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Coronary Calcium Score Benefits of Aged Garlic

Coronary Calcium Score Benefits of Aged Garlic

How to Reduce Calcium Scores  ?

Jim has an elevated coronary calcium score in the 95% percentile indicating high risk for future heart attack.  He is being treated by his cardiologist with daily aspirin and atorvastatin (lipitor), a statin drug to reduce cholesterol.

Currently we are following a number of similar patients with elevated coronary calcium score treated with statin drugs by their cardiologist.  The elevated calcium score indicates higher risk for future coronary event such as chest pain, angina, heart attack etc.  Current cardiology dogma dictates treatment with statin drugs to lower cholesterol, thus preventing heart disease.

Cholesterol Theory has Been Falsified

The problem with this cardiology dogma is the cholesterol theory of atherosclerotic disease has been falsified by many studies which are summarized nicely by Dr. William R Ware from the University of Ontario.  Dr Ware’s fine article in Medical Hypotheses 2009, reveals there is no correlation between serum cholesterol and the amount of atherosclerotic plaque when reviewing either autopsy studies or coronary calcium score studies.(9)  Thus, the theory that elevated cholesterol  causes atherosclerotic plaque is essentially falsified.

Statin Drugs Disappointing for Calcium Score

Two randomized trials using statin drugs to reduce calcium scores showed  disappointing results.(10,11)  Left Image CAT scan showing calcified coronary artery (yellow arrow).

In Dr. Houslay’s trial published in Heart 2006, 102 patients were randomized and treated for two years with either 80 mg/d atorvastatin (lipitor) or placebo.(10)  As expected, the statin treated group had a 53% reduction in LDL cholesterol, while the placebo group had no change in theirs.  The researchers were expecting benefit from the statin treatment.  They found the opposite.  Paradoxically, the statin group had greater increase in calcium score (26%) than the placebo group (only 18%).  The authors concluded:“statin treatment does not have a major effect on the rate of progression of coronary artery calcification.”(10)

The second trial by Dr Schmermund in Circulation 2006 randomized 471 patients with no pre-existing coronary artery disease, treated for one year with either  low dose (10mg/d) or high dose (80 mg/d) atorvastatin therapy.  In the high dose group (80 mg/d) the LDL cholsterol was reduced from 106 to 87 mg/dL (approximately 20% reduction).  However, the low dose statin  group  had no change in LDL cholesterol from baseline (108 vs 109 mg/dL).   The authors were expecting reduction in progression of calcium score in the high dose statin group with a 20% reduction in LDL cholesterol.  They were surprised to find no difference in calcium scores between the two groups.  The high dose atorvastatin group actually had slightly greater progression of calcium score (27%) vs (25%) for the low dose group.  The authors concluded,”Coronary artery calcification (CAC) progression showed no relationship with on-treatment LDL cholesterol levels.”  (11)

According to Dr. Gill in a 2010 report: as of the year 2010 there had been five randomized controlled studies showing that statin drug treatment does not reduce coronary calcium score.  Worse, the statin treatment showed progression of coronary calcium score indistinguishable from the non-treated placebo group.

What Interventions Have Been Successful in Reduced Calcium Score ?

As we can see from the above studies, statin drugs are quite effective for lowering cholesterol, yet fail to reduce or slow progression of calcium score.  Again, this provides even more evidence falsifying the cholesterol theory of atherosclerotic heart disease.  Perhaps we should look elsewhere for a treatment modality in the patient with elevated calcium score. Left image courtesy of Matthew J Budoff MD and OCWeekly Magazine.

Dr. Matthew J Budoff did just this, exploring the use of Aged Garlic in retarding progression of calcium score in three studies. (1-3)

In the first study published in 2006 Journal of Nutrition, twenty three “high risk” patients maintained on a stable dose of statin drug and aspirin were randomized to either placebo or 4 mL of Aged Garlic (1200 mg KYOLIC Aged Garlic Liquid) After one year of treatment, the Aged Garlic group showed a 7.5 % progression of calcium score, considerably lower than the 22.2% progression in the placebo group. (1) Remember that both groups were maintained on statin drugs during the one year study.

In the second study by Dr Budoff published in Preventive Medicine 2009, sixty five “intermediate risk” patients, all maintained on statins,  were randomized and treated for one year with either placebo or Aged Garlic Extract (250 mg). (2)  In addition, the garlic group was vitamins: Vitamin B12 (100 microg), folic acid (300 microg),Vitamin B6 (12.5 mg) and l-arginine (100 mg) . (The product used was: Kyolic 108 Aged Garlic by Wakunaga) After one year of treatment, the Aged Garlic Group had significantly less Coronary Artery Calcification progression (6.8%)  compared to the placebo group (26.5%). (see Table 2, Budoff Preventive Medicine 2009).     In addition the Garlic Group had “favorable improvement in oxidative biomarkers and vascular function”(1)

Left Image: Fig 2 showing Aged Garlic Group left and placebo right.  Aged Garlic Group(left bars) shows lower progression of calcium score (blue bar), reduction in IgG IgM MDA LDL, IC/apoB oxidative bio-markers and reduction in Homocysteine (red bar) compared to placebo (right). Courtesy of Aged garlic extract retards progression of atherosclerosis Budoff Preventive medicine 2009 .

A third study by Dr Matt Budoff  in the 2012 Journal of Cardiovascular Research randomized 65 firefighters to one year treatment with either Aged Garlic plus Co-Q-10 (Kyolic Aged Garlic-Co-Q10 Formula 110, Wakunaga ) or to placebo. (3)  Some were taking statin drugs. About 25% of the Aged Garlic CoQ10 were on statins, compared to 31% of placebo group were on statins.

After one year of treatment the aged Garlic group showed less progression of calcium score (32 vs. 58 absolute) and (18.9% vs 27.4%).  CRP was also lower in the Garlic group.  See Left Image :Table One courtesy Budoff 2012 (3).

 

Additional Benefits of Garlic

In a 2013 study by  Dr. Kumar, Garlic was found beneficial as an adjunct to Metformin 500 mg twice a day (BID) in obese diabetics.(12)  Garlic lowers blood pressure has been found useful in hypertensive patients.(13) In addition, Garlic has anti-microbial properties and has uses as an anti-microbail agent (4-8).

Garlic Reduces Calcium Score Progression, Mechanism of Action

My previous article discussed the failure of the cholesterol hypothesis, and recent revelations about atherosclerotic plaque as infected biofilm, and the association with increased gut permeability, also called “Leaky Gut”.   This would certainly explain our somewhat paradoxical findings in the three studies by Dr Matthew Budoff showing Garlic more effective than statin drugs.  A natural antimicrobial agent, the lowly Garlic bulb, shows ability to retard progression of calcium score while the high and mighty statin drug fails,  even though cholesterol is reduced.

Garlic as Anti-Microbial

Although various mechanisms have been proposed to explain the benefits of Garlic in cardiovascular disease, I would like to concentrate on Garlic as an anti-microbial agent.(4-8)  Unlike conventional antibiotics which may disrupt the normal intestinal flora, Garlic’s antimicrobial properties act against pathogenic gut bacteria with relative sparing of the beneficial, “friendly” gut bacteria.(4)   Dr Bayan in 2014 says: “garlic exerts a differential inhibition between beneficial intestinal microflora and potentially harmful enterobacteria”(4)   Dr Rees studied Garlic’s antimicrobial activity finding broad spectrum activity against  “many  bacteria, yeasts, fungi and virus. All microorganisms tested were susceptible to garlic.”(5)  Dr Filocamo in 2012 studied Garlic in a bacterial population representative of the colonic microbiota.   Lacto-baccillus was more resistant to Garlic compared to the Clostridial which was was more susceptible.   The author suggested the “consumption (of garlic) may favor the growth of these beneficial bacterial species in the gut. Garlic intake has the potential to temporarily modulate the gut microbiota.”(6)  A full discussion of the antimicrobial spectrum of Garlic can be found in an excellent article in 2015 by Dr Packia Lekshmi  (7) Mark Slevin’s  2012 article  reported on natural products with vascular protective properties and significant anti-atherogenic potential.  Dr Slevin mentions Aged Garlic, Resveratrol and Green Tea extract (ECGC ) as the most promising (8)

Pseudomonas BioFilm in Atherosclerotic Plaque Material

Dr Bernard Lanter studied athersclerotic plaque specimens, identifying Pseudomonas 16S rRNA genes in 6 of 15 cases, indicating colonization by Pseudomonas biofims. (14) The virulence of Pseudomonas is attributed to Quorum Sensing, the ability of the bacterial cells to communicate with one another to form Bio-Films. (16) Dr. Bjarnsholt considers disruption of this Quorum Sensing to be the key to controlling Psudomonas Biofilm infections.  That is exactly what Garlic does.  In Vitro and In Vivo animal studies show Garlic inhibits quorum sensing and virulence of Pseudomonas. (15)  An excellent way to study the effect of Allicin, the active ingredient in Garlic, on the PSeudomonas organism is to tag the bacteria with the Green Flourscent Protein (GFP).  This was done published in the 2013 with an elegant series of in-vitro experiemnts using Allicin treated GFP-modified Pseudomonas organisms.(17) Dr. Lihua’s group showed that:

“Allicin treatment not only reduced the adhesion ratio of P. aeruginosa, but also inhibited EPS (extracellular polysaccharide) secretion and down-regulates production of some Quorum Sensing -controlled virulence factors.  These results imply that allicin can disturb the formation and

maturation of P. aeruginosa biofilm, and suggest that allicin may represent a promising therapeutic candidate for the management of P. aeruginosa biofilms.”(17)

Poly-Microbial Colonization

Others have found diverse colonies of bacterial, fungal and protozoal life-forms colonizing biofilms in atherosclerotic plaque specimens (18-20),  In view of this,  investigating other botanical agents with known antimicrobial activity might also be useful, such as Olive Leaf extract, Oregano Oil, Berberine, etc.   Perhaps a combination of such natural products would have a more powerful synergistic effect. Other natural anti-microbials such as colloidal silver, and Iodine should be considered as well.   This would be a fertile area for future research.

Our program for Elevated Calcium Score:

Aged Garlic,

Co-Q-10,

L-Arginine

Reveratrol, Pterostilbene

Homocysteine reducing program (B6, B12, Methylfolate)

LinusPauling Protocol (Lysine, Proline, Vitamin C, Tocotrienols)

William Davis Track Your Plaque Protocol (Niacin, Omega-3 Fish Oil, Vitamin D3, Vitamin K2, Eliminate Wheat products)

Weight Reduction,

Hormone Optimization (optimize thyroid, testosterone, estrogen progesterone)

Heal the Leaky Gut (Probiotics, Glutamine, Colostrum)

Eliminate NSAIDS, PPI’s which cause dysbiosis and leaky gut.

Eliminate Pesticides,  Glyphosate and GMO food, eat Organic.

Articles With related Interest:

Atherosclerotic Plaque as Infected Biofilm

Preventing Heart Attacks with Ouabain

Thyroid Pills Prevent Heart Attacks

How to Reverse Heart Disease with the Coronary Calcium Score

Heart Disease Vitamin C and Linus Pauling

Jeffrey Dach MD

7450 Griffin Road Suite 180

Davie FL 33314

954-792-4663

www.jeffreydachmd.com

Links and References

1) http://jn.nutrition.org/content/136/3/741S.full

Budoff, Matthew. “Aged garlic extract retards progression of coronary artery calcification.” The Journal of nutrition 136.3 (2006): 741S-744S. Aged garlic extract retards progression of atherosclerosis Budoff Preventive medicine 2009

2) http://www.ncbi.nlm.nih.gov/pubmed/19573556

Budoff, M. J., et al. “Aged garlic extract supplemented with B vitamins, folic acid and L-arginine retards the progression of subclinical atherosclerosis: a randomized clinical trial.” Preventive medicine 49.2-3 (2009): 101.

Previous studies demonstrated that aged garlic extract reduces multiple cardiovascular risk factors. This study was designed to assess whether aged garlic extract therapy with supplements (AGE S) favorably affects inflammatory and oxidation biomarkers, vascular function and progression of atherosclerosis as compared to placebo.

METHODS: In this placebo-controlled, double-blind, randomized trial (conducted 2005-2007), 65 intermediate risk patients (age 60 /-9 years, 79% male) were treated with a placebo capsule or a capsule containing aged garlic extract (250 mg) plus Vitamin B12 (100 microg), folic acid (300 microg), Vitamin B6 (12.5 mg) and l-arginine (100 mg) given daily for a 1 year. All patients underwent coronary artery calcium scanning (CAC), temperature rebound (TR) as an index of vascular reactivity using Digital Thermal Monitoring (DTM), and measurement of lipid profile, autoantibodies to malondialdehyde (MDA)-LDL, apoB-immune complexes, oxidized phospholipids (OxPL) on apolipoprotein B-100 (OxPL/apoB), lipoprotein (a) [Lp (a)], C-reactive protein (CRP), homocysteine were measured at baseline and 12 months. CAC progression was defined as an increase in CAC>15% per year and an increase in TR above baseline was considered a favorable response.

RESULTS: At 1 year, CAC progression was significantly lower and TR significantly higher in the AGE S compared to the placebo group after adjustment of cardiovascular risk factors (p

CONCLUSION: AGE S is associated with a favorable improvement in oxidative biomarkers, vascular function, and reduced progression of atherosclerosis.

3) http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3425023/

Zeb, Irfan, Budoff M  et al. “Aged Garlic Extract and Coenzyme Q10 Have Favorable Effect on Inflammatory Markers and Coronary Atherosclerosis Progression: A Randomized Clinical Trial.” Journal of Cardiovascular Disease Research 3.3 (2012): 185–190. PMC. Web. 11 June 2015.

Aged garlic extract (AGE) and coenzyme Q10 (CoQ10) have been shown to affect multiple cardiovascular risk factors. The current study evaluates the effect of AGE combined with CoQ10 on inflammatory markers and progression of coronary atherosclerosis compared with placebo.

Methods and Results: In this placebo-controlled, double-blind, randomized trial, 65 intermediate risk firefighters (age 55 ± 6 years) were treated with a placebo capsule or a capsule containing AGE and CoQ10 (AGE CoQ10, 1200 and 120 mg, respectively) daily for 1 year. All participants underwent coronary artery calcium (CAC) scanning and C-reactive protein (CRP) at baseline and at 12 months. At 1 year, mean CAC progression was significantly lower in AGE CoQ10 (32 ± 6 vs. 58 ± 8, P = 0.01) than placebo. Similarly, CRP were significantly decreased in AGE CoQ10 compared with placebo (-0.12 ± 0.24 vs. 0.91 ± 0.56 mg/L, P < 0.05). After adjustment for age, gender, conventional cardiac risk factors, and statin therapy, AGE CoQ10 was associated with 3.99 fold (95% 1.3–12.2, P = 0.01) lack of CAC progression compared with the placebo.

4) http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4103721/

Bayan, Leyla, Peir Hossain Koulivand, and Ali Gorji. “Garlic: A Review of Potential Therapeutic Effects.” Avicenna Journal of Phytomedicine 4.1 (2014): 1–14. Print.

It has been documented that garlic exerts a differential inhibition between beneficial intestinal microflora and potentially harmful enterobacteria

5) http://www.ncbi.nlm.nih.gov/pubmed/24420031/

World J Microbiol Biotechnol. 1993 May;9(3):303-7. doi: 10.1007/BF00383068.

A quantitative assessment of the antimicrobial activity of garlic (Allium sativum).

Rees LP1, Minney SF, Plummer NT, Slater JH, Skyrme DA.

An aqueous extract of freeze-dried garlic (Allium sativum), when incorporated into growth media, inhibited many representative bacteria, yeasts, fungi and a virus. All microorganisms tested were susceptible to garlic. Quantitative assessment of the minimum inhibitory concentrations for bacteria and yeasts showed values ranging from 0.8 to 40.0 mg garlic ml(-1). Fungal radial colony growth was inhibited by at least 25% at concentrations as low as 2.0 mg garlic ml(-1). The 50% endpoint neutralization titre for rotavirus was 2.4 to 2.8 μg ml(-1). Lactic acid bacteria were the least sensitive microorganisms to the inhibitory effects of garlic. In mixed culture studies of Lactobacillus acidophilus and Escherichia coli, garlic prevented the establishment of E. coli, although the final outcome of competition was not affected.

6) http://www.ncbi.nlm.nih.gov/pubmed/22480662

Filocamo, Angela, et al. “Effect of garlic powder on the growth of commensal bacteria from the gastrointestinal tract.” Phytomedicine 19.8 (2012): 707-711.

Garlic (Allium sativum) is considered one of the best disease-preventive foods. We evaluated in vitro the effect of a commercial garlic powder (GP), at concentrations of 0.1% and 1% (w/v), upon the viability of representative gut bacteria. In pure culture studies, Lactobacillus casei DSMZ 20011 was essentially found to be resistant to GP whereas a rapid killing effect of between 1 and 3 log CFU/ml reduction in cell numbers was observed with Bacteroides ovatus, Bifidobacterium longum DSMZ 20090 and Clostridium nexile A2-232. After 6h incubation, bacterial numbers increased steadily and once the strains became resistant they retained their resistant phenotype upon sub-culturing. A colonic model was also used to evaluate the effect of GP on a mixed bacterial population representing the microbiota of the distal colon. Lactic acid bacteria were found to be more resistant to GP compared to the clostridial members of the gut microbiota. While for most bacteria the antimicrobial effect was transient, the lactobacilli showed a degree of resistance to garlic, indicating that its consumption may favour the growth of these beneficial bacterial species in the gut. Garlic intake has the potential to temporarily modulate the gut microbiota.

7) Antimicrobial Spectrum Allium Garlic Packia Lekshmi 2015

Packia Lekshmi, N. C. J., et al. “Antimicrobial Spectrum of Allium Species–A Review.” History 15.44 (2015): 1-5.

8) pdf vascular protective supplements anti_atherosclerotic Slevin Mark Vasc Cell 2012  .  Slevin, Mark, et al. “Unique vascular protective properties of natural products: supplements or future main-line drugs with significant anti-atherosclerotic potential.” Vasc Cell 4.1 (2012): 9.

9) cholesterol atherosclerosis falsified coronary artery plaque Ware Medical Hypotheses 2009 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.

10)  Houslay, E S et al. “Progressive Coronary Calcification despite Intensive Lipid‐lowering Treatment: A Randomised Controlled Trial.” Heart 92.9 (2006): 1207–1212. PMC. Web. 11 June 2015.

To evaluate the effect of intensive lipid‐lowering treatment on coronary artery calcification in a substudy of a trial recruiting patients with calcific aortic stenosis.

Methods In a double blind randomised controlled trial, 102 patients with calcific aortic stenosis and coronary artery calcification were randomly assigned by the minimisation technique to atorvastatin 80 mg daily or matched placebo. Coronary artery calcification was assessed annually by helical computed tomography.

Results 48 patients were randomly assigned to atorvastatin and 54 to placebo with a median follow up of 24 months (interquartile range 24–30). Baseline characteristics and coronary artery calcium scores were similar in both groups. Atorvastatin reduced serum low density lipoprotein cholesterol (−53%, p  0.95 for both). The rate of change in coronary artery calcification was 26%/year (0.234 (SE 0.037) log arbitrary units (AU)/year; n  =  39) in the atorvastatin group and 18%/year (0.167 (SE 0.034) log AU/year; n  =  49) in the placebo group, with a geometric mean difference of 7%/year (95% confidence interval −3% to 18%, p  =  0.18). Serum low density lipoprotein concentrations were not correlated with the rate of progression of coronary calcification (r  =  0.05, p  =  0.62).

Conclusion In contrast to previous observational studies, this randomised controlled trial has shown that, despite reducing systemic inflammation and halving serum low density lipoprotein cholesterol concentrations, statin treatment does not have a major effect on the rate of progression of coronary artery calcification.

11)  Schmermund, Axel, et al. “Effect of Intensive Versus Standard Lipid-Lowering Treatment With Atorvastatin on the Progression of Calcified Coronary Atherosclerosis Over 12 Months A Multicenter, Randomized, Double-Blind Trial.” Circulation 113.3 (2006): 427-437.

Background— Recent clinical trials have suggested that intensive versus standard lipid-lowering therapy provides for additional benefit. Electron-beam computed tomography provides the opportunity to quantify the progression of coronary artery calcification (CAC) in serial measurements.

Methods and Results— In a multicenter, randomized, double-blind trial, 471 patients (age 61±8 years) who had no history of coronary artery disease and no evidence of high-grade coronary stenoses (>50% diameter reduction) were randomized if they had ≥2 cardiovascular risk factors and moderate calcified coronary atherosclerosis as evidenced by a CAC score ≥30. Patients were assigned to receive 80 mg or 10 mg of atorvastatin per day over 12 months. Progression of CAC volume scores could be analyzed in 366 patients. After pretreatment with 10 mg of atorvastatin for 4 weeks, 12 months of study medication reduced LDL cholesterol from 106±22 to 87±33 mg/dL in the group randomized to receive 80 mg of atorvastatin (P

12) Kumar, Rahat et al. “Antihyperglycemic, Antihyperlipidemic, Anti-Inflammatory and Adenosine Deaminase– Lowering Effects of Garlic in Patients with Type 2 Diabetes Mellitus with Obesity.” Diabetes, Metabolic Syndrome and Obesity: Targets and Therapy 6 (2013): 49–56. PMC. Web. 12 June 2015.

13) Xiong, X. J., et al. “Garlic for hypertension: A systematic review and meta-analysis of randomized controlled trials.” Phytomedicine 22.3 (2015): 352-361.

14) Lanter, Bernard B., Karin Sauer, and David G. Davies. “Bacteria present in carotid arterial plaques are found as biofilm deposits which may contribute to enhanced risk of plaque rupture.” MBio 5.3 (2014): e01206-14.

15) Harjai, K., R. Kumar, and S. Singh. “Garlic blocks quorum sensing and attenuates the virulence of Pseudomonas aeruginosa.” FEMS immunology and medical microbiology 58.2 (2010): 161.

16) Bjarnsholt, Thomas, and Michael Givskov. “The role of quorum sensing in the pathogenicity of the cunning aggressor Pseudomonas aeruginosa.” Analytical and bioanalytical chemistry 387.2 (2007): 409-414.


17) Allicin_Pseudomonas_BioFilm_Quorum-Sensing Microbiology Lihua 2013
Lihua, Lin, et al. “Effects of allicin on the formation of Pseudomonas aeruginosabiofinm and the production of quorum-sensing controlled virulence factors.” Pol J Microbiol 62 (2013): 243-51.

18)  Ott, Stephan J., et al. “Detection of diverse bacterial signatures in atherosclerotic lesions of patients with coronary heart disease.” Circulation 113.7 (2006): 929-937.

19) Ott, S. J., et al. “Fungal rDNA signatures in coronary atherosclerotic_Ott_2007_Athrosclerosis  Fungal rDNA signatures in coronary atherosclerotic plaques.” Environmental microbiology 9.12 (2007): 3035-3045.

20)  Putative biofilm-forming organisms in the human vasculature: expanded case reports and review of the literature. Stephen Eugene Fry, Jeremy Eugene Ellis, Matthew Andrew Shabilla, Delyn Lorene Martinez, Renatta Schwarz, Richard Heuser, Constantine Moschonas . Phlebological Review 2014; 22, 1: 24–37 Biofilm_forming organisms human vasculature Stephen Eugene Fry Phlebological Review 2014

Jeffrey Dach MD

7450 Griffin Road Suite 190

Davie, Fl 33314

954-792-4663

www.jeffreydachmd.com

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Atherosclerotic Plaque as Infected Biofilm

Atherosclerotic Plaque

as Infected Biofilm

I first met Stephen Fry M.D.  a couple of years ago at his booth at the ACAM meeting at the Diplomat Hotel in Hollywood, and enjoyed an interesting conversation about his work.  We met a second time last month again at his booth at a medical meeting.  Dr. Stephen Fry runs his own microbiology lab where he examines high powered views of biofilms in atherosclerotic plaque material obtained from surgical specimens. (1-2) These biofilms are colonized by multiple bacterial, fungal and protozoal organisms identified by DNA and  ribosomal RNA sequencing.  A true pioneer in the field, Dr Fry has identified a new organism not listed in the gene databank, which he named “Protomyxzoa Rheumatica”.   Left image courtesy of Stephen Fry MD Web site.

Leaky Gut and LPS

With the recent revelations of Allesio Fasano et al about the increased permeability of the gut wall called “Leaky Gut” which allows bacterial organisms, and undigested food particles into the blood stream, the next logical thought in this sequence is: What happens to all these micro-organisms which are leaking into the blood stream? 

Undoubtedly there is an immune response with release of inflammatory markers cytokines, myeloperoxidase etc.  In addition, this may trigger autoimmune disease through the wonders of “molecular mimicry”.  Some of these microbial organisms possess similar amino acid sequences shared by our own tissues, thereby creating autoimmune disease.  However, my question is : What happens when these microrganisms set up house ?  Where do they go and what do they do?   Left Image from Stephen Fry Lab showing bright staining of micro-organism identified as Protomyxzoa in Biofilm background.Courtesy of Music of the Spheres.

The Endothelium as the Innocent Bystander

Of course, all the blood from the gut enters the portal venous system which goes directly to the liver and spleen.  The reticuloendothelial system of the liver and spleen serve as a giant filtering system for all this “goop” leaking into the blood stream from our permeable small bowels.   This is protective.  However, assuming this filtering system has been overwhelmed allowing a bolus of slimy micro-organisms to gain entry to circulation, where does it go ?  Setting up house in the endothelium is not difficult to imagine.  The endothelium is the inner lining of our blood vessels and this layer is in direct contact our evil bolus of micro-organisms. Left image portal venous system showing splenic vein thrombosis courtesy of Internet J Surg.

Injury Leading to Infection

If one pauses for a minute to think about skin infections in kids,  the skin seems immune to infection until there is an injury, a scrape, laceration  or  some break in the dermal barrier.   This injury allows entry of micro-organisms which then form an infection with the usual hallmarks of pus and inflammation.  Same can be said for the vascular system.  Formation of atherosclerotic plaque tends to occur at sites of injury, such as at bifurcations where shear forces are maximal, and at sites of movement such as the coronary arteries imbedded in the moving surface of the left ventricle.  So, the idea of atherosclerotic plaque as infected biofilm certainly fits the pattern of commonly affected sites in the arterial tree.  Left Image Carotid Plaque courtesy of wikimedia commons.

Uffe Ravnskov and Killmer McKully

Uffe Ravnskov and Killmer McKully have been writing about this for at least 8 years now.(5-6)  In multiple publications listed below, the two doctors list research studies clearly  falsifying the cholesterol theory of atherosclerotic disease, while at the same time massing evidence that atherosclerotic plaque is an infected biofilm colonized with a diverse flora of bacterial, fungal and protozoal organisms.  Left Image Courtesy of Uffe Ravnskov MD

Th e End For Statins ?

If this is true, then this represents a paradigm shift our thinking about the etiology of atherosclerotic vascular disease, and the end of the anti-cholesterol statin drug era.   OOPS ! The drug industry is not going to be happy about this one.

Left image: Tight stenosis of internal carotid origin. Carotid  angiogram courtesy of jeffrey dach md.

Jeffrey Dach MD

7450 Griffin Road Suite 180

Davie, Florida 33314

954-792-4663

Articles with Related interest:

Biofilms in Chronic Sinusitis

Preventing Heart Attacks with Ouabain

Does High Cholesterol Cause Heart Disease?

Links and References:

1) Putative biofilm-forming organisms in the human vasculature: expanded case reports and review of the literature. Stephen Eugene Fry, Jeremy Eugene Ellis, Matthew Andrew Shabilla, Delyn Lorene Martinez, Renatta Schwarz, Richard Heuser, Constantine Moschonas . Phlebological Review 2014; 22, 1: 24–37 Biofilm_forming organisms human vasculature Stephen Eugene Fry Phlebological Review 2014

2) Stephen Fry Interview on Biofilms and Protomyxzoa Rheumatica Marc Braman

3) Lanter, Bernard B., Karin Sauer, and David G. Davies. “Bacteria present in carotid arterial plaques are found as biofilm deposits which may contribute to enhanced risk of plaque rupture.” MBio 5.3 (2014): e01206-14.

4) Bacterial Growth in Arteries Implicated in Heart Attacks Stress, biofilms, and cardiovascular disease By Jacob Schor, ND, FABNO, and Lise Alschuler, ND, FABNO

5) http://mbio.asm.org/content/5/5/e01717-14.full.pdf

Ravnskov, Uffe, and Kilmer S. McCully. “Biofilms, Lipoprotein Aggregates, Homocysteine, and Arterial Plaque Rupture.” mBio 5.5 (2014): e01717-14.

Biofilms Arterial Plaque Rupture Ravnskov Uffe Kilmer McCully 2014

6)  Ravnskov, U., and K. S. McCully. “Infections may be causal in the pathogenesis of atherosclerosis.” The American journal of the medical sciences 344.5 (2012): 391.  Infections May be Causal in the Pathogenesis of Atherosclerosis Ravnskov McCully 2012

7)  Ott, Stephan J., et al. “Detection of diverse bacterial signatures in atherosclerotic lesions of patients with coronary heart disease.” Circulation 113.7 (2006): 929-937.

8) Ott, S. J., et al. “Fungal rDNA signatures in coronary atherosclerotic_Ott_2007_Athrosclerosis  Fungal rDNA signatures in coronary atherosclerotic plaques.” Environmental microbiology 9.12 (2007): 3035-3045.

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The reader is advised to discuss the comments on these pages with his/her personal physicians and to only act upon the advice of his/her personal physician. Also note that concerning an answer which appears as an electronically posted question, I am NOT creating a physician — patient relationship. Although identities will remain confidential as much as possible, as I can not control the media, I can not take responsibility for any breaches of confidentiality that may occur.

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Shaken Baby Syndrome Imprisonment by Misdiagnosis

Shaken Baby Syndrome Imprisonment by Misdiagnosis

by Jeffrey Dach MD

Over the past 30 years thousands of parents have been falsely accused, found guilty and imprisoned for “shaken baby syndrome”, a diagnosis  of child abuse based on Xrays showing fractures, intracerebral and retinal bleeding.  Left image shows  old rib fractures (yellow arrow) on chest xray of infant.  Is this diagnostic of child abuse ? What other diagnostic possibilities should be considered?  Courtesy of Radiology Assistant.

John Caffey Pediatric Radiologist Invented “Shaken Baby Syndrome”

John Caffey, author of the1946 authoritative textbook of pediatric radiology,  coined the name “shaken infant syndrome”.(15)  Left Image 12th edition Caffey’s Pediatric Diagnostic Imaging.

“In 1946, John Caffey described multiple fractures in the long bones of infants suffering from chronic subdural hematoma. None of the parents reported any knowledge of falls or physical injury, but Caffey suspected child abuse to explain the injuries. Following this retrospective, radiological study by Caffey, the diagnosis of shaken baby syndrome (including retinal petechiae, multiple fractures of the long bones, and subdural hematomas) evolved and has resulted in many men and women being convicted of child abuse, all without any meaningful consideration of a differential diagnosis”.(6) (Clemetson 2006)

Radiologists Now Questioning John Caffey’s Authoritative Bible

Illinois radiologist David Ayoub MD and pediatrician Edward Yazbak MD have studied the issue and found that many of these cases are not child abuse.  Rather, many of these unfortunate babies have underlying metabolic bone disease associated with prematurity, chronic pneumonia, maternal and fetal Vitamin D3 deficiency, Vitamin C deficiency, Vitamin K deficiency, all aggravated by aluminum adjuvants in multiple vaccinations given early in the first few months of life.  The underlying metabolic bone disease predisposes these babies to fracture.  Coagulation disorders, and hypoxia predispose to intracerebral bleeding which may occur in-utero or associated with traumatic birth.

Fractured Femur: Wife Abuse or Metabolic Bone Disease?

The left image is an Xray showing  a mid femur fracture.  Is this a traumatic fracture caused by wife beating,  “Battered Wife Syndrome”? Or Metabolic Bone disease?:  If you guessed metabolic bone disease, you would be correct.   This middle aged female had been treated many years with a bisphosphonate drug which created a metabolic bone disease, with a spontaneous mid-femur fracture occurring with NO trauma.

Left image : Cortical Thickening, and obvious Tranverse Mid Femur Fracture in a patient on osteoporosis drugs-  Bisphosphonate. Image courtesy of Dr Jörg Schilcher and Per Aspenberg, Acta Orthop . 2009 August 7; 80(4): 413–415. Incidence of stress fractures of the femoral shaft in women treated with bisphosphonates.

Child Abuse Does Exist

Needless to say, child abuse does exist.  Some children are unwanted, and there are no doubt many cases of infanticide by parents who consider killing their child more convenient than caring for a demanding infant.

However, to incarcerate innocent parents and caregivers based on a false medical diagnosis of “Shaken Baby Syndrome”  is equally unjust.  The diagnosis of child abuse vs. metabolic bone disease requires appropriate testing for metabolic bone disease, and applying thought and consideration to the case.  Hopefully pediatric radiologists and pediatricians can be educated quickly enough to bring a halt to the unjust imprisonment of innocent parents. Its bad enough to grieve over a lost infant.  To grieve from inside a prison cell wrongly convicted of killing your own child is a bit too much.  Wrongful Imprisonment image courtesy of David Feldman Web Site.

Overturning the Convictions

After many long years of imprisonment, parents wrongly convicted of “shaken baby” are now being released, and convictions overturned,  thanks to Drs.  David Ayoub and Edward Yazbak who have devoted themselves to helping these innocent people.

Jeffrey Dach MD

7450 Griffin Road

Suite 180/190

Davie, Florida 33314

954-792-4663

Links and References

1)  Blumenthal, I. “Shaken Baby Syndrome.” Postgraduate Medical Journal 78.926 (2002): 732–735. PMC. Web. 1 June 2015.

2)  Tissue scurvy misdiagnosed as shaken baby syndrome Michael Innis 2014 Clinical Medicine Research 2014; 3(1): 6-8   Tissue scurvy misdiagnosed as shaken baby syndrome homicide Michael D. Innis

Retired Haematologist Princess Alexandra Hospital Brisbane Australia

Michael D. Innis, Tissue Scurvy Misdiagnosed as Shaken Baby Syndrome Homicide, Clinical Medicine Research. Vol. 3, No. 1, 2014, pp. 6-8.

“Tissue Scurvy” is an autoimmune disorder in which there is an abundance of Vitamin C in the body(unlike the Seafarer Scurvy of yesteryear) but it is inhibited from entering the tissue cells to perform its functions of maintaining the integrity of the blood vessels and skeletal tissue and partaking in several enzymatic reactions because of the lack of insulin which is essential for the transfer of Vitamin C into the cell. The result is the development of fractures, hemorrhages and other lesions of Scurvy. Here it is shown a child alleged to have been murdered by being shaken to death was found to have hyperglycemia, implying insulin deficiency and concomitant Tissue Scurvy. It is concluded that the diagnosis Shaken Baby Syndrome, and all examples of unexplained fractures, bruises, retinal and subdural hemorrhages with encephalopathy – the so-called “TRIAD” – are in fact an autoimmune disorder following antigenic stimulation in a genetically susceptible child. Vaccines administered within 4 weeks of the onset of symptoms are the most common cause. The Shaken Baby Syndrome is a fabricated diagnosis and has no place in medical jurisprudence.

3) Is Shaken Baby Syndrome Often Misdiagnosed and Caused by Vaccine-Induced Rickets?  By: TLB Staff  Published January 8, 2015, in HEALTH

The Journal of American Physicians and Surgeons, Vol. 11, No. 1, spring 2006 issue.  Also available at http://www.jpands.org/

4) J.E. Leestma. Shaken Baby Syndrome”: Do Confessions by Alleged Perpetrators Validate the Concept? J Am Phys Surg. 2006; 11(1): 14-16. Also available at http://www.jpands.org/vol11no1/leestma.pdf

5) MD Innis. Vaccines, Apparent Life-Threatening Events, Barlow’s Disease, and Questions about “Shaken Baby Syndrome. J Am Phys Surg. 2006; 11(1): 17-19. Also available at http://www.jpands.org/vol11no1/innis.pdf

6) C.A.B. Clemetson. Caffey Revisited: A Commentary on the Origin of “Shaken Baby Syndrome” J Am Phys Surg. 2006; 11(1): 20-21. Also available at http://www.jpands.org/vol11no1/clemetson.pdf

7) J.E. Leestma. “Case analysis of brain-injured admittedly shaken infants: 54 cases, 1969-2001.” Am J Forensic Med Pathol. September 2005. 26(3): 199-212. Review.

8) F.E. Yazbak. Shaken Baby Syndrome: Pitfalls in Diagnosis and Demographics. Red Flags,February 2006.

Available at  http://www.redflagsdaily.com/yazbak/2006_feb17.php

9)  Child Abuse or Rickets Interview David Ayoub

10)  Shaking Wrong Beliefs By: Dr. F. Edward Yazbak

11) Shaken Baby Syndrome AAPS online

12) “Shaken baby” conviction overturned. The case of Alan Yurko 07 September 2004 Mark Struthers GP Bedfordshire, UK

13) Geddes, J. F., and John Plunkett. “The evidence base for shaken baby syndrome: We need to question the diagnostic criteria.” BMJ: British Medical Journal 328.7442 (2004): 719.

14) Reece, Robert M. “The evidence base for shaken baby syndrome: response to editorial from 106 doctors.” BMJ: British Medical Journal 328.7451 (2004): 1316.

15) Caffey, John. “The Classic: Multiple Fractures in the Long Bones of Infants Suffering From Chronic Subdural Hematoma.” Clinical Orthopaedics and Related Research 469.3 (2011): 755–758. PMC. Web. 1 June 2015.  Reprint from 1946 article.

16) Shaken Baby Syndrome: A Differential Diagnosis of Justice By Ken Strutin, Published on February 21, 2015

 

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Health Insurance CEO’s Rewarded for Denying Care

Health Insurance CEO’s Rewarded for Denying Care

by Jeffrey Dach MD

The CEO for United Healthcare received a $66 million compensation package.  This is a reward for denying care to sick people. This is outrageous.  Why does America allow this?   Every time we pay a monthly premium to the health insurance company, we are funding the exorbitant salaries of the CEO’s.

Above image courtesy of doctors for single payer.

See my article on this topic: Making Your health Insurance Company Pay Up.

Jeffrey Dach MD

Links and References:

Health Reform The Inevitability Of Single Payer May 18, 2015 by admin The Bitchy Pundit

Top Execs At “Big Five’’ Health Insurers Each Pull In Millions

By: Barbara Nagy | June 10, 2013

Wendell Potter  Center for Public Integrity and healthinsurance.org

The Higher Health Insurers’ Claim Denial Rate, the Higher the CEO Pay

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The reader is advised to discuss the comments on these pages with his/her personal physicians and to only act upon the advice of his/her personal physician. Also note that concerning an answer which appears as an electronically posted question, I am NOT creating a physician — patient relationship. Although identities will remain confidential as much as possible, as I can not control the media, I can not take responsibility for any breaches of confidentiality that may occur.

Link to this article

Copyright (c) 2015 Jeffrey Dach MD All Rights Reserved. This article may be reproduced on the internet without permission, provided there is a link to this page and proper credit is given.

FAIR USE NOTICE: This site contains copyrighted material the use of which has not always been specifically authorized by the copyright owner. We are making such material available in our efforts to advance understanding of issues of significance. We believe this constitutes a ‘fair use’ of any such copyrighted material as provided for in section 107 of the US Copyright Law. In accordance with Title 17 U.S.C. Section 107, the material on this site is distributed without profit to those who have expressed a prior interest in receiving the included information for research and educational purposes.

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Fecal Transplantation and the Sweet Smell of Success

Fecal Transplantation, the Sweet Smell of Success

by Jeffrey Dach MD

A recent medical meeting I attended covered the “microbiome”, the friendly bacteria in our gut.  Apparently these little microbes are doing a lot more than we thought.

Dybiosis is disruption of our normal microbial flora.  One example is the dreaded complication,  Clostrida Difficile entero-colitis,  resulting from over-use of antibiotics allowing the pathogenic Clostridia Difficile to dominate.

There are hundred of strains of Clostridia, and some produce toxins which disrupt neurotransmitter function in the brain.  Hence the interest in probiotic therapy and fecal transplantation for neurological disease.  Left Image: Air Contrast Barium Xray of Colon courtesy of How Fecal Transplants Work.

When Probiotics Are Not Enough

Restoring our normal gut flora with probiotics usually gets things back to normal.   If the probiotic capsules from the health food store are not enough, then the next step is fecal transplantation.  This more drastic measure “transplants” the microbial flora from a normal person into the colon of the recipient.  The procedure is done with a large syringe filled with colon contents (fecal material) which is injected into the colon of the recipient.  As disgusting as this might sound, it works remarkably well for  Clostridia Difficile entero-colitis, used when antibiotics such as Flagyl and Vancomycin are ineffective and stop working.  More than 100 US hospitals are offering fecal transplantation for Clostridia difficile.  Here is a list of providers and trials.  Above left image Electron Microscope view of Clostridia Difficile

Fecal Transplantation for Inflammatory Bowel Disease

Crohn’s Disease: Dr David Suskind at Seattle Children’s Hospital  reported success using fecal transplant in ten children with Crohn’s Disease in the first FDA-approved study of its type.   Seven of ten actually went into “remission” after the procedure. Left image: Typical apthous ulcers of crohn’s colitis on air contrast barium Xray of colon.  Crohn’s usually involves the terminal ileum, yet can also involve the colon as well.

Ulcerative Colitis: Thomas Borody MD reported in 2003 his experience with fecal transplant for Ulcerative Colitis. He concluded the procedure is capable of reversing the ulcerative colitis in “selected patients” (7)

Left image: air contrast barium enema of colon typical findings of ulcerative colitis with granular mucosal pattern.

Fecal Transplant for Autism, Parkinson’s and other Neurological Disease

Lately, fecal transplantation has been proposed as a treatment for many other  diseases.  For example, there have been case reports with favorable outcomes in autism,  “Parkinson’s disease, multiple sclerosis, myoclonus dystonia, chronic fatigue syndrome, and idiopathic thrombocytopenic purpura” (1)

The well known neurologist, Dr David Perlmutter was one of the keynote speakers at the meeting.  He presented video clips of remarkable recoveries in two cases after fecal transplantation.  The first case was Jason, a 10 year old autistic youngster with documented dysbiosis from frequent bouts of antibiotics.  Jason and his mom, Melinda, traveled to Europe for a series of fecal transplants with remarkable recovery.

Parkinson’s Case

The second case was a Parkinson’s patient unable to walk because of his neurological disorder  After a series of  fecal transplants in Europe, his video showed him walking nonchalantly down the hall of his hotel.(2)  This certainly got my attention.

Conclusion

One should be cautious and not too hasty in placing too many expectations on a new therapy.  Perhaps the field of “targeted” probiotcs and fecal transplantation will prove to be the next great discovery of modern medicine.  On the other hand it may not pan out as advertised, in which case, we would be “sh_t out of luck.”

Jeffrey Dach MD

Articles with Related Interest

Curing Autism with Antibiotics Probiotics

Links and References

1) Xu, Meng-Que et al. “Fecal Microbiota Transplantation Broadening Its Application beyond Intestinal Disorders.” World Journal of Gastroenterology : WJG 21.1 (2015): 102–111. PMC. Web. 22 May 2015.

Intestinal dysbiosis is now known to be a complication in a myriad of diseases. Fecal microbiota transplantation (FMT), as a microbiota-target therapy, is arguably very effective for curing Clostridium difficile infection and has good outcomes in other intestinal diseases. New insights have raised an interest in FMT for the management of extra-intestinal disorders associated with gut microbiota. This review shows that it is an exciting time in the burgeoning science of FMT application in previously unexpected areas, including metabolic diseases, neuropsychiatric disorders, autoimmune diseases, allergic disorders, and tumors. A randomized controlled trial was conducted on FMT in metabolic syndrome by infusing microbiota from lean donors or from self-collected feces, with the resultant findings showing that the lean donor feces group displayed increased insulin sensitivity, along with increased levels of butyrate-producing intestinal microbiota. Case reports of FMT have also shown favorable outcomes in Parkinson’s disease, multiple sclerosis, myoclonus dystonia, chronic fatigue syndrome, and idiopathic thrombocytopenic purpura. FMT is a promising approach in the manipulation of the intestinal microbiota and has potential applications in a variety of extra-intestinal conditions associated with intestinal dysbiosis.

2) Ananthaswamy, Anil. “Faecal transplant eases symptoms of Parkinson’s disease.” New Scientist 209.2796 (2011): 8-9.

3)  Fecal Flora Transplantation February 20, 2011 Jacob Schor ND, FABNO

4) Vindigni, Stephen M., Elizabeth K. Broussard, and Christina M. Surawicz. “
intestinal microbiome fecal transplant probiotics Clostridium difficile Vindigni 2013
Alteration of the intestinal microbiome: fecal microbiota transplant and probiotics for Clostridium difficile and beyond.” (2013): 615-628.

5) Borody, Thomas J., Sudarshan Paramsothy, and Gaurav Agrawal. “Fecal microbiota transplantation: indications, methods, evidence, and future directions.” Current gastroenterology reports 15.8 (2013): 1-7. Fecal transplantation Borody Current gastroenterology reports 2013

6) Borody, Thomas J., Lawrence J. Brandt, and Sudarshan Paramsothy. “Therapeutic faecal microbiota transplantation: current status and future developments.” Current opinion in gastroenterology 30.1 (2014): 97.

7) Borody, Thomas J., et al. “Treatment of ulcerative colitis using fecal bacteriotherapy.” Journal of clinical gastroenterology 37.1 (2003): 42-47.Treatment ulcerative colitis fecal bacteriotherapy Borodny Journal of clinical gastroenterology 2003

8) Does it All Begin W/ Vitamin K in the Gut? Vitamin K ⇆ Gut Interactions Link in Intestinal Dysbiosis, Prostate Health and an Emerging Cause of Severe Pregnancy Complications?  from muscle jenny titanium pro x.

9) Autism Case David Permutter

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www.bioidenticalhormones101.com

www.truemedmd.com

Click Here for: Dr Dach’s Online Store for Pure Encapsulations Supplements

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The reader is advised to discuss the comments on these pages with his/her personal physicians and to only act upon the advice of his/her personal physician. Also note that concerning an answer which appears as an electronically posted question, I am NOT creating a physician — patient relationship. Although identities will remain confidential as much as possible, as I can not control the media, I can not take responsibility for any breaches of confidentiality that may occur.

Link to this article

Copyright (c) 2015 Jeffrey Dach MD All Rights Reserved. This article may be reproduced on the internet without permission, provided there is a link to this page and proper credit is given.

FAIR USE NOTICE: This site contains copyrighted material the use of which has not always been specifically authorized by the copyright owner. We are making such material available in our efforts to advance understanding of issues of significance. We believe this constitutes a ‘fair use’ of any such copyrighted material as provided for in section 107 of the US Copyright Law. In accordance with Title 17 U.S.C. Section 107, the material on this site is distributed without profit to those who have expressed a prior interest in receiving the included information for research and educational purposes.

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Lung Cancer Screening for Smokers Major Breakthrough

Lung Cancer Screening Major Breakthrough

During my days working as a radiologist, one of my jobs was early detection of lung cancer on chest Xrays and CAT scans. Left Image shows CAT scan of chest shows typical lung cancer (red circle) courtesy of Duke Lung Cancer Screening.

Although we occasionally found a mass or nodule on a chest Xray, the prognosis for lung cancer was poor even with the best of treatment. Since the 980’s clinical trials using palin chest Xrays for lung cancer screening were disappointing.  Not only was there no reduction in mortality in the screened population, many lung cancers could be found in retrospect on the previous X-ray which had been “missed ” six months before.  This was an embarrassment best avoided.  The large study which finally answered the question was the PLCO in JAMA.  Again, this showed no  reduction in mortality, and Lung Cancer Screening with the plain chest X-Ray never took off.

Lung Cancer Sc reening with (Computerized Axial Tomography) CAT Scan

Since the plain old fashioned Chest Xray is a failure for lung cancer screening, perhaps by upgrading to the latest technology, the CAT Scanner, and we might have better luck.  The CAT scan is a more sensitive and accurate imaging device compared to the plain chest Xray.

Favorable Clinical Study

The latest clinical study was favorable.  The National Lung Screening Trial,  enrolling heavy smokers, showed a 20% reduction in mortality in the screened population.(8)  However there was a high price to pay in terms of a 96% false positive rate.  These false positive cases may then undergo invasive procedures such as percutaneous lung biopsy which can cause a pneumothorax (air in the chest cavity and collapsed lung).  A pneumothorax requires a hospital admission and chest tube placement.(8-10)

Reducing the False Positive Rate

A false positive means the CAT scan detects a suspicious nodule which later is discovered to be “nothing”, just a benign nodule or scar tissue.  This is quite common in heavy smokers with COPD (chronic obstructive lung disease) and many years of chronic cough and inflammation.  Needless to say, such a high false positive rate is alarming, and can lead to harming the patient with unnecessary invasive procedures. Left Image shows pneumothorax on the right courtesy of Aukland hospital.

Enter The Circulating Tumor Cell Test.

What if we had a test that could reduce the 96% false positive rate? The Circulating Tumor Cell (CTC) test finds the tumor cells circulating in the patient’s blood stream.  The presence of the circulating tumor cells predicts which patient harbors an occult malignancy. (1-3)

The CTC test uses an ingenious technique which coats the tumor cells with beads, microscopic iron nano-particles, and then uses a strong magnetic to separate the tumor cells from the remaining blood components.  Once separated, the tumor cell can be examined under the microscope, and even grown in cell culture.(4-5)  Left image circulating tumor cell (upper left) covered with attached beads courtesy of Angewandte Chemie

Using the CTC Test at the Pasteur Hospital, Nice, France

A research group from the Pasteur Hospital in Nice, France reported in Oct 2014  their experience using CTC testing on COPD patients.  They were able to find lung cancers before clinically apparent on CAT scans.(1-3) Left Image Pasteur Hospital Nice France courtesy of Ingerhop.

In this study, Circulating Tumor Cell testing (CTC) was done on 168 COPD patients.  Even though clinically negative for cancer,  five (3%) of the 168 COPD patients had a positive CTC test indicating they harbored an undetected early malignancy.  Later, over the next few years, annual CAT scans revealed lung cancer in all five patients who then underwent surgical resection with good outcome.  The authors concluded,”Monitoring “sentinel” CTC-positive COPD patients may allow early diagnosis of lung cancer.”(3)

Other Cancer Markers:  By combing cancer markers such as hCG (human chorionic gonadotropin), PHI (phosphohexose isomerase) and CEA (carcino-embryonic antigen), Dr Emil Schandl has reported excellent results for early detection of lung and other cancers.(11-12).  Perhaps incorporating these additional markers along with CTC testing prior to Lung CAT screening might prove even more useful.

Conclusion: Utilizing the CTC test before initiating screening with annual CAT scan surveillance avoids the unacceptable 96% false positive rate and holds promise as a superior technique for early lung cancer detection in high risk smokers.

The CTC test is available at Quest.  It is called Cell Search.

Articles with Related Interest:

Cancer as a Metabolic Disease

How Does Cannabis Kill Cancer Cells?

How Does Cannabis Kill Cancer Cells PArt two

Jeffrey Dach MD

7450 Griffin Road, Suite 180/190

Davie, Fl 33314

954-792-4663

Links and References:

1) http://www.isetbyrarecells.com/circulating-tumor-cells-narrow-lung-cancer-screening-greatest-risk/

Could Circulating Tumor Cells Narrow Lung Cancer Screening to Those at Greatest Risk ?  On Nov. 10,2014,  the U.S. Centers for Medicare & Medicaid Services (CMS) announced that it will fund low-dose helical computerized tomography (CT) screening for those at high risk for lung cancer, specifically those aged 55-74 who are defined at “heavy smokers” (1 pack per day for the last 30 years). All told, 9 million Americans will be covered for annual screening.

The decision is based on the 2010 National Lung Screening Trial, which looked at 53,000 smokers in the U.S. aged 55-74. These patients were screened annually with low-dose helical CT and X-rays.  When compared to patients who were screened using X-ray alone, the cohort screened with CT had overall reduction in mortality of 20%.

The decision is not without critics. Many worry about the radiation exposure from annual CT scans. Another risk comes from false positives. CT scanning is not perfect, often providing images that are nebulous. The 2010 National Lung Screen Trial revealed that invasive action taken as a result of a positive CT scan—such as biopsy or surgery—caused a significant number of deaths.  Cost is another factor. The new Medicare benefit is expected to cost $9 billion in the first five years.

In the recent INSERM study, “Sentinel Circulating Tumor Cells Allow Early Diagnosis of Lung Cancer in Patients with Chronic Obstructive Pulmonary Disease,” researchers first screened high-risk lung cancer patients (COPD patients and smokers) with the ISET by Rarecells Circulating Tumor Cell (CTC) detection system. Five of the COPD patients tested positive and were prioritized for annual CT screening.  Within 1-4 years, nascent lung tumors were detected in all five patients and quickly removed.

These patients were diagnosed and treated while in the very earliest stages of lung cancer: Stage 1A. And all five remain in remission 16 months after the surgery. Spiral CT screening can save many lives. But in the INSERM study, researchers were able to first identify those high risk patients at the greatest risk of lung cancer by testing for CTC using ISET.

2) http://lungcancernewstoday.com/2014/11/05/early-detection-lung-cancer-using-circulating-tumor-cells-blood/

Early detection of Lung Cancer Using Circulating Tumor Cells In The Blood  November 5th, 2014

3) http://www.ncbi.nlm.nih.gov/pubmed/25360587  PLoS One. 2014 Oct 31;9(10):e111597.  “Sentinel” circulating tumor cells allow early diagnosis of lung cancer in patients with chronic obstructive pulmonary disease.  Ilie M1, Hofman V1, Long-Mira E2, Selva E3, Vignaud JM4, Padovani B5, Mouroux J6, Marquette CH7, Hofman P1.

Chronic obstructive pulmonary disease (COPD) is a risk factor for lung cancer. Migration of circulating tumor cells (CTCs) into the blood stream is an early event that occurs during carcinogenesis. We aimed to examine the presence of CTCs in complement to CT-scan in COPD patients without clinically detectable lung cancer as a first step to identify a new marker for early lung cancer diagnosis. The presence of CTCs was examined by an ISET filtration-enrichment technique, for 245 subjects without cancer, including 168 (68.6%) COPD patients, and 77 subjects without COPD (31.4%), including 42 control smokers and 35 non-smoking healthy individuals. CTCs were identified by cytomorphological analysis and characterized by studying their expression of epithelial and mesenchymal markers. COPD patients were monitored annually by low-dose spiral CT.  CTCs were detected in 3% of COPD patients (5 out of 168 patients). The annual surveillance of the CTC-positive COPD patients by CT-scan screening detected lung nodules 1 to 4 years after CTC detection, leading to prompt surgical resection and histopathological diagnosis of early-stage lung cancer. Follow-up of the 5 patients by CT-scan and ISET 12 month after surgery showed no tumor recurrence. CTCs detected in COPD patients had a heterogeneous expression of epithelial and mesenchymal markers, which was similar to the corresponding lung tumor phenotype. No CTCs were detected in control smoking and non-smoking healthy individuals. CTCs can be detected in patients with COPD without clinically detectable lung cancer. Monitoring “sentinel” CTC-positive COPD patients may allow early diagnosis of lung cancer.

4) http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3506783/  full free  Wong, Maria P. “Circulating Tumor Cells as Lung Cancer Biomarkers.” Journal of Thoracic Disease 4.6 (2012): 631–634. PMC. Web. 21 May 2015.

5) http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3461065/

Taenzer, Aline et al. “Circulating Tumor-Derived Biomarkers in Lung Cancer.” Journal of Thoracic Disease 4.5 (2012): 448–449. PMC. Web. 21 May 2015

6) For Lung Cancer Screening, a Small Dose of Hope By Jane E. Brody December 8, 2014 New York Times

7) On Medicare and Assessing the Value of Lung Cancer Screening MAY 8, 2015 New York Times

8) N Engl J Med. 2011 Aug 4;365(5):395-409.

Reduced lung-cancer mortality with low-dose computed tomographic screening. National Lung Screening Trial Research Team, Aberle DR, Adams AM, Berg CD, Black WC, Clapp JD, Fagerstrom RM, Gareen IF, Gatsonis C, Marcus PM, Sicks JD.

The aggressive and heterogeneous nature of lung cancer has thwarted efforts to reduce mortality from this cancer through the use of screening. The advent of low-dose helical computed tomography (CT) altered the landscape of lung-cancer screening, with studies indicating that low-dose CT detects many tumors at early stages. The National Lung Screening Trial (NLST) was conducted to determine whether screening with low-dose CT could reduce mortality from lung cancer.

METHODS:

From August 2002 through April 2004, we enrolled 53,454 persons at high risk for lung cancer at 33 U.S. medical centers. Participants were randomly assigned to undergo three annual screenings with either low-dose CT (26,722 participants) or single-view posteroanterior chest radiography (26,732). Data were collected on cases of lung cancer and deaths from lung cancer that occurred through December 31, 2009.

RESULTS:  The rate of adherence to screening was more than 90%. The rate of positive screening tests was 24.2% with low-dose CT and 6.9% with radiography over all three rounds. A total of 96.4% of the positive screening results in the low-dose CT group and 94.5% in the radiography group were false positive results. The incidence of lung cancer was 645 cases per 100,000 person-years (1060 cancers) in the low-dose CT group, as compared with 572 cases per 100,000 person-years (941 cancers) in the radiography group (rate ratio, 1.13; 95% confidence interval [CI], 1.03 to 1.23). There were 247 deaths from lung cancer per 100,000 person-years in the low-dose CT group and 309 deaths per 100,000 person-years in the radiography group, representing a relative reduction in mortality from lung cancer with low-dose CT screening of 20.0% (95% CI, 6.8 to 26.7; P=0.004). The rate of death from any cause was reduced in the low-dose CT group, as compared with the radiography group, by 6.7% (95% CI, 1.2 to 13.6; P=0.02).

CONCLUSIONS:  Screening with the use of low-dose CT reduces mortality from lung cancer. (Funded by the National Cancer Institute; National Lung Screening Trial ClinicalTrials.gov number, NCT00047385.).

9) N Engl J Med. 2014 Nov 6;371(19):1813-20. Clinical practice. Lung-cancer screening with low-dose computed tomography.  Gould MK.

10) Bach, Peter B. et al. “Benefits and Harms of CT Screening for Lung Cancer: A Systematic Review.” JAMA : the journal of the American Medical Association 307.22 (2012): 2418–2429. PMC. Web. 22 May 2015.

11) Cancer Detect Prev. 1987;10(3-4):197-203.

Comparison of serum CEA, PHI, and TPA as tumor markers in breast cancer patients. Paulick R, Caffier H, Paulick M.

Abstract

The purpose of this study was to evaluate the clinical significance of different serum tumor markers in patients with breast cancer who developed recurrent disease. Determined were tissue polypeptide antigen (TPA), carcinoembryonic antigens (CEA), and phosphohexose isomerase (PHI). Serum samples of 411 breast cancer patients with either locoregional or metastatic recurrence were analyzed. Positive rates of all three markers depended on the clinical stage of the disease, with highest rates of elevated titers in advanced disease. In comparison, CEA and TPA are more sensitive markers than PHI. According to the site of recurrence, CEA exhibited the highest rate of elevated titers in patients with bone metastases and PHI in patients with visceral metastases. Using PHI in combination with CEA, sensitivity (ie, at least one marker is elevated) was increased by 6-20% compared to the results obtained with single marker analysis. However, for easier interpretation of the tumor marker results in clinical practice, it may be helpful to employ a product value of CEA and PHI.

12) Int J Biol Markers. 1988 Apr-Jun;3(2):113-22.

Phosphohexose isomerase and carcinoembryonic antigen in the sera of patients with primary lung cancer.Santabárbara P1, Molina R, Estapé J, Ballesta AM.

Phosphohexose isomerase (PHI) and carcinoembryonic antigen (CEA) were measured at the time of diagnosis in 300 patients with lung cancer. Serum levels were high in 75.7% and 53.0% of patients respectively. PHI levels were higher in large cell and small cell carcinomas (p less than 0.001). CEA levels were higher in adenocarcinomas (p less than 0.001). Metastatic carcinomas showed higher levels on PHI and CEA than localized cases. Survival was significantly longer in patients with normal PHI (p less than 0.001) and normal CEA (p less than 0.005) than in cases with elevated markers. The prognostic significance of PHI persisted in the different pathological types and stages, whereas CEA only had prognostic impact in non-small cell cases. Serial PHI determinations were useful for follow-up in 82.4% of cases with initial abnormal values and in 55.4% of cases with a normal value. Serial CEA was useful in 41% of cases with initially high value but in less than 15% of those with baseline normal. We conclude that PHI has prognostic significance independently of pathology and stage, whereas CEA was a prognostic indicator only in non-small cell cases; serial PHI determinations were useful more often than CEA for follow-up.

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Copyright (c) 2015 Jeffrey Dach MD All Rights Reserved. This article may be reproduced on the internet without permission, provided there is a link to this page and proper credit is given.

FAIR USE NOTICE: This site contains copyrighted material the use of which has not always been specifically authorized by the copyright owner. We are making such material available in our efforts to advance understanding of issues of significance. We believe this constitutes a ‘fair use’ of any such copyrighted material as provided for in section 107 of the US Copyright Law. In accordance with Title 17 U.S.C. Section 107, the material on this site is distributed without profit to those who have expressed a prior interest in receiving the included information for research and educational purposes.

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Dr Mehmet Oz Smear Campaign Back Fires

Dr Mehmet Oz Smear Campaign Back-Fires

In round one of the war between Monsanto and Dr OZ, a poisoned pen letter was mailed to Columbia University.  Here is a quote:

“We are surprised and dismayed that Columbia University’s College of Physicians and Surgeons would permit Dr. Mehmet Oz to occupy a faculty appointment, let alone a senior administrative position in the Department of Surgery.”

Round Two – The Goon Squad

In round two, Dr Oz did his own Google search on the ten signatories of the letter, discovering they were part of a “goon squad” with financial ties to Monsanto, and the chemical/pesticide industry.  Dr Oz then posted his own video revealing the names and backgrounds of this “goon squad”, revealing the financial ties to Monsanto.  Some of the people who signed the letter actually had criminal convictions for medical related fraud.(6-8) 

Dr. Oz announced to his critics: “We are not going anywhere”.

Left image Round Up Label Courtesy of Monsanto 

Repeating the Rachel Carson Story ?

The title of Rachel Carson’s 1962 book, “Silent Spring”, refers to the mass extermination of birds from indiscriminate spraying of DDT over agricultural fields. The Spring months were “silent” because the song-birds all died from the toxic pesticide exposure.  Left Image: Rachel Carson

Taking On the Chemical Industry

Rachel Carson bravely took on the entire Chemical Industry which fought her by hiring their own “experts”, goons with scientific credentials, to attack her work. The attacks back fired, providing even more media attention to her work and the health dangers of pesticides. DDT was banned in 1972.

Dr. Mehmet Oz – History Repeats Itself.

Now history repeats itself.  A recent World Health Organisation report, the IARC, labels Monsanto’s herbicide, Glyphosate, a “probable human carcinogen”.  Dr Oz discussed the IARC report, pointing out the environmental dangers of herbicides on the air during his show.

Dr. Oz might as well have painted a large bulls-eye on his forehead, because  Immediately after this show aired, he became the primary target of a chemical industry goon squad.  launching a smear campaign to discredit him.   Just as in the case of Rachel Carson, I predict these attacks will back fire, and we will see more public awareness and a major turning point in the battle against toxic chemicals in our environment and food.

World Health Organization Report Labels Glyphosate as “probably” Ca rcinogenic

A recent report from IARC labels Monsanto’s herbicide, Round-up, chemical name, Glyphospate as “probably carcinogenic”.

Glyphosates Linked to Renal Disease, and Renal Failure in Farmers.

Perhaps more disturbing than causing cancer, numerous reports have linked glyphosate to kidney disease and renal failure. (1)(12-23)   The toxicity is based on the  chelating ability of glyphosate, and the formation of  glyphosate-heavy metal complexes which damage the kidneys.  A number of countries such as Sri Lanka and El Salvador have already banned or limited its use. (12-23)  Left image heavy metal toxic nephropathy renal biopsy slide courtesy of emedicine.

Glyphosate Residues in Food and In Humans

Since Glyphosate is a commonly used herbicide, and it is sprayed over agricultural areas copiously, a number of alarming studies show high levels of glyphosate residue in our food.  Further testing of human blood and urine shows we are all contaminated by Glyphosate residues. (24-25)  Left Image Glyphosate Spraying from airplane.

Conclusion: Like it or not, we are all experiencing the health consequences of Glyphosate contamination, thanks and credit goes to Monsanto, also known as “Mon-Satan”

Jeffrey Dach MD

7450 Griffin Road Suite 190

Davie, Fl 33314

954-792-4663

link to this article: http://wp.me/p3gFbV-2Rp

Articles with Related Interest

Rachel Carson Fights The Chemical Industry

GMO FOOD, the Great Scandal

Links and References

1) http://www.i-sis.org.uk/Glyphosate_Probably_Carcinogenic_to_Humans.php

ISIS Report 24/03/15

Glyphosate ‘Probably Carcinogenic to Humans’ Latest WHO Assessment.  The world authority on cancer’s evidence-based assessment is pitched against the Monsanto-led corrupt approvals in US and Europe Dr Mae-Wan Ho and Dr Nancy Swanson

Renal Failure and Kidney Disease Caused by Glyphosate

Sri Lanka had originally imposed a total ban based on evidence of glyphosate link to a deadly kidney disease, with prevalence estimated at 15 % affecting a total of 400 000 patients with an estimated death toll of around 20 000. Under pressure from industry, it has now a partial ban in certain districts [19].

El Salvador, stricken with the same lethal kidney disease epidemic, has voted to ban glyphosate along with 52 other chemicals since 2013 [20], though it has yet to be written into law, again under great pressure from industry.

Brazil’s Federal Public Prosecutor has requested the Justice Department to ban glyphosate along with 8 other chemicals [21]. Finally, the Dutch Parliament voted for a ban on non-agricultural uses [22].

2) http://www.thelancet.com/journals/lanonc/article/PIIS1470-2045(15)70134-8/abstract

Carcinogenicity of tetrachlorvinphos, parathion, malathion, diazinon, and glyphosate by Kathryn Z Guyton , Dana Loomis , Yann Grosse , Fatiha El Ghissassi  , Lamia Benbrahim-Tallaa  , Neela Guha , Chiara Scoccianti  , Heidi Mattock  , Kurt Straif , on behalf of the International Agency for Research on Cancer Monograph Working Group, IARC, Lyon, France .  Published Online: 20 March 2015

In March, 2015, 17 experts from 11 countries met at the International Agency for Research on Cancer (IARC; Lyon, France) to assess the carcinogenicity of the organophosphate pesticides tetrachlorvinphos, parathion, malathion, diazinon, and glyphosate (table). These assessments will be published as volume 112 of the IARC Monographs.1

3) IARC_Monograph_20_March_2015_Volume_112_Glyphosate_Carcinogen_Dr_Oz

4) http://www.mintpressnews.com/monsanto-launches-smear-campaign-against-doctor-oz-and-the-world-health-organization/204652/

Monsanto Launches Smear Campaign Against Doctor Oz And The World Health Organization.  About a week after TV’s popular but controversial Dr. Oz devoted most of an episode to new findings that suggest Monsanto’s Roundup causes cancer, he came under attack from medical professionals with agrichemical industry ties. By Kit O’Connell

Dr. Mehmet Oz, a cardiothoracic surgeon, who hosts a popular but controversial TV health program, devoted several segments of his April 7 program to a discussion of the glyphosate cancer risk.

Glyphosate, created in the 1970s, is the key ingredient in the Roundup and many other herbicides. Much of Monsanto’s business model depends on the sale of its “Roundup Ready” seeds, which grow crops that are genetically modified for resistance to glyphosate.

5) http://www.doctoroz.com/episode/how-outsmart-identity-thieves-after-your-money-and-medical-data?video_id=4158724753001

How to Know if Your Weed Killer Could Cause Cancer. Originally aired on 4/07/2015.  Dr. Oz discusses the safety of the chemical glyphosate, which is found in a popular weed killer. Find out more about this product and if it is carcinogenic.  Guests: Jon Sileo , Nikki Burton , Scott Faber , Dr. Alan Greene , Robyn O’Brien , Carole Radziwill , Luann De Lesseps , Sonja Morgan , Kristen Taekman , Dorinda Medley , Vic Dibetto , Monica Reinagel

WHO: Round-Up (Glyphosate) might Cause Cancer- new report

IARC report on Glyphosate.

Netherlands has banned glyphospate.

6) http://time.com/3831926/dr-oz-criticism-answers/

Exclusive: Dr. Oz Says ‘We’re Not Going Anywhere’      Dr. Mehmet Oz April 23, 2015

7) http://www.huffingtonpost.com/joel-fuhrman-md/unjust-attacks-against-dr_b_7103640.html?utm_source=Social&utm_medium=FBTwitter&utm_campaign=4.23.15_DrOzUnjustAttack

Joel Fuhrman, M.D. Unjust Attacks Against Dr. Oz 04/23/2015

8) http://eatlocalgrown.com/article/14470-gmo-fight-dr-oz.html

GMO FIGHT: Dr. Oz Says ‘We’re Not Going Anywhere’ after Monsanto Launches Smear Campaign New  by Rick D

9) http://www.doctoroz.com/episode/dr-oz-fights-back-his-exclusive-reaction-his-critics

Dr. Oz Fights Back: His Exclusive Reaction to His Critics

Dr. Oz Breaks His Silence

Originally aired on 4/23/2015

Dr. Oz addresses the 10 doctors who signed the headline-grabbing letter calling for Columbia University to fire him.

10)  http://www.cnn.com/2015/04/17/health/dr-oz-columbia-letter/

Physicians to Columbia University: ‘Dismayed’ that Dr. Oz is on faculty

By Debra Goldschmidt, CNN  April 22, 2015

11) http://www.nytimes.com/2015/04/24/business/media/dr-mehmet-oz-responds-to-critics-on-his-television-show.html?_r=0

Dr. Oz Responds to Critics on His Television Show

By SYDNEY EMBERAPRIL 23, 2015

12) Glyphosate modern diseases Celiac sprue gluten intolerance samsel seneff Toxicol 2013

13) http://www.mdpi.com/1660-4601/11/2/2125/htm

Int. J. Environ. Res. Public Health 2014, 11(2), 2125-2147;

Hypothesis …Glyphosate, Hard Water and Nephrotoxic Metals: Are They the Culprits Behind the Epidemic of Chronic Kidney Disease of Unknown Etiology in Sri Lanka?

Channa Jayasumana 1,2,* , Sarath Gunatilake 2,†

and Priyantha Senanayake 3,†

– Authors’ affiliations

1 Department of Pharmacology, Faculty of Medicine, Rajarata University, Anuradhapura 50008, Sri Lanka 2 Health Science Department, California State University, Long Beach, CA 90840, USA 3 Hela Suwaya Organization, Malabe 10115, Sri Lanka †

The current chronic kidney disease epidemic, the major health issue in the rice paddy farming areas in Sri Lanka has been the subject of many scientific and political debates over the last decade. Although there is no agreement among scientists about the etiology of the disease, a majority of them has concluded that this is a toxic nephropathy. None of the hypotheses put forward so far could explain coherently the totality of clinical, biochemical, histopathological findings, and the unique geographical distribution of the disease and its appearance in the mid-1990s. A strong association between the consumption of hard water and the occurrence of this special kidney disease has been observed, but the relationship has not been explained consistently. Here, we have hypothesized the association of using glyphosate, the most widely used herbicide in the disease endemic area and its unique metal chelating properties. The possible role played by glyphosate-metal complexes in this epidemic has not been given any serious consideration by investigators for the last two decades. Furthermore, it may explain similar kidney disease epidemics observed in Andra Pradesh (India) and Central America. Although glyphosate alone does not cause an epidemic of chronic kidney disease, it seems to have acquired the ability to destroy the renal tissues of thousands of farmers when it forms complexes with a localized geo environmental factor (hardness) and nephrotoxic metals.

14) http://www.glyphosate.eu/glyphosate-and-chronic-kidney-disease-sri-lanka

Glyphosate and Chronic Kidney Disease – Sri Lanka

15) http://www.truth-out.org/news/item/24876-monsantos-herbicide-linked-to-fatal-kidney-disease-epidemic-will-ckdu-topple-monsanto

Monsanto’s Herbicide Linked to Fatal Kidney Disease Epidemic: Could It Topple the Company?  Thursday, 10 July 2014 09:18 By Jeff Ritterman, M.D., Truthout |

16) http://www.globalresearch.ca/chronic-kidney-failure-5-times-higher-in-glyphosate-ridden-monsanto-roundup-areas-study-confirms/5434947

Chronic Kidney Failure 5 Times Higher in Glyphosate-Ridden (Monsanto Roundup) Areas, Study Confirms Yet Monsanto claims it is safe

By Christina Sarich  Global Research, March 05, 2015 Natural Society

17) http://www.greenmedinfo.com/blog/dramatic-increase-kidney-disease-us-and-abroad-linked-roundup-glyphosate

Dramatic Increase in Kidney Disease in the US and Abroad Linked To Roundup (Glyphosate) ‘Weedkiller’  Friday, March 14th 2014 Sayer Ji, Founder

18) http://panswiss.org/newsroom/glyphosate-linked-to-epidemic-of-kidney-failure-but-regulation-obstructed/

Glyphosate linked to epidemic of kidney failure, but regulation obstructed

19) http://www.npr.org/blogs/health/2014/04/30/306907097/mysterious-kidney-disease-slays-farmworkers-in-central-america

Mysterious Kidney Disease Slays Farmworkers In Central America

April 30, 2014 3:30 AM ET

20) http://grist.org/news/is-monsantos-roundup-linked-to-a-deadly-kidney-disease/   Is Monsanto’s Roundup linked to a deadly kidney disease?

By John Upton on 1 May 2014

21) http://naturalsociety.com/doctor-discusses-truth-glyphosate-chronic-kidney-disease/   Doctor Discusses Truth About Glyphosate and Chronic Kidney Disease

Christina Sarich     July 21, 2014

22)  Newly Released: Study Confirms Chronic Kidney Failure 5 Times Higher in Glyphosate-Ridden Areas  Yet Monsanto claims it is safe

Read more: http://naturalsociety.com/chronic-kidney-failure-5-times-higher-glyphosate-areas/#ixzz3YGIjCG2Y

23) http://permaculturenews.org/2014/04/09/sri-lanka-partially-bans-glyphosate-deadly-kidney-disease-epidemic/

Sri Lanka Partially Bans Glyphosate for Deadly Kidney Disease Epidemic

Posted April 9, 2014 by I-SIS & filed under GMOs, Health & Disease, Soil Erosion & Contamination, Water Contaminaton & Loss.

Glyphosate’s metal-chelating activity causes bioaccumulation of toxic metals in the body, resulting in an estimated 400 000 cases in Sri Lanka and 20 000 deaths.  by Dr Eva Sirinathsinghji

24) http://www.independentsciencenews.org/news/how-extreme-levels-of-roundup-in-food-became-the-industry-norm/

How “Extreme Levels” of Roundup in Food Became the Industry Norm

March 24, 2014 Environment, Health, News 6 Comments By Thomas Bøhn and Marek Cuhra

25) Human contamination by glyphosate Friends of the Earth Europe 2013

Jeffrey Dach MD

7450 Griffin Road, Suite 190

Davie, Fl 33314

954-792-4663

www.jeffreydachmd.com

www.drdach.com

www.naturalmedicine101.com

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The reader is advised to discuss the comments on these pages with his/her personal physicians and to only act upon the advice of his/her personal physician. Also note that concerning an answer which appears as an electronically posted question, I am NOT creating a physician — patient relationship. Although identities will remain confidential as much as possible, as I can not control the media, I can not take responsibility for any breaches of confidentiality that may occur.

Copyright (c) 2015 Jeffrey Dach MD All Rights Reserved. This article may be reproduced on the internet without permission, provided there is a link to this page and proper credit is given.

FAIR USE NOTICE: This site contains copyrighted material the use of which has not always been specifically authorized by the copyright owner. We are making such material available in our efforts to advance understanding of issues of significance. We believe this constitutes a ‘fair use’ of any such copyrighted material as provided for in section 107 of the US Copyright Law. In accordance with Title 17 U.S.C. Section 107, the material on this site is distributed without profit to those who have expressed a prior interest in receiving the included information for research and educational purposes.

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New Attack on BioIdentical Hormones by Drug Industry

BioIdentical Hormones Attacked Again

Article in Huffington Post by SWHR.

Just when things have calmed down, the Drug Industry opens a new salvo in its war against bioidentical hormones, perceived as unfairly stealing market share from their flaghip hormone pill, Prempro, a synthetic chemical currently in litigation for causing cancer and heart disease.

This time the attack appeared in the Huffington Post, with an article by Phyllis Greenberger, CEO of Society for Women’s Health Research, an industry sponsored mouthpiece which funnels money from the drug industry to doctors for research grants, speaking engagements, meetings and even gala celebrations. Upper left image courtesy of Huffington Post, Phyllis Greenberger,and SWHR.

Hot Flash and Cold Cash by Alicia Mundy

A 2003 expose by journalist Alicia Mundy in the Washington Monthly spills the beans on the Society for Women’s Health Research (SWHR).  Here is a quote from Alicia Mundy’s 2003 article:

“We do know the companies that sit on the (SWHR) society’s 40-member “corporate advisory board,” created since Greenberger took over. They include Eli Lilly, Johnson & Johnson, Merck, Pfizer, and Wyeth–all of which market popular women’s drugs. “

Serving Your Corporate Master

Although I am grateful to Phyllis Grenberger for giving me a topic to write about, I must confess astonishment with such a twisted and distorted collection of untruths, and deception nonsense all in one place.    Apparently, having the drug industry as one’s corporate master requires regurgitation of old marketing propaganda, even if it doesn’t make any sense.  Even to the most casual observer, this Huffing Post piece is a blatant attempt to discredit bioidentical hormones using fallacies, innuendo, and misinformtion.  Much of this material was covered in my previous book, Bioidentical Hormones 101.

 Let’s Take A Look At the Huff Post Article



The author,  Phyllis Greenberger M.S.W.,  states, “Bioidentical Hormones are not FDA approved.”

This is blatantly incorrect. There are twenty or so FDA approved bioidentical hormone preparations widely available at corner drug stores. Here are a few examples: Vivelle-Dot, Estrace, Climara, Prometrium, Androgel, etc.

The author Phyllis Greenberger states: “Bioidentical Hormones made by compounding pharmacies are Non-FDA approved.”

This is misleading and deceptive.  Compounding pharmacies are regulated at the state level, and do not fall under FDA jurisdiction. So, of course compounding is not FDA approved. No FDA approval is required or even desired. Your local hospital pharmacy is a compounding pharmacy that makes up life-saving medication such as IV antibiotics with no FDA oversight or approval. The FDA approval process is designed for manufacturer capsules and tablets, and is impractical and unnecessary for compounded medications prepared to order by hand. Are we going to reject IV antibiotics from the hospital pharmacy because these are non-FDA approved compounded medication? Of course not. Compounding is here to stay.

66 Cases of Endometrial Cancer on Prempro

The author, Phyllis Greenberger brings up a 2007 report of three cases of endometrial cancer in women on bioidentical hormones, implying that synthetic PremPro prevents endometrial cancer wheras biodentical hormones do not.  This is a blatant lie.  Prempro contains a synthetic progestin which reduces the incidence of endometrial cancer.  However, this is not reduced to zero. The author conveniently neglected to mention the 66 cases of endometrial cancer in Prempro treated women.as reported in the Women’s Health Initiative Study.  Dr. Rowan T. Chlebowski reported on the WHI data after 13.2 years of follow-up.  He said there were 66 endometrial cancers among women given PremPro (premarin and medroxyprogesterone).  There were 95 cases of endometrial cancer in the placebo group.

A “Bad Drug”  in Litigation ?

One easy way to determine if you are dealing with a “bad drug” is to ask the question:  Is this drug in litigation ?  For Prempro and synthetic “FDA approved” women’s hormones, the answer is yes, Prempro has been in litigation for years now.  Pfizer, the company that bought Wyeth, has paid almost a billion dollars to settle 6,000 lawsuits by women who claimed the drug caused their breast cancer.  This information should have been included, yet was conveniently omitted from the Huffington Post article by Phyllis Greenberger.

A Quote from June 19, 2012 Bloomberg News:

June 19 (Bloomberg) by Jef Feeley — Pfizer Inc. has paid $896 million to resolve about 60 percent of the cases alleging its menopause drugs caused cancer in women.  Pfizer has now settled about 6,000 lawsuits that claim Prempro and other hormone-replacement drugs caused breast cancer, and it has set aside an additional $330 million to resolve the remaining 4,000 suits, according to a filing with the U.S. Securities and Exchange Commission.

The reserve means New York-based Pfizer has committed more than $1.2 billion to resolving claims that its Wyeth and Pharmacia & Upjohn units failed to properly warn women about the menopause drugs’ health risk. Based on the May 10 filing, the company is paying an average of about $150,000 a case.

Abandoning Synthetic Hormones

The Women’s Health Initiative (WHI) study was terminated early in 2002, because the data showed increased risk of breast cancer and heart disease in the synthetic hormone treated group given Prempro. This information prompted intelligent women to abandon synthetic hormones. Instead they switched to bioidentical hormones, same as estrogen and progesterone produced by the ovary.  The massive switch to bioidentical hormones produced an immediate decline in breast cancer rates of about nine per cent.(9,10)  Left image: Abandoning the Sinking Ship courtesy of wikimedia commons.

Wake up From the Synthetic Hormone Nightmare

It is time to awaken from the nightmare of synthetic hormones, known for decades to cause cancer and heart disease. The drug industry can spin, and deceive us with misinformation and propaganda, however, the truth is clearly seen. Synthetic hormones remain monsters that should be avoided. Sadly, nowhere in this Huffington Post article was this important message stated.

Link to Op Ed News Version of this article.

Jeffrey Dach MD

7450 Griffin Rd

Suite 190

Davie Florida 33314

954-792-4663

Articles with Related Interest:

Synthetic Hormones Lose in Court

The Safety of Bioidentical Hormones

The Importance of Bioidentical Hormones

Newsweek Attacks Bioidentical Hormones



10 Bioidintical Hormone Fallacies of Staness Jonekos

Bioidentical Hormones According to the LA Times

Bioidientical Hormones Trashed by AP News

Waking Up From the Synthetic Hormone Nightmare

Links and References:

1) Non_Profit_Organisations with Ties to Industry_Integrity_in_Science

2) A Hot Flush for Big Pharma British Medical Journal Clark 2003

3) http://www.obgmanagement.com/home/article/hormone-therapys-protection-against-endometrial-cancer-persists-in-womens-health-initiative-follow-up-study/9feb2e22640ae61f8e62891f93de2547.html

Hormone therapy’s protection against endometrial cancer persists in Women’s Health Initiative follow-up study

After a median of 13.2 years’ follow-up, there were 35% fewer endometrial cancers among women given combined estrogen and progestin vs. placebo (hazard ratio, 0.65; P = .007). A total of 66 women treated with the hormone therapy (HT) and 95 given placebo had developed endometrial cancer, yielding annual incidences of 0.06% and 0.10%, respectively.

“We do not feel that this effect on endometrial cancer changes the overall balance of risk and benefit of estrogen plus progestin,” Dr. Rowan T. Chlebowski stated at the multidisciplinary European cancer congresses.

4) http://www.sourcewatch.org/index.php/Society_for_Women%27s_Health_Research

The Society for Women’s Health Research (SWHR) is a Washington, DC nonprofit organization which claims that its “sole mission is to improve the health of women through research.” However, it has received substantial funding from the Wyeth-Ayerst drug company, and rose to Wyeth’s defense when research showed that Wyeth’s hormone replacement therapy hurts women.

In July 2002, the US National Institutes of Health (NIH) announced that it was abandoning its study of the effects of Prempro, Wyeth’s market-leading hormone replacement therapy (HRT) drug. NIH had originally planned an eight-year trial of the drug, but it only took five years to accumulate conclusive evidence of increased health damage to women who use the drug over time. The announcement was reported with shock in media outlets around the world, which had long been accustomed to glowing reports of HRT.  Women’s health and consumer groups welcomed the decision, but the SWHR condemned the NIH decision and distributed op-eds and letters to newspapers around the country. Reporting in Washington Monthly, Alicia Mundy noted that Wyeth and other drug companies are represented on the group’s corporate advisory board, but details of the group’s funding remain obscure. “Our attorney says it is confidential information that we don’t distribute,” Mundy was told when she inquired.

The SWHR website notes, however, that Wyeth has been a corporate sponsor of its annual fundraising ball at the Washington Ritz-Carlton. In fact, Wyeth underwrote the entire glitzy affair, which promoted Prempro so enthusiastically that one attendee complained it was “like they were doing an ad for Wyeth.”

5) http://www.huffingtonpost.com/phyllis-greenberger/

Phyllis Greenberger, MSW, is the president and CEO of the Society for Women’s Health Research (SWHR®), a national nonprofit organization based in Washington, D.C., widely recognized as the thought leader in research on biological differences in disease, and dedicated to transforming women’s health through science, advocacy and education. Greenberger is the first and only president and CEO of SWHR since its founding in 1990. Through her leadership, dedication and promotion of women’s health, sex differences is now widely known and recognized as a critical factor in women’s health.

6) http://www.washingtonmonthly.com/features/2001/0301.mundy.html

Hot Flash, Cold Cash, How a once-respected women’s group went through The Change–with the help of drug industry money.By Alicia Mundy

7) http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1126827/

Clark, Jocalyn. “A Hot Flush for Big Pharma.” BMJ : British Medical Journal 327.7411 (2003): 400.

8) http://web18.superb.net/womenshealthresearch.org/rf/pfizer.htm

The Society/Pfizer Women’s Health Research Scholars Grants for Faculty Development in Women’s Health Program represents the mutual commitment of the Society for Women’s Health Research and Pfizer to the scientific and academic advancement of M.D. or D.O. medical school faculty members interested in advancing the science of women’s health. The Scholars Grants Program provides research and training opportunities for physician researchers who wish to pursue basic study in biologic mechanisms of diseases that affect women.

(9) http://www.nejm.org/doi/full/10.1056/NEJMsr070105 The Decrease in Breast-Cancer Incidence in 2003 in the United States. Peter M. Ravdin, Ph.D., M.D et al. N Engl J Med 2007; 356:1670-1674 April 19, 2007.  A comparison of incidence rates in 2001 with those in 2004 (omitting the years in which the incidence was changing) showed that the decrease in annual age-adjusted incidence was 8.6% .

(10) http://jnci.oxfordjournals.org/content/early/2010/09/23/jnci.djq345.abstract Breast Cancer Incidence and Hormone Replacement Therapy in Canada by Prithwish De, C. Ineke Neutel, Ivo Olivotto and Howard Morrison. JNCI J Natl Cancer Inst (2010) . This drop occurred concurrently with a 9.6% decline in the incidence rate of breast cancer

Jeffrey Dach MD

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Progesterone for PMS Part Two

Progesterone for PMS, and irregular menstrual cycles. Part Two

For part one, click here.

For over a million years, now, estrogen and progesterone has been key players in the female menstrual cycle, ovulation and fertility.  Left Image: Iconic 1966 theatrical poster of Raquel Welch in One Million Years BC. later featured in the Shawshank Redemption covering the escape tunnel.

Understanding the Normal Menstrual Cycle – Hormone Charts

The chart below from college level biology class, showing the idealized normal menstrual cycle.Estrogen and Progesterone

To understand progesterone and estrogen,  one must review the above chart showing the major events of the menstrual cycle.  Estrogen and progesterone are natural human hormones produced in harmony by the ovary. Estrogen is produced throughout most of the month, from days 5-26 with a peak just before ovulation (day 11) and another peak around day 19.

The Corpus Luteum

Progesterone is produced the last two weeks of the monthly cycle by the corpus luteum,  a specialized ovarian structure, representing the remnant of the ovulatory follicle after ovulation.  During ovulation, the egg (aka ovum, oocyte) is expelled from the ovarian follicle, and starts its long journey down the fallopian tube to the endometrial cavity where fertilization and  implantation may occur (aka ovulation).  Ovulation usually occurs on day 11 (vertical dotted line on chart), so progesterone levels start rising on day 12, peaking on day 19-20 or so.

Sudden Decline in Hormone Levels Leads to Bleeding

Both progesterone and estrogen levels decline suddenly around day 26 of the menstrual cycle.  This sudden drop in hormone levels initiates menstrual bleeding, the endometrial lining has lost hormonal support and sloughs off (aka menstrual bleeding).  Left image shows microscopic view of ovary and corpus luteum courtesy of UNSW Embryology.

Idealized Normal Menstrual Cycle

The above schematic diagram  shows the idealized menstrual cycle in the normal female.  Firstly, look at the top row.  The yellow do-nut like-structure  is the corpus luteum in the ovary which makes progesterone.  The next row down is body temperature which spikes up at the time of ovulation around day 11.  The vertical dotted line represents ovulation around day 11.  The next row down we see that FSH and LH spike at the time of ovulation.  These are pituitary hormones.  FSH is follicle stimulating hormone, and LH is leutinizing hormone. The next row down, we see charts of serum estrogen (yellow) and progesterone (purple).  Estrogen spikes just before ovulation, and then has a second peak around day 19.  Progesterone starts rising after ovulation, peaks around day 19 and then falls off around day 26.  The bottom row shows a schematic of the endometrial lining which thickens with hormonal stimulation, and then sloughs off as hormone levels drop off at day 26.

Anovulation, Estreogen Dominance and Menstrual Irregularities

The chart shows a normal ovulatory cycle.  What happens if ovulation does not occur?  This is called anovulation, a common problem in young women. in which the ovum is not expelled, no corpus luteum is formed, and no progesterone is produced.  Without ovulation, menstrual bleeding becomes irregular, and the cycle length is variable.   This leads to a condition known as “estrogen dominance” in which body tissues respond to estrogenic stimulation without progesterone to counter act the estrogen..

PMS – PreMenstrual Syndrome – Estrogen Dominance

Estrogen causes fluid retention and breast tissue stimulation.  In the absence of enough progesterone to counter balance the estrogen,  the patient may experience bloating, breast enlargement and tenderness, and fluid retention.  Estrogen also causes psycho-stimulation, so the patient may complain of insomnia and mood disorders, migraine headaches etc..   As estrogen levels drop, the serum binding protein levels also drop, thus liberating testosterone to cause acne, oily skin and aggressive, “snappy” behavior.

In some cases, ovulation occurs , yet progesterone production is insufficient to balance  the massive amounts of estrogen.  Similarly these patients suffer from “estrogen dominance” and a similar symptom complex also called “PMS”. premenstrual syndrome.

Treatment for PMS and Irregular Menstrual Cycles

Since progesterone is the missing or deficient element in the PMS syndrome, it would be logical to assume providing progesterone in the form of creams or capsules would benefit the patient.  In fact, many doctors and patients report dramatic resolution of PMS symptoms with progesterone capsules and creams.  Of course, an annual pelvic exam by the local gynecologist as well as pelvic sonogram is warranted for pre-menopausal women prior to treatment with natural progesterone.   Although we will typically perform laboratory testing of hormone levels on day 19 of the menstrual cycle, this type of lab testing is not required by mainstream medicine, and in fact rarely done for treatment of PMS or irregular menstrual bleeding.  For more on this, see my article on the importance of the pelvic sonogram.

Still Not Accepted by Mainstream Medicine

Although progesterone is an FDA approved drug, mainstream medicine has yet to accept bioidentical natural human progesterone as a treatment for PMS and irregular menstrual cycles. Instead, mainstream medicine relies on synthetic forms of progesterone called “progestins” such as medroxyprogesteron (Provera) which was shown to cause breast cancer and heart disease in the ill fated Women’s Health Initiative Study.  Why hasn’t mainstream medicine accepted progesterone as a valid treatment for PMS?  This is explained by the “War Against Natural Medicine”.

The War Against Natural Medicine

In my first book,  Natural medicine 101, I delved into the reasons for the information war between natural medicine and mainstream medicine.  In short, mainstream medicine is dominated by the drug industry whose profits are dependent on the patented drug system.  A patented drug is a natural molecule whose chemical structure has been altered in order to obtain a patent.  Molecular structures naturally occurring in the human body or in nature by definition cannot be patented, and are therefore of no interest to the drug industry.  Rather, these natural substances such as progesterone represent economic competition to the patented counterparts.  That is why progesterone has not taken its rightful place in mainstream medicine treatment of PMS.  Left Image courtesy of SheKnows Left image courtesy of Dysfunctional uterine bleeding.

John R Lee MD and Uzzi Reiss M

Thanks and credit goes to  Uzzi Reiss MD and John R Lee MD, Most of the material in this article can be found in John R Lees’ chapter on progesterone in his book, What the doctor wont tell you about premenopause.   Also Uzzi Reiss’s chapter on progesterone and PMS from his book, Natural Superwoman was another source for this article.

Jeffrey Dach MD

7450 Griffin Road

Suite 180/190

Davie, Florida  33314

954-792-4663

Links and References:

Progesterone FDA Approval Prevention Endometrial Hyperplasia

Carlo Campagnoli Progestins progesterone hormone replacement risk breast cancer steroid biochemistry 2005

Mood Biochemistry of Women at Mid-life Phyllis Bronson 2001 J Ortho Mol Med

progesterone Katharina Dalton MD

Conservative management of endometrial hyperplasia Childs OBG MANAGEMENT 2003  Childs, A. J., W. E. Check, and W. J. Hoskins. “Conservative management of endometrial hyperplasia: New strategies, experimental options.” OBG MANAGEMENT 15.9 (2003): 15-26.

Progesterone for Symptomatic Perimenopause Prior 2011  Prior, J. C. “Progesterone for Symptomatic Perimenopause Treatment–Progesterone politics, physiology and potential for perimenopause.” Facts, Views & Vision in ObGyn 3.2 (2011): 109.

Natural progesterone Jane Murray Womens Health Primary Care 1998  Murray, Jane L. “Natural progesterone: what role in women’s health care.” Women’s Health Primary Care 1.8 (1998): 671-87.

progesterone_booklet Lawley Pharmaceuticals 2010

Estrogen carcinogenesis in breast cancer James Yager New England Journal of Medicine 2006

Dose dependent effects oral progesterone oestrogenised postmenopausal endometrium Lane BMJ 1983

Oral micronized progesterone de Lignières Clinical therapeutics 1999  de Lignières, Bruno. “Oral micronized progesterone.” Clinical therapeutics 21.1 (1999): 41-60.

Premenstrual Syndrome Chart American Family Physician

Endometrial_Hyperplasia_Progesterone_ACOG_Brochure

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http://www.thelancet.com/pdfs/journals/lancet/PIIS0140673604173005.pdf

Katharina Dorothea Dalton

A gynaecologist who popularised the concept of premenstrual syndrome and wrote the best- selling book Once a Month.  . Born in London, UK, on Nov 11, 1916, she died on Sept 17, 2004, aged 87 years

Letter containing basic incorrect statements about progesterone

http://www.bmj.com/rapid-response/2011/10/30/katharina-dalton-and-progesterone-dangers

Obituaries Katharina Dorothea Dalton

BMJ 2004; 329 doi: http://dx.doi.org/10.1136/bmj.329.7473.1048-b (Published 28 October 2004) Cite this as: BMJ 2004;329:1048

Removal of the ovaries has long been used to prevent endogenous progesterone production as a treatment for breast cancer. Recent studies confirm that progesterones cause more breast cancer than oestrogens. Progesterone is also potentially teratogenic.

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Freeman, ELLEN W., et al. “A placebo‐controlled study of effects of oral progesterone on performance and mood.” British journal of clinical pharmacology 33.3 (1992): 293-298.

http://www.drkaslow.com/html/progesterone.html

Jeremy E. Kaslow, MD, FACP, FACAAI Physician and Surgeon

Board Certified Internal Medicine

Hormones and the Menstrual Cycle

http://www.ncbi.nlm.nih.gov/pubmed/8726605

Pharmacotherapy. 1996 May-Jun;16(3):453-7.

Oral administration of micronized progesterone: a review and more experience.

McAuley JW1, Kroboth FJ, Kroboth PD.

Historically, oral progesterone has been regarded clinically ineffective because of its poor absorption and rapid clearance. Recent evidence suggests that an oral micronized form of natural progesterone is readily absorbed, produces luteal phase serum concentrations, provokes an end-organ response, and has no detrimental effect on the lipoprotein profile. Thus it is considered by many to be an attractive alternative to synthetic progestin. We evaluated the effects of a single oral dose of micronized progesterone 300 mg in eight healthy postmenopausal women. The maximum serum concentration ranged from 15.72-625.98 ng/ml.

http://www.ncbi.nlm.nih.gov/pubmed/7473442

Efficacy of oral micronized progesterone in the treatment of luteal phase defects.

Frishman GN1, Klock SC, Luciano AA, Nulsen JC.

Vaginal progesterone suppositories are an accepted treatment for infertility attributed to luteal phase defects. Although oral micronized progesterone may be preferable to suppositories for many patients, there are no studies on its use for patients with luteal phase defects. This study evaluated the efficacy of oral micronized progesterone for the treatment of luteal phase defects.

STUDY DESIGN:  Seven women with luteal phase defects previously corrected by vaginal suppositories were administered oral micronized progesterone (200 mg by mouth three times a day). Endometrial biopsies were performed to evaluate treatment efficacy. Questionnaires were used to assess side effects, including sedation.

RESULTS:  On oral micronized progesterone, all patients had in-phase endometrial biopsies. Despite complaints of drowsiness, the majority of patients preferred the oral formulation over the vaginal route of administration.

CONCLUSION:  We conclude that oral micronized progesterone is efficacious in the treatment of luteal phase defects.

http://www.bmj.com/content/287/6401/1241.short

Dose dependent effects oral progesterone oestrogenised postmenopausal endometrium Lane, G., et al. “Dose dependent effects of oral progesterone on the oestrogenised postmenopausal endometrium.” BMJ 287.6401 (1983): 1241-1245.

Full free-  BEST

http://www.fertstert.org/article/S0015-0282%2899%2900272-1/fulltext

Fitzpatrick, Lorraine A., and Andrew Good. “Micronized progesterone: clinical indications and comparison with current treatments.” Fertility and sterility 72.3 (1999): 389-397.

Objective: To integrate and evaluate the pharmacokinetic, endocrine, and clinical effects of micronized progesterone formulations.

Design: Published articles concerning the pharmacokinetics of orally administered progesterone and the potential clinical uses of oral micronized progesterone were reviewed. Results concerning their use for secondary amenorrhea, premenopausal bleeding disorders, luteal phase dysfunction, termination of premature labor, hormone replacement therapy, and premenopausal syndrome are summarized. Critical issues to be resolved through ongoing preclinical and clinical research are highlighted.

Result(s): Because of the enhanced bioavailability of oral micronized progesterone, the compound may be useful for a variety of therapeutic indications. Oral micronized progesterone is available in France, and a formulation recently has been approved in the United States for the treatment of secondary amenorrhea and postmenopausal hormone replacement therapy. A large body of evidence, including the Postmenopausal Estrogen/Progestin Interventions study, suggests that the use of a combination of estrogen and oral micronized progesterone is optimal for long-term hormone replacement therapy. There also are data indicating that oral micronized progesterone could be of potential use for the treatment of premenopausal bleeding disorders, luteal phase disorders, and premature labor.

Conclusion(s): Oral micronized progesterone has widespread clinical potential, particularly for the treatment of secondary amenorrhea and dysfunctional premenopausal bleeding, and as a component of postmenopausal hormone replacement therapy.

In summary, oral micronized progesterone has the potential for widespread clinical utility. For indications in which oral delivery of the synthetic progestins currently are used, the theoretic benefits of oral delivery of the natural form of the hormone are obvious. In addition to the decreased potential for adverse effects, there are clear advantages in convenience, cost, compliance, and quality of life.

Acknowledgements

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Li, Quanxi, et al. “The antiproliferative action of progesterone in uterine epithelium is mediated by Hand2.” Science (New York, Ny) 331.6019 (2011): 912.

 

P counteracts E-induced endometrial hyperplasia.

pdf available

Munro, Malcolm G., et al. “medroxyprogesterone for acute uterine bleeding Munro Oral medroxyprogesterone acetate and combination oral contraceptives for acute uterine bleeding: a randomized controlled trial.” Obstetrics & Gynecology 108.4 (2006): 924-929.

Bitzer, Johannes, et al. “Medical Management of Heavy Menstrual Bleeding: A Comprehensive Review of the Literature.” Obstetrical & gynecological survey 70.2 (2015): 115-130.

Quinn, Stephen, and Jenny Higham. “Available management options for heavy menstrual bleeding.” Prescriber 25.18 (2014): 18-25.

Matteson, Kristen A., et al. “Nonsurgical management heavy menstrual bleeding systematic review Nonsurgical management of heavy menstrual bleeding: a systematic review.” Obstetrics & Gynecology 121.3 (2013): 632-643.

Matteson, Kristen A., et al. “Practice patterns and attitudes about treating abnormal uterine bleeding: a national survey of obstetricians and gynecologists.” American journal of obstetrics and gynecology 205.4 (2011): 321-e1.

Kaunitz, A. M., et al. “Levonorgestrel-releasing intrauterine system or medroxyprogesterone for heavy menstrual bleeding: a randomized controlled trial.” Obstetrics and gynecology 116.3 (2010): 625.

Managing acute heavy menstrual bleeding

Recommendations for hormonal regimens to halt blood loss in the outpatient

January 01, 2014  By Anita L. Nelson, MD

Aksu, M. Feridun, et al. “High‐Dose Medroxyprogesterone Acetate for the Treatment of Dysfunctional Uterine Bleeding in 24 Adolescents.” Australian and New Zealand journal of obstetrics and gynaecology 37.2 (1997): 228-231.

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PMS

Once a Month: Understanding and Treating PMS Paperback – March 23, 1999  Katharina Dalton (Author)

http://www.johnleemd.com/store/drphil_anderson.html

Dr. Phil Interview with Holly Anderson: Treating PMS Symptoms With Natural Progesterone  .   The treatment that works is vaginal or rectal natural progesterone. [Progesterone cream works just as well or better because it’s not messy and drippy! It is delivered to cells throughout the body within minutes of application.] Oral [pill] progesterone does not work for PMS. […because it stresses the liver and creates a lot of metabolites or byproducts, and also only delivers about 20 percent of the dose to the cells].

http://www.aafp.org/afp/2003/0415/p1743.html

Premenstrual Daily Symptom Diary.

Premenstrual Syndrome

LORI M. DICKERSON, PHARM.D., PAMELA J. MAZYCK, PHARM.D., and MELISSA H. HUNTER, M.D., Medical University of South Carolina, Charleston, South Carolina.  Am Fam Physician. 2003 Apr 15;67(8):1743-1752.

http://www.ncbi.nlm.nih.gov/pubmed/3924191

Br Med J (Clin Res Ed). 1985 Jun 1;290(6482):1617-21.

Progesterone and the premenstrual syndrome: a double blind crossover trial.

Dennerstein L, Spencer-Gardner C, Gotts G, Brown JB, Smith MA, Burrows GD.

A double blind, randomised, crossover trial of oral micronised progesterone (two months) and placebo (two months) was conducted to determine whether progesterone alleviated premenstrual complaints. Twenty three women were interviewed premenstrually before treatment and in each month of treatment. They completed Moos’s menstrual distress questionnaire, Beck et al’s depression inventory, Spielberger et al’s state anxiety inventory, the mood adjective checklist, and a daily symptom record. Analyses of data found an overall beneficial effect of being treated for all variables except restlessness, positive moods, and interest in sex. Maximum improvement occurred in the first month of treatment with progesterone. Nevertheless, an appreciably beneficial effect of progesterone over placebo for mood and some physical symptoms was identifiable after both one and two months of treatment. Further studies are needed to determine the optimum duration of treatment.

http://www.amazon.com/Emerita-Pro-Gest-Cream-tube-PACKAGING/product-reviews/B000IMQE5U

Emerita Pro-Gest Cream, 4 oz. tube (PACKAGING MAY VARY)

byEmerita on Amazon

http://www.drnorthrup.com/heavy-menstrual-bleeding-menorrhagia/

Heavy Menstrual Bleeding (Menorrhagia) Christiane Northrup, M.D.

Although I prefer to try natural progesterone first, if that doesn’t work, a strong synthetic progestin such as medroxyprogesterone acetate (Provera) can help. (This is the only circumstance in which I recommend the synthetic.) T – See more at: http://www.drnorthrup.com/heavy-menstrual-bleeding-menorrhagia/#sthash.6GlJCGzW.dpuf

http://www.pmstreatmentclinic.com/services.html

PMS Treatment Clinic using bioidentical hormones to treat premenstrual syndrome.

Treatment of Premenstrual Syndrome

Premenstrual Syndrome is a condition of estrogen dominance-progesterone deficiency. It occurs in the two weeks before the period and goes away when the period is over. 150 emotional and physical symptoms can occur. Symptoms may include headaches, migraines, menstrual cramps, depression, irritability, fatigue, emotional outbursts, low blood sugar, rage, out of control behavior, dizziness, decreased resistance to infection and epileptic seizures. An underactive thyroid is commonly an underlying disorder that is present.

Patients can become symptom-free on natural progesterone therapy. If the patient is hypothyroid, treatment involves thyroid supplements.

https://www.womentowomen.com/pms/severe-pms-and-pmdd-treatment/

by Marcelle Pick, OB/GYN NP

Advanced Premenstrual Syndrome (PMS) and Premenstrual Dysphoric Disorder (PMDD) Treatment

http://www.womenlivingnaturally.com/articlepage.php?id=29

Dysfunctional Uterine Bleeding

http://www.georgiahormones.com/Progesterone-Use-For-Cycle-Regulation.aspx

Progesterone Use for Cycle Regulation

If you are reading this flyer, it is likely that you are having problems with irregular, heavy or abnormal periods and have been given a prescription for Progesterone supplementation. The most common cause of these problems is irregular or inadequate production of progesterone.

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http://www.mountainspringsmedicine.com/14.html

UNOPPOSED ESTROGEN AND THE PERI-MENOPAUSAL TRANSITION

http://press.endocrine.org/doi/abs/10.1210/edrv.21.1.0386

Is Estradiol a Genotoxic Mutagenic Carcinogen? Joachim G. Liehr July 01, 2013  Endocrine Reviews

Yager, James D., and Nancy E. Davidson. “Estrogen carcinogenesis in breast cancer.” New England Journal of Medicine 354.3 (2006): 270-282.

Campagnoli, Carlo, et al. “Progestins and progesterone in hormone replacement therapy and the risk of breast cancer.” The Journal of steroid biochemistry and molecular biology 96.2 (2005): 95-108.

 

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HGH Human Growth Hormone Medical Research Studies

HGH Human Growth Hormone Medical Research Studies This is a compilation of articles on HGH Human Growth hormone, and the Diagnosis and Treatment of adult human growth hormone deficiency. Link to article with related interest: Dr Andrew Weil AARP Human … Continue reading →

The post HGH Human Growth Hormone Medical Research Studies appeared first on Jeffrey Dach MD .