurgical Adhesions in a Chimeric Mouse Model of Experimental Endometriosis.” Fertility and sterility 95.4 (2011): 1295.

To examine the impact of a recent surgery on development of endometriosis-related adhesions in a chimeric model and to determine the therapeutic efficacy of pioglitazone (PIO).

Design

Human endometrial biopsies were maintained in estradiol (E) with or without PIO for 24 hrs prior to intraperitoneal injection into immunocompromised mice at multiple timepoints following peritoneal surgery. The presence and extent of adhesions was examined in animals relative to the initial establishment of experimental endometriosis.

Setting

Medical School Research Center

Patients Endometrial biopsies for experimental studies described herein were provided by normally cycling women without a medical history indicative of endometriosis or adhesions.

Examination of the development of endometriosis-related adhesions in an experimental model.

Results without therapeutic intervention, injection of E-treated human endometrial tissue into mice near the time of peritoneal surgery resulted in multiple adhesions and extensive endometriotic-like disease. In contrast, PIO treatment reduced adhesive disease and experimental endometriosis related to surgical injury.

Conclusions The presence of human endometrial tissue fragments in the peritoneal cavity of mice with a recent surgical injury promoted development of both adhesive disease and experimental endometriosis. Targeting inflammation and angiogenesis with PIO therapy limited the development of postsurgical adhesions associated with ectopic endometrial growth.

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https://www.ncbi.nlm.nih.gov/pubmed/2...

Eur J Obstet Gynecol Reprod Biol. 2017 Feb;209:61-66. doi: 10.1016/j.ejogrb.2016.05.032. Epub 2016 May 27.

Hormonal therapy for endometriosis: from molecular research to bedside.

Tosti C1, Biscione A1, Morgante G1, Bifulco G2, Luisi S1, Petraglia F3.

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Rapamycin – Itraconazole ?

https://www.ncbi.nlm.nih.gov/pmc/arti...

Br J Pharmacol. 2006 Sep; 149(2): 137–144.

Rapamycin induces regression of endometriotic lesions by inhibiting neovascularization and cell proliferation M W Laschke,1,* A Elitzsch,1 C Scheuer,1 J H Holstein,1 B Vollmar,2 and M D Menger1

Rapamycin is a widely used drug with antifungal, immunosuppressant and antiangiogenic effects. Herein, we studied whether immunosuppressive doses of rapamycin are capable of influencing endometriotic lesions.

Experimental approach: We tested in vitro the potential of rapamycin to inhibit endothelial cell sprouting using the aortic ring assay and we further studied its effect on the expression of proliferating cell nuclear antigen (PCNA), apoptotic cell death-associated activated caspase-3 and vascular endothelial growth factor (VEGF) in cultured endometrial tissue fragments. In addition, we analyzed the drug in vivo after induction of endometriotic lesions by transplanting isolated endometrial fragments into the dorsal skinfold chamber of Syrian golden hamsters. Using intravital fluorescence microscopy, we repetitively analyzed angiogenesis, neovascularization and microcirculatory parameters over a time period of 14 days in rapamycin-treated animals and DMSO-treated controls.

Itraconazole

https://www.pnas.org/content/112/52/E...

Itraconazole, a clinically used antifungal drug, was found to possess potent antiangiogenic and anticancer activity that is unique among the azole antifungals. Previous mechanistic studies have shown that itraconazole inhibits the mechanistic target of rapamycin (mTOR) signaling pathway, which is known to be a critical regulator of endothelial cell function and angiogenesis. However, the molecular target of itraconazole that mediates this activity has remained unknown. Here we identify the major target of itraconazole in endothelial cells as the mitochondrial protein voltage-dependent anion channel 1 (VDAC1), which regulates mitochondrial metabolism by controlling the passage of ions and small metabolites through the outer mitochondrial membrane. VDAC1 knockdown profoundly inhibits mTOR activity and cell proliferation in human umbilical vein cells (HUVEC), uncovering a previously unknown connection between VDAC1 and mTOR. Inhibition of VDAC1 by itraconazole disrupts mitochondrial metabolism, leading to an increase in the cellular AMP:ATP ratio and activation of the AMP-activated protein kinase (AMPK), an upstream regulator of mTOR. VDAC1-knockout cells are resistant to AMPK activation and mTOR inhibition by itraconazole, demonstrating that VDAC1 is the mediator of this activity. In addition, another known VDAC-targeting compound, erastin, also activates AMPK and inhibits mTOR and proliferation in HUVEC. VDAC1 thus represents a novel upstream regulator of mTOR signaling in endothelial cells and a promising target for the development of angiogenesis inhibitors.

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Anti-angiogenic treatment

free pdf

https://academic.oup.com/humupd/artic...

Laschke, M. W., and M. D. Menger. “Anti-angiogenic treatment strategies for the therapy of endometriosis.” Human reproduction update 18.6 (2012): 682-702.

initiation of the disease by retrograde menstruation of highly angiogenic endometrial fragments into the peritoneal cavity. Based on these findings, endometriosis has been classified as a typical angiogenic disease, such as cancer, psoriasis or diabetic retinopathy (Healy et al., 1998).

Several studies report that COX-2 is also crucially involved in the pathogenesis of endometriosis. COX-2 over-expression is found in both endometriotic lesions and eutopic endometrium of patients with endometriosis when compared with controls

treatment with COX-2 inhibitors prevents the implantation of endometrium to ectopic sites and induces the regression of established endometriotic lesions

Dopamine agonists

A decade ago, Basu et al. (2001) made the interesting discovery that the neurotransmitter dopamine selectively inhibits the vascular permeabilizing and angiogenic activity of VEGF at non-toxic levels, revealing a new link between the nervous system and angiogenesis. This led to the idea to use dopamine agonists for anti-angiogenic therapy. In gynaecology, dopamine agonists, such as cabergoline, are currently used for the suppression of breast-feeding and treatment of hyperprolactinaemia (Gillam et al., 2006; Colao et al., 2007; Buhendwa et al., 2008). Importantly, cabergoline treatment during pregnancy does not increase the risk of spontaneous miscarriage, premature delivery or congenital abnormalities (Robert et al., 1996; Ricci et al., 2002).

cabergoline

Based on these reports, the Pellicer research group analysed the effect of cabergoline on growth and vascularization of endometriotic lesions in the nude mouse model (Novella-Maestre et al., 2009). They found that daily oral treatment with cabergoline over 14 days causes the regression of endometriotic lesions by suppression of cell proliferation and VEGF-mediated angiogenesis. They could further demonstrate that cabergoline treatment results in a significantly lower expression of VEGF and VEGFR-2 in endometriotic lesions (Novella-Maestre et al., 2010). Thus, they concluded that dopamine agonists may be successful in the treatment of peritoneal endometriosis. However, chronic cabergoline treatment is known to be associated with an increased incidence of cardiac valve regurgitation (Schade et al., 2007). Therefore, in an additional study they compared the efficacy of the non-ergot-derived dopamine agonist quinagolide with that of cabergoline in inhibiting angiogenesis and vascularization of endometriotic lesions (Delgado-Rosas et al., 2011). Because both compounds were equally effective, they decided to perform a clinical pilot study with quinagolide in hyperprolactinemic patients with endometriosis, who required a first surgical intervention and underwent a second-look laparoscopy (Gómez et al., 2011). Of interest, treatment with the dopamine agonist quinagolide induced a 70% reduction of endometriotic lesions, with 35% of lesions vanishing completely. Further histological analyses revealed that this was associated with a down-regulation of VEGF/VEGFR-2, pro-angiogenic cytokines and plasminogen activator inhibitor-1 within the lesions. These highly promising results and the beneficial side effect profile of quinagolide suggest that this compound should now be tested in larger clinical multicenter trials for its applicability in patients with endometriosis.

fenofibrate

PPAR agonists have been developed for the treatment of hypertrigliceridemia and type 2 diabetes mellitus in the form of fibrates and thiazolidinediones (Lalloyer and Staels, 2010).

Onalan et al. (2009) demonstrated for the first time in a rat model that treatment with the PPAR-α agonist fenofibrate causes regression of endometriotic lesions, which is associated with reduced VEGF levels in the peritoneal fluid.

Lebovic et al. (2007) demonstrated in the baboon endometriosis model that the size and overall number of endometriotic lesions is significantly reduced in animals treated with rosiglitazone and pioglitazone (Lebovic et al., 2010) when compared with placebo-treated controls.

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celecoxib

https://www.ncbi.nlm.nih.gov/pubmed/2...

Fertil Steril. 2011 Aug;96(2):428-33. The inhibitory effect of celecoxib and rosiglitazone on experimental endometriosis. Olivares C1, Ricci A, Bilotas M, Barañao RI, Meresman G.

To evaluate the effects of celecoxib and rosiglitazone on the implantation and growth of endometriotic-like lesions in a murine model of endometriosis.

DESIGN:Prospective experimental study.

SETTING:Animal research and laboratory facility.

ANIMAL(S):Two-month-old female BALB/c mice.

INTERVENTION(S):Surgically induced endometriosis in female BALB/C mice; 28 days of treatment with celecoxib, rosiglitazone, or their combination; counting, measuring, excising, and fixing lesions.

MAIN OUTCOME MEASURE(S):Immunohistochemical examination for proliferating cell nuclear antigen (PCNA), CD31, and CD34 to assess cell proliferation and vascularization, with the terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) technique for apoptosis evaluation.

RESULT(S):Celecoxib and the combined treatment (celecoxib and rosiglitazone) statistically significantly reduced the mean number of lesions established per mouse, and all treatments diminished the implant volume. In addition, cell proliferation within the implants was statistically significantly reduced, and apoptosis was statistically significantly enhanced by all treatments. Also, we found that all treatments diminished the vascularized area in the lesion.

CONCLUSION(S):These results are promising and reveal that celecoxib and rosiglitazone, combined or separately, have a beneficial effect on overall endometriotic growth.

curcumin

https://www.ncbi.nlm.nih.gov/pubmed/2...

Int J Mol Med. 2011 Jan;27(1):87-94. doi: 10.3892/ijmm.2010.552. Epub 2010 Nov 8.

Inhibitory effect of curcumin on angiogenesis in ectopic endometrium of rats with experimental endometriosis.Zhang Y1, Cao H, Hu YY, Wang H, Zhang CJ.

The aim of this study was to observe the inhibitory effect of curcumin on endometriosis (EMS) and to determine its influence on vascular endothelial growth factor (VEGF) and microvessel density (MVD) in eutopic and ectopic endometrium of experimental rats, thus exploring the pathogenesis of EMS offering more experimental evidence for the clinical use of curcumin. Forty-eight female virgin rats were subjected to autotransplantation of endometrium during the estrus stage. After four weeks, 8 rats were randomly sacrificed to confirm that the rat model was successful. The remaining rats were randomly divided into four groups. Three groups were intragastrically administered curcumin (50, 100 and 150 mg/kg), and the model group was intragastrically administered vehicle alone. All rats were treated daily for four continuous weeks and examined by histology and immunohistochemical staining for MVD of eutopic and ectopic endometrium. Our results revealed that the cubic capacity of focal tissue in gross appearance was high in the model group and dose-dependently diminished after treatment with curcumin (P

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Dipyridimole

Pathophysiology- platelet-derived endothelial growth factor

https://www.ncbi.nlm.nih.gov/pmc/arti...

Fertil Steril. 2012 Sep; 98(3): 10.1016/j.fertnstert.2012.06.029.

Pathogenesis and Pathophysiology of Endometriosis

Richard O. Burney, M.D., M.Sc.a and Linda C. Giudice, M.D., Ph.D.b

Evidence for VEGF as the prominent angiogenic factor is compelling. Other angiogenic factors implicated in disease pathophysiology include angiogenin (70), platelet-derived endothelial growth factor (71), and macrophage migration inhibitory factor (72).

dipyridimole – antiplatelet agents

https://academic.oup.com/jcem/article...

https://www.ncbi.nlm.nih.gov/pubmed/9...

J Clin Endocrinol Metab. 1999 Jan;84(1):359-62.

Expression of platelet-derived endothelial cell growth factor (PD-ECGF) related to angiogenesis in ovarian endometriosis.

Fujimoto J1, Sakaguchi H, Hirose R, Tamaya T.

Platelet-derived endothelial cell growth factor (PD-ECGF) is expressed in the lining epithelial cells of ovarian endometriomas, and in interstitial cells of the subepithelial area with angiogenesis. The expression of PD-ECGF persists in endometriotic endometrium during the menstrual cycle. This might suggest that PD-ECGF contributes to the growth of ovarian endometriomas via subepithelial angiogenesis independently of the sex steroidal milieu.

Published on May 19th, 2019 by
Jeffrey Dach MD

The post Fenofibrate for Endometriosis, Part Two appeared first on Jeffrey Dach MD.

Measles Outbreak Fake News

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Published on May 19, 2019 08:17

May 1, 2019

WaPo Says Anti-Vaxxers Are Dangerous Should be Arrested

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WaPo Says Anti-Vaxxers Are Dangerous Should be Arrested

by Jeffrey Dach MD

You may have noticed a recent article in the Washington Post by Juliette N. Kayyem entitled, “Anti-vaxxers are dangerous. Make them face isolation, fines, arrests.“(1)

My initial reaction was the article must have been written by a moron. However, my opinion changed when I discovered the author, Ms. Kayyem, graduated Harvard law school in 1995. So, it appears this article is a carefully crafted piece of pro-vaccine industry propaganda. In other words, a large pile of nonsense and misinformation masquerading as authoritative information. Propaganda pieces typically contain nonsense and blatant lies. That’s OK because the “Big Lie” becomes believable if repeated often enough. (Who Said That?) Let’s take a look at the main point and the most glaring falsehood in the article: “Anti-Vaxxers Are Dangerous.”

What is An Anti-Vaxxer ?

The catch word, “anti-vaxxer” has become popular in the vaccine industry propaganda machine as a pejorative term for children who have been vaccine injured, and whose mothers no longer vaccinate them. This is aptly described by Barbara Low Fisher in her article: “No Mercy for Mothers Or Their Vaccine Injured Children“(2)

The Big Lie: Unvaccinated Are Dangerous

The easiest way to demonstrate the Big Lie: “Unvaccinated are Dangerous”, is to ask the CDC, the US Government Center for Disease Control.

It is universally agreed those most susceptible to the ravages of infectious disease are the immuno-compromised, such as those undergoing bone marrow transplantation. If the “Unvaccinated Are A Danger”, then one would expect the CDC to advise keeping the unvaccinated away from the immunocompromised, those having bone marrow transplants. Quite to the contrary, the CDC says the exact opposite. The recently vaccinated, not the unvaccinated, must be kept away from the transplant ward.(3)

The CDC document, ”Guidelines for Preventing Opportunistic Infections Among Hematopoietic Stem Cell Transplant Recipients.” contains this quote.(3)

“Visitors who might have communicable infectious diseases (e.g., URIs, flu-like illnesses, recent exposure to communicable diseases, an active shingles rash whether covered or not, a VZV-like rash (note: VZV is Varcella, chickenpox) within 6 weeks of receiving a live-attenuated VZV vaccine, or a history of receiving an oral polio vaccine within the previous 3–6 weeks) should not be allowed in the HSCT center (note HSCT is hematopoetic stem cell transplant center) or allowed to have direct contact with HSCT recipients or candidates undergoing conditioning therapy (AII).”(3)

Not sure you want to believe the CDC ? Instead, lets ask the University of Kentucky Transplant Service (4). Are the unvaccinated a danger? and should they be kept away from the transplant ward? Again, they say the exact opposite, adults and children who are recently vaccinated with the chickenpox or polio vaccine are a danger and should be kept away from immunocompromised transplant patients.

Still Dont Believe it? Maybe the University of Kentucky is an exception ? All transplant wards across the nation follow the American Society for Blood and Bone Marrow Transplantation Guidelines. (5) What do they say? Are the unvaccinated a danger to be kept from visiting the transplant ward? No, again they say quite the opposite. Those who have been recently vaccinated are a danger. Nowhere in this document do they say the unvaccinated are a danger. Quite to the contrary they say those recently vaccinated with the following vaccinations are a danger to the transplant ward: MMR (measles mumps rubella) Polio vaccine (OPV), Varicella Vaccine, Rotavirus vaccine, Influenza Vaccine (LAIV).(5)

The reality is that healthy unvaccinated individuals are NOT DANGEROUS, and are allowed visitation rights on the transplant wards across the country. It is the recently vaccinated who are “dangerous’ and are restricted from visiting the transplant ward.

The Unvaccinated Are Causing the Measles Outbreaks

Another BIG Lie in this Washington Post article by Juliette N. Kayyem is the blame for the recent measles outbreak falls squarely on the unvaccinated. For this reason, the unvaccinated should be branded as criminals to be arrested, found guilty and sent to prison. For the moment lets ignore the obvious contrary argument that persecuting the unvaccinated like this is a violation of just about every form of national and international human rights and civil liberties laws you can think of.

Measles Outbreaks Are Caused by the Vaccine Program Itself

Lets take a look at what Dr Levy in 1984 J Epidemiology has to say about this in his article: “The future of measles in highly immunized populations.”(6) Dr Levy is not alone in stating the obvious. Because of limitations and failures in the measles vaccine program ( i.e. primary and secondary vaccine failure), we are creating a larger population of susceptible individuals, than before the vaccine era. (6) Dr Levy is saying the measles vaccine program itself is creating a larger population of people susceptible to contracting measles, and this is the reason we are seeing periodic measles outbreaks which are predicted to increase.

Dr Levy says:

“despite short-term success in eliminating the disease (measles), long-range projections demonstrate that the proportion of susceptibles in the year 2050 may be greater than in the prevaccine era. Present vaccine technology and public health policy must be altered to deal with this eventuality.”(6)

What Dr Levy is saying is that the unvaccinated are NOT to blame for periodic recurrent measles outbreaks. We will be seeing more and more of these outbreaks as a result of primary and secondary vaccine failure. This is discussed in more detail in my previous article.

Conclusion: Pro Vaccine Industry Propaganda has reached a new extreme which threatens to label the unvaccinated as criminals to be arrested and sent to prison. In case you haven’t noticed, its official, you are now living in a police state.

Push Back by Rep Daryl D. Metcalfe Pennsylvania

At least one Pennsylvania congressman, Rep. Daryl D. Metcalfe, R-Cranberry, is introducing House Bill 286, also known as the Informed Consent Protection Act : watch this video of the News Conference :

Articles with Related Interest:

GMO Food and Forced Vaccination Its a Great Country

Aluminum in Vaccines Cause Autism

Which is Greater threat Measles or Measles Vaccine?

Measles and Somalis in Minnesota

Financial Kickbacks to Pediatricians is Illegal and Harms Children

HPV Vaccine the Greatest Scandal of Our Time

Italy Overturns Mandatory Vaccination

Jeffrey Dach MD

7450 Griffin Road

Suite 180/190

Davie, Florida 33314

954-792-4663

Header Featured Image Courtesy of Wikipedia:in the public domain.

Links and references

1) Anti-vaxxers are dangerous. Make them face isolation, fines, arrests.

Juliette N. Kayyem Wasington Post Harvard Law School with a Juris Doctor degree in 1995.

We are viewing the measles outbreak though a public health lens. We need to change our orientation. This is a public safety crisis and hopes for people to “get the shot” are well past the pretty please stage. My latest for the Washington Post

In the same way we have created sex-offenders lists to protect our children, communities can inventory families that choose not to be vaccinated, notifying employers of these parents as well as neighbors who may choose not to expose their children.

2) No Mercy for Mothers Or Their Vaccine Injured Children

by Barbara Loe Fisher Published April 25, 2019 | Opinion

3) CDC Guidelines for Preventing Opportunistic Infections Among Hematopoietic Stem Cell Transplant Recipients

Recommendations of CDC, the Infectious Disease Society of America, and the American Society of Blood and Marrow Transplantation

HSCT Center Visitors

Visitors who might have communicable infectious diseases (e.g., URIs, flu-like illnesses, recent exposure to communicable diseases, an active shingles rash whether covered or not, a VZV-like rash within 6 weeks of receiving a live-attenuated VZV vaccine, or a history of receiving an oral polio vaccine within the previous 3–6 weeks) should not be allowed in the HSCT center or allowed to have direct contact with HSCT recipients or candidates undergoing conditioning therapy (AII).

4) Univ Kentucky Visiting Patients on the Transplant Unit 2012

University of Kentucky Markey Center Patient Care Standards Chapter 4: Visiting Patients on the Transplant Unit Reviewed May 2012 Page 1 of 3 Chapter Four: Visiting Patients on the Transplant Unit Purpose: To provide visitation guidelines which are designed to minimize the risk of transmission of bacterial, fungal, viral, and other infectious organisms from visitors to patients in the transplant unit.

Allowed Visitors:

1. A patient’s nurse will assess all visitors for signs and symptoms of infectious diseases or organisms.

2.Anyone with evidence of even a mild communicable illness or infection, or who has been exposed to one, will not be allowed to visit patients.

3.Adults who meet the following requirements:

a)Have not received a live polio vaccine in the previous 3 months

b) Have not received live chicken pox vaccine in the previous 2 weeks

c) Have not been exposed to chicken pox in the previous 4 weeks

d) Do not have a fever, cold of any sort, cough, sneezing, conjunctivitis, sore throat, ear infection, wheezing, cold sores, or any skin rash.e)Have not been exposed to TB

f)Do not have shingles

4.Children who meet the following requirements:

a)Must be at least 10 years of age or receive special permission from staff

b) Children must be under the direct supervision of a responsible adult at all times.The responsible adult must not be the patient.

c) Have not received a live polio vaccine in the previous 3 months

d) Have not received live chicken pox vaccine in the previous 2 weeks

e) Have not been exposed to chicken pox in the previous 4 weeks

f) Do not have a fever, cold of any sort, cough, sneezing, conjunctivitis, sore throat, ear infection, wheezing, cold sores, or any skin rash.g)Have not been exposed to TB

h) Do not have shinglesi) During the RSV/Flu season (December –March) children less than 10 years old may not visit patients in the transplant unit

5) Amer Soc Blood Bone Marrow Transplantation Guidelines for Preventing Infectious Complications

American Society for Blood and Bone marrow transplantation GUIDELINES Guidelines for Preventing Infectious Complications among Hematopoietic Cell Transplantation Recipients:A Global Perspective Marcie Tomblyn, Tom Chiller, Hermann Einsele, Ronald Gress, Kent Sepkowitz, Jan Storek,John R. Wingard, Jo-Anne H. Young, Michael A. BoeckhBiol Blood Marrow Transplant 15: 1143-1238 (2009)Ó2009 American Society for Blood and Marrow Transplantation

Infants and children who have recently received the OPV vaccine should be excluded from visiting the HCT unit for 4 to 6 weeks after receipt of vaccine to minimize the risk of transmission and vaccine-associated paralytic poliomyelitis among HCT recipients (AII)[734]

Until further data on the risks of transmission of vaccine virus become available,HCT units may wish to exclude infants who have re-cently received rotavirus vaccine from visiting for 2to 4 weeks after receiving a vaccine dose (CIII).

Health care center personnel and HCT center visitors who receive LAIV Live-attenuated influenza vaccine (LAIV) instead of TIV shouldavoid contact with severely immunosuppressed per-sons for 7 days after vaccination (CIII)[307]

However, HCT centers should exclude visitors who develop a varicella- or zoster-like rash aftervaccination (AIII). If a household member developsa varicella or zoster-like rash after vaccination, closecontact with the HCT recipient should be avoidedand affected areas should be covered (AIII).

Individuals who experience a vaccine-associatedrash within 1 month after varicella vaccinationshould be excluded from visiting the HCT centerand should avoid close contact with HCT recipientsin the home setting (BIII).

Measles, mumps, rubella (MMR) vaccine (AIII):Household members should receive age-appropri-ate MMR vaccination as recommended. However,vaccine recipients who develop a fever and/or rash postvaccination should be excluded from visiting the HCT center while symptomatic and should avoid close contact with HCT recipients in the home setting (BIII)

6) Am J Epidemiol. 1984 Jul;120(1):39-48.

The future of measles in highly immunized populations. A modeling approach. Levy DL.

Little is known about how an intensive measles elimination program changes the overall immune status of the population. A computer model was created to study the effect of the measles elimination program in the United States on the number of susceptibles in the population. The simulation reveals that in the prevaccine era, approximately 10.6% of the population was susceptible to measles, most of whom were children less than 10 years of age. With the institution of the measles immunization program, the proportion of susceptibles in the population fell to 3.1% from 1978 through 1981, but then began to rise by approximately 0.1% per year to reach about 10.9% in the year 2050. The susceptibles at this time were distributed evenly throughout all age groups. The model did not consider the potential effect of waning immunity. The results of this study suggest that measles elimination in the United States has been achieved by an effective immunization program aimed at young susceptibles combined with a highly, naturally immunized adult population. However, despite short-term success in eliminating the disease, long-range projections demonstrate that the proportion of susceptibles in the year 2050 may be greater than in the prevaccine era. Present vaccine technology and public health policy must be altered to deal with this eventuality.

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Link to this Article

Published on May 1st, 2019 by
Jeffrey Dach MD

The post WaPo Says Anti-Vaxxers Are Dangerous Should be Arrested appeared first on Jeffrey Dach MD.

Ann Nicole Smith and Hypothyroidism

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Published on May 01, 2019 05:50

April 14, 2019

Gigi Hadid and Hashimotos Autoimmune Thyroiditis

[image error]

Gigi Hadid and Hashimotos Autoimmune Thyroiditis by Jeffrey Dach MD

Gigi Hadid is a supermodel celebrity who spends her day doing photo shoots for high end magazine covers. One day she discovered for no obvious reason, she was gaining weight and looked “puffy”. Her skin seemed to change as well, becoming thick and coarse, no longer soft and smooth. Her previously shiny thick hair became thin, dry and brittle.

[image error]Needless to say, Gigi was very concerned. After all, this could affect her modeling career. Shortly after, Gigi announced she has Hashimotos Auto-Immune Thyroid Disease, and the unwanted changes in her face and body were attributed to a low thyroid condition caused by thyroid disease. Fortunately for Gigi, and others like her, modern medicine has thyroid pills, which restores Gigi’s appearance and saves her modeling career. Thank goodness for thyroid hormone pills. The puffy face, thickened skin, hair loss all promptly resolve with thyroid hormone replacement. Link to this article.

Myxedema of the Skin

The skin changes associated with Hashimotos thyroid disease are due to a condition called “Myxedema” in which the skin is infiltrated by a gelatinous substance causing thickening of the skin. The photos below are illustrative.

Myxedema Before and After Treatment with Thyroid Hormone

[image error]

The above image: Note “Puffy ” appearance of face typical for Myxedema (left image) which resolves completely after treatment with thyroid hormone (right image). Images from Popular Science Monthly 1897 in public domain courtesy of wikimedia commons.

Conclusion: Whether or not you happen to be a high priced celebrity, the unwanted skin changes called “Myxedema” from thyroid disease can be reversed by the judicious use of thyroid hormone medication.

Link to this article

Jeffrey Dach MD

7450 Griffin Road Suite 180/190

Davie, Florida 33314

954-792-4663

For articles with related interest see:

Antonio Bianco TSH Inadequate for Thyroid Dosing

Chronic Fatigue, The Non-Mystery

Errors in Modern Thyroid Endocrinology

Finding the Right Thyroid Doctor

Hashimotos Thyroiditis, Manic Depression, Psychosis and Psychiatric Manifestations

Hashimotos Thyroiditis and Selenium Part One

Hashimotos, Selenium and Iodine, Part Two

Hashimotos Thyroid Disease and Molecular Mimicry

Hashimotos Thyroiditis and Selenium Part One

Hashimotos Selenium and Iodine Part Two

Hashimotos and Iodine Part Three

Iodine and Bromine Detox With Unrefined Salt

Iodine and Unrefined Sea Salt Part two

Iodine and Hashimotos Thyroid Disease

Low Thyroid Hashimotos and Pregnancy

New Study Shows Natural Thyroid is Better

Paradigm Shift from Levothyroxine to Combination T3 T4

Production of Thyroid Hormone

Myo-Inositol for PCOS and Hashimotos

Selenium and the Thyroid More Good News

TSH Suppression Benefits and Adverse Effects

Unexplained Infertility Linked to Low Thyroid Function

Which Thyroid is Best, Natural Synthetic or Combination?

Why Natural Thyroid is Better than Synthetic Part One

Why Natural Thyroid is Better Part Two

Links and References:

Images of Gigi Hadid Courtesy of Wikimedia commons public domain PIC1 and PIC2.

1) Gigi Hadid on How Her Health Has Affected Her Body: “If I Could Choose, I Would Have My Ass Back”

7:57 AM PDT 4/11/2018 by Sam Reed

The supermodel reflects on how her shape has transformed following a diagnosis of Hashimoto’s disease, an autoimmune disorder.

2) Gigi Hadid Slams Body Shamers by Revealing She Suffers From Thyroid Disease FEBRUARY 12, 2018 12:59 PM by BROOKE BOBB

On Sunday, Gigi Hadid sent out a series of tweets aimed at the social media communities who have been bashing her for being too thin (this, after she was shamed for being “too fat” as a teenager starting off in the business). She wrote: “For those of you so determined to come up with why my body has changed over the years, you may not know that when I started at 17, I was not yet diagnosed with Hashimoto’s disease; those of you who called me ‘too big for the industry’ were seeing inflammation and water retention due to that.”

3) Gigi Hadid Says Hashimoto’s Disease Changed Her Body

She slammed critics of her size on Twitter.

By Korin Miller Feb 12, 2018

Gigi Hadid put her body-shamers to, well, shame on Sunday in a series of tweets addressing speculation about her weight.

“For those of you so determined to come up w why my body has changed over the years, you may not know that when I started @ 17 I was not yet diagnosed w/Hashimoto’s disease,” Gigi wrote. “Those of u who called me ‘too big for the industry’ were seeing inflammation & water retention due to that.” She said that since her diagnosis, she’s been taking medication for her condition and has worked to adopt a healthier lifestyle. ”

Gigi Hadid first revealed her Hashimoto’s diagnosis in December 2016. “My metabolism actually changed like crazy this year,” Gigi revealed at Reebok’s #PerfectNever event in New York City, according to People. “I have Hashimoto’s disease. It’s a thyroid disease, and it’s now been two years since taking the medication for it.”

Her disease played a role in how she prepared for the Victoria’s Secret Fashion Show. “I didn’t want to lose any more weight, she said. “I just want to have muscles in the right place, and if my butt can get a little perkier, then that’s good.”

4) 13 Celebs Who’ve Been Super-Honest About Their Thyroid Conditions

“I woke up with a giant bulge in my neck the size of a golf ball.”

5) The little-known disease that affects millions of women

Supermodel Gigi Hadid has been busy on Twitter setting the record straight about her apparent weight loss and her experience with a little-known autoimmune disorder called Hashimoto’s disease.

“For those of you so determined to come up with why my body has changed over the years, you may not know that when I started at 17 I was not yet diagnosed with Hashimoto’s disease, those of you who called me ‘too big for the industry’ were seeing inflammation and water retention due to that,” she tweeted in February.

===============================

6) Michelle Madrigal: I have Hashimoto’s disease

ABS-CBN News

Posted at May 11 2018 06:01 PM | Updated as of May 11 2018 08:40 PM

MANILA — Michelle Madrigal is on a journey of “healing naturally” after she was recently diagnosed with Hashimoto’s disease, the former Kapamilya actress revealed Thursday.

On Instagram, the 29-year-old actress explained to her followers the illness she has to battle, “along with other millions of young and older women who suffer from it.”

She wrote: “It is an autoimmune disorder that can cause hypothyroidism, or underactive thyroid. It means that my immune system makes antibodies that attack the thyroid gland. The thyroid becomes damaged and can’t make enough thyroid hormones.”

7) Gina Rodriguez on Hashimoto’s, Equal Pay, and Learning to Fight For Herself

Rodriguez, 33, has Hashimoto’s disease, an autoimmune condition that wages war on the thyroid gland, which produces hormones that influence how your body uses energy. Hashimoto’s can lead to an underactive thyroid that doesn’t produce enough of these hormones, and symptoms can be devastating and wide-ranging, including fatigue, joint pain, memory issues, and weight gain, to name a few.

8) Hashimoto’s Disease, Gigi Hadid, and Me What you need to know about the disease that is affecting one of America’s top models … and me. By Maggie May Ethridge | January 2, 2017 | 2:30pm

Photo by Dimitrios Kambouris/Getty

9) Hashimoto’s Disease, Gigi Hadid, Hotze Wellness

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April 8, 2019

Does Cholesterol Cause Coronary Artery Disease ?

[image error] Does Cholesterol Cause Coronary Artery Disease ?

Part Two, for part one click here.

A Reappraisal of the Lipid Hypothesis

In the Sept 2018 Amer J Med, Dr Robert Dubroff points out an inconvenient truth. Since clinical trial regulations were tightened in 2004, there have been 29 major randomized controlled trials of cholesterol reduction. (1) Only 2 of 29 show a mortality benefit, and 66% of the studies show no cardiovascular benefit at all. (1) Dr Dubroff says:

“only 2 of these 29 studies reported a mortality benefit, while nearly two-thirds reported no cardiovascular benefit at all. These unfavorable outcomes and inconsistent results suggest that the lipid hypothesis has failed the test of time…. Three decades of RCTs (randomized controlled trials), however, have yielded inconsistent and contradictory results. We must acknowledge these anomalies and either modify or reject the lipid hypothesis…. the pathogenesis of atherosclerosis is far more complex than originally thought.“(1) End quote

Jeffrey Dach MD

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Articles with related interest:

LDL Particle Sizeand Number What Gives ?

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Header Image: Cholesterol Crystals in Synovial Fluid Courtesy of Wikimedia Commons.

Links and References:

1) DuBroff, Robert. “A Reappraisal of the Lipid Hypothesis” (2018). American Journal of Medicine, September 2018, Volume 131, Issue 9, Pages 993–997

The randomized controlled trial (RCT) is the gold standard for validating or rejecting a medical hypothesis. Initial proof of the lipid hypothesis came from some of the earliest RCTs of cholesterol reduction, such as the Coronary Primary Prevention Trial of cholestyramine and the first statin trials (Scandinavian Simvastatin Survival Study [4S], West of Scotland Coronary Prevention Study [WOSCOPS], and Cholesterol and Recurrent Events [CARE]).

More widespread trials over the next 20 years produced mixed results, however.2 Regrettably, some clinical trials prior to 2004 have been tainted by scandals that led to new clinical trial regulations intended to safeguard patients and lend credibility to subsequent trials.3, 4 The table summarizes 29 major RCTs of cholesterol reduction reported after the publication of these regulations (Table). Notably, only 2 of these 29 studies reported a mortality benefit, while nearly two-thirds reported no cardiovascular benefit at all. These unfavorable outcomes and inconsistent results suggest that the lipid hypothesis has failed the test of time. Alternatively, some have suggested that this lack of benefit could be due to inadequate intensity or duration of treatment, insufficiently powered studies, targeting LDL-C instead of apolipoprotein B, or perhaps these trials are attempting to lower LDL-C too late in the course of the disease.

Final Thoughts: LDL-C is considered the primary constituent of atherosclerotic plaque. Therefore, it stands to reason that lowering serum LDL-C should prevent cardiovascular disease. Three decades of RCTs, however, have yielded inconsistent and contradictory results. We must acknowledge these anomalies and either modify or reject the lipid hypothesis. Clearly, some individuals do benefit from lipid-modifying therapy. I believe the real question is how to identify them. Our current approach of focusing almost exclusively on lowering LDL-C for everyone does not consistently work, may result in unnecessary treatment of some healthy individuals, and likely reflects the fact that the pathogenesis of atherosclerosis is far more complex than originally thought. Our LDL-C-centric approach to cardiovascular disease prevention may have distracted us from investigating other pathophysiologic mechanisms and treatments. Last, we should not ignore the benefits of a healthy lifestyle. Although changing our patients’ lifestyle is more difficult than prescribing a pill, the benefits are far more robust.22

2) DuBroff, Robert. “Cholesterol paradox: a correlate does not a surrogate make.” BMJ Evidence-Based Medicine 22.1 (2017): 15-19.

Abstract

The global campaign to lower cholesterol by diet and drugs has failed to thwart the developing pandemic of coronary heart disease around the world. Some experts believe this failure is due to the explosive rise in obesity and diabetes, but it is equally plausible that the cholesterol hypothesis, which posits that lowering cholesterol prevents cardiovascular disease, is incorrect. The recently presented ACCELERATE trial dumbfounded many experts by failing to demonstrate any cardiovascular benefit of evacetrapib despite dramatically lowering low-density lipoprotein cholesterol and raising high-density lipoprotein cholesterol in high-risk patients with coronary disease. This clinical trial adds to a growing volume of knowledge that challenges the validity of the cholesterol hypothesis and the utility of cholesterol as a surrogate end point. Inadvertently, the cholesterol hypothesis may have even contributed to this pandemic. This perspective critically reviews this evidence and our reluctance to acknowledge contradictory information.

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April 5, 2019

Plant Based Diet Health Benefits for Coronary Artery Disease

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Plant Based Diet, Health Benefits for Coronary Artery Disease

by Jeffrey Dach MD

At the recent ICM meeting “Matters of the Heart” in Philadelphia March 6-8, 2019, one of the little known secrets of integrative cardiology was revealed. The plant based diet can prevent and reverse coronary artery disease.

Case Reports

A few case reports in the medical literature are illustrative: In 2015, Dr Massera reported on a 60 year old male with typical angina and a positive stress test who declined both drug therapy and invasive treatment. His symptoms resolved promptly on a plant based diet. (13)

” A 60-year-old man presented with typical angina and had a positive stress test. He declined both drug therapy and invasive testing. Instead, he chose to adopt a whole-food plant-based diet, which consisted primarily of vegetables, fruits, whole grains, potatoes, beans, legumes, and nuts. His symptoms improved rapidly, as well as his weight, blood pressure, and cholesterol levels.” endquote(13)

Here is another 2017 case report from Dr Daniela Massera of a 77 year old female with unstable angina who declined bypass surgery. Her symptoms resolved on a plant based diet.: (12)

“A 77-year-old hypertensive female with unstable angina was taking atenolol 50 mg and simvastatin 20 mg daily. She had chest pain (angina) with mild exercise whihc resolved at rest. Coronary angiography showed severe triple vessel disease with normal left ventricular unction (Normal EF). The patient declined treatment with Cardiac bypass surgery. Instead she changed her diet from a “healthy western” to a whole-food plant-based diet, (all vegetables, fruits, whole grains, potatoes, beans, legumes and nuts. She avoided all animal products, eggs, dairy, meat. One month later, symptoms had resolved and the patient could walk on treadmill form 50 minutes without chest pain.”(12)

A third case is a 79 year old male who has an improvement in Left Ventricular function on a plant based diet.(11) Three more case reports were published by Dr Esselstyn in 2004.(14)

40% Reduction in Mortality from Cardiovascular Disease

According to Dr Kahleova in 2018, Plant Based Diet reduces mortality from Cardiovascular Disease by 40%, the only diet to reverse coronary artery disease, as well as beneficial for weight loss, metabolic syndrome, and type 2 diabetes.(3-4)(9):

“Vegetarian dietary patterns reduce CVD mortality and the risk of coronary heart disease (CHD) by 40%. Plant-based diets are the only dietary pattern to have shown reversal of CHD. Additionally, evidence suggests benefits of vegetarian dietary patterns in both the prevention and the treatment of heart failure and cerebrovascular disease. Plant-based diets are associated with lower blood pressure, lower blood lipids, and reduced platelet aggregation than non-vegetarian diets and are beneficial in weight management, reduce the risk of developing metabolic syndrome, and type 2 diabetes. They have also been shown an effective treatment method in diabetes management.” (3-4)

What is a Plant Based Diet ?

Dr Robert Ostfeld in Geriatric Cardiology 2017 gives us the definition of a Plant Based Diet: “All minimally processed fruits, vegetables, whole grains, legumes, nuts and seeds, herbs, and spices and excludes all animal products, including red meat, poultry, fish, eggs, and dairy products.”(5)

Benefits for Weight Loss, and Obesity

In 2017 Dr Turner-McGrievy reports that:

“Both clinical trials and observational research indicate advantage of PBDs (Plant Based Diets) for preventing obesity and promoting weight loss.”(6)

A 2017 study in New Zealand showed Plant Based Diet was excellent for weight loss.(7) Another study in 2017 by Dr. Haghighatdoost, showed reduction in CRP for those on plant based diet.(8)

Caldwell B Esselstyn Jr. Advocate of Plant Based Diet

Perhaps Dr Esselstyn is one of the strongest and most dedicated advocates of the Plant Based Diet over many years now.(10)(14)(17-19)(22-23) His many studies and publications extolling the benefits of the plant based diet for preventing and reversing heart disease, and argue for implementing the plant based diet for patients with coronary artery disease as the most logical and rational alternative to invasive procedures. In spite of Dr Esselstyn’s valiant efforts to convince mainstream cardiologists of the merits of a plant based diet, his message has been largely ignored. Another advocate of the Plant Bases Diet is Dr Phillip Tuso.(15-16) He says:

“Changing from a Western diet to a plant-based diet may be a simple, low-cost intervention that prevents atherothrombotic CAD…..Physicians should consider recommending a plant-based diet to all their patients, especially those with high blood pressure, diabetes, cardiovascular disease, or obesity.”(15-16)

My previous articles discuss the idea that coronary artery disease is caused by infection, and that atherosclerotic plaque is polymicrobial biofilm caused by endotoxemia arising from “leaky gut” and periodontal disease.(29) Indeed, the enteric bacteria, E. Coli, has been found in atherosclerotic plaques.(26) Metabolic endotoxemia has other pathological effects, one of which we see commonly is low testosterone in males caused by hypothalamic dysfunction.(27-28)

Fatty Meal Causes Endotoxemia – no Animal Fat in Plants

Consumption of animal products, especially animal fat has been associated with postprandial endotoxemia. Diabetics and the obese seem most sensitive to this.(31-38) Needless to say, a plant based diet avoids these episodes of excess postprandial endotoxemia, since no animal products or fats are consumed.

Anti-Inflammatory and Antimicrobial Substances in Plants

Another benefit of the plant based diet is the anti-inflammatory and antimicrobial substances in plants.(8)

Conclusion

In conclusion, here is a quote from Dr Esselstyn. He says: (10)

“Despite overwhelming evidence for the safety, simplicity, and efficacy of plant nutrition to halt and prevent coronary artery disease, the cardiovascular medicine community has failed to embrace this option of therapy and persists in palliative treatments associated with high morbidity, mortality, and expense. It is long overdue to question why.”(10)

Jeffrey Dach MD

7450 Griffin Road Suite 180/190

Davie, Florida 33314

954-792-4663

Articles With Related Interest

Books:

Kahn, Joel K. The Plant-based Solution: America’s Healthy Heart Doc’s Plan to Power Your Health. Sounds True, 2018

Above Header image courtesy of : Prev Cardiol. 2001 Autumn;4(4):171-177. Resolving the Coronary Artery Disease Epidemic Through Plant-Based Nutrition. Esselstyn CB Jr1. Fig 1 LAD Before (Red) and after (green) Plant based diet for 32 months without cholesterol lowering medication.

.links and references

1) 6 Ways to Kick Off a Plant-Based Diet by Joel Kahn MD

2) 5 Questions with Dr. Joel Kahn, Leading Cardiologist and Author of The Plant-Based Solution Max Goldberg February 11, 2018 living max well

The love of animal products raised on grass or grain-fed is a dinosaur that will be soon be considered barbaric and primitive, like 8-track tape players. Slowly the functional medicine world will get it.

2018

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3) Prog Cardiovasc Dis. 2018 May – Jun;61(1):54-61.Vegetarian Dietary Patterns and Cardiovascular Disease. Kahleova H, Levin S1, Barnard ND2.

Cardiovascular (CV) disease (CVD) is the leading global cause of mortality, being responsible for 46% of non-communicable disease deaths. It has been estimated that about 85.6 million Americans are living with some form of CVD, which continues to rise. Healthy lifestyle choices may reduce the risk of myocardial infarction by >80%, with nutrition playing a key role. Vegetarian dietary patterns reduce CVD mortality and the risk of coronary heart disease (CHD) by 40%. Plant-based diets are the only dietary pattern to have shown reversal of CHD. Additionally, evidence suggests benefits of vegetarian dietary patterns in both the prevention and the treatment of heart failure and cerebrovascular disease. Plant-based diets are associated with lower blood pressure, lower blood lipids, and reduced platelet aggregation than non-vegetarian diets and are beneficial in weight management, reduce the risk of developing metabolic syndrome, and type 2 diabetes. They have also been shown an effective treatment method in diabetes management. Well planned vegetarian diets provide benefits in preventing and reversing atherosclerosis and in decreasing CVD risk factors and should be promoted through dietary guidelines and recommendations.

4) Kahleova, Hana, Susan Levin, and Neal Barnard. “Cardio-Metabolic Benefits of Plant-Based Diets.” Nutrients 9.8 (2017).

Cardio-metabolic disease, namely ischemic heart disease, stroke, obesity, and type 2 diabetes, represent substantial health and economic burdens. Almost one half of cardio-metabolic deaths in the U.S. might be prevented through proper nutrition. Plant-based (vegetarian and vegan) diets are an effective strategy for improving nutrient intake. At the same time, they are associated with decreased all-cause mortality and decreased risk of obesity, type 2 diabetes, and coronary heart disease. Evidence suggests that plant-based diets may reduce the risk of coronary heart disease events by an estimated 40% and the risk of cerebral vascular disease events by 29%. These diets also reduce the risk of developing metabolic syndrome and type 2 diabetes by about one half. Properly planned vegetarian diets are healthful, effective for weight and glycemic control, and provide metabolic and cardiovascular benefits, including reversing atherosclerosis and decreasing blood lipids and blood pressure. The use of plant-based diets as a means of prevention and treatment of cardio-metabolic disease should be promoted through dietary guidelines and recommendations.

Plant-based diets are associated with decreased all-cause mortality and decreased risk of obesity, type 2 diabetes, and coronary heart disease [6].Plant-based diets are characterized by a reduction or elimination of animal product consumption. They are typically based on the consumption of grains, legumes, vegetables, fruits, and nuts. Vegan diets contain only plant foods, while lacto-ovo-vegetarian diets include dairy and/or egg products.

Plant-based diets have been shown to be a particularly effective dietary approach for weight loss [29,30]. A recent study showed a mean BMI reduction of 4.4 kg/m2 with a 6-month, whole-food, plant-based diet with no energy restrictions, compared with usual care (0.4 kg/m2), in overweight or obese subjects [31].

Plant-based diets appear to reduce the risk of developing metabolic syndrome by about one half [33].

Vegetarian diets have been shown to be helpful not only in prevention but also in the treatment of type 2 diabetes in several clinical trials.

A recent meta-analysis of six randomized controlled trials showed that consumption of vegetarian diets was associated with a significant reduction in HbA1c by 0.4 absolute percentage points, compared with conventional diets in patients with type 2 diabetes [41].

In randomized controlled trials, vegetarian diets decreased both systolic and diastolic blood pressure by 4.8 and 2.2 mm Hg, respectively [78].

2017

Definition of a plant-based diet

5) Ostfeld, Robert J. “Definition of a plant-based diet and overview of this special issue.” Journal of geriatric cardiology: JGC 14.5 (2017): 315.

1. Definition of a plant-based diet: A plant-based diet consists of all minimally processed fruits, vegetables, whole grains, legumes, nuts and seeds, herbs, and spices and excludes all animal products, including red meat, poultry, fish, eggs, and dairy products.

6) Turner-McGrievy, Gabrielle, Trisha Mandes, and Anthony Crimarco. “A plant-based diet for overweight and obesity prevention and treatment.” Journal of geriatric cardiology: JGC 14.5 (2017): 369.

The goal of this paper is to review the evidence related to the effect of plant-based dietary patterns on obesity and weight loss, including both observational and intervention trials. Literature from plant-based diets (PBDs) epidemiological and clinical trial research was used to inform this review. In addition, data on dietary quality, adherence, and acceptability were evaluated and are presented. Both clinical trials and observational research indicate an advantage to adoption of PBDs for preventing overweight and obesity and promoting weight loss. PBDs may also confer higher levels of diet quality than are observed with other therapeutic diet approaches, with similar levels of adherence and acceptability. Future studies should utilize health behavior theory to inform intervention development and delivery of PBDs studies and new technologies to bring interventions to scale for greater public health impact. Research examining PBDs and weight loss is also needed with more diverse populations, including older adults. Based on the available evidence, PBDs should be considered a viable option for the treatment and prevention of overweight and obesity.

7) Wright, N., et al. “The BROAD study: A randomised controlled trial using a whole food plant-based diet in the community for obesity, ischaemic heart disease or diabetes.” Nutrition & Diabetes 7.3 (2017): e256.

PBD – Lower CRP Levels

8) Haghighatdoost, Fahimeh, et al. “Association of vegetarian diet with inflammatory biomarkers: a systematic review and meta-analysis of observational studies.” Public health nutrition 20.15 (2017): 2713-2721.

Objective: Vegetarian diets contain various anti-inflammatory components. We aimed to investigate the effects of vegetarianism on inflammatory biomarkers when compared with omnivores.

Literature search was conducted in Science Direct, Proquest, MEDLINE and Google Scholar up to June 2016. Summary estimates and corresponding 95 % CI were derived via the DerSimonian and Laird method using random effects, subgroup analyses were run to find the source of heterogeneity and a fixed-effect model examined between-subgroup heterogeneity.

Subjects Studies were included if they evaluated effects of any type of vegetarianism compared with omnivores on circulating levels of inflammatory biomarkers. No restriction was made in terms of language or the date of study publications.

Results Eighteen articles were included. Pooled effect size showed no difference in high-sensitivity C-reactive protein (hs-CRP) levels in vegetarians v. omnivores (Hedges’ g=−0·15; 95 % CI −0·35, 0·05), with high heterogeneity (I 2=75·6 %, Plower hs-CRP levels v. omnivores (Hedges’ g=−0·29; 95 % CI −0·59, 0·01), with moderate heterogeneity (I 2=68·9 %, P

Conclusions The meta-analysis provides evidence that vegetarianism is associated with lower serum concentrations of hs-CRP when individuals follow a vegetarian diet for at least 2 years. Further research is necessary to draw appropriate conclusions regarding potential associations between vegetarianism and IL-6 levels. A vegetarian diet might be a useful approach to manage inflammaging in the long term.

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9) Harland, J., and L. Garton. “An update of the evidence relating to plant‐based diets and cardiovascular disease, type 2 diabetes and overweight.” Nutrition bulletin 41.4 (2016): 323-338.

Recent findings from meta‐analyses, European cohorts and randomised controlled trials (RCTs) evaluating the relationship between plant‐based dietary regimes (i.e. those with an emphasis on plant foods, such as vegetarian, vegan, Mediterranean or combination diets), and the incidence of, or risk factors for, cardiovascular disease (CVD), type 2 diabetes (T2D) and obesity are considered in this review. Evidence from meta‐analyses of epidemiological studies indicates that those following plant‐based dietary regimes have around 20–25% lower risk of developing CVD and a similar reduced risk of developing T2D. Evidence from RCTs indicates that those following plant‐based dietary regimes have lower total cholesterol, low‐density lipoprotein‐cholesterol and blood pressure, and modest reductions in inflammatory and endothelial markers. Higher intake of plant foods has been associated with lower incidence of obesity, lower BMI and smaller waist circumference. For weight loss, it seems that following a plant‐based dietary regime results in weight loss comparable to that achieved on conventional reduced calorie diets, but with better overall weight management. The totality of evidence indicates there are benefits for cardiovascular health, risk of developing T2D and weight management from following a plant‐based dietary regime. From a nutritional perspective, plant‐based diets tend to be lower in saturated fatty acids, higher in unsaturated fatty acids and fibre, and lower in energy density than typical ‘Western’ diets. These qualities may be at the core of the health benefits reported and/or it may be simply a greater proportion of plant foods in the diet that is beneficial in its own right.

Esselstyn

10) Esselstyn Jr, Caldwell B. “Defining an Overdue Requiem for Palliative Cardiovascular Medicine.” American journal of lifestyle medicine 10.5 (2016): 313-317.

During the past 40 years, we have witnessed significant advances in the pharmaceutical and interventional treatment of cardiovascular disease (CVD), which have helped achieve a decrease in morbidity and mortality for this illness. Nevertheless, CVD remains the number 1 killer of women and men in Western civilizations. This fact is in stark contrast to the scenario in multiple whole food, plant-based nutrition (WFPBN) cultures, where CVD is virtually nonexistent. The utility of plant-based nutrition to halt and prevent CVD has been demonstrated epidemiologically, during wartime deprivation, in large cohort and population transitioning studies, and through prospective randomized and nonrandomized investigations. A basic scientific study confirms that omnivores have intestinal bacteria capable of converting animal food to trimethylamine oxide (TMAO), which injures blood vessels, whereas those eating plants only do not have intestinal bacteria capable of producing TMAO. Despite this overwhelming evidence for the safety, simplicity, and efficacy of plant nutrition to halt and prevent coronary artery disease, the cardiovascular medicine community has failed to embrace this option of therapy and persists in palliative treatments associated with high morbidity, mortality, and expense. It is long overdue to question why.

2017 case report

11) Choi, Evan Y., et al. “A plant-based diet and heart failure: case report and literature review.” Journal of geriatric cardiology: JGC 14.5 (2017): 375.

2016

12) Massera, Daniele, et al. “Angina rapidly improved with a plant-based diet and returned after resuming a Western diet.” Journal of geriatric cardiology: JGC 13.4 (2016): 364.

In summary, a whole-food plant-based diet was associated with reversing angina symptoms in our patient with severe coronary atherosclerotic disease Her angina returned when she resumed consuming a ‘healthy’ Western diet.

2015 CASE REPORT !!!!!!!!!!

13) Case Rep Cardiol. 2015;2015:978906. A Whole-Food Plant-Based Diet Reversed Angina without Medications or Procedures. Massera D1, Zaman T2, Farren GE3, Ostfeld RJ1.

A 60-year-old man presented with typical angina and had a positive stress test. He declined both drug therapy and invasive testing. Instead, he chose to adopt a whole-food plant-based diet, which consisted primarily of vegetables, fruits, whole grains, potatoes, beans, legumes, and nuts. His symptoms improved rapidly, as well as his weight, blood pressure, and cholesterol levels. Plant-based diets have been associated with improved plasma lipids, diabetes control, coronary artery disease and with a reduction in mortality. Adoption of this form of lifestyle therapy should be among the first recommendations for patients with atherosclerosis.

free pdf

14) Esselstyn, Caldwell, and Mladen Golubic. “The Nutritional Reversal of Cardiovascular Disease “Fact or Fiction? Three Case Reports.” (2014). Nutritional Reversal of Cardiovascular Disease Fact or Fiction Esselstyn Three Case Reports 2014

15) Tuso, Phillip, Scott R. Stoll, and William W. Li. “A plant-based diet, atherogenesis, and coronary artery disease prevention.” The Permanente Journal 19.1 (2015): 62.

A plant-based diet is increasingly becoming recognized as a healthier alternative to a diet laden with meat. Atherosclerosis associated with high dietary intake of meat, fat, and carbohydrates remains the leading cause of mortality in the US. This condition results from progressive damage to the endothelial cells lining the vascular system, including the heart, leading to endothelial dysfunction. In addition to genetic factors associated with endothelial dysfunction, many dietary and other lifestyle factors, such as tobacco use, high meat and fat intake, and oxidative stress, are implicated in atherogenesis. Polyphenols derived from dietary plant intake have protective effects on vascular endothelial cells, possibly as antioxidants that prevent the oxidation of low-density lipoprotein. Recently, metabolites of L-carnitine, such as trimethylamine-N-oxide, that result from ingestion of red meat have been identified as a potential predictive marker of coronary artery disease (CAD). Metabolism of L-carnitine by the intestinal microbiome is associated with atherosclerosis in omnivores but not in vegetarians, supporting CAD benefits of a plant-based diet. Trimethylamine-N-oxide may cause atherosclerosis via macrophage activation. We suggest that a shift toward a plant-based diet may confer protective effects against atherosclerotic CAD by increasing endothelial protective factors in the circulation while reducing factors that are injurious to endothelial cells. The relative ratio of protective factors to injurious endothelial exposure may be a novel approach to assessing an objective dietary benefit from a plant-based diet. This review provides a mechanistic perspective of the evidence for protection by a plant-based diet against atherosclerotic CAD.

changing from a Western diet to a plant-based diet may be a simple, low-cost intervention that prevents atherothrombotic CAD.

16) Tuso, Philip J., et al. “Nutritional update for physicians: plant-based diets.” The Permanente Journal 17.2 (2013): 61.

We present a case study as an example of the potential health benefits of such a diet. Research shows that plant-based diets are cost-effective, low-risk interventions that may lower body mass index, blood pressure, HbA1C, and cholesterol levels. They may also reduce the number of medications needed to treat chronic diseases and lower ischemic heart disease mortality rates. Physicians should consider recommending a plant-based diet to all their patients, especially those with high blood pressure, diabetes, cardiovascular disease, or obesity.

2014

Nice images !!!!!

17) J Fam Pract. 2014 Jul;63(7):356-364b. A way to reverse CAD? Esselstyn CB Jr1, Gendy G, Doyle J, Golubic M, Roizen MF.

Plant-based nutrition achieved coronary artery disease (CAD) arrest and reversal in a small study. However, there was skepticism that this approach could succeed in a larger group of patients. The purpose of our follow-up study was to define the degree of adherence and outcomes of 198 consecutive patient volunteers who received counseling to convert from a usual diet to plant-based nutrition.

METHODS: We followed 198 consecutive patients counseled in plant-based nutrition. These patients with established cardiovascular disease (CVD) were interested in transitioning to plant-based nutrition as an adjunct to usual cardiovascular care. We considered participants adherent if they eliminated dairy, fish, and meat, and added oil.

RESULTS:Of the 198 patients with CVD, 177 (89%) were adherent. Major cardiac events judged to be recurrent disease totaled one stroke in the adherent cardiovascular participants—a recurrent event rate of .6%, significantly less than reported by other studies of plant-based nutrition therapy. Thirteen of 21 (62%) nonadherent participants experienced adverse events.

CONCLUSION:Most of the volunteer patients with CVD responded to intensive counseling, and those who sustained plant-based nutrition for a mean of 3.7 years experienced a low rate of subsequent cardiac events. This dietary approach to treatment deserves a wider test to see if adherence can be sustained in broader populations. Plant-based nutrition has the potential for a large effect on the CVD epidemic.

18) Prev Cardiol. 2001 Autumn;4(4):171-177. Resolving the Coronary Artery Disease Epidemic Through Plant-Based Nutrition. Esselstyn CB Jr1.

The world’s advanced countries have easy access to plentiful high-fat food; ironically, it is this rich diet that produces atherosclerosis. In the world’s poorer nations, many people subsist on a primarily plant-based diet, which is far healthier, especially in terms of heart disease. To treat coronary heart disease, a century of scientific investigation has produced a device-driven, risk factor-oriented strategy. Nevertheless, many patients treated with this approach experience progressive disability and death. This strategy is a rear-guard defensive one. In contrast, compelling data from nutritional studies, population surveys, and interventional studies support the effectiveness of a plant-based diet and aggressive lipid lowering to arrest, prevent, and selectively reverse heart disease. In essence, this is an offensive strategy. The single biggest step toward adopting this strategy would be to have United States dietary guidelines support a plant-based diet. An expert committee purged of industrial and political influence is required to

19) Esselstyn Jr, Caldwell B. “Is the Present Therapy for Coronary Artery Disease the Radical Mastectomy of the Twenty-First Century?.” Curr Surg 60 (2003): 329-337. Present Therapy for Coronary Artery Disease the Radical Mastectomy of the Twenty First Century Caldwell B Esselstyn

20) JAMA. 1998 Dec 16;280(23):2001-7. Intensive lifestyle changes for reversal of coronary heart disease. Ornish D1, Scherwitz LW, Billings JH, Brown SE, Gould KL, Merritt TA, Sparler S, Armstrong WT, Ports TA, Kirkeeide RL, Hogeboom C, Brand RJ.JAMA 1999 Apr 21;281(15):1380.

The Lifestyle Heart Trial demonstrated that intensive lifestyle changes may lead to regression of coronary atherosclerosis after 1 year.

OBJECTIVES: To determine the feasibility of patients to sustain intensive lifestyle changes for a total of 5 years and the effects of these lifestyle changes (without lipid-lowering drugs) on coronary heart disease.

DESIGN: Randomized controlled trial conducted from 1986 to 1992 using a randomized invitational design.

PATIENTS: Forty-eight patients with moderate to severe coronary heart disease were randomized to an intensive lifestyle change group or to a usual-care control group, and 35 completed the 5-year follow-up quantitative coronary arteriography.

SETTING: Two tertiary care university medical centers.

INTERVENTION: Intensive lifestyle changes (10% fat whole foods vegetarian diet, aerobic exercise, stress management training, smoking cessation, group psychosocial support) for 5 years.

MAIN OUTCOME MEASURES: Adherence to intensive lifestyle changes, changes in coronary artery percent diameter stenosis, and cardiac events.

RESULTS: Experimental group patients (20 [71%] of 28 patients completed 5-year follow-up) made and maintained comprehensive lifestyle changes for 5 years, whereas control group patients (15 [75%] of 20 patients completed 5-year follow-up) made more moderate changes. In the experimental group, the average percent diameter stenosis at baseline decreased 1.75 absolute percentage points after 1 year (a 4.5% relative improvement) and by 3.1 absolute percentage points after 5 years (a 7.9% relative improvement). In contrast, the average percent diameter stenosis in the control group increased by 2.3 percentage points after 1 year (a 5.4% relative worsening) and by 11.8 percentage points after 5 years (a 27.7% relative worsening) (P=.001 between groups. Twenty-five cardiac events occurred in 28 experimental group patients vs 45 events in 20 control group patients during the 5-year follow-up (risk ratio for any event for the control group, 2.47 [95% confidence interval, 1.48-4.20]).

CONCLUSIONS: More regression of coronary atherosclerosis occurred after 5 years than after 1 year in the experimental group. In contrast, in the control group, coronary atherosclerosis continued to progress and more than twice as many cardiac events occurred.

21) Circulation. 1999 Feb 16;99(6):779-85.Mediterranean diet, traditional risk factors, and the rate of cardiovascular complications after myocardial infarction: final report of the Lyon Diet Heart Study.

de Lorgeril M1, Salen P, Martin JL, Monjaud I, Delaye J, Mamelle N.

The Lyon Diet Heart Study is a randomized secondary prevention trial aimed at testing whether a Mediterranean-type diet may reduce the rate of recurrence after a first myocardial infarction. An intermediate analysis showed a striking protective effect after 27 months of follow-up. This report presents results of an extended follow-up (with a mean of 46 months per patient) and deals with the relationships of dietary patterns and traditional risk factors with recurrence.

METHODS AND RESULTS:

Three composite outcomes (COs) combining either cardiac death and nonfatal myocardial infarction (CO 1), or the preceding plus major secondary end points (unstable angina, stroke, heart failure, pulmonary or peripheral embolism) (CO 2), or the preceding plus minor events requiring hospital admission (CO 3) were studied. In the Mediterranean diet group, CO 1 was reduced (14 events versus 44 in the prudent Western-type diet group, P=0.0001), as were CO 2 (27 events versus 90, P=0.0001) and CO 3 (95 events versus 180, P=0. 0002). Adjusted risk ratios ranged from 0.28 to 0.53. Among the traditional risk factors, total cholesterol (1 mmol/L being associated with an increased risk of 18% to 28%), systolic blood pressure (1 mm Hg being associated with an increased risk of 1% to 2%), leukocyte count (adjusted risk ratios ranging from 1.64 to 2.86 with count >9×10(9)/L), female sex (adjusted risk ratios, 0.27 to 0. 46), and aspirin use (adjusted risk ratios, 0.59 to 0.82) were each significantly and independently associated with recurrence.

CONCLUSIONS: The protective effect of the Mediterranean dietary pattern was maintained up to 4 years after the first infarction, confirming previous intermediate analyses. Major traditional risk factors, such as high blood cholesterol and blood pressure, were shown to be independent and joint predictors of recurrence, indicating that the Mediterranean dietary pattern did not alter, at least qualitatively, the usual relationships between major risk factors and recurrence. Thus, a comprehensive strategy to decrease cardiovascular morbidity and mortality should include primarily a cardioprotective diet. It should be associated with other (pharmacological?) means aimed at reducing modifiable risk factors. Further trials combining the 2 approaches are warranted.

22) Dr. Esselstyn’s landmark heart disease reversal program. Success Stories

23) Esselstyn Jr, Caldwell B. “The Hoffman Centre for Integrative Medicine.” Patient Handout 2011

http://www.hoffmancentre.com/wp-conte...

24) Kahn, Joel K. The Plant-based Solution: America’s Healthy Heart Doc’s Plan to Power Your Health. Sounds True, 2018.

Probiotic Reduces Endotoxemia

free pdf

25) Sabico, Shaun, et al. “Effects of a 6-month multi-strain probiotics supplementation in endotoxemic, inflammatory and cardiometabolic status of T2DM patients: A randomized, double-blind, placebo-controlled trial.” Clinical Nutrition (2018).

Multi-strain probiotics supplementation for 6 months caused a significant decrease in circulating levels of endotoxin by almost 70% over 6 months, as well as glucose (38%), insulin (38%), HOMA-IR (64%), triglycerides (48%), total cholesterol (19%), total/HDL-cholesterol ratio (19%), TNF-a (67%), IL-6 (77%), CRP (53%), resistin (53%), and a significant increase in adiponectin (72%) as compared with baseline. Only HOMA-IR had a clinically significant reduction (-3.4, 64.2%) in the probiotics group as compared to placebo group at all time points. No other clinically significant changes were observed between the probiotic or placebo group at 3 and 6 months in other markers.

Conclusion: Multi-strain probiotic supplementation over 6 months as a monotherapy significantly decreased HOMA-IR in T2DM patients, with the probiotic treatment group highlighting reduced inflammation and improved cardiometabolic profile. As such, multi-strain probiotics is a promising adjuvant anti-diabetes therapy.

The probiotics group was allocated with sachets [2 g freeze-dried powder of the probiotic mixture Ecologic®Barrier (Winclove probiotics, the Netherlands) (2.5 × 109 cfu/g)] which contains the following strains: Bifidobacterium bifidum W23, Bifidobacterium lactis W52, Lactobacillus acidophilus W37, Lactobacillus brevis W63, Lactobacillus casei W56, Lactobacillus salivarius W24, Lactococcus lactis W19 and L. lactis W58. This probiotic combination has been previously investigated for its ability to improve endothelial barrier and its potency to inhibit mast cell activation, inhibit pro-inflammatory cytokines decrease endotoxin load [20].

Finding LPS from E Coli in Atherosclerotic Plaque

26) Carnevale, Roberto, et al. “Localization of lipopolysaccharide from Escherichia Coli into human atherosclerotic plaque.” Scientific reports 8.1 (2018): 3598.

Experimental studies showed that gut-derived lipopolysaccharide (LPS) is pro-atherogenic, however, its relationship with human atherosclerosis is still to be defined. We investigate if gut-derived LPS from Escherichia Coli localizes in human carotid plaque and its potential role as pro-inflammatory molecule in the atherosclerotic lesion. LPS from Escherichia Coli and Toll-like receptor 4 (TLR4) were studied in specimens from carotid and thyroid arteries of 10 patients undergoing endarterectomy and 15 controls matched for demographic and clinical characteristics. Blood LPS were significantly higher in patients compared to controls. Immunochemistry analysis revealed positivity for antibodies against LPS and TLR4 coincidentally with positivity for CD68 only in the atherosclerotic plaque of carotid arteries but not in thyroid arteries; the positivity for LPS and TLR4 was greater in the area with activated macrophages. LPS concentration similar to that detected in atherosclerotic plaque resulted in a dose-dependent TLR4-mediated Nox2 up-regulation by human monocytes. These data provide the first evidence that LPS from Escherichia Coli localizes in human plaque and may contribute to atherosclerotic damage via TLR4-mediated oxidative stress.

Endotoxemia and HPA Dysfunction

27) Tremellen, Kelton, Natalie McPhee, and Karma Pearce. “Metabolic endotoxaemia related inflammation is associated with hypogonadism in overweight men.” Basic and clinical andrology 27.1 (2017): 5.

28) Tremellen, Kelton. “Gut Endotoxin Leading to a Decline IN Gonadal function (GELDING)-a novel theory for the development of late onset hypogonadism in obese men.” Basic and Clinical Andrology 26.1 (2016): 7.

Gut LPS Increased Risk of CV Event

29) Pastori, Daniele, et al. “Gut-Derived Serum Lipopolysaccharide is Associated With Enhanced Risk of Major Adverse Cardiovascular Events in Atrial Fibrillation: Effect of Adherence to Mediterranean Diet.” Journal of the American Heart Association 6.6 (2017): e005784.

Postprandial Endotoxemia

30) Vors, Cécile, et al. “Postprandial endotoxemia linked with chylomicrons and lipopolysaccharides handling in obese versus lean men: a lipid dose-effect trial.” The Journal of Clinical Endocrinology & Metabolism 100.9 (2015): 3427-3435.

High Fat Meal and Endotoxemia

Hi Fat Intake CAuses Endotoxemia

31) Lyte, Joshua M., Nicholas K. Gabler, and James H. Hollis. “Postprandial serum endotoxin in healthy humans is modulated by dietary fat in a randomized, controlled, cross-over study.” Lipids in health and disease 15.1 (2016): 186.

32) Harte, Alison L., et al. “High fat intake leads to acute postprandial exposure to circulating endotoxin in type 2 diabetic subjects.” Diabetes care 35.2 (2012): 375-382.

These studies have highlighted that exposure to a high-fat meal elevates circulating endotoxin irrespective of metabolic state, as early as 1 h after a meal. However, this increase is substantial in IGT and type 2 diabetic subjects, suggesting that metabolic endotoxinemia is exacerbated after high fat intake. In conclusion, our data suggest that, in a compromised metabolic state such as type 2 diabetes, a continual snacking routine will cumulatively promote their condition more rapidly than in other individuals because of the greater exposure to endotoxin.

33) Erridge, Clett, et al. “A high-fat meal induces low-grade endotoxemia: evidence of a novel mechanism of postprandial inflammation.” The American journal of clinical nutrition 86.5 (2007): 1286-1292.

34) Clemente-Postigo, Mercedes, et al. “Endotoxin increase after fat overload is related to postprandial hypertriglyceridemia in morbidly obese patients.” Journal of lipid research 53.5 (2012): 973-978.

35) Michalski, Marie-Caroline, et al. “Dietary lipid emulsions and endotoxemia.” OCL 23.3 (2016): D306.

36) Piya, Milan K., Alison L. Harte, and Philip G. McTernan. “Metabolic endotoxaemia: is it more than just a gut feeling?.” Current opinion in lipidology 24.1 (2013): 78-85.

37) Hamilton, M. Kristina, et al. “Changes in intestinal barrier function and gut microbiota in high-fat diet fed rats are dynamic and region-dependent.” American Journal of Physiology-Heart and Circulatory Physiology (2015).

38) Neves, Ana Luísa, et al. “Metabolic endotoxemia: a molecular link between obesity and cardiovascular risk.” Journal of molecular endocrinology 51.2 (2013): R51-R64.

39) Mani, Venkatesh, James H. Hollis, and Nicholas K. Gabler. “Dietary oil composition differentially modulates intestinal endotoxin transport and postprandial endotoxemia.” (2013).

Intestinal derived endotoxin and the subsequent endotoxemia can be considered major predisposing factors for diseases such as atherosclerosis, sepsis, obesity and diabetes. Dietary fat has been shown to increase postprandial endotoxemia. Therefore, the aim of this study was to assess the effects of different dietary oils on intestinal endotoxin transport and postprandial endotoxemia using swine as a model. We hypothesized that oils rich in saturated fatty acids (SFA) would augment, while oils rich in n-3 polyunsaturated fatty acids (PUFA) would attenuate intestinal endotoxin transport and circulating concentrations.

Methods Postprandial endotoxemia was measured in twenty four pigs following a porridge meal made with either water (Control), fish oil (FO), vegetable oil (VO) or coconut oil (CO). Blood was collected at 0, 1, 2, 3 and 5?hours postprandial and measured for endotoxin. Furthermore, ex vivo ileum endotoxin transport was assessed using modified Ussing chambers and intestines were treated with either no oil or 12.5% (v/v) VO, FO, cod liver oil (CLO), CO or olive oil (OO). Ex vivo mucosal to serosal endotoxin transport permeability (Papp) was then measured by the addition of fluorescent labeled-lipopolysaccharide.

Results Postprandial serum endotoxin concentrations were increased after a meal rich in saturated fatty acids and decreased with higher n-3 PUFA intake. Compared to the no oil control, fish oil and CLO which are rich in n-3 fatty acids reduced ex vivo endotoxin Papp by 50% (P?

Conclusion

Overall, these results indicate that saturated and n-3 PUFA differentially regulate intestinal epithelial endotoxin transport. This may be associated with fatty acid regulation of intestinal membrane lipid raft mediated permeability.

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Published on April 5th, 2019 by
Jeffrey Dach MD

The post Plant Based Diet Health Benefits for Coronary Artery Disease appeared first on Jeffrey Dach MD.

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Published on April 05, 2019 08:30

March 21, 2019

Coronary Calcium Score Paradigm Shift Podcast Jeffrey Dach MD

[image error] Coronary Calcium Score Paradigm Shift Podcast Jeffrey Dach MD

This is 15 minute podcast – a short version of my talk at the Phillie meeting (ICIM Heart ) recorded by Kirk Hamilton who works with Dr Matthew Budoff.

Here is a link to my slides given at the talk: Heart_ICIM_Philli 2019_JDach_PDF_M6

Thanks to Kirk Hamilton PA-C

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Jeffrey Dach MD Podcast Calcium Score Paradigm Shift in Cardiology

Replacing the “Cholesterol Theory of Atherosclerosis” with the “LPS (Low Level Endotoxemia) Theory of Coronary Artery Disease” – An Interview with Jeffrey Dach, MD

Published on March 21st, 2019 by
Jeffrey Dach MD

The post Coronary Calcium Score Paradigm Shift Podcast Jeffrey Dach MD appeared first on Jeffrey Dach MD.

Measles Hysteria and Fake News

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Published on March 21, 2019 17:50

March 19, 2019

Forced Vaccination GMO Food Its A Great Country

[image error]

Forced Vaccination GMO Food Its A Great Country

By Jeffrey Dach MD

I ran across this cartoon graphic by Ben Garrison and just had to share it with you. This just about sums up what is happening right now in America, “its a Great Country”. Could someone please tell me exactly how we find ourselves in this mess? Am I misinformed ? I thought this was a country governed by the People and for the People? How did this happen? Debt Slaves living in a Police State, eating at the trough of GMO Food with Forced Vaccinations at the Rear !

Articles with related interest:

Which is Greater threat Measles or Measles Vaccine?

Measles and Somalis in Minnesota

Financial Kickbacks to Pediatricians is Illegal and Harms Children

HPV Vaccine the Greatest Scandal of Our Time

Mitch Daniels Says Anti-GMO is Immoral

GMO Food Fight From Senate Floor

GMO Food, The Great Scandal

Jeffrey Dach MD

7450 Griffin Road Suite 180

Davie, Florida 33314

954-792-4663

References and Links:

1) Above header image courtesy of Ben GarriChildren’s Health Defense Teamson at GRRRGraphics.com

2) Taking No Prisoners in the Vaccine Culture War. Posted: 3/13/2019 8:44:49 PM By Barbara Loe Fisher

3) March 19, 2019 Real-Life Data Show that the CDC Vaccine Schedule is Causing Harm Children’s Health Defense Team

Published on March 19th, 2019 by
Jeffrey Dach MD

The post Forced Vaccination GMO Food Its A Great Country appeared first on Jeffrey Dach MD.

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Published on March 19, 2019 13:24

February 22, 2019

Calcium Score Determines Who to Treat With Statin Drug

Decision to Start Statin Based on Calcium Score

by Jeffrey Dach MD

Have you ever wondered why statin drugs seem to be effective for secondary prevention, (people with known heart disease), and not effective for primary prevention (people without heart disease)? A new study by Joshua Mitchell explains explains why. Current practice dictates that Cardiologists prescribe statin drugs based on a cholesterol over 200. This has been changed by the Joshua Mitchell study from the Walter Reed Registry which supports a new decision tree. Instead of using the cholesterol level, the decision to give a statin drug should be based on the Calcium Score.

Calcium Score Has Replaced the Cholesterol Panel

The chart below shows that for a Calcium score of 0 to 100, there is no benefit for taking a statin drug. For a score above 100, however, the chart shows considerable reduction in MACE (major adverse cardiac event) for the statin users. Notice cholesterol level is not mentioned in this study.

Pleotropic Effects

The Mitchell study does something else. It supports the conclusion that benefits of statin drugs are due to Pleotropic effects (anti-inflammatory and antimicrobial), not due to cholesterol lowering effects of the statin drug.

The Power of Zero

The key study is The Mitchell study from JACC 2018. Dr. Mitchell followed 13,644 patients from the Walter Reed Army Medical Center (mean age 50 years; 71% men) for 9.4 years.

Dr Mitchell concluded,

“the presence and severity of CAC (Coronary Artery Calcium) identified patients most likely to benefit from statins for the primary prevention of cardiovascular diseases.”

[image error]

Above chart, upper panels, shows no benefit for statin drug for Calcium Score of Zero to 100 (Green Line) Both Statin user and non-user lines are super-imposed. Bottom two panels: For Calcium Score over 100, statin user line is nicely separated from non-statin user (Red Arrow) indicating reduction in Major Adverse cardiac Events (MACE) Statin user dotted red line.

Conclusion:

One of the remarkable paradigm shifts in cardiology is the shift away from the cholesterol panel. The calcium score has emerged as a better decision making tool to decide which patients should be treated with statins, and which patients should not. The old method of prescribing a statin drug based on elevated cholesterol level is no longer valid, and has been replaced by Calcium Score.

Jeffrey Dach MD

7450 Griffin Road Suite 180

Davie, Fl 33314

954-792-4663

References:

Society of Cardiovascular Computed Tomography consensus statement using a CAC threshold of 100 for treatment

Mitchell, Joshua D., et al. “Impact of statins on cardiovascular outcomes following coronary artery calcium scoring.” Journal of the American College of Cardiology 72.25 (2018): 3233-3242.

Raggi, Paolo. “Coronary calcium is all we need for risk assessment, yet we do not use it often enough.” Atherosclerosis (2019).

The most fatal flaw of CAC detection for risk assessment, in the eye of physicians opposed to its use, is that there are no randomized clinical trials to demonstrate that by treating only patients with CAC, as opposed to those with an (no ?) indication for treatment, the risk of events is reduced. However, the circumstantial evidence that this is true is overwhelming, and it is simply logical to predict that antibiotics will work best in patients with lobar pneumonia than in those at “risk of developing pneumonia”.

Published on February 22nd, 2019 by
Jeffrey Dach MD

The post Calcium Score Determines Who to Treat With Statin Drug appeared first on Jeffrey Dach MD.