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17) https://www.ncbi.nlm.nih.gov/pubmed/4005876

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Published on October 20, 2017 14:18

September 26, 2017

Salicinium Non-Toxic Anti-Cancer Agent

[image error] Salicinium Non-Toxic Anti-Cancer Agent by Jeffrey Dach MD

A few recent articles in Townsend Letter for Doctors discuss Salicinium as a non-toxic anticancer agent.(1-2) Salicinium was patented in 2011 by Joe Brown as a glyco-benzaldehyde, by adding glucose to benzaldehyde.(19)

Below image: Chemical structure of Glyco-Benzaldehyde (Salicinium) courtesy of Joe Brown Patent (19). Benzaldehyde (left) is attached to a glucose molecule(right)

See chemical formula at below (19):

[image error]Benzaldehyde is present in the plant world, as an extract from figs for example, and has been studied going back to the 1980’s as a potent anticancer agent.(7-14) In addition to direct cytotoxicity to cancer cells, a second benefit of benzaldehyde is the enhancement of the host immune system with increased numbers of Killer T Cells observed after treatment. (15)

Since cancer cells have increased glucose uptake to support fermentation (aerobic glycolysis, or Warburg Effect), it makes sense to conjugate the benzaldehyde to a glucose molecule, insuring avid uptake by the cancer cell, while sparing normal cells.

Previous work conjugating benzaldehyde to ascorbic acid was promising, “rapidly necrotized inoperable human lung cancer, and induced degeneration of rat hepatocellular carcinoma”.(12) Glucose and Ascorbate are very similar in molecular structure and both seen by the cancer cell as glucose with avid uptake. Previous work on Benzadehyde-Glucose conjugates showed promising results.(17-18)

[image error] Left Image: Two Basal Cell cancer Lesions of the EAR (dark areas) Before Treatment. Courtesy of Townsend Letter(2).

Nagalase is a cell surface protein secreted by cancer cells which allows immune evasion, preventing activation of MAF(Macrophage Activating Factor) . Recent studies measuring Nagalase levels before and after Salcinium reveals profound reduction in serum Nagalase in treated patients. This allows immune system to activate Macrophages which then attack the cancer cells.(2)

The routine protocol is a 15 session course of IV Salcinium infusions followed by Oral salicinium (Orasal). No toxicities have been reported (3)

Conclusion: Salicinium may represent a promising non-toxic anticancer agent.

[image error] Left Image , same lesions after 18 days Salicinium. Lesions are healing, smaller and less vascular. Courtesy of Townsend Letter (2)

Jeffrey Dach MD

7450 Griffin Road suite 190

Davie, Fl 33314

954-792-4663

Header Image: Salicinium Logo courtesy of Perfect Balance.

Links and References

Salicinium – glyco benzaldehyde

1) http://www.townsendletter.com/AugSept2017/salicinium0817.html

http://www.townsendletter.com/AugSept2017/salicinium0817_2.html

Salicinium – Disrupting Anaerobic Glycolosis and Improving GcMAF Immune Response

by Virginia Osborne, ND

2) http://www.townsendletter.com/AugSept2016/salicinium0816.html

Salicinium: An Excellent Addition to My Armamentarium for Cancer Patients

by Carol M. Brown, DO, PhD, FAARFM’

3) http://www.naturodoc.com/salicinium_guidelines.htm

Guidelines for the Use of Salicinium (OraSal)

By Thomas S. Lee NMD, APH

free pdf

3) Matamoros, Morales Eric. “GcMAF: a polemic or a highly promising molecule?.” World Scientific News 65 (2017): 20-36.

4) https://www.erowid.org/culture/characters/lemaire_darrell/

Darrell Lemaire In 2005, Joe Brown and Forrest Niccum hired Lemaire to help them with investigating the potential medicinal applications for some phytochemicals. Together they discovered that salicinium—a glucoside of 4-hydroxy-benzaldehyde, extracted from the plant Helicia nilagirica—shows great promise as a cancer treatment, with a survival rate in Stage 4 cancer patients of nearly 85%.

5) Orasal 250 http://forperfectbalance.com/order-now/

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benzaldehyde.

7) http://www.medicinacomplementar.com.br/biblioteca/pdfs/Cancer/ca-1732.pdf

Cancer Treat Rep. 1980 Jan;64(1):21-3.

Antitumor activity of benzaldehyde. Kochi M, Takeuchi S, Mizutani T, Mochizuki K, Matsumoto Y, Saito Y.

Ninety patients with inoperable carcinoma in the terminal stages and 12 patients in serious condition with other tumor types were given benzaldehyde in the form of beta-cyclodextrin benzaldehyde inclusion compound (CDBA) orally or rectally at a daily dose of 10 mg/kg divided in four doses. Toxic effects, including hematologic or biochemical disturbances, were not seen during long-term successive administration of CDBA. Fifty-seven of the patients treated were evaluable; 19 patients responded completely and ten patients responded partially (greater than 50% regression). For all responding patients longer response durations were associated with longer CDBA treatment periods. Treatment of squamous cell carcinoma induced the cancer cells to change into a conglomeration of pearls (the well-known product of differentiation) which consisted of keratinized normal squamous cells.

8) http://ar.iiarjournals.org/content/30/12/5069.long

Anticancer Res. 2010 Dec;30(12):5069-76.

Tumor-specific cytotoxicity and type of cell death induced by benzaldehyde.

Ariyoshi-Kishino K1, Hashimoto K, Amano O, Saitoh J, Kochi M, Sakagami H.

We have previously reported that sodium 5,6-benzylidene-L-ascorbate (SBA) induced dramatic antitumor activity in inoperable cancer patients, but induced only marginal tumor specificity in vitro. Here the tumor specificity and type of cell death induced by benzaldehyde (BA), a degradation product of SBA, was investigated, using human tumor cell lines (oral squamous cell carcinoma [OSCC], glioblastoma, myelogenous leukemia) and human normal oral cells (gingival fibroblast, pulp cell, periodontal ligament fibroblast). BA showed much higher tumor-specific cytotoxicity than SBA. BA induced the formation of autophagosomes, the destruction of mitochondrial structure and digestion of broken organelles, without any apparent induction of internucleosomal DNA fragmentation and caspase activation in an OSCC cell line HSC-2, in a similar manner to SBA. However, pretreatment with 3-methyladenine or bafilomycin A(1), autophagy inhibitors, did not completely rescue the cells from the cytotoxicity induced by BA. The study suggests that BA may play an important role in the induction of antitumor activity of SBA in vivo, although the autophagic phenotypes induced by BA may be involved in both cell death and survival.

9) http://cancerres.aacrjournals.org/content/76/14_Supplement/4758

Abstract 4758: Benzaldehyde suppresses multiple signal pathways in cancer cells by regulating 14-3-3ζ-mediated protein-protein interactions Jun Saitoh and Hideyuki Saya

DOI: 10.1158/1538-7445.AM2016-4758 Published July 2016

Proceedings: AACR 107th Annual Meeting 2016; April 16-20, 2016; New Orleans, LA

Abstract Benzaldehyde is the simplest aromatic aldehyde constituent of almonds and many fruits. Anticancer effect of Benzaldehyde was first reported in 1980, and multi-institutional clinical trials were performed in those days in Japan. However trial was over without determination of effectiveness, only its safety was confirmed. The underlying mechanism why Benzaldehyde specifically suppresses growth of some particular cancer cells but not that of normal cells has not been elucidated. Therefore, we attempted to clarify the mechanism of anticancer effect of Benzaldehyde. In pancreatic cancer cell BxPC3 and in non-small cell lung cancer cell A549, we found that Benzaldehyde inhibits PI3K/AKT/mTOR, STAT3, NFκB and ERK pathways, those are major signaling pathways activated in cancer cells. Effects of Benzaldehyde on multiple signaling pathways are found to be derived from regulation of 14-3-3 family proteins which interact with phosphorylation sites of various proteins of multiple signals. In BxPC3 cells, Benzaldehyde treatment reduced the phosphorylation levels of 14-3-3-binding sites. Furthermore, we ectopically expressed seven isoforms of 14-3-3 in HEK293T cells and found that Benzaldehyde treatment significantly suppressed association of 14-3-3ζ with client proteins such as mTOR, Rictor, cRaf, STAT3 and FOXOs. The interaction of other isoforms of 14-3-3 with their client proteins was also partially reduced. But, the expression levels of those seven 14-3-3 isoforms were not significantly changed. Those data indicate that Benzaldehyde suppresses the interaction of 14-3-3ζ with its client proteins. Recent reports have shown that 14-3-3ζ is overexpressed in many cancers and acts as a signaling hub controlling the network of oncogenic pathways, suggesting that 14-3-3ζ associates with carcinogenesis, metastasis and resistance for chemotherapy and radiation. Hence, Benzaldehyde is considered to be a new class of anti-cancer agent inhibiting 14-3-3ζ-mediated tumor promoting and/or maintaining signals.

Citation Format: Jun Saitoh, Hideyuki Saya. Benzaldehyde suppresses multiple signal pathways in cancer cells by regulating 14-3-3ζ-mediated protein-protein interactions. [abstract]. In: Proceedings of the 107th Annual Meeting of the American Association for Cancer Research; 2016 Apr 16-20; New Orleans, LA. Philadelphia (PA): AACR; Cancer Res 2016;76(14 Suppl):Abstract nr 4758.

Benzaldehyde

full pdf

10) Takeuchi, Setsuo, et al. “Benzaldehyde as a carcinostatic principle in figs.” Agricultural and Biological Chemistry 42.7 (1978): 1449-1451.

11) Kochi, Mutsuyuki, et al. “Antitumor activity of a benzaldehyde derivative.” Cancer treatment reports 69.5 (1985): 533-537.

12) Sakagami, H., et al. “Induction of tumor degeneration by sodium benzylideneascorbate.” Anticancer research 11.4 (1991): 1533-1538.

Anticancer Res. 1991 Jul-Aug;11(4):1533-8.

Induction of tumor degeneration by sodium benzylideneascorbate.

Sakagami H1, Asano K, Fukuchi K, Gomi K, Ota H, Kazama K, Tanuma S, Kochi M.

Intravenous administration of sodium benzylideneascorbate (SBA) rapidly necrotized inoperable human lung cancer, and induced degeneration of 3′-methyl-4-dimethylaminoazobenzene-induced rat hepatocellular carcinoma (vacuolar, eosinophilic degeneration, nuclear debris) without affecting the serum glutamic oxaloacetic transaminase, gamma-glutamyl transpeptidase and total protein levels. Cultured normal human lung and skin fibroblasts, and human glioma and glioblastoma cell lines were relatively resistant to SBA, when compared to human myelogenous leukemic cell lines. SBA had no apparent host immunopotentiation activity such as stimulation of cytokine action or production; activation of monocyte or polymorphonuclear cells; or modulation of poly (ADP-ribose) glycohydrolase activity. The data suggest that the antitumor activity of SBA might be produced by direct action of authentic SBA or its metabolized form(s), rather than by immunopotentiation of the hosts.

13) http://journals.sagepub.com/doi/pdf/10.1177/34.2.3003181

Chieco, P. A. S. Q. U. A. L. E., et al. “Quantitative histochemistry of benzaldehyde dehydrogenase in hepatocellular carcinomas of vinyl chloride-treated rats.” Journal of Histochemistry & Cytochemistry 34.2 (1986): 151-158.

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14) Ochiai, Hiroshi, Seihachiro Niwayama, and Kiichi Masuyama. “Inhibition of experimental pulmonary metastasis in mice by β-cyclodextrin-benzaldehyde.” Journal of cancer research and clinical oncology 112.3 (1986): 216-220. J Cancer Res Clin Oncol. 1986;112(3):216-20.

Inhibition of experimental pulmonary metastasis in mice by beta-cyclodextrin-benzaldehyde.

Ochiai H, Niwayama S, Masuyama K.

The effect of beta-cyclodextrin-benzaldehyde (CDBA) on experimental pulmonary metastasis in C3H/He mice was examined. In an in vitro assay, the growth of RCT(+) cells was inhibited by 1200 micrograms/ml CDBA using unrenewed media, and by 600 micrograms/ml CDBA in that using daily renewed media. When mice were treated daily with CDBA, 3 weeks later the number of lung nodules developing after i.v. injection of 1 X 10(6) RCT(+) cells was significantly decreased in a dose-dependent manner, i.e., 73.8%, 85.6%, and 95.7% inhibition was observed following 0.5, 5, and 25 mg CDBA/mouse per day p.o. administration, respectively. The same mice showed almost as much natural killer (NK) activity as normal mice. Therefore, experiments were designed to evaluate the effect of CDBA on the NK activity of tumor-free mice whose immunity had been suppressed by 5-fluorouracil (5FU). Injections of 5FU only suppressed this activity to about 50% of normal mice, but the combined treatment with CDBA negated the suppressive effect of 5FU on NK activity. The results suggested that the inhibition of experimental pulmonary metastasis might be induced by the possible combined effects of CDBA; that is, the direct inhibition of tumors and the augmentation of NK cell activity.

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15) https://www.ncbi.nlm.nih.gov/pubmed/2007609

J Cancer Res Clin Oncol. 1991;117(2):109-14.

Augmentation of murine lymphokine-activated killer cell cytotoxicity by beta-cyclodextrin-benzaldehyde. Kuroki Y1, Ochiai H, Kurokawa M, Niwayama S, Kishimoto C, Tazawa K, Fujimaki M.

We investigated the effect of beta-cyclodextrin-benzaldehyde (CDBA) on lymphokine-activated killer (LAK) cell activity of spleen cells from normal or RCT(+)H-2(+)-sarcoma-bearing C3H/He mice. CDBA augmented the induction of LAK cytotoxicity in vitro against RCT(+)H-2+ tumor cells by IL-2, whereas the culture with CDBA alone did not. In a LAK cytotoxicity assay in vitro, the augmentative effect of CDBA was strongly exerted against spleen cells originating from 2-week-tumor-bearing mice, rather than those from normal mice or mice that had born tumors for 5 weeks. Such an augmentative effect was not observed against other tumor cells (YAC-1, D-6, Colon-26 and EL-4 cells) non-specifically. When the intravenous adoptive transfer of LAK cells was carried out in the mice, LAK cells from tumor-bearing mice induced by combined culture with interleukin-2 (IL-2) and CDBA markedly inhibited the pulmonary metastases of RCT(+)H-2+ tumor, while neither LAK cells from the same tumor-bearing mice induced by only IL-2 nor those from normal mice inhibited the pulmonary metastasis. The majority of LAK cells induced either by IL-2 plus CDBA or by IL-2 alone were found to be Thy1.2+ and asialoGM1+ cells by flow-cytometric analysis, but no obvious phenotypical difference was observed between them. However, the most significant effect of CDBA might be the maintenance of the Lyt-2+ cell level in the spleen cells from tumor-bearing mice. These results suggested that the costimulation of spleen cells with IL-2 and CDBA might induce cytotoxic T cells specific for syngeneic tumor cells.

16) http://www.bloodjournal.org/content/bloodjournal/73/5/1351.full.pdf?sso-checked=true

Reittie, Joyce E., et al. “Endogenously generated activated killer cells circulate after autologous and allogeneic marrow transplantation but not after chemotherapy.” Blood 73.5 (1989): 1351-1358.

Cancer Treat Rep. 1985 May;69(5):533-7. Antitumor activity of a benzaldehyde derivative.

Kochi M, Isono N, Niwayama M, Shirakabe K.

Benzaldehyde, in the form of 4,6-benzylidene-alpha-D-glucose (BG), was given iv at a daily dose of 720-1800 mg/m2 to 65 patients with inoperable carcinoma in the advanced stages. The overall objective response rate was 55%; seven patients achieved complete response, 29 achieved partial response, 24 remained stable, and five showed progressive disease. Response was seen in various cell types. Prolongation of survival was apparent for the patients. Toxic reactions were not observed during long-term injection with BG.

18) https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1971458/

Br J Cancer. 1990 Sep;62(3):436-9. 4, 6-0-benzylidene-D-glucopyranose (BG) in the treatment of solid malignant tumours, an extended phase I study. Tatsumura T1, Tsujimoto M, Koyama S, Furuno T, Komori Y, Sato H, Yamamoto K, Kitagawa M, Kagamimori S.

4, 6-0-Benzylidene-D-glucopyranose (BG), a derivative of benzaldehyde (BA), whose anti-tumour action has often been reported, showed responses in 10 out of 24 patients (41.7%). These patients consisted of 11 cases of primary lung cancer, 4 of metastatic lung cancer, 5 of gastric cancer, and one each of cancer of the sigmoid colon, liver, pancreas and prostate. There were two complete responses (one each of ipsilateral lung metastasis from breast cancer and metastatic liver lesions due to gastric cancer). The mean total dose of BG was 392.6 g, given by intravenous infusion of 1.2 g BG in 100 ml saline twice daily. The treatment was discontinued when no response was observed after two months. Careful monitoring showed no toxic action of BG at these large doses. Complete necrotic liquefaction of tumour, without any damage to surrounding tissue, was seen in 2 of 3 cases in which histological examination was feasible. It is apparent that BG, like BA, is not a cytotoxic agent in the ordinary sense, but its mechanism of action is still unknown.

19) Infusion Treatment Methods And Compositions Using Salicinium For Treating Cellular Proliferative Disorders And Immune Deficiencies

US 20110311477 A1 Publication date Dec 22, 2011 Inventors Joe Ernest BROWN

Chemical Structure of Salicinium

Link to this article: http://wp.me/p3gFbV-5bQ

Jeffrey Dach MD

7450 Griffin Road, Suite 190

Davie, Fl 33314

954-792-4663

www.jeffreydachmd.com

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Antonio Bianco TSH Inadequate for Levothyroxine Dosage

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Published on September 26, 2017 07:43

September 3, 2017

Errors in Modern Thyroid Endocrinology

[image error] Errors in Modern Thyroid Endocrinology

by Jeffrey Dach MD

Web Sites like Janie Bowthorpe’s, Stop the Thyroid Madness and Dana Trentini’s, Hypothyroid Mom are very popular for a very good reason. They identify and alert readers to the errors in modern thyroid endocrinology. Before we discuss these errors in detail, you might first ask the question, “How is this possible, that there could be errors in modern thyroid medical practice?”

How Are Errors in Thyroid Medical Practice Possible?

The answer to this question becomes obvious considering the money flowing from the drug industry to thyroid societies and doctors. In various forms, your doctor might be taking financial incentives (AKA bribes) from the drug industry. For example the American Thyroid Association and the Endocrine Society, the Endocrine Journals, Endocrine Research Grants, Endocrine Speakers Fees and Endocrine Meetings are all heavily funded by the Major Drug Companies, including the ones that make Synthroid, Levothyroxine and T4 only thyroid medications. This is all public information.

Creating Guidelines For the Benefit of the Benefactors

In 2012, the American Association of Endocrinologists and the American Thyroid Association, (ATA), published Guidelines for prescribing thyroid pills, which says:

“There is no evidence to support using desiccated thyroid hormone in preference to L-thyroxine monotherapy in the treatment of hypothyroidism and therefore desiccated thyroid hormone should not be used for the treatment of hypothyroidism.”

[image error]By some strange coincidence. the ATA (American Thyroid Association) receives substantial financial support from three drug companies: Pfizer, AbbVie, and Akrimax, makers of Levothyroxine, the same drug which is “Standard of Care” according to their “Guidelines”.

Endocrine Society is proud to publicly disclose their funding which comes from (among others) :

AbbVie Inc. Akrimax Pharmaceuticals Alexion Pharmaceuticals, Inc. Amarin Pharma Inc. Bayer HealthCare Boehringer Ingelheim Pharmaceuticals, Inc. & Lilly USA, LLC Burroughs Wellcome Fund Corcept Therapeutics Incorporated Dexcom, Inc. Eisai Inc. Endo Pharmaceuticals Inc. Esaote North America, Inc. Ethicon Endo-Surgery, Inc. FNA Path Genentech, Inc. Janssen Pharmaceuticals, Inc. Lilly USA, LLC Merck & Co., Inc. Mindray Thyroid Ultrasound by CSD Novartis Pharmaceuticals Corporation Noven Pharmaceuticals, Inc. Novo Nordisk Inc. NPS Pharmaceuticals, Inc. Pfizer, Inc. Salix Pharmaceuticals, Inc. sanofi-aventis U.S. Inc sanofi-aventis U.S. Inc, Regeneron Pharmaceuticals Alliance Takeda Pharmaceuticals U.S.A., Inc. Toshiba Head and Neck Ultrasound Veracyte, Inc.

I think you are starting to get the idea. You might be surprised to know that these Guidelines are wrong, a fact admitted by the ATA when they came up with different guidelines in 2014. nonetheless, the new Guidelines still serve the Drug Industry by rejecting natural desiccated thyroid in favor of T4 only medications, a recommendation having no basis in medical science. We will discuss this in detail below.

Medical practice in the US is strongly influenced by guidelines promulgated by the medical societies. So when the leading Thyroid Endocrinology societies issue incorrect guidelines, you can understand how this leads to errors in the practice of thyroid endocrinology.

[image error]Why Wont My Endocrinologist Listen to Me ?

A frequent question that comes up a few times a day in my office is: “Why won’t my endocrinologist listen to me?” Many of these patients are actually escapees from the endocrinology office, having been ignored and mistreated by a succession of “cookie cutter” endocrinologists who give them minuscule amounts of T4 only medication (usually Levothyroxine), which keeps the TSH in the “reference range” These poor miserable souls finally arrive in my office where we switch them from Levothyroxine to natural desiccated thyroid in a dosage that gives them some relief from low thyroid symptoms. We use Natural Desiccated Thyroid from RLC Labs called Naturthroid, One Grain Tab (65mg) contains 38 Mcg T4 and 9 mg T3 per tab, the same ratio produced by the normal thyroid gland.

Shorter Half Life Makes Natural Thyroid Safer

[image error]T3 has a shorter half life (T1/2) of one day (24 hrs), compared to the 7 day half life of T4 (Levothyroxine). This difference explains why NDT is a safer choice compared to T4 only meds such as levothyroxine. Symptoms of thyroid excess dissipate within a few hours of stopping NDT, while for the T4 only Levothyroxine, it may take a week for symptoms to resolve. We check labs prior to starting and aftert 6 weeks: TSH, FT4, FT3, TPO and Thyroglobulin Abs. We also routinely check serum selenium and spot urinary iodine.

Thyroid Physiology

The Thyroid Gland Produces T3 and T4 in 1:4 ratio, same as the T3/T4 ratio in NDT. Thyroid hormone is made by organifying iodine to thyroglobulin in the follicle at the apical membrane of the thyrocyes. This organification requires oxidation of Iodine by the TPO enzyme using hydrogen peroxide as a substrate. Various thyroid pathologies can be explained by overproduction and lack of degradation of H2O2, such as thyroiditis, cancer etc. This T3/T4 ratio of 1:4 is found in Natural Dessicated Thyroid which has 9 Mcg T3 and 38 Mcg T4 in each one grain tablet.

The List of Errors in Thyroid Endocrinology

Reliance on TSH Only to Monitor Treatment. .(Bianco 2016)
TSH Suppression may be needed for Adequate Treatment.(Ito 2012)
Reliance of T4 Only-Monotherapy (Levo or Synthoid) (Gullo,2011)
NDT –Natural Dessicated Thyroid Better Choice. (Hoang, 2013)

Shorter Half Life-makes NDT safer choice.

NDT Combines T3 and T4 – more robust for poor converters.

TSH Can Be Unreliable

The TSH can be unreliable in a number of medical conditions such as: Hypothalamic Dysfunction, Chronic Fatigue, Fibromyalgia Patients (Teitelbaum, Holtorf, Skinner)

Relying on TSH WIthin Reference RAnge

Dr Antonio Bianco’s study: 469 Levothyroxine (T4) treated patients were compared to controls. The Levothyroxine treated patients more likely to have lower serum T3:T4 ratios,

Higher BMI(Weight), more likely to be taking Beta-Blockers drugs, Statin drugs, and SSRI Anti-depressant drugs. And they were more likely to suffer from cognitive Impairment. (Peterson, Sarah J., Antonio C. Bianco. (2016).

Dr Antonio C. Bianco, MD, PhD, past president of the American Thyroid Association and professor of medicine at Rush Medical School says this:

Despite normal TSH tests, these patients still have many nagging symptoms of hypothyroidism. “Patients complain of being depressed, slow and having a foggy mind,” said “They have difficulty losing weight. They complain of feeling sluggish and have less energy. Yet we doctors keep telling them, ‘I’m giving you the right amount of medication and your TSH is normal. You should feel fine.’”

“Better medications (than Levo) are needed to treat hypothyroidism…. Patients who continue to have symptoms on Levothyroxine monotherapy might try a pill that contains both T3 and T4. “ (Antonio Bianco MD 12-Oct-2016)(Peterson, Sarah J., Antonio C. Bianco. (2016)

TSH Suppression May be Needed for Adequate Treatment

TSH Suppressive doses of Levothyoxine may be needed to achieve pre-operative T3 levels after thyroidectomy (Ito, 2012). More than 20% of patients, despite normal TSH levels, do not maintain FT3 or FT4 values in the reference range, reflecting the inadequacy of peripheral deiodination to compensate for the absent T3 secretion.” (Gullo, 2011)(Ito,2012)(deCastro, 2015)

Levothyroxine-T4 Alone does not resolve symptoms of Hypothyroidism

“Unfortunately therapy with L-T4 alone does not resolve symptoms in all hypothyroid patients, with approximately 12% of the patients remaining symptomatic despite normalization of serum TSH and TH levels. Impaired cognition, fatigue, and difficulty losing weight are the main residual symptoms of these patients, for which we lack understanding and have no mechanistic explanation.” Quote from: (McAninch 2015)

Conclusion: Errors in Modern Thyroid Endocrinology are understandable considering the corrupting influence of industry funding of thyroid endocrine societies, meeting, research and key opinion leaders. The main error is dogmatically insisting the TSH stay within the reference range when TSH suppression may be required for adequate therapy. The second error is dogmatically insisting on T4 monotherapy when natural desiccated thyroid (containing both T3 and T4) is more effective and safer than T4 monotherapy.

Link to this article: http://wp.me/p3gFbV-5b4

Jeffrey Dach MD

7450 Griffin Road, Suite 190

Davie, Fl 33314

954-792-4663

Articles with related interest:

TSH Suppression Benefits and Adverse effects

Natural Thyroid is Better than Synthroid Part One

Natural Thyroid is Better than Synthroid Part Two

Links and References

Peterson, Sarah J., Elizabeth A. McAninch, and Antonio C. Bianco. “Is a Normal TSH Synonymous With “Euthyroidism” in Levothyroxine Monotherapy?.” The Journal of Clinical Endocrinology & Metabolism 101.12 (2016): 4964-4973.

McAninch, Elizabeth A., et al. “Prevalent polymorphism in thyroid hormone-activating enzyme leaves a genetic fingerprint that underlies associated clinical syndromes.” The Journal of Clinical Endocrinology & Metabolism 100.3 (2015): 920-933.

Ito, Mitsuru, et al. “TSH-suppressive doses of levothyroxine are required to achieve preoperative native serum triiodothyronine levels in patients who have undergone total thyroidectomy.” European Journal of Endocrinology 167.3 (2012): 373-378.

Center for Excellence in Thyroid Care, Kuma Hospital, 8-2-35, Shimoyamate-Dori, Chuo-Ku, Kobe-City, Hyogo 650-0011, Japan

Gullo, Damiano, et al. “Levothyroxine monotherapy cannot guarantee euthyroidism in all athyreotic patients.” PloS one 6.8 (2011): e22552..

de Castro, Joao Pedro Werneck, et al. “Differences in hypothalamic type 2 deiodinase ubiquitination explain localized sensitivity to thyroxine.” The Journal of clinical investigation 125.125 (2) (2015): 0-0. quote:“normalization of serum TSH with L-T4 monotherapy results in relatively low serum 3,5,3′-triiodothyronine (T3) and high serum thyroxine/T3 (T4/T3) ratio”

Song, Yue, et al. “Roles of hydrogen peroxide in thyroid physiology and disease.” The Journal of Clinical Endocrinology & Metabolism 92.10 (2007): 3764-3773.

Hydrogen peroxide is degraded by seleno-proteins such as (Glutathione) GSH peroxidase and thioredoxin reductase. Selenium deficiency is associated with thyroid damage from excess hydrogen peroxide. We routinely check the serum selenium level and give selenium supplements to those in need.

Iodine Excess and Selenium Deficiency

In the face of selenium deficiency, excessive iodine intake will Induce Goiter, lead to thyroiditis, worsen lymphocytic infiltration, and damage the thyroid follicular structure in a dose-dependent manner in autoimmune mice.

Teng, X., et al. “Experimental study on the effects of chronic iodine excess on thyroid function, structure, and autoimmunity in autoimmune-prone NOD. H-2h4 mice.” Clinical and experimental medicine 9.1 (2009): 51.

However, supplemental Selenium alleviates the toxic effects of excessive Iodine on thyroid.”

Xu, Jian, et al. “Supplemental selenium alleviates the toxic effects of excessive iodine on thyroid.” Biological trace element research 141.1-3 (2011): 110-118.

Iodine Suppresses Thyroid Function

Occasionally a patient will walk into the office after taking high dose iodine for a few months, and report they feel fine, however, their thyroid labs are “out of wack” which disturbs their endocrinologust or primary care doctor. The TSH may be quite elevated (in the 50-70 range), caused by the suppressive effect of Iodine on the thyroid. This reverses upon stopping the high dose iodine, and labs return to normal in a few weeks. High dose Iodine reduces TPO activity, reduces Iodine Uptake and reduces Iodine organification by the thyroid gland. Autoimmune thyroid patients with Hashimotos or Graves are more sensitive to this suppressive effect of Iodine.

Man, N., et al. “Long-term effects of high iodine intake: inhibition of thyroid iodine uptake and organification in Wistar rats.” Zhonghua yi xue za zhi 86.48 (2006): 3420-3424.

TAJIRI, JUNICHI, et al. “Studies of Hypothyroidism in Patients with High Iodine Intake.” The Journal of Clinical Endocrinology & Metabolism 63.2 (1986): 412-417.

[image error]Peripheral Conversion of T4 to T3

The deiodinase enzyme is responsible for the peripheral conversion of T4 to its more biologically active cousin, T3. This is done by removing of an iodine molecule from the tyrosine skeleton. About 20% of patient have difficulty with peripheral conversion of T4 to T3. These are the patients who do well by switching from Levothyroxine to NDT which contains T3 as well as T4.

Medical Model Determines Thyroid Usage

CASH Model-NDT: More Time w Pt. 30 min. Suppressed TSH May be required for adequeate treatment. Labs: Look at TSH, and FT3, FT4. Spend 5 min explaining risks and adverse effects of thyroid pills.

Insurance Model – Synthroid Levo : Less Time w Pt. 3-10 min. Keep TSH in Range, Adjust T4 Dosage based on TSH in range. No time to explain adverse effects,

Jeffrey Dach MD

7450 Griffin Road, Suite 190

Davie, Fl 33314

954-792-4663

www.jeffreydachmd.com

www.drdach.com

www.naturalmedicine101.com

www.bioidenticalhormones101.com

www.truemedmd.com

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Published on September 03, 2017 10:33

ICU Nurse Assaulted by Police Thugs While Treating Patient

ICU Nurse Assaulted by Police Thugs While Treating Patient

Alex Wubbels, an ICU nurse in the Burn Unit, was assaulted and falsely arrested for refusing a blood draw blood on her comatose patient. She was handcuffed and dragged out of the hospital screaming by police detectives while video cameras recorded the event.

State and constitutional law is very clear that blood samples may not be obtained without satisfying one of three criteria, 1) the patient is under arrest, 2) the patient gives consent, or 3) there is a warrant for the procedure. Since the police officer admitted none of these criteria were fulfilled, the nurse stood her ground and refused the blood draw on her comatose patient.

Above image: Angry protesters assembled in front of Salt Lake Police Department demanding that Detective Jeff Payne be fired for arresting without cause and manhandling ICU nurse Alex Wubbels. Courtesy of Salt Lake tribune.

The video from the police body camera, (now public domain), clearly shows the police office assaulting and manhandling the nurse who is led away in handcuffs screaming. The hospital security police stood by without lifting a finger to protect the ICU nurse from the overly aggressive police officer.

Utah Nurse DRAGGED out of Hospital by Police ‘This isn’t right”

In her interview, Alex Wubbels, the ICU nurse was incredibly restrained saying, “The police should be respectful of health care workers”. In the old days when I worked the emergency room, and occasionally did procedures in the ICU, this type of event was unheard of, and it would be unthinkable this would ever happen. The police were very respectful of health care workers in the hospital for a very good reason. They knew they could easily be injured on duty, and they relied on the Emergency Room staff to save their lives. In the event of a gunshot injury or trauma, ER health care could be depended upon. Police department chief Mike Brown reiterated this sentiment in his public statement :

“We know that if we are ever hurt in the line of duty, it is their (the ER nurses) caring hands that will perhaps save our lives one day.”

Obviously, times have changed. This lack of respect for health care workers by the police is a danger sign for our society and culture. When health care workers can be intimidated, assaulted and falsely arrested by the police, then all of us are at risk. This type of incident really worries me because it may represent a marker for a general trend toward greater militarization of the police, increased police use of force, increased police killings, and increased police action claims and settlements (see charts below with this data). This is not good and we need to reverse this trend before it becomes too late..

Below Image : In this July 26, 2017, frame grab from video taken from a police body camera and provided by attorney Karra Porter, nurse Alex Wubbels is arrested by a Salt Lake City police officer at University Hospital in Salt Lake City. The officer dragged Wubbels out of the hospital in handcuffs (screaming) when she refused to allow blood to be drawn from an unconscious patient. (Salt Lake City Police Department/Courtesy of Karra Porter via AP)

[image error]Who Are the Winners and Losers?

The obvious winner here is Alex Wubbels, the ICU nurse who will no doubt eventually collect 10 million dollars in damages from the city. The assumption here is that the police department carries insurance for this type of thing. As for the two police officers in question who were given administrative leave, Detective Jeff Payne and Lt. James Tracy, they may no longer be popular with their fellow officers who go out into the field every day wondering if the ER staff will react unfavorably when they arrive needing medical care. These are the big losers in all this.

Make a few calls and send a few emails to express your feelings:

Gov. Gary Herbert

send an email to the Governor https://www.utah.gov/governor/contact/

The Office of Governor Gary R. Herbert

350 North State Street, Suite 200

PO Box 142220

Salt Lake City, Utah 84114-2220

Phone: 801-538-1000

Toll Free: 800-705-2464

Salt Lake County District Attorney Sim Gill

email: districtattorney@slco.org.

Mayor Jackie Biskupski

http://www.slcmayor.com/contact/

801-535-7704

mayor@slcgov.com

Chief of Police Mike Brown

askthechief@slcgov.com

The two police officers in question who were given leave:

Detective Jeff Payne and Lt. James Tracy

Above Left Image: Use of Force Arrests Have Skyrocketed in Salt lake City: This is not an isolated incident.

Left Image: Police Action Claims and Settlements Going Up in NYC

This is not an isolated incident.

Washington Post Story on ICU Nurse Arrested

……..

Above Left Image Killings by Police Going UP Dramatically. This is not an isolated incident.

Jeffrey Dach MD

7450 Griffin Road Suite 190

Davie, Fl 33314

954-792-4663

Links and References

By all accounts, the head nurse at the University of Utah Hospital’s burn unit was professional and restrained when she told a Salt Lake City police detective he wasn’t allowed to draw blood from a badly injured patient.

The detective didn’t have a warrant, first off. And the patient wasn’t conscious, so he couldn’t give consent. Without that, the detective was barred from collecting blood samples — not just by hospital policy, but by basic constitutional law.

Still, Detective Jeff Payne insisted that he be let in to take the blood, saying the nurse would be arrested and charged if she refused.

Nurse Alex Wubbels politely stood her ground. She got her supervisor on the phone so Payne could hear the decision loud and clear. “Sir,” said the supervisor, “you’re making a huge mistake because you’re threatening a nurse.”

Payne snapped. He seized hold of the nurse, shoved her out of the building and cuffed her hands behind her back. A bewildered Wubbels screamed “help me” and “you’re assaulting me” as the detective forced her into an unmarked car and accused her of interfering with an investigation.

‘This is crazy,’ sobs Utah hospital nurse as cop roughs her up, arrests her for doing her job

By Derek Hawkins September 2 at 12:16 AM

https://www.reuters.com/article/us-ut...

Utah nurse claims police assault after she refused patient blood sample Reuters Staff

A nurse at a Utah hospital was assaulted by a police officer last month after declining to allow him to obtain a sample of an unconscious patient’s blood because he had neither a warrant nor the patient’s consent, media reported.

Prosecutors in Utah will consider criminal charges against the officer, an official said on Friday.

Video of the July 26 incident from Salt Lake City police officers’ body-worn cameras showed Alex Wubbels, dressed in blue medical scrubs, consulting with colleagues before showing the waiting officers a printout of the University of Utah Hospital’s policy on providing blood samples to test for alcohol or drugs.

The patient was a truck driver who was comatose when he was brought to the hospital burns unit after a crash with a vehicle being driven by someone fleeing police, the Deseret News reported.

Wubbels explained to the officers that under the policy, which she said was agreed to by the police department, she would need a warrant, the patient’s consent or the patient would need to be under arrest.

Utah Nurse DRAGGED out of Hospital by Police ‘This isn’t right”

KUTV exclusive interview with U of U nurse

“The police should be respectful of health care workers”

Detective Jeff Payne: 5 Fast Facts You Need to Know

Video shows Utah nurse screaming, being handcuffed after refusing to take blood from unconscious victim

A nurse says she was assaulted and illegally arrested by a Salt Lake City police detective for following a hospital policy that does not allow blood draws from unconscious patients.

Footage from University Hospital and officer body cameras shows Detective Jeff Payne and nurse Alex Wubbels in a standoff over whether the policeman should be allowed to get a blood sample from a patient who had been injured in a July 26 collision in northern Utah that left another driver dead.

Wubbels says blood cannot be taken from an unconscious patient unless the patient is under arrest, unless there is a warrant allowing the draw or unless the patient consents. The detective acknowledges in the footage that none of those requirements is in place, but he insists that he has the authority to obtain the draw, according to the footage.

At one point, Payne threatens to take Wubbels to jail if he doesn’t get the sample, and he accuses her of interfering with a criminal case.

“I either go away with blood in vials or body in tow,” Payne says.

After Wubbels consults with several hospital officials and repeats the policy, Payne tells her she is under arrest and grabs her, pulling her arms behind her back and handcuffing her. The footage shows the detective dragging Wubbels out of the hospital and putting her inside a patrol car as she screams, “Help! Help! Somebody help me! Stop! Stop! I did nothing wrong!”

A University of Utah police officer and other officers, who provide security for the hospital, were present at time of the arrest and did not intervene.

As he stands in the hospital parking lot after the arrest, Payne says to another officer that he wonders how this event will affect an off-duty job transporting patients for an ambulance company.

“I’ll bring them all the transients and take good patients elsewhere,” Payne says.

Officer placed on leave as DA launches criminal investigation into arrest of Utah nurse

Posted 3:24 pm, September 1, 2017, by Mark Green, Updated at 08:09PM, September 1, 2017

How Many Americans Do the Cops Kill Each Year?

By Daniel Bier On 7/16/16 at 11:00 AM

NYC to Step Up Defense of Police Misconduct Cases

The filing of police brutality, and the Violation of Civil Rights, cases against the City of New York, have been on the rise in recent years. Now the legal division of the City, the Corporation Counsel, is forming a new legal task force to more diligently fight what the consider those case they consider without merit or frivolous. In the past, according to the City’s top lawyer, the City was more likely to settle those cases for small amounts rather than fight them. This graph clearly shows the rise in cases arising from police misconduct and the increased payout by the City to settle them.

Police Chief Interview

We know that if we are ever hurt in the line of duty, it is their caring hands that will perhaps save our lives one day.

SLC mayor, police chief apologize for officer who arrested nurse; criminal investigation to follow

Police department places two officer on leave as internal investigation continues.

Gov. Gary Herbert

send an email to the Governor

https://www.utah.gov/governor/contact/

The Office of Governor Gary R. Herbert

350 North State Street, Suite 200

PO Box 142220

Salt Lake City, Utah 84114-2220

Phone: 801-538-1000

Toll Free: 800-705-2464

Salt Lake County District Attorney Sim Gill

email: districtattorney@slco.org.

Mayor Jackie Biskupski

http://www.slcmayor.com/contact/

801-535-7704

mayor@slcgov.com

Chief Mike Brown

askthechief@slcgov.com

The two police officer in question who were suspended

Detective Jeff Payne

Lt. James Tracy

link to this article: http://wp.me/p3gFbV-5be

Jeffrey Dach MD

7450 Griffin Road, Suite 190

Davie, Fl 33314

954-792-4663

www.jeffreydachmd.com

www.drdach.com

www.naturalmedicine101.com

www.bioidenticalhormones101.com

www.truemedmd.com

Disclaimer click here: www.drdach.com/wst_page20.html

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Published on September 03, 2017 05:41

July 30, 2017

Statin Denialism Internet Cult with Deadly Consequences

[image error] Statin Denialism: an Internet Cult with Deadly Consequences

An editorial by Cleveland Clinic cardiologist Steven Nissen (above image) appeared in the Annals of Internal Medicine this week lamenting the problem of “Statin Denialism” on the Internet.(1-2)

Yesterday, I received this reply to the editorial from Alfred E Hackenbush, an anonymous blogger who somehow found my email address and sent me the following enlightening message:

[image error]Quote Alfred E Hackenbush: Dr Steve Naissan is my hero because his excellent editorial reveals the evil Mom and Pop bloggers operating out of their basements who have convinced millions of American to stop taking their statin drugs. We all know that statins are miracle drugs, and millions of gullible Americans are just dropping off like flies because they have been hoodwinked into stopping their miracle Statin Drug. However, let me be clear. I suggest this is not the “Real Problem”. The real problem is “Statin Drug Denialists” lurking in the academic medical community, and publishing their “Statin Denialism” articles in the mainstream medical literature. Above two images of Steven E Nissen MD courtesy of New York Times and Cleveland Clinic.

[image error] Statin Denialists in the academic cardiology community such as Dr Edward Gill Professor of Cardiology at University of Colorado actually have DENIED that statin drugs have any benefit for reducing calcium score.

I just can’t believe that!

Left image photo of Alfred E Hackenbush courtesy of Mad Magazine.

Dr Gill states:

“five randomized controlled trials have demonstrated that not only does statin treatment not reduce coronary calcium, but in fact, the progression of coronary calcium by CT scanning is indistinguishable from placebo treatment.” (Curr Atheroscler Rep. 2010 Mar;12(2):83-7.).

Another denialist is William R Ware, PhD, Emeritus Professor University of Western Ontario Canada, who wrote in 2009 that modern imaging studies have falsified the cholesterol theory of atherosclerosis. Dr Ware says:

“Contrary to the conventional wisdom, total cholesterol (TC) and LDL cholesterol in asymptomatic individuals are not associated

with either the extent or progression of coronary plaque, as quantified either by electron beam tomography (EBT) or coronary CT angiography” (Med Hypotheses. 2009 Oct;73(4):596-600.)

Dr Ware also says this data has been largely ignored by mainstream cardiology. He says,

“The evidence falsifying the hypothesis that LDL drives atherosclerosis has been largely ignored.”

These denialists are not mom and pop bloggers on the internet. These Statin Denialists are in the mainstream medical literature!!! They must be identified and reported to the thought police ! Denialists… we know who you are and we are coming for you!![image error]

Signed: Alfred E Hackenbush,

Grand Wizard of DenialismWatch.com

442 Fruitcake Street

Nuttsville, Pennsylvania

Above left image courtesy of Statin DenialismWatch.com

Donations to Statin DenialismWatch.com may be sent by carrier pigeon to: DenialismWatch.com at 4123 Waco Nut Drive, Elephant Butte, New Mexico, 87935. (by the way, that’s the name of a real city)

Links and References:

1) Nissen, Steven E. “Statin Denial: An Internet-Driven Cult With Deadly ConsequencesStatin Denial: An Internet-Driven Cult With Deadly Consequences.” Annals of Internal Medicine.

2) Steve Nissen says the battle for patients’ hearts and minds is being lost by Larry Husten, CardioBrief July 24, 2017

3) Gill, Edward A. “Does statin therapy affect the progression of atherosclerosis measured by a coronary calcium score?.” Current atherosclerosis reports 12.2 (2010): 83-87.

4) Ware, William R. “The mainstream hypothesis that LDL cholesterol drives atherosclerosis may have been falsified by non-invasive imaging of coronary artery plaque burden and progression.” Medical hypotheses 73.4 (2009): 596-600. cholesterol atherosclerosis falsified coronary artery plaque Ware Medical Hypotheses 2009

5) Steven Nissen conflicts of interest disclosure: Dr. Nissen reports grants from Esperion Therapeutics, during the conduct of the study; grants from Amgen, grants from Pfizer, grants from Astra Zeneca, outside the submitted work; .

6) Nissen reported receiving research support from Amgen, Abbvie, AstraZeneca, Cerenis, Eli Lilly, Esperion Therapeutics, Novo-Nordisk, The Medicines Company, Orexigen, Pfizer, and Takeda and consulting for a number of pharmaceutical companies without financial compensation (all honoraria, consulting fees, or any other payments from any for-profit entity are paid directly to charity, so neither income nor any tax deduction is received).

7) Cleveland Clinic Dr. Shamelessly Promotes Statin Drugs Calling Side Effects ‘Imagined’ Wednesday, July 26th 2017 at 11:00 am Sayer Ji, Founder GreenMEdINFO

8) I Admit It: I’m A Member Of The Cult Posted by Tom Naughton in Bad Science, Media Misinformation, Random Musings…special note: to Tom Naughton…I hate you because your post is actually a lot funnier than mine…

9) Will Stopping Statins Kill People? The statin skirmishes of recent years have turned into bitter conflict. Dr. Nissen says stopping statins will lead to many deaths. What about side effects? Joe Graedon July 27, 2017

Laughing All the Way to the Bank

[image error] Left image : Doctor Receiving Financial Stipends, Research awards, speaking fees etc from statin drug makers: Courtesy of the best you magazine

Laughing all the way to the bank

Jeffrey Dach MD

7450 Griffin Road

Suite 190

Davie, Fl 33314

954 792 4663

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Published on July 30, 2017 06:27

July 3, 2017

Cancer Immune System Evasion with Progesterone-Induced Blocking Factor

Cancer Immune System Evasion with Progesterone-Induced Blocking Factor

In part one of this series, we discussed strategies to eradicate cancer stem cells using Doxycycline, and high dose vitamin C. Unfortunately, a few cancer stem cells, however small in number, will always remain behind at the end of treatment. These will again grow into sizable tumor masses capable of metastasis to remote areas of the body. The new tumors may even be more treatment resistant and more aggressive than the original cell type. How can we avoid this scenario ?

You might ask the question, why doesn’t the immune system recognize these cancer cells as “foriegn invaders” and kill them as they do for other invaders? After all, the cancer cells are genetically different from the host cells. How do the cancer cells evade the immune system?

The answer lies in the observation made over a hundred years ago by Dr Beard, of the similarity between embryo implantation and tumor metastasis.(1) Cancer cells invade and induce new blood vessels similar to trophoblast growth into the endometrium during pregnancy, and both are governed by a protein called PIBF, progesterone inducing blocking factor. PIBF suppresses the activity of NK killer cells of the immune system, allowing the cancer cells to evade surveillance by the immune system.

Treatment of cancer cells with progesterone upregulates PIBF, while blocking progesterone receptors with a drug called Mifepristone, prevents secretion of PIBF, and renders the cancer cell vulnerable to attack by the immune system.

Dr Wan in his 2015 Oncotarget article suggested Mifepristone together with a platelet inhibitor and the antibiotic doxycycline could prevent metastatic disease.(1) Mifepristone inhibits adhesion of Circulating Tumor Cells to vascular endothelium.

Working with a Glioblastoma brain cancer cell model, Dr Gutiérrez-Rodríguez found that PIBF promotes proliferation, migration, and invasion of human glioblastoma cells.(2) Likewise for Leukemia cell types, Dr. Check in 2009 found that 100% of human leukemia cell lines express mRNA for the PIBF protein.(3) PIBF protein expression was inhibited by the progesterone receptor blocker, mifepristone.

Links and References

1) https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4742096/

Wan, Liyuan et al. “Aspirin, Lysine, Mifepristone and Doxycycline Combined Can Effectively and Safely Prevent and Treat Cancer Metastasis: Prevent Seeds from Gemmating on Soil.” Oncotarget 6.34 (2015): 35157–35172.

Recent scientific advances have increased our understanding of the cancer metastatic complexities and provided further impetus for new combination therapies to prevent cancer metastasis. Here, we demonstrated that a combination (HAMPT) of aspirin, lysine, mifepristone and doxycycline can effectively and safely prevent cancer metastasis. The pharmaceutically-formulated HAMPT inhibited adhesion of cancer cells to either endothelial cells or extracellular matrix via down-regulating cell adhesion molecules ICAM-1 and a4-integrin. HAMPT inhibited the cloak effect by activated platelets on cancer cells, thereby interfering adhesion and invasion of cancer cells to the underlying stroma. At the effective concentration, HAMPT induced cancer cells into dormancy with minor inhibition on cell viability. Four-day pretreatment followed by 30-day oral administration of HAMPT (33.5-134 mg/kg) to the mice inoculated with cancer cells produced significant inhibition on cancer metastasis dose-dependently without marked side effects. Fifty-day rat toxicity study with HAMPT at doses (335-1340 mg/kg) 20-fold higher than its therapeutic dose produced no significant toxicity. Interestingly, the acute toxic death could not be reached at the maximum administrable dose (5 g/kg). This proof-of-concept study provides the first conceptual evidence that cancer metastasis can be controlled by using affordable old drugs to restrain circulating tumor cells from gemmating on the metastatic soil without the need for cytotoxicity.

metapristone (the active mifepristone metabolite) has a safe and effective profile as a cancer metastasis chemopreventive agent by inhibiting adhesion of CTCs to vascular endothelium

We proposed that the initiation of CTC adhesion to the local vascular endothelium is the first and important step for CTCs to start the metastatic cascade.HAMPT prevents cancer cells from cloaked or aggregated by platelets

As the molecular understanding of the biological functions necessary for metastasis increases, it becomes important to develop a comprehensive cancer metastasis chemoprevention strategy that targets not only the intrinsic growth of disseminated CTCs, but also their necessary adhesion and invasion to endothelial layer in the distant metastatic organs, including the bone marrow. Most of CTCs die in the circulation, presumably due to the loss of matrix-derived survival signals, circulatory shear stress, or anoikis [16]. Mifepristone, aspirin, lysine and doxycycline hyclate work differently at distinct metastatic targets and pathways.

metapristone

Interestingly, it seems like that there are some similarity between embryo implantation and tumor metastasis [34], which constructs the base for the abortifacient mifepristone to act as a metastatic chemopreventive. Patients already took mifepristone for as long as 14 years [35]. The safety profile of mifepristone makes it well-suited for a safe metastatic chemopreventive candidate.

2) https://www.hindawi.com/journals/bmri/2017/1295087/

Gutiérrez-Rodríguez, Araceli, Valeria Hansberg-Pastor, and Ignacio Camacho-Arroyo. “Proliferative and Invasive Effects of Progesterone-Induced Blocking Factor in Human Glioblastoma Cells.” BioMed research international 2017 (2017).

These data suggest that PIBF promotes proliferation, migration, and invasion of human glioblastoma cells.

3) https://www.ncbi.nlm.nih.gov/pubmed/18842348

Med Hypotheses. 2009 Jan;72(1):87-90. doi: 10.1016/j.mehy.2008.05.042. Epub 2008 Oct 7.

Support for the hypothesis that successful immunotherapy of various cancers can be achieved by inhibiting a progesterone associated immunomodulatory protein.Check JH1, Dix E, Sansoucie L.

A hypothesis was proposed that cancer cells may utilize a pre-existing mechanism that pregnant mammals use to avoid natural killer cell immune surveillance of the fetus. The hypothesis suggested that those cancer cells that are able to proliferate may have found a way to cause the expression of the immunomodulatory protein known as the progesterone induced blocking factor (PIBF). The cancer cells could find an alternate pathway to make this protein that does not require progesterone secretion, or the cancer cells may actually utilize progesterone and thus make PIBF in a similar fashion to normal pregnancy. If the former mechanism was operational, then one could develop monoclonal antibody type therapy directed to this unique protein not needed for normal body functions. However, if the latter pathway involving progesterone secretion is operational, then there would be drugs already on the market, e.g., the progesterone receptor antagonist mifepristone that could be used to treat these cancers. In vitro data has shown that 100% of human leukemia cell lines express mRNA for the PIBF protein. Some leukemia cell lines have been found that actually express the PIBF protein. In fact adding progesterone to the culture media upregulated PIBF protein expression and mifepristone inhibited it. Controlled studies in various murine spontaneous cancers not known to be associated with progesterone receptors showed increased length and quality of life following mifepristone therapy. Anecdotal improvement in advanced widely metastatic human cancers has also been found. Thus there is now experimental data to support this hypothesis and a new door to a completely different type of cancer therapy has been opened.

4) Szekeres-Bartho, Julia, and Beata Polgar. “PIBF: the double edged sword. Pregnancy and tumor.” American Journal of Reproductive Immunology 64.2 (2010): 77-86. PIBF the double edged sword Pregnancy and tumor Szekeres-Bartho Julia Beata Polgar A J Reproductive Immunology 2010

!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!

5) http://ar.iiarjournals.org/content/29/8/2977.full

Check, Jerome H., et al. “Mifepristone treatment improves length and quality of survival of mice with spontaneous leukemia.” Anticancer research 29.8 (2009): 2977-2980.

Mifepristone was found to suppress expression of the progesterone-induced blocking factor (PIBF). Progesterone-induced blocking factor suppresses natural killer cell activity.

The objective of the present study was to determine if treatment of mice with spontaneous murine lymphocyte leukemia with the progesterone receptor antagonist mifepristone could improve length and quality of life. Materials and Methods: Sixty-one mice were gavaged with mifepristone and 33 controls with olive oil. Quality of life was determined by body conditioning score (BCS). Treatment was initiated when the mice were 6 months old. Results: Within 2 weeks of therapy only 11.4% of the mifepristone treated mice died vs. about 50% of controls. The BCS was 5 (highest quality) in 82% of treated mice vs. 11% of controls after 2 weeks of therapy. Conclusion: Mifepristone therapy should be further evaluated for treating leukemia and lymphoma.

6) http://ar.iiarjournals.org/content/34/5/2413.full

Check, Jerome H., et al. “Mifepristone Causing Complete Remission of Rapidly Advancing Leukemia with Measurement of Progesterone-induced Blocking Factor.” Anticancer research 34.5 (2014): 2413-2416.

one of the theories of how PIBF can aid malignant tumors to escape immune surveillance is that the tumor influences gamma/delta T-cells in the tumor microenvironment to secrete PIBF, which in turn inhibits NK cell cytolytic activity in the tumor microenvironment

!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!

see Figure 7: PIBF is sensitive to nocodazole (similar to mebendazole) and colocalizes with the centrosomal protein ?-tubulin.

7) http://onlinelibrary.wiley.com/doi/10.1002/ijc.20326/full

Lachmann, Margit, et al. “PIBF (progesterone induced blocking factor) is overexpressed in highly proliferating cells and associated with the centrosome.” International journal of cancer 112.1 (2004): 51-60.

PIBF (Progesterone Induced Blocking Factor) was discovered in the context of reproductive immunology as a secreted product of human pregnancy lymphocytes and described as an immunomodulatory molecule relevant for the maintenance of pregnancy

The disappearance of the PIBF signal upon nocodazole treatment and the appearance of two PIBF signals on opposite sides of the nuclei in dividing cells suggested that PIBF might associate with the microtubule organizing center (MTOC) or centrosome.

In CMAP, the MBZ-induced gene expression profile correlated strongly with nocodazole a well-known tubulin inhibitor with chemical structure similarity to MBZ (mebendazole)

Association of PIBF with the centrosomes is clearly demonstrated in the present study. The nocodazole-sensitivity of the PIBF-centrosome interaction suggests that PIBF is not an integral component of the centrosome but rather a microtubule-associated protein. This is supported by preliminary copurification studies with ?-tubulin, where no direct interaction of PIBF with ?-tubulin was detected (data not shown).

nocodazole Progesterone Induced Blocking Factor

8) https://www.ncbi.nlm.nih.gov/pubmed/27919975

Anticancer Res. 2016 Dec;36(12):6511-6513.

Long-term High-quality Survival with Single-agent Mifepristone Treatment Despite Advanced Cancer. Check JH1,2, Check D2, Wilson C2, Lofberg P2.

We show long-term high-quality survival following single-agent treatment with a progesterone receptor antagonist in two cases of advanced metastatic cancer. Because no biopsy was performed (patient refused) the exact type of lung cancer was not determined but the majority of oncologists who evaluated the patient thought that the rapid onset and syndrome of inappropriate anti-diuretic hormone was more consistent with small-cell lung cancer. The US Food and Drug Association granted a compassionate-use investigational new drug approval for use of single-agent 200 mg mifepristone orally/day to a moribund woman with never-treated metastatic lung cancer and a male with bilateral renal cell carcinoma who had undergone only a unilateral hemi-nephrectomy. Both had long-term high-quality survival (5 years for the patient with lung cancer with complete remission of all lung lesions, and 12 years for the male patient with kidney cancer). Neither patient had any side-effects from mifepristone therapy.

CONCLUSION:These cases helped influence the US Food and Drug Association in granting an investigator-initiated investigational new drug study on advanced non-small cell lung cancer.

9) http://www.tandfonline.com/doi/abs/10.1080/17446651.2017.1314783

Check, Jerome H. “The role of progesterone and the progesterone receptor in cancer.” Expert Review of Endocrinology & Metabolism 12.3 (2017): 187-197.

There is an abundance of accumulating data strongly suggesting there is a key role for the progesterone receptor in the molecular events effecting the growth or containment of a variety of cancers. This knowledge should lead to novel new strategies to combat various cancers, including drugs classified as progesterone receptor modulators or monoclonal antibodies against some of the key proteins needed for cancer proliferation by suppressing immune surveillance.

Expert commentary: Discussion is made about a unique immunomodulatory protein called the progesterone induced blocking factor (PIBF). The role of this protein, that is unique to rapidly growing cells, may hold a key to how the cancer cells escape immune surveillance. Thus, techniques to suppress the intracytoplasmic isoforms of PIBF may play a significant role in the fight against all cancers, not just the ones with the classic nuclear progesterone receptors.

10) https://www.ncbi.nlm.nih.gov/pubmed/18225679

Clin Exp Obstet Gynecol. 2007;34(4):207-11.

Evidence that progesterone receptor antagonists may help in the treatment of a variety of cancers by locally suppressing natural killer cell activity.Check JH, Sansoucie L, Chern J, Amadi N, Srivastava M, Larece K.

To propose a novel concept that progesterone receptor antagonists, e.g., mifepristone, may prove effective in treating a variety of cancers–even those not shown to be hormonally dependent or possessing progesterone receptors.

METHODS:Multiple human leukemia cell lines were evaluated for mRNA expression of an immunomodulatory protein called the progesterone-induced blocking factor (PIBF) that suppresses natural killer (NK) cell activity during normal pregnancy. Furthermore, we evaluated the effects of progesterone (P) and mifepristone in PIBF protein expression. Finally, the effect of mifepristone treatment of mice with advanced leukemia was evaluated.

RESULTS:All tumor cell lines evaluated were found to express mRNA for PIBF and some were found to even express the PIBF protein. The addition of PROGESTERONE to the media increased the expression of PIBF and mifepristone downregulated its expression. Treatment of mice with spontaneous leukemia when they already had extensive disease seemed to increase the length and quality of their life.

CONCLUSIONS:These data and other experience with mice with lung cancer and some anecdotal human cancer experience suggest that various cancers may utilize similar mechanisms used by the fetus to escape NK cell surveillance. Mifepristone and other progesterone receptor antagonists may deserve a clinical trial in human cancer even where there is no knowledge of the presence of progesterone receptors.

11) http://ar.iiarjournals.org/content/34/5/2385.full

Check, Jerome H., et al. “Evidence that mifepristone, a progesterone receptor antagonist, can cross the blood brain barrier and provide palliative benefits for glioblastoma multiforme grade IV.” Anticancer research 34.5 (2014): 2385-2388.

It has been hypothesized that an immunomodality protein expressed by gamma delta thymic (T) cells with up-regulation of progesterone receptors will be produced after these cells have been exposed to a high concentration of progesterone. It has been hypothesized that this protein, known as the progesterone-induced blocking factor (PIBF) suppresses natural killer cell activity in the tumor microenvironment and thus provides one mechanism allowing cancer cells to escape immune surveillance, similar to the immunosuppressant effect that this protein has on natural killer cells during normal pregnancy

This hypothesis was supported by the demonstration of PIBF mRNA expression in all human leukemia cell lines tested in one study, including T-cell leukemia, seven myeloid leukemia and 10 B-cell leukemia cell lines (7). In that same study, 4 out of 10 leukemia cell lines tested for expression of this PIBF protein exhibited up-regulation of PIBF expression when extra progesterone was added to the culture medium, and down-regulation of PIBF expression was found with use of the progesterone receptor antagonist mifepristone

12) https://www.ncbi.nlm.nih.gov/pubmed/17701593

Leuk Lymphoma. 2007 Aug;48(8):1610-7.

Expression and modulation of progesterone induced blocking factor (PIBF) and innate immune factors in human leukemia cell lines by progesterone and mifepristone.

Srivastava MD1, Thomas A, Srivastava BI, Check JH.

Progesterone (P), required for successful pregnancy, influences autoimmune, infectious, and malignant diseases via adaptive and innate immune effects. P induces NK inhibitor progesterone induced blocking factor (PIBF) in CD8+ T cells. PIBF isoforms could permit solid tumor immune escape. Expression and modulation of PIBF and innate immune proteins by P in leukemia cells and leukocyte subpopulations have not been reported. Ten T, seven myeloid, six B, five epithelial, fibroblast BG9, G-CSF mobilized CD34+ stem cells, and peripheral blood mononuclear cells were screened for PIBF mRNA by RT-PCR, and protein by immunohistochemistry in SRIK-NKL, MOT, U937, HL60, R-CLL, MD-E, 729pH6neo, SRIH-B(ATL), SRIK-B(T-PLL), and MeWo. Cell lines expressing PIBF and exemplifying myeloid/monoblast, natural killer/T, and B lineages were cultured with and without 0.5 – 5 microM P or 0.5 – 0.05 microM mifepristone (RU486) for 24 h. Subsequently they were examined for changes in the expression of mRNA by RT-PCR and protein by immunohistochemistry for PIBF and some innate immune factors. All cells expressed PIBF mRNA; protein only in four (SRIK-NKL, U937, SRIK-B(T-PLL) and HL60) out of 10 cell lines tested. P increased and RU486 decreased PIBF in U937, SRIK-B(T-PLL) and SRIK-NKL. P upregulated TLR-4 in U937, and HNP1 – 3, LL-37, IRAK-2, and IRAK-4 in multiple lines and RU486 down regulated these. PIBF may be used by some leukemias to evade immune surveillance and is a potential therapeutic target. P may impact infection and autoimmunity via effects on LPS receptor, TLR signaling, and antimicrobial peptides.

13) https://bmccancer.biomedcentral.com/articles/10.1186/1471-2407-13-35

Brandhagen, BreeAnn N., et al. “Cytostasis and morphological changes induced by mifepristone in human metastatic cancer cells involve cytoskeletal filamentous actin reorganization and impairment of cell adhesion dynamics.” BMC cancer 13.1 (2013): 35.

Cytostatic concentrations of mifepristone induced alterations in the cellular structure of a panel of aggressive, highly metastatic cancer cells of different tissues of origin. Such changes were associated with re-distribution of actin fibers that mainly form non-adhesive membrane ruffles, leading to dysregulated cellular adhesion capacity.

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

Progesterone Receptor Blocker for Uterine Fibroids

14) https://www.glowm.com/Critical_current_issue/page/5

Ulipristal Acetate: a novel medical therapy for uterine fibroids

Vikram Sinai Talaulikar MD, MRCOG

Clinical Fellow in Reproductive Endocrinology and Assisted Reproduction, University College London Hospital, London, UK

Uterine fibroids – current management options and the need for an effective medical therapy

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

Platelets and Metastases

15) https://www.ncbi.nlm.nih.gov/pubmed/21258396/

Nat Rev Cancer. 2011 Feb;11(2):123-34. doi: 10.1038/nrc3004.

Contribution of platelets to tumour metastasis.

Gay LJ1, Felding-Habermann B.

Extensive experimental evidence shows that platelets support tumour metastasis. The activation of platelets and the coagulation system have a crucial role in the progression of cancer. Within the circulatory system, platelets guard tumour cells from immune elimination and promote their arrest at the endothelium, supporting the establishment of secondary lesions. These contributions of platelets to tumour cell survival and spread suggest platelets as a new avenue for therapy.

16) http://www.tldp.com/issue/202/LettersMartin.htm

Anti-Cancer Effect of Dipyridamole

17) https://www.ncbi.nlm.nih.gov/pubmed/9834413

dipyridamole daily orally (75 mg)

18) https://www.ncbi.nlm.nih.gov/pubmed/17470859

Dipyridamole 75 mg was administered orally three times daily during the FU administration.

Mantle Cell Lymphoma

19) https://www.ncbi.nlm.nih.gov/pubmed/11293905

Am J Clin Pathol. 2001 Apr;115(4):567-70.

Platelet satellitism as presenting finding in mantle cell lymphoma. A case report.

Cesca C1, Ben-Ezra J, Riley RS.

Platelet satellitism surrounding polymorphonuclear neutrophils has been observed almost exclusively in EDTA-treated blood at room temperature. The mechanism underlying this phenomenon is not understood fully. We report a case of platelet rosetting around atypical lymphocytes in peripheral blood smears made from EDTA-treated and untreated blood. Flow cytometry of the peripheral blood sample and immunohistochemical stains of the subsequent bone marrow biopsy specimen revealed a monoclonal B-cell population positive for CD5, CD20, and cyclin D1 and negative for CD3 and CD23; cytogenetic findings revealed a complex karyotype that included t(11;14). These findings were consistent with mantle cell lymphoma. To our knowledge, the finding of platelet satellitism involving mantle cell lymphoma cells in peripheral blood has not been reported previously.

20) Rhodes, E. L., et al. “Dipyridamole for treatment of melanoma.” The Lancet 325.8430 (1985): 693.

21) Spano, Daniela, et al. “Dipyridamole prevents triple-negative breast-cancer progression.” Clinical & experimental metastasis 30.1 (2013): 47-68.

22) https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3829204/

Wang, Chunmei, et al. “Chemoprevention activity of dipyridamole in the MMTV-PyMT transgenic mouse model of breast cancer.” Cancer Prevention Research 6.5 (2013): 437-447. Cancer Prev Res (Phila).in PMC 2014 May 1.

Dipyridamole (DPM) is widely used to prevent strokes and vascular thrombosis. Combination therapy of DPM and antimetabolites has shown synergistic anticancer activity. This study investigated the chemopreventive effects of DPM in the mouse mammary tumor virus promoter driven polyoma middle T oncoprotein (MMTV-PyMT) metastatic breast cancer model. We also investigated the effects of DPM on gene and miRNA expression. Chemopreventive activity was assessed by comparing the time to onset of palpable lesions, primary tumor growth kinetics and the number of lung metastases in transgenic mice treated with DPM or vehicle. Gene expression and microRNA (miRNA) expression profiles of mammary tumor tissues were then analyzed using the Affymetrix GeneChip® or miRNA 2.0 arrays. Real-time quantitative PCR (qPCR) was used to confirm changes in gene expression. Treatment with DPM beginning at the age of four weeks delayed the onset of palpable lesions, delayed tumor progression and suppressed lung metastasis. Microarray gene expression analysis identified 253 genes differentially expressed between DPM-treated and control mammary tumors. miRNA expression analysis revealed that 53 miRNAs were altered by DPM treatment. The results indicate that DPM has chemoprevention activity against breast cancer tumorigenesis and metastasis in mice. The array analyses provide insights into potential mechanisms of DPM’s chemopreventive effects, involving upregulation of several genes and miRNAs known to suppress cancer growth and/or metastasis and downregulation of genes known to promote cancer. Some of these genes have not been previously studied in breast cancer and may serve as novel molecular targets for breast cancer chemoprevention.

23) https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5209474/

Ge, Shu-Min, et al. “Reverse screening approach to identify potential anti-cancer targets of dipyridamole.” American journal of translational research 8.12 (2016): 5187.

Platelets histamine

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24) http://www.lyos.fr/wp-content/uploads/2016/10/Leblanc-blood-2016.pdf

Leblanc, Raphael, and Olivier Peyruchaud. “Metastasis: new functional implications of platelets and megakaryocytes.” Blood 128.1 (2016): 24-31.

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25) https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4186918/

Cancer Metastasis Rev. 2014 Mar; 33(1): 231–269.

Platelets and cancer: a casual or causal relationship: revisited

David G. Menter, Stephanie C. Tucker, Scott Kopetz, Anil K. Sood, John D. Crissman, and Kenneth V. Honn

26) https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4160963/

Front Oncol. 2014; 4: 245. Published online 2014 Sep 11.

Involvement of Platelet–Tumor Cell Interaction in Immune Evasion. Potential Role of Podocalyxin-Like Protein 1. Laura Amo,1,† Estíbaliz Tamayo-Orbegozo,1,† Natalia Maruri,1 Cristina Eguizabal,2 Olatz Zenarruzabeitia,3 Marta Riñón,1 Arantza Arrieta,1 Silvia Santos,2 Jorge Monge,2 Miguel Angel Vesga,2 Francisco Borrego,3,4 and Susana Larrucea1,*

1Regulation of the Immune System Group, BioCruces Health Research Institute, Hospital Universitario Cruces, Barakaldo, Spain

27) https://pdfs.semanticscholar.org/c955/12465e6e7a6ba95355969d91ff14a15e1cd5.pdf

[CANCER RESEARCH 59, 1295–1300, March 15, 1999]

Lysis of Tumor Cells by Natural Killer Cells in Mice Is Impeded by Platelets1

Bernhard Nieswandt, Michael Hafner, Bernd Echtenacher, and Daniela N. Ma ¨ nnel2

Department of Pathology, Tumor Immunology, University of Regensburg, 93042 Regensburg, Germany

Cimetidine Histamine receptor Blocker

28) Saxena, Satya P., et al. “Histamine is an intracellular messenger mediating platelet aggregation.” Science 243.4898 (1989): 1596-1600.

29) https://www.ncbi.nlm.nih.gov/pubmed/9657253

Inflamm Res. 1998 May;47(5):211-20.

The role of histamine in platelet aggregation by physiological and immunological stimuli.

Masini E1, Di Bello MG, Raspanti S, Ndisang JF, Baronti R, Cappugi P, Mannaioni PF.

Platelets participate in allergic and inflammatory processes beside their role in haemostasis and thrombosis. This paper reports the level, the uptake, the metabolism and the release of histamine in human platelets. The effects of exogenous histamine, as well as the receptor and signal transduction of these effects, are also described.

METHODS: Purified suspensions of platelets, prepared from healthy volunteers and from atopic patients, were exposed in vitro to physiological and immunological stimuli. Platelet aggregation was measured by the increase in light transmission; histamine content and release, as well as cytosolic free Ca2+ concentration, were measured fluorimetrically. Platelet histamine forming capacity, and the uptake of exogenous histamine, were measured with a radioisotopic method.

RESULTS: Human platelets contain 72.5 +/- 9.6pmoles of histamine x 10(9) platelets, and their capacity to form histamine is 18.7 +/- 3.5pmoles h(-1)g(-1) protein, which is reduced by alpha-fluoromethylhistidine (10(-5) M) a selective inhibitor of the specific histidine decarboxylase. Human platelets take up the preformed amine by a calcium and energy-dependent process, and the uptake of histamine is reduced by mepyramine, an H1-receptor antagonist, and N,N-diethyl-2-[4-(phenylmethyl) phenoxyl] ethanamine (10(-6) M), a blocker of intracellular histamine receptors. Histamine is also metabolized by human platelets. The exposure of platelets to thrombin (10-60 mUml(-1)) produced a progressive aggregation, associated with histamine release. The same is observed in platelets isolated from atopic patients exposed to anti-IgE antibodies. Exogenous histamine dose-dependently potentiates the aggregation induced by physiological and immunological stimuli. In resting platelets cytosolic calcium level (207 +/- 4.2 nM/10(8) platelets) is increased by thrombin as well as by anti-IgE; this effect is potentiated by 10(-5) M histamine.

CONCLUSIONS: The synergistic effect between histamine and other monoamines on platelet aggregation may explain some aspects of allergic vasculitis in which platelet aggregation is present.

Histamine and platelets

30) https://www.ncbi.nlm.nih.gov/pubmed/2928797

Science. 1989 Mar 24;243(4898):1596-9.

Histamine is an intracellular messenger mediating platelet aggregation.

Saxena SP1, Brandes LJ, Becker AB, Simons KJ, LaBella FS, Gerrard JM.

Author information Department of Pediatrics, University of Manitoba, Winnipeg, Canada.

The results indicate a role for histamine as an intracellular messenger, which in platelets promotes aggregation.

32) https://www.ncbi.nlm.nih.gov/pubmed/20632959

Inflamm Allergy Drug Targets. 2010 Jul;9(3):146-57.

Histamine and histamine receptor antagonists in cancer biology.

Blaya B1, Nicolau-Galmés F, Jangi SM, Ortega-Martínez I, Alonso-Tejerina E, Burgos-Bretones J, Pérez-Yarza G, Asumendi A, Boyano MD.

Histamine has been demonstrated to be involved in cell proliferation, embryonic development, and tumour growth. These various biological effects are mediated through the activation of specific histamine receptors (H1, H2, H3, and H4) that differ in their tissue expression patterns and functions. Although many in vitro and in vivo studies of the modulatory roles of histamine in tumour development and metastasis have been reported, the effect of histamine in the progression of some types of tumours remains controversial; however, recent findings on the role of histamine in the immune system have shed new light on this question. This review focuses on the recent advances in understanding the roles of histamine and its receptors in tumour biology. We report our recent observations of the anti-tumoural effect of H1 histamine antagonists on experimental and human melanomas. We have found that in spite of exogenous histamine stimulated human melanoma cell proliferation, clonogenic ability and migration activity in a dose-dependent manner, the melanoma tumour growth was not modulated by in vivo histamine treatment. On the contrary, terfenadine-treatment in vitro induced melanoma cell death by apoptosis and in vivo terfenadine treatment significantly inhibited tumour growth in murine models. These observations increase our understanding of cancer biology and may inspire novel anticancer therapeutic strategies.

33) https://www.ncbi.nlm.nih.gov/pubmed/10888267/

Semin Cancer Biol. 2000 Feb;10(1):15-23.

Histamine as an autocrine growth factor: an unusual role for a widespread mediator.

Rivera ES1, Cricco GP, Engel NI, Fitzsimons CP, Martín GA, Bergoc RM.

34) https://www.ncbi.nlm.nih.gov/pubmed/7741034

Agents Actions. 1994 Nov;43(1-2):17-20.

Histamine as an autocrine growth factor in experimental mammary carcinomas.

Cricco GP1, Davio CA, Martin G, Engel N, Fitzsimons CP, Bergoc RM, Rivera ES.

35) https://www.ncbi.nlm.nih.gov/pubmed/7605350

Biochem Pharmacol. 1995 Jun 29;50(1):91-6.

H1 and H2 histamine receptors in N-nitroso-N-methylurea (NMU)-induced carcinomas with atypical coupling to signal transducers.

Davio CA1, Cricco GP, Bergoc RM, Rivera ES.

Two specific binding sites for histamine were characterized in the cell membrane of N-nitroso-N-methylurea (NMU)-induced tumors. The first one, with higher affinity (Kd = 4 +/- 2 nM), was further identified as an H2 type, while the lower affinity one (35 +/- 10 nM) corresponded to an H1 receptor. Histamine concentrations up to 50 nM, as well as H2 agonists, significantly enhanced the phosphoinositide turnover by acting through higher affinity H2 receptors. On the other hand, histamine at concentrations over 50 nM and H1 agonists produced a 100% increase in cAMP levels in a response specifically blocked by mepyramine. These H1 and H2 histamine receptors that exhibit different linkages to second messenger systems may prove to be a characteristic of cells with a high proliferating capacity, such as undifferentiated or transformed cells.

36) https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2992892/

Br J Pharmacol. 2010 Oct; 161(4): 755–767.

Histamine receptors and cancer pharmacology

Vanina A Medina1,2 and Elena S Rivera1

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

PIBF and trophoblast invasiveness

37) J Reprod Immunol. 2011 Jun;90(1):50-7.

Progesterone-induced blocking factor (PIBF) and trophoblast invasiveness.

Miko E1, Halasz M, Jericevic-Mulac B, Wicherek L, Arck P, Arató G, Skret Magierlo J, Rukavina D, Szekeres-Bartho J.

Controlled trophoblast invasion is a key process during human placentation and a prerequisite for successful pregnancy. Progesterone is one of the factors to regulate trophoblast invasiveness. Progesterone-induced blocking factor (PIBF) is a progesterone-induced molecule expressed by the trophoblast, and also by tumors. The distribution of PIBF within the first-trimester decidua coincides with sites of trophoblast invasion. Another molecule that has been implicated in the control of trophoblast invasiveness is placental leptin. Leptin inhibits the secretion of progesterone by cytotrophoblast. The aim of this work was to investigate the possible interaction of PIBF and leptins in regulating trophoblast invasion. Paraffin-embedded sections from normal first-trimester placentae, partial moles, complete moles, and choriocarcinomas were reacted with PIBF, leptin, and leptin receptor specific antibodies. PIBF-deficient trophoblast cells were generated using siRNA and leptin receptor was detected on Western blot analysis. The lysates of PIBF-treated cells were used for detecting leptin expression in a protein array. PIBF was expressed in both normal first-trimester villous trophoblast and in partial mole. Compared with this, PIBF expression was markedly decreased in complete mole and absent in choriocarcinoma. Neither leptinR nor leptin were detected in partial mole, whereas both of these molecules were present in complete mole and choriocarcinoma. Leptin receptor expression was upregulated in PIBF-deficient cells, while leptin expression was decreased in PIBF-treated cells. These data suggest that PIBF affects the expression of leptin and its receptor, and that PIBF expression is inversely related to trophoblast invasiveness.

Jerome Check MD

38) Study of Oral Mifepristone as Salvage Therapy in Patients With Advanced or Metastatic Non-Small Cell Lung Cancer Check, Jerome H., M.D., Ph.D.

Collaborator: Corcept Therapeutics

Experimental: mifepristone

mifepristone 300 mg capsule per day, orally in 28-day cycles

39) Check, Jerome H., et al. “Efficacy of the progesterone receptor antagonist mifepristone for palliative therapy of patients with a variety of advanced cancer types.” Anticancer research 30.2 (2010): 623-628.

Mifepristone has been demonstrated to improve longevity and quality of life in mice with spontaneous murine cancer without progesterone receptors and in human colon cancer. The present study evaluated the palliative effect of mifepristone in a variety of different types of human cancer. Patients and Methods: Mifepristone was given at 200 mg daily orally with permission from the Food and Drug Administration to people with widely metastatic human cancer no longer responsive to other chemotherapy regimens. Results: Improvement in pain and energy and/or length of life was found in thymic epithelial cell carcinoma, transitional cell carcinoma of the renal pelvis, leiomyosarcoma, pancreatic carcinoma, malignant fibrous histiocytoma and another case of adenocarcinoma of the colon. Conclusion: Our data demonstrate a palliative role for the use of mifepristone in cancer therapy. Progesterone receptor antagonists should be given a therapeutic trial in larger controlled studies of various malignancies in humans.

All patients reported significant decrease in pain and improved energy within 2 weeks of starting the medication. No one reported any side-effects.

In the United States mifepristone is a restricted drug. It can only be used by licensed abortionists. One needs special permission from the Food and Drug Administration to use it off-label. Approval can only be obtained for cases where no known approved therapy exists or the patient has proven resistant at this time to standard therapy.

40) Check, Jerome H., et al. “Mifepristone may halt progression of extensively metastatic human adenocarcinoma of the colon-case report.” Anticancer research 29.5 (2009): 1611-1613.

The post Cancer Immune System Evasion with Progesterone-Induced Blocking Factor appeared first on Jeffrey Dach MD.

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Published on July 03, 2017 12:19

June 15, 2017

Doxycycline Vitamin C Anti Cancer Synergy

[image error] Doxycycline Vitamin C Anti-Cancer Synergy

Eradicates Cancer Stem Cells

I was simply astounded by a publication appearing last week in Oncotarget on anti-cancer synergy of Doxycyline and vitamin C.(1) This is a really huge breakthrough in cancer research, in our quest for effective non-toxic cancer treatment. Working with MCF7 Breast cancer cell cultures, Lisanti’s group showed the combined use of Doxycycline and Vitamin C was a “lethal metabolic strategy for eradicating cancer stem cells”.(1)

Doxycycline

[image error]Doxycline is a safe common antibiotic used for 50 years. I have seen patients coming into the office on doxycycline for months or even years for treatment of acne or rosacea. Likewise Vitamin C is about as safe as a substance as you can get. Safety studies on lymphoma patients receiving 75 grams of vitamin C Intravenously had no adverse effects. Left image doxycycline courtesy of National Library of Medicine

Cancer Stem Cells Escape from Doxycycline Become Purely Glycolytic Phenotype

In an elegant study, Lisanti’s group created Doxycycline resistant cancer stem cells by successive passage of the cells through higher doses of Doxycycline treatments. Most of the cells were killed by the doxycycline. However the few surviving cells were then allowed to multiply and repopulate, and were again treated with higher doses of doxyxycline. This process was repeated until final cells were indeed Doxycyline resistant, they were immune to the antibiotic.

[image error]Lisanti’s group then did next generation molecular studies on the Dox-R cancer stem cells showing they had assumed a purely glycolytic phenotype.

Above left image Figure 12 from Lisanti (1)

The Dox-Resistant cancer cells were now sensitive to eradication with metabolic perturbation from high dose vitamin C. Vitamin C acts as a glycolysis inhibitor, by targeting (GAPDH) Glyceraldehyde 3-phosphate dehydrogenase, 6th step in glycolysis. Vitamin C also and depletes the (NAD) nicotinamide adenine dinucleotide pool. High dose IV vitamin C easily reached serum concentrations for these lethal effects in the clinical setting.

A few other drugs and natural substances were also effective, namely Berberine, Chloroquin, Atovaquone, Niclosamide etc. ) The authors state, “understanding the metabolic basis of Doxycycline-resistance has ultimately helped us to develop a new synthetic lethal strategy, for more effectively targeting Cancer Stem Cells (CSCs). ”

[image error]Left Image figure 10 from Lisanti(1) Fig A effect of 2DG (2-de-oxyglucose) on both plain MC7 breast cancer stem cells and Dox-resistant cells. Fig B: effect of Vitamin C on Dox Resistant breast cancer stem cells. 100% (complete) cell death at 500 micromolar=0.5 millimolar.

Cancer Stem Cells

Cancer stem cells are the reason why chemotherapy fails for rapidly proliferating cancers. A temporary remission, or reduction in tumor size can be achieved followed by cancer relapse within months.

Conclusion: This Doxycycline/ Vitamin C combination is a dramatic breakthrough in finding an effective targeted cancer stem cell eradication strategy. My hat comes off in admiration and thanks to Michael Lisanti and his group.

Articles with related interest:

My previous report covered Intravenous high dose Vitamin C as effective cancer chemotherapy. My previous report covered use of common antibiotics to target cancer stem cells.

Jeffrey Dach MD

7450 Griffin Road, Suite 190

Davie, Fl 33314

954-792-4663

References

1) http://www.impactjournals.com/oncotarget/index.php?journal=oncotarget&page=article&op=view&path[]=18428&path[%5D=59195

Ernestina Marianna De Francesco, Gloria Bonuccelli, Marcello Maggiolini, Federica Sotgia, Michael P. Lisanti. Vitamin C and Doxycycline: A synthetic lethal combination therapy targeting metabolic flexibility in cancer stem cells (CSCs). Oncotarget, 2015; DOI: 10.18632/oncotarget.18428

2) http://www.medicalnewstoday.com/articles/317902.php

Combining vitamin C with antibiotics destroys cancer stem cells

By Honor Whiteman published Tuesday 13 June 2017 670

3) http://www.worldhealth.net/news/antibiotics-and-vitamin-c-cancer-stem-cells/

Vitamin C and Antibiotic Combo Can Kill Cancer Cells

Posted on June 13, 2017, 6 a.m. in Cancer Immune System Vitamins

Researchers have shown that a combination of antibiotics and Vitamin C can destroy cancer stem cells before they promote the growth of fatal tumors.

4) http://www.nhs.uk/news/2017/06June/Pages/Antibiotics-and-vitamin-C-could-kill-cancer-cells.aspx

Antibiotics and vitamin C could kill cancer cells

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5) https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4558116/

Pulvino, Mary, et al. “Inhibition of COP9-signalosome (CSN) deneddylating activity and tumor growth of diffuse large B-cell lymphomas by doxycycline.”

In searching for small-molecule compounds that inhibit proliferation and survival of diffuse large B-cell lymphoma (DLBCL) cells and may, therefore, be exploited as potential therapeutic agents for this disease, we identified the commonly used and well-tolerated antibiotic doxycycline as a strong candidate. Here, we demonstrate that doxycycline inhibits the growth of DLBCL cells both in vitro and in mouse xenograft models. In addition, we show that doxycycline accumulates in DLBCL cells to high concentrations and affects multiple signaling pathways that are crucial for lymphomagenesis. Our data reveal the deneddylating activity of COP-9 signalosome (CSN) as a novel target of doxycycline and suggest that doxycycline may exert its effects in DLBCL cells in part through a CSN5-HSP90 pathway. Consistently, knockdown of CSN5 exhibited similar effects as doxycycline treatment on DLBCL cell survival and HSP90 chaperone function. In addition to DLBCL cells, doxycycline inhibited growth of several other types of non-Hodgkin lymphoma cells in vitro. Together, our results suggest that doxycycline may represent a promising therapeutic agent for DLBCL and other non-Hodgkin lymphomas subtypes.

nice image

http://pubmedcentralcanada.ca/pmcc/articles/PMC4637276/

Barbie, David A., and Brian K. Kennedy. “Doxycycline: new tricks for an old drug.” Oncotarget 6.23 (2015): 19336.

also images

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4580062/

Peiris-Pagès, Maria, Federica Sotgia, and Michael P. Lisanti. “Doxycycline and therapeutic targeting of the DNA damage response in cancer cells: old drug, new purpose.” Oncoscience 2.8 (2015): 696.

Saikali, Zeina, and Gurmit Singh. “Doxycycline and other tetracyclines in the treatment of bone metastasis.” Anti-cancer drugs 14.10 (2003): 773-778.

Onoda, Toshinao, et al. “Tetracycline analogues (doxycycline and COL‐3) induce caspase‐dependent and‐independent apoptosis in human colon cancer cells.” International journal of cancer 118.5 (2006): 1309-1315.

Iwasaki, Hiromichi, et al. “Doxycycline induces apoptosis by way of caspase-3 activation with inhibition of matrix metalloproteinase in human T-lymphoblastic leukemia CCRF-CEM cells.” Journal of Laboratory and Clinical Medicine 140.6 (2002): 382-386.

Sun, Tao, et al. “Doxycycline inhibits the adhesion and migration of melanoma cells by inhibiting the expression and phosphorylation of focal adhesion kinase (FAK).” Cancer letters 285.2 (2009): 141-150.

Lokeshwar, Bal L. “Chemically modified non-antimicrobial tetracyclines are multifunctional drugs against advanced cancers.” Pharmacological research 63.2 (2011): 146-150.

breast CAncer

Zhang, Le, et al. “Doxycycline inhibits the cancer stem cell phenotype and epithelial-to-mesenchymal transition in breast cancer.” Cell Cycle just-accepted (2016): 00-00.

Tang, Xiaoyun, et al. “Doxycycline attenuates breast cancer related inflammation by decreasing plasma lysophosphatidate concentrations and inhibiting NF-κB activation.” Molecular cancer 16.1 (2017): 36.

Fife, Rose S., and George W. Sledge Jr. “Effects of doxycycline on in vitro growth, migration, and gelatinase activity of breast carcinoma cells.” The Journal of laboratory and clinical medicine 125.3 (1995): 407-411.

Rubins, Jeffrey B., et al. “Inhibition of mesothelioma cell growth in vitro by doxycycline.” Journal of Laboratory and Clinical Medicine 138.2 (2001): 101-106.

Shen, Ling-Chang, et al. “Anti-invasion and anti-tumor growth effect of doxycycline treatment for human oral squamous-cell carcinoma–in vitro and in vivo studies.” Oral oncology 46.3 (2010): 178-184.

Wang-Gillam, Andrea, et al. “Anti-tumor effect of doxycycline on glioblastoma cells.” Journal of Cancer Molecules 3.5 (2007): 147-153.

Tolomeo, Manlio, et al. “Effects of chemically modified tetracyclines (CMTs) in sensitive, multidrug resistant and apoptosis resistant leukaemia cell lines.” British journal of pharmacology 133.2 (2001): 306-314.

Liu, Jian, Charles A. Kuszynski, and B. Timothy Baxter. “Doxycycline induces Fas/Fas ligand-mediated apoptosis in Jurkat T lymphocytes.” Biochemical and biophysical research communications 260.2 (1999): 562-567.

Onoda, Toshinao, et al. “Doxycycline inhibits cell proliferation and invasive potential: combination therapy with cyclooxygenase-2 inhibitor in human colorectal cancer cells.” Journal of Laboratory and Clinical Medicine 143.4 (2004): 207-216.

Fife, Rose S., et al. “Effects of tetracyclines on angiogenesis in vitro.” Cancer letters 153.1 (2000): 75-78.

Sagar, Jayesh, et al. “Doxycycline in mitochondrial mediated pathway of apoptosis: a systematic review.” Anti-Cancer Agents in Medicinal Chemistry (Formerly Current Medicinal Chemistry-Anti-Cancer Agents) 10.7 (2010): 556-563.

Richards, Christopher, Liron Pantanowitz, and Bruce J. Dezube. “Antimicrobial and non-antimicrobial tetracyclines in human cancer trials.” Pharmacological research 63.2 (2011): 151-156.

van den Bogert, Coby, et al. “Arrest of the proliferation of renal and prostate carcinomas of human origin by inhibition of mitochondrial protein synthesis.” Cancer research 46.7 (1986): 3283-3289.

Kroon, Albert M., et al. “The mitochondrial genetic system as a target for chemotherapy: tetracyclines as cytostatics.” Cancer letters 25.1 (1984): 33-40.

van den Bogert, Coby, Bert HJ Dontje, and Albert M. Kroon. “The antitumour effect of doxycycline on a T-cell leukaemia in the rat.” Leukemia research 9.5 (1985): 617-623.

Antibiotics Eradicate Cancer Stem Cells

2015 OncoTarget

73) Lamb, Rebecca, et al. “Antibiotics that target mitochondria effectively eradicate cancer stem cells, across multiple tumor types: Treating cancer like an infectious disease.” Lamb Rebecca Antibiotics that target mitochondria effectively eradicate cancer stem cells 2015 OncoTarget

Finally, recent clinical trials with doxycycline and azithromycin (intended to target cancer-associated infections, but not cancer cells) have already shown positive therapeutic effects in cancer patients, although their ability to eradicate cancer stem cells was not yet appreciated.

Doxycycline for Lymphoma

2015

74) Ann Hematol. 2015 Apr;94(4):575-81. Long-term outcomes of first-line treatment with doxycycline in patients with previously untreated ocular adnexal marginal zone B cell lymphoma.

Han JJ1, Kim TM, Jeon YK, Kim MK, Khwarg SI, Kim CW, Kim IH, Heo DS.

Author information 1Department of Internal Medicine, Seoul National University Hospital, 101 Daehak-ro, Jongno-gu, Seoul, 110-744, South Korea.

Ocular adnexal lymphoma (OAL) has been associated with Chlamydophila psittaci infection, for which doxycycline has been suggested as a treatment option. We conducted this study to evaluate the long-term results of first-line doxycycline treatment in patients with OAL. Ninety patients withhistologically confirmed OAL with marginal zone B cell lymphoma were enrolled. Each patient received one or two cycles of doxycycline (100 mg bid) for 3 weeks. After a median follow-up period of 40.5 months (8-85), the 5-year progression-free survival (PFS) rate was 60.9 %. All patients were alive at the last follow-up date. Thirty-one patients (34 %) showed local treatment failure without systemic spread. However, PFS rate in these patients was 100 % after salvage chemotherapy and/or radiotherapy.

PFS was independently predicted in multivariate analysis by the tumor-node-metastasis (TNM) staging (hazard ratio [HR], 4.35; 95 % confidence interval [CI], 2.03-9.32; P

Patients who failed to respond to doxycycline therapy were successfully salvaged with chemotherapy and/or radiotherapy without compromising long-term outcomes. Patients with T1N0M0 disease could be considered good candidates for first-line doxycycline.

2015

13 patients antibiotics alone for gastric lymphoma – HP eradication regimen

75) Ann Hematol. 2015 Jun;94(6):969-73. doi: 10.1007/s00277-014-2298-3. Epub 2015 Jan 13. Antibiotic treatment as sole management of Helicobacter pylori-negative gastric MALT lymphoma: a single center experience with prolonged follow-up. Raderer M1, Wöhrer S, Kiesewetter B, Dolak W, Lagler H, Wotherspoon A, Muellauer L, Chott A.

Relatively little is known about the long-term outcome of patients with Helicobacter pylori (HP)-negative gastric lymphoma of mucosa-associated lymphoid tissue (MALT lymphoma) with antibiotic therapy as sole management. We have analyzed all patients with HP-negative gastric MALT lymphoma undergoing antibiotic therapy as sole management of their disease. HP negativity was defined as negative histology, breath test and serology, and response to treatment, survival and long-term outcome was assessed together with clinico-pathological characteristics including t(11; 18) (q21; q21) translocation. Out of 97 patients with gastric MALT lymphoma, 24 were HP-negative, and 13 (5 females and 8 males) underwent only antibiotic management for initial therapy. Eight had stage I and five were found to have stage II disease, with three patients suffering from an underlying autoimmune disease. Antibiotic therapy consisted of standard HP eradication regimens consisting of clarithromycin in all patients, along with metronidazole in seven and amoxicillin in six plus a proton-pump inhibitor. After a median follow-up of 95 months (42-, 181 ), 12/13 patients are alive. Six patients with stage I disease achieved an objective response (five complete (CR) and one partial remission, 46 %), four had stable disease (lasting 11-27 months), and three progressed. All patients with stable disease received chemotherapy, but only one patient due to clear cut progression. One patient relapsed 23 months after initial CR, and achieved a second CR with antibiotics now lasting 87 months. These results indicate that a relevant percentage of patients with HP-negative gastric MALT lymphoma may benefit from antibiotic therapy and do not require additional oncological therapies. Our data suggest that the remissions seen in these patients might be durable as evidenced by prolonged follow-up in our series.

2013

76) Kiesewetter, Barbara, and Markus Raderer. “Antibiotic therapy in nongastrointestinal MALT lymphoma: a review of the literature.” Blood 122.8 (2013): 1350-1357.

A single course of oral doxycycline at a dose of 100 mg given twice a day for 3 weeks was the most popular regimen and was used by most investigators.14⇓⇓-17,19⇓⇓-22 By contrast, Kim and coworkers19 added a second course after an interval of 3 weeks for patients with residual eye-related symptoms after the initial cycle. The activity of a 6-month oral application of 500 mg clarithromycin twice a day was assessed in an Italian pilot study,18 assuming potential additional direct anticancer effects of macrolide antibiotics through changes in apoptotic mechanisms of tumor cells. In addition, 1 patient received HP eradication as first-line treatment of OAML. CR was achieved in 23 patients (18%) out of the collective of all 131 patients reported. Thirty-six (27%) had a PR

2006

77) Ferreri, Andrés JM, et al. “Bacteria-eradicating therapy with doxycycline in ocular adnexal MALT lymphoma: a multicenter prospective trial.” Journal of the National Cancer Institute 98.19 (2006):1375-1382.

Background: An association between ocular adnexal MALT lymphoma (OAL) and Chlamydia psittaci (Cp) infection has been proposed, and recent reports suggest that doxycycline treatment causes tumor regression in patients with Cp-related OAL. The effectiveness of doxycycline treatment in Cp-negative OAL has not been tested. Methods: In a prospective trial, 27 OAL patients (15 newly diagnosed and 12 having experienced relapse) were given a 3-week course of doxycycline therapy. Objective lymphoma response was assessed by computerized tomography scans or magnetic resonance imaging at 1, 3, and 6 months after the conclusion of therapy and every 6 months during follow-up. Cp infection in patients was determined by touchdown enzyme time-release polymerase chain reaction (TETR-PCR). Statistical tests were two-sided. Results: Eleven patients were Cp DNA–positive and 16 were Cp DNA negative. Doxycycline was well tolerated. At a median follow-up of 14 months, lymphoma regression was complete in six patients, and a partial response (≥50% reduction of all measurable lesions) was observed in seven patients (overall response rate [complete and partial responses] = 48%). Lymphoma regression was observed in both Cp DNA–positive patients (seven of 11 experienced regression) and Cp DNA–negative patients (six of 16 experienced regression) (64% versus 38%; P = .25, Fisher’s exact test). The three patients with regional lymphadenopathies and three of the five patients with bilateral disease achieved objective response. In relapsed patients, response was observed both in previously irradiated and nonirradiated patients. The 2-year failure-free survival rate among the doxycycline- treated patients was 66% (95% confidence interval = 54 to 78), and 20 of the 27 patients were progression free. Conclusions: Doxycycline is a fast, safe, and active therapy for Cp DNA–positive OAL that was effective even in patients with multiple failures involving previously irradiated areas or regional lymphadenopathies. The responses observed in PCR-negative OAL may suggest a need for development of more sensitive methods for Cp detection and investigation of the potential role of other doxycycline-sensitive bacteria.

Ferreri et al conducted a prospective phase 2 clinical trial of 27 patients (15 newly diagnosed and 12 relapsed) with OAML, using doxycycline 100 mg orally twice daily for 3 weeks. Partial or complete lymphoma regression after antibiotic therapy was observed in 7 of 11 Cp-positive and 6 of 16 Cp-negative patients, with an overall response rate of 48%. The 2-year failure-free survival rate among patients treated with doxycycline was 66%

Abramson et al84 treated 3 patients with biopsy-proven conjunctival MALT lymphoma with antibiotic therapy, resulting in 2 complete remissions and 1 partial response.

Husain et al43 conducted a meta-analysis, identifying 4 studies with a total of 42 patients who had

been treated with oral doxycycline.

———————————-

full free pdf

78) Husain, Amina, et al. “Meta–analyses of the association between Chlamydia psittaci and ocular adnexal lymphoma and the response of ocular adnexal lymphoma to antibiotics.” Cancer 110.4 (2007): 809-815.

Abramson DH, Rollins I, Coleman M. Periocular mucosa-associated lymphoid/low grade lymphomas: treatment with antibiotics. Am J Ophthalmol. 2005;140:729–730. Am J Ophthalmol. 2005 Oct;140(4):729-30.

Periocular mucosa-associated lymphoid/low grade lymphomas: treatment with antibiotics. Abramson DH1, Rollins I, Coleman M.

To report on the treatment of primary mucosa-associated lymphoid tumors (MALT)/low grade lymphomas of the conjunctiva/orbit treated solely with systemic antibiotics. DESIGN: Retrospective interventional case series.

METHODS: Three adult patients with biopsy/marker proven MALT lymphomas of the conjunctiva/orbit were treated with systemic antibiotics and followed for signs of local or systemic relapse.

RESULTS: All three patients showed a response to antibiotics based on clinical, ultrasonographic, and MRI/CT imaging studies. Two patients have had complete remissions (42 months follow-up) and one a partial remission (18 months). No systemic relapses have occurred.

CONCLUSION: MALT/low grade lymphomas of the conjunctiva/orbit respond to systemic antibiotic therapy and may have complete remissions.

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

http://cancerres.aacrjournals.org/con...

Chatzispyrou, Iliana A., et al.

“Tetracycline antibiotics impair mitochondrial function and its experimental use confounds research.” Cancer research 75.21 (2015): 4446-4449.

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

Moullan, Norman, et al. “Tetracyclines disturb mitochondrial function across eukaryotic models: a call for caution in biomedical research.” Cell reports 10.10 (2015): 1681-1691.

Lamb, Rebecca, et al. “Antibiotics that target mitochondria effectively eradicate cancer stem cells, across multiple tumor types: treating cancer like an infectious disease.” Oncotarget 6.7 (2015): 4569-4584.

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Published on June 15, 2017 08:00

June 6, 2017

Disaster Medicine in America

[image error] Disaster Medicine in America

by Jeffrey Dach MD

No, I am not referring to heroic doctors who parachute into remote areas to help victims of earthquake disasters. I am talking about the current state of Medicine in America which is quite simply, a disaster. Above Left image china earthquake disaster courtesy of irevolutions.

1) Thyroid Endocrinology is a Disaster with reliance on T4 only thyroid meds, and TSH test for monitoring treatment, dogmatically insisting the TSH be “within the range”. Treatment of hypothyroidism with natural thyroid ignored and rejected. Treatment of Graves’ disease with Lithium and iodine ignored and rejected.

2) Hormone Replacement for Post Menopausal Women and Aging Males is a Disaster. Our medical system has failed our post-menopausal women creating an unnecessary burden of suffering.

3) Modern Oncology: Cancer Chemotherapy by conventional oncology is a disaster. The cancer patient suffers horribly from adverse effect of highly toxic chemotherapy, only to have cancer recurrence a few short months after treatment because chemotherapy fails to address cancer stem cells. Oncology rejects and ignores non-toxic therapies such as Artemisinin, IV vitamin C, alpha lipoic acid, Mebendazole, Ivermectin, Chinese Skullcap, Medicinal cannabis Oil etc.

4) Statin Drugs, Stents Bypass Surgery: Cardiology is a disaster. The cholesterol theory of heart disease has been falsified. Statin drugs provide no health benefit for most people taking them. Stenting and bypass surgery do not prevent progression of heart disease.

5) Modern Psychiatry with its poly pharmacy of Psych Meds is a Disaster.

6) Vaccination, ADD/ADHD: Modern Pediatrics with its ballooning vaccination schedules is a disaster. The overdiagnosis of ADD/ADHD with obligatory over-use of amphetamines is a disaster.

7) Autism: The medical system ignores the exponential increasing autism in children challenging the capacity of our schools, hospitals and social services. The medical system claims there is no known cause and no cure. This is a disaster.

8) Modern Agriculture with its GMO Food, Glyphosate Weed Killer, Wheat Gluten Sensitive is a Disaster.

9) Fast Food in hospital lobbies has created a health disaster.

10) Revolving door policy between FDA and Drug industry, Monsanto and Big Agriculture has created a disaster.

11) Over the Counter NSAID Pain Pills, NSAIDS and Tylenol consumed glibly by millions is a Disaster causing leaky gut, heart disease and Parkinsonism.

12) Antibiotics and Antivirals: Increasing antibiotic resistant organisms and rapidly mutating viral pathogens evade the drugs offered by the pharmaceutical industry. However, the medical system ignores and rejects highly effective botanicals which are more effective as antibacterial and antiviral agents. This is a disaster.

13) Overuse of antibiotics has created the C Diff epidemic. This is a Disaster.

14) Overuse of fluoroquinolone antibiotics adverse effects has created a disaster.

15) Cancer Screening for Breast Cancer, Prostate Cancer Thyroid Cancer is a disaster.

16) Autoimmune Disease: Endocrinology,Rheumatology, GI, Neuro treatment for Hashimotos, Rheumatoid Arthritis, Inflammatory Bowel Disease, and Multiple Sclerosis all a DISASTER. Medial system ignores and rejects LDN, Gluten Free diet, and vitamin D3 for autoimmune disease.

17) False Flag Viral Epidemics, Zika Virus, HIV, etc. This is a Disaster. Unreliable HIV blood yielding false positives testing is a disaster.

18) Syntheric hormones. DES (diethyl-stilbestrol), medroxyprogesterone , Oral contraceptives and other synthetic hormones are a disaster. OB/Gyne docs ignore and reject natural progesterone and

bioidentical hormones.

19) Shaken Baby Syndrome and the Disaster of Imprisonment by Misdiagnosis.

20) Health Insurance in America is a Criminal Enterprise, making profits by denying health care to sick people. This is a Disaster.

21) Drug Industry is an organized crime syndicate involved in deceiving the public and their doctors, paying 35 billion in criminal and civil violations. This is a Disaster.

22) Massive use of osteoporosis drugs called bisphosphonates cause an epidemic of jaw necrosis, and spontaneous femur fractures. This is a disaster.

23) Ignoring Iodine supplementation to prevent thyroid cancer, gastric cancer, breast cancer has created a disaster.

24) Ignoring Maternal iodine and thyroid levels has created a disaster of poor pregnancy outcomes and reduced IQ I newborns.

25) Long term overuse of PPI antacids which turns off gastric acid production. The adverse effects of dysbiosis, B12 deficiency, pneumonia, C diff enterocolitis has created a disaster.

26) Environmental endocrine disruptors and increasing PCOS (poly cystic ovary syndrome) , a disaster.

27) False studies denying micronutrient deficiencies in the population, advising people not to take vitamins which are ignored and rejected by medical system. This is a disaster.

28) One of Five New Drugs are “Bad Drugs”, which are FDA approved and later withdrawn or given black box warning. This is a disaster.

Jeffrey Dach MD

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Atherosclerotic Plaque as Infected Biofilm

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Published on June 06, 2017 06:36

May 26, 2017

NSAIDS Leaky Gut and Heart Attacks

[image error] NSAIDS Leaky Gut and Heart Attacks

By Jeffrey Dach MD

Jim takes Naproxen, an NSAID pain pill, on a regular basis for relief of arthritis pain. In addition, Jim’s Calcium Score is very high, and in fact, Jim had a coronary stent placed about 5 years ago during cardiac catheterization for chest pain. Jim wants to know why he should stop the NSAID arthritis drugs, and switch to a safer and more effective botanical alternative such as Zyflamend by New Chapter.

[image error]NSAID drugs have been associated with increased heart attacks for many years now.(1-9)

The 2000 Vioxx Scandal was due to increased heart attack rate discovered years later after a introduction of a new NSAID drug called Vioxxx (Rofecoxib). In November 2007, Merck announced a $4.85 billion settlement with 47,000 plaintiffs claiming Vioxx caused their heart attack, the largest drug settlement in drug history.(10)

All NSAIDS Cause Heart Attacks

However, this problem is not restricted to Vioxx. In fact, all NSAID drugs are associated with increased heart attack risk according to a recent publication in the British Medical Journal.(1)

What is the mechanism by which NSAIDS cause heart attacks ? None of the medical publications take the next step of explaining the mechanism by which NSAIDS cause heart attacks.(2-9) In my opinion, the obvious explanation is “LEAKY GUT” with low level endotoxemia.

NSAIDS Cause Leaky Gut

[image error]My previous article on NSAIDS and Leaky Gut discusses the overwhelming evidence that NSAIDS cause leaky gut. Animal studies show NSAID induced damage to the small bowel intestinal brush border, with increased intestinal permeability and “Leaky Gut” in virtually all animals treated with NSAIDS. Left Image: Brush Border of Small Bowel

NSAIDS Cause Leaky Gut Which Causes Heart Disease

[image error]My previous article on the Low Level Endotoxemia – LPS theory of heart disease explains the mechanism by which Leaky Gut causes low level endotoxemia, a known risk factor for coronary artery disease and increased risk for heart attacks. Low level endotoxemia is the fancy medical name for leakage of gut bacteria into the blood stream. This has been directly linked to causing atherosclerotic plaque, a form of infected biofilm as discussed in my previous article on this topic.

Conclusion: The obvious mechanism by which NSAID drugs cause coronary artery disease and increased heart attack risk is “Leaky Gut”. This allows leakage of LPS and gram negative bacteria into the blood stream, a form of “low level endotoxemia”, directly linked to atherosclerotic disease. Avoiding NSAID drugs is essential for healing the gut and preventing coronary artery disease.

Jeffrey Dach MD

Articles with Related Interest

NSAIDS, Small Bowel and Leaky Gut

Low Level Endotoxemia LPS Theory of Coronary Artery Disease

Low Level Endotoxemia, Depression, Endocrinopathy and Coronary Artery Disease by Jeffrey Dach MD

Links and References:

1) NSAIDS, Small Bowel and Leaky Gut by Jeffrey Dach MD

2) Bally, Michèle, et al. “Risk of acute myocardial infarction with NSAIDs in real world use: bayesian meta-analysis of individual patient data.” bmj 357 (2017): j1909. Objective To characterise the determinants, time course, and risks of acute myocardial infarction associated with use of oral non-steroidal anti-inflammatory drugs (NSAIDs).

Results A cohort of 446 763 individuals including 61 460 with acute myocardial infarction was acquired. Taking any dose of NSAIDs for one week, one month, or more than a month was associated with an increased risk of myocardial infarction. With use for one to seven days the probability of increased myocardial infarction risk (posterior probability of odds ratio >1.0) was 92% for celecoxib, 97% for ibuprofen, and 99% for diclofenac, naproxen, and rofecoxib. The corresponding odds ratios (95% credible intervals) were 1.24 (0.91 to 1.82) for celecoxib, 1.48 (1.00 to 2.26) for ibuprofen, 1.50 (1.06 to 2.04) for diclofenac, 1.53 (1.07 to 2.33) for naproxen, and 1.58 (1.07 to 2.17) for rofecoxib. Greater risk of myocardial infarction was documented for higher dose of NSAIDs. With use for longer than one month, risks did not appear to exceed those associated with shorter durations.

Conclusions All NSAIDs, including naproxen, were found to be associated with an increased risk of acute myocardial infarction. Risk of myocardial infarction with celecoxib was comparable to that of traditional NSAIDS and was lower than for rofecoxib. Risk was greatest during the first month of NSAID use and with higher doses.

Data from nearly half a million patients – a total cohort of 446,763 people – showed that any dose of NSAIDs is associated with an increased risk of heart attack, even within the first week of use. Comparing people who took painkillers to those who didn’t, the team found an increase of heart attack risk of about 20-50 percent, with a similar result for all the different NSAIDs they looked at.

3) Johnsen, Søren P., et al. “Risk of hospitalization for myocardial infarction among users of rofecoxib, celecoxib, and other NSAIDs: a population-based case-control study.” Archives of internal medicine 165.9 (2005): 978-984.

Conclusions :Current and new users of all classes of non- aspirin NSAIDs had elevated relative risk estimates for

MI. Although the increased risk estimates may partly re-flect unmeasured bias, they indicate the need for fur-ther examination of the cardiovascular safety of all nonaspirin NSAIDs.

4) Olsen, Anne-Marie Schjerning, et al. “Long-term cardiovascular risk of NSAID use according to time passed after first-time myocardial infarction: a nationwide cohort study.” Circulation (2012): CIRCULATIONAHA-112.

5) Leaky Gut Syndrome Isn’t Only Scary, But Extremely Dangerous to Your Health – This is More Than a Poop Issue!

by Jordan Reasoner

6) Kohli, Payal, et al. “NSAID use and association with cardiovascular outcomes in outpatients with stable atherothrombotic disease.” The American journal of medicine 127.1 (2014): 53-60.

Among patients with stable atherothrombosis, NSAID use is associated with a higher risk of myocardial infarction, stroke, and hospitalizations for both ischemia and heart failure.

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

7) The Guardian – Common painkillers may raise risk of heart attack by 100% – study. Risk of myocardial infarction is greatest in first month of taking NSAIDs such as ibuprofen if dose is high, say researchers

For the paper, published in the BMJ on Tuesday, the researchers analysed results on 446,763 people on healthcare databases in countries including Canada, Finland and the UK, of whom 61,460 had a heart attack.

They said the potential increase in risk was 75% for ibuprofen and naproxen and more than 100% for rofecoxib but that uncertainty about the extent of the increased risk was greatest for ibuprofen and naproxen.

8) The Guardian – Calls for ibuprofen sale restrictions after study finds cardiac arrest risk

Over-the-counter drug linked to 31% increased cardiac arrest risk, with the figure rising to 50% for diclofenac, says research

9) FDA strengthens warning that NSAIDs increase heart attack and stroke risk July 13, 2015 Gregory Curfman, MD, Editor in Chief, Harvard Health Publications

10) 1999 Vioxx Scandal

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Jeffrey Dach MD

7450 Griffin Road, Suite 190

Davie, Fl 33314

954-792-4663

www.jeffreydachmd.com

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Which is Greater Threat, Measles or Measles Vaccine?

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Published on May 26, 2017 14:01

May 18, 2017

Measles Autism and Vaccination in Somalis in Minnesota

[image error] Measles Autism and Vaccination in Somalis in Minnesota

A recent outbreak of measles in the Somali community in Minnesota has the main stream media riled up, blaming anti-vaccination activists. There is so much rancor on this topic, a Boston Herald editorial calls for hanging execution of anti-vaccination activists. Why are these extremes of opinion published in the mainstream media against people who are questioning a medical procedure? I find this bizarre and disturbing.

[image error]Canary in the Coal Mine

The Somali Migrant community in Minnesota is the canary in the coal mine regarding MMR vaccination and autism. Having the highest MMR vaccination rates for many years, the Somali community was also afflicted with the highest autism rates of any community. Notice the fact that for Somalis living in Somalia, autism is nonexistent. Clearly, there is some environmental factor in the US sparking the high autism rate for Somalis who immigrate to Minnesota. Somali mothers in Minnesota became concerned and began to decline the measles vaccination. Canary Image Courtesy of Share America Gov.

Boston Herald Wants to HANG YOU

To give you an idea of the type of inflammatory rhetoric found in the mainstream media, take a look at this Boston Herald editorial:

“These are the facts: Vaccines don’t cause autism. Measles can kill. And lying to vulnerable people about the health and safety of their children ought to be a hanging offense.“ Boston Herald Editorial

With all due respect to the editorial staff of the Boston Herald, I would like to see their omitted data on this question. According to William Thomson, a whistle blower at the CDC, this data set showing increased autism in African American children after MMR vacccine was intentionally destroyed by the CDC.

Secondly, asserting that “measles can kill” is a deceptive statement, as there has been only one reported death from measles in the US in the last 10 years. One can also say that a glass of water can kill if you aspirate it. Mortality from measles is a greater problem in malnourished children in third world countries. However, these kids need food and water, not vaccination.

David Brownstein MD Speaks Out

Perhaps the best summary of the Somali autism vaccine debate can be found in this excellent article by David Brownstein MD. Firstly, Dr Brownstein reminds us that measles is a benign childhood disease. TV sitcoms such as the Brady Bunch have expressed this fact.

Secondly, having childhood measles confers life long immunity to the virus. Newborns receive antibodies from their mothers and are protected. Vaccination confers only temporary immunity, and mothers who were vaccinated in childhood, no longer have antibodies to transmit to their newborns who are no longer protected. This is a huge issue.

Death from Measles or Death from Measles Vaccine?

According to Dr Brownstein,

“During the last 10 years, there has been one death from measles, but that patient was an adult woman who was on immunosuppressive medications and had other serious health problems.”

However, there are 156 deaths related to MMR vaccine reported by the Vaccine Adverse Event Reporting System (VAERS) from 2000 to 2017

Corruption and Fraud at the CDC

A CDC scientist with whistleblower status has stated under oath, “that the CDC destroyed, hid and falsified data that showed a clear link between the MMR vaccine and autism. And, the altered CDC data revealed that the most affected group of children were African American boys.”

“A CDC whistleblower, Dr. William Thompson co-authored a 2004 CDC study which claimed the MMR vaccine was not associated with autism. In 2014, Dr. Thompson admitted that the 2004 CDC study was altered to hide a 240% increase in autism in African American children who were vaccinated before 36 months of age when compared to those vaccinated later. Furthermore, there was a 69% increase risk in autism in all male children who received the MMR vaccine before 36 months. (1) Under emotional and mental distress over what happened, Dr. Thompson contacted Brian Hooker, PhD who has a son with autism caused by vaccine injury. Dr. Thompson gave Dr. Hooker the missing 2004 data which Dr. Hooker published in August, 2014 in the Translational Neurodegeneration Journal. (2) ” Quote from David Brownstein MD Note: the 2014 Brian Hooker study published in Translational Neurodegeneration was later retracted by the editors.

Conclusion: It is quite obvious the mainstream media is a mouthpiece for pro-vaccine corporate interests. These shrill outcries against vaccine activists by the mainstream media represent propaganda and yet another example of the information war between vaccine manufacturers and the public. Don’t be deceived and fooled by the propaganda.

Articles with Related Interest

The Failure of Global Polio Eradication

Jeffrey Dach MD

Links and references

http://blog.drbrownstein.com/somali-measles-epidemic-and-the-brady-principle/

Somali Measles Epidemic and The Brady Principle by David Brownstein MD

http://www.jabfm.org/content/27/4/458.full

Wolff, Emily R., and Diane J. Madlon-Kay. “Childhood vaccine beliefs reported by Somali and non-Somali parents.” The Journal of the American Board of Family Medicine 27.4 (2014): 458-464.

https://www.nytimes.com/aponline/2017/05/03/us/ap-us-measles-somalis.html

Retracted Article

Measles Outbreak Sickens Dozens of Minnesota Somalis – The New York Times …

https://www.nytimes.com/aponline/2017/05/03/us/ap-us-measles-somalis.html

May 3, 2017 – An outbreak of measles in Minnesota has sickened more than 30 children in … and special offers for The New York Times’s products and services. … “We did a presentation that helped the Somalis put the measles and the …

http://www.breitbart.com/big-government/2017/04/25/measles-outbreak-in-minnesotas-somali-community/

Measles Outbreak in Minnesota’s Somali Community

by Michael Patrick Leahy25 Apr 2017

http://www.cnn.com/2017/05/08/health/measles-minnesota-somali-anti-vaccine-bn/

Anti-vaccine groups blamed in Minnesota measles outbreak

By Jacqueline Howard, CNN Updated 8:28 PM ET, Mon May 8, 2017

http://www.ageofautism.com/2017/05/deliberate-ignorance-minnesota-measles-spotty-reporting-is-contagious.html

Deliberate Ignorance: Minnesota Measles’ Spotty Reporting is Contagious Twisted By Anne Dachel

http://propaganda.news/2017-05-11-truth-somalian-refugees-are-responsible-for-the-minnesota-measles-outbreak-not-anti-vaxxers.html

TRUTH: What is really behind the measles outbreak among Somali-Americans in Minnesota?

http://www.ageofautism.com/2017/05/boston-herald-editorial-staff-calls-vaccine-choice-hanging-offense.html

Boston Herald “Editorial Staff” Calls Vaccine Choice “Hanging Offense” By Kim Stagliano

http://www.bostonherald.com/opinion/editorials/2017/05/editorial_preying_on_parents_fear

Editorial: Preying on parents’ fear Boston Herald editorial staff Monday, May 08, 2017

William Thompson, Brian Hooker

https://www.ncbi.nlm.nih.gov/pubmed/14754936

DeStefano, Frank, et al. “Age at first measles-mumps-rubella vaccination in children with autism and school-matched control subjects: a population-based study in metropolitan Atlanta.” Pediatrics 113.2 (2004): 259-266.

https://translationalneurodegeneration.biomedcentral.com/articles/10.1186/2047-9158-3-16

Hooker, Brian S. “Measles-mumps-rubella vaccination timing and autism among young african american boys: a reanalysis of CDC data.” Translational neurodegeneration 3.1 (2014): 16.

free pdf

Miller, Neil Z. “Minority Report: A Covert CDC Program Inoculated Black Babies.” CDC Fraud and Cover Up Brian Hooker WIlliam Thompson Vaxxed_Minority_Report_2014 _Neil Miller

Major vaccine danger uncovered: Media blackout

Posted on December 28, 2015 by William M. Wentworth, Ph.D

Garenne, Michel, et al. “Child mortality after high-titre measles vaccines: prospective study in Senegal.” The Lancet 338.8772 (1991): 903-907.

video infowars

Measles, Vaccines, and Somolians in Minnesota

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