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Thoughts On Coca, Cannabis, Opium & Tobacco – Gifts Of The Great Spirit


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Did Mom Give You Testicular Cancer?

             Stu Kraft – Brother, Friend, Artist, Beloved Fisher

I dedicate this post to our brother Stu Kraft, a mountain man full of joy, talent, energy and life whose mother was a heavy smoker from the 1950’s until her death of lung cancer. Stu was born with reproductive system issues, and turned even that into art. He loved to make his friends uncomfortable by joking about his “monoball”, and once serenaded a large party with an impromptu and delightfully bawdy song about a sailor with one ball and the feats he manfully managed to perform. It turned out that Stu’s monoball must have been attacked in the womb by the hidden DDT in his Mom’s cigarettes, because when he was in his early 50’s monoball turned on him and killed him.

Researchers have long known there is a connection between smoking and testicular cancer. They just couldn’t explain what it is.

But when you examine a secret tobacco industry study from 1972 (see more below) then we can see that it’s more than just possible that a lot of 2019’s testicular cancer will arise from a genetic hit in the womb from the DDT in a mother’s (or grandmother’s) cigarettes in the 1960’s or 70’s. That genetic hit occurred because with every puff she was inhaling massive doses of hidden organochlorine pesticides.

Mothers weren’t being irresponsible by smoking in those days – many doctors even advised it. Mothers smoked because they believed it would help to keep their weight from getting out of control and to deal with the stress of Motherhood. Everybody did it.

Here’s How Mothers & Fetuses Were Exposed To DDT in the 1970’s

The problem with looking at DDT in Tobacco products is that all the DDT exposure studies ever done deal only with the health consequences of environmental exposure to DDT and ingestion in food or water. Nobody has ever studied the health effects of smoking pesticide contaminated tobacco products because the Tobacco industry knew about the problem and actively and completely suppressed that kind of research. It just hasn’t been done.  But DDT and other organochlorines have been there in heavy concentrations since 1955, and we now know that genetic damage caused by organochlorine pesticides is transgenerational, and targets specific parts of the genome in order to accomplish this stealth transmission of genetic disease.

Bottom line – if that mother or grandmother we referred to above was pregnant and smoking cigarettes between 1955-1980 she was without any question micro-dosing herself and her unborn child with DDT.

I referred to a confidential RJR report above. It’s from 1972, with all the original signatures, and reports on tests of DDT contamination of three RJR brands. All three brands show heavy contamination, and other research I’ve done shows that the entire tobacco product supply in the US in those days was loaded with enough chemicals to explain nearly all the smoking-related disease we see today.

If the anti-tobacco forces weren’t barely disguised Victorian moralists moralists, under the weight of factual evidence of pesticide contamination they would have to recognize that there is a legitimate question about whether it is actually tobacco that is responsible for all smoking-related disease and if not, what else is responsible and in what proportion? The fact is that there was DDT in every US cigarette in 1972, and that the sons of mothers born to mothers who smoked in those days are now known to be at high risk of testicular (and other) cancer in 2019. I’ll link you to peer-reviewed journal research on this below but first here’s a table summarizing the data on DDT in those three RJR brands in 1972. This is what millions of grandmothers of today’s middle-age men were inhaling. (BTW – this report only covered DDT – there were many other heavy organochlorine residues in 1972 cigarettes.)

RJR Confidential June 21, 1972

Project 2358 – Cigarette Development; Notebook Pages: 250701-250719

In The Cigarette DDT – Range PPM (20 samples) DDT – Avg PPM (20 Samples)
4841 – Regular Unfiltered 4.14 – 7.96 6.06 +/- 0.99
4842 – Filter King 3.38 – 6.65 4.95 +/- 0.90
4843 – Filter King 4.86 – 6.82 5.89 +/- 0.61
In The Cigarette Smoke    
4841 – Regular Unfiltered 0.35 – 0.57 0.42 +/- 0.06
4842 – Filter King 0.16 – 0.35 0.025 +/- 0.05
4843 – Filter King 0.24 – 0.46 0.35 +/- 0.05

 

Here’s What’s Happening To Male Children Today

J Natl Cancer Inst. 2008 May 7;100(9):663-71.

Persistent organochlorine pesticides and risk of testicular germ cell tumors

https://www.ncbi.nlm.nih.gov/pubmed/18445826

CONCLUSIONS:

Increased exposure to p,p’-DDE may be associated with the risk of both seminomatous and nonseminomatous TGCTs, whereas exposure to chlordane compounds and metabolites may be associated with the risk of seminoma. Because evidence suggests that TGCT is initiated in very early life, it is possible that exposure to these persistent organic pesticides during fetal life or via breast feeding may increase the risk of TGCT in young men.

Here’s Why Even Tiny, Steady Doses Of DDT Matter

Male Reproductive Health and Environmental Xenoestrogens

https://ehp.niehs.nih.gov/doi/pdf/10.1289/ehp.96104s4741

Long-term exposure to small amounts of organochlorine contaminants leads to the accumulation of considerable burdens in animal and human tissues. It is therefore not the amount of DDT to which a mother is exposed during pregnancy that is critical but rather her lifetime exposure that will determine the level of exposure of the fetus and the breast-fed infant.

Here’s Evidence That This Is Happening Worldwide

Human Reproduction, Volume 16, Issue 5, 1 May 2001, Pages 972–978

Testicular dysgenesis syndrome: an increasingly common developmental disorder with environmental aspects: Opinion

https://academic.oup.com/humrep/article/16/5/972/2913494

This article summarizes existing evidence supporting a new concept that poor semen quality, testis cancer, undescended testis and hypospadias are symptoms of one underlying entity, the testicular dysgenesis syndrome (TDS), which may be increasingly common due to adverse environmental influences.

Experimental biological investigations and epidemiological studies leave little doubt that the TDS can be a result of disruption of embryonal programming and gonadal development during fetal life. As the rise in the incidence of the various symptoms of TDS occurred rapidly over few generations, the aetiological impact of adverse environmental factors such as hormone disrupters, probably acting upon a susceptible genetic background, must be considered.

While the focus of this post is on DDT and TDS, take a look at the pesticide contaminants that we just found in a sample of tobacco brands purchased off-the-shelf at out Portland-area minimarts, The first thing that stands out is the number of contaminants and – look at that – the cheaper the brand the higher the contamination and the worse the contaminants. In fact, the cheaper the brand the more Testicular disrupting/damaging chemicals there are – look at the Carbendazim in the Swisher Sweets. Combined with the action of DDT on Testicular tissues and hormones Carbendazim is equally well-documented as a male reproductive system poison and carcinogen.

Carbendazim is a broad-spectrum benzimidazole antifungal with potential antimitotic and antineoplastic activities. Although the exact mechanism of action is unclear, carbendazim appears to binds to an unspecified site on tubulin and suppresses microtubule assembly dynamic. This results in cell cycle arrest at the G2/M phase and an induction of apoptosis.

The point of this is to say that the brand of tobacco product your mother smoked matters more than just about any other factor in determining your risk of Testicular cancer as an adult. This means staying alert and getting checked often – which Stu did not do. I would end this with RIP, but there’s no way that “Tiny Ball” is laying around resting, wherever he is.

CURATED BLOG POSTS ON RELATED TOPICS

Hidden Causes Of HIV/AIDS Treatment Failure

https://wp.me/p48Z9A-nOD

The Korean Genome + Smoking + (DDT) = Diabetes Epidemic

https://wp.me/p48Z9A-nO6

Ancestral DDT Exposure & Trans-generational Obesity

https://wp.me/p48Z9A-nNO

Smoking & Breast Cancer – A New Link?

https://wp.me/p48Z9A-nNl

Little Cigars And High Liver Cancer Rates In Marginalized Communities

https://wp.me/p48Z9A-nMy

Sweet Cheap Poison At The Bodega

https://wp.me/p48Z9A-nLj

Prostate Cancer & Tobacco Pesticides: Hidden Links

https://wp.me/p48Z9A-nKy

Obesity & Obesogens: The Tobacco Connection

https://wp.me/p48Z9A-nJ4

Tobacco Pesticides & Childhood Leukemia

https://wp.me/p48Z9A-nIL


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Smoking & Breast Cancer – A New Link?

Because of the heavy concentrations of DDT and other endocrine disrupting pesticide residues we recently detected contaminating popular tobacco brands, I’ve been thinking a lot about the fact that beginning with the 1950s every tobacco product being smoked, puffed, dipped or chewed in America had extremely heavy concentrations of organochlorine pesticides. Heavy use of xenobiotic “crop protection” agents for tobacco began in the 1950s with DDT and quickly included aldrin, endrin, dieldrin, chlordane and other byproducts of wartime toxic gas research.

With that in mind, please check this:

DDT Exposure in Utero and Breast Cancer  The Journal of Clinical Endocrinology & Metabolism, Volume 100, Issue 8, 1 August 2015, Pages 2865–2872,

Maternal o,p′-DDT predicted daughters’ breast cancer (odds ratio fourth quartile vs first = 3.7, 95% confidence interval 1.5–9.0). Mothers’ lipids, weight, race, age, and breast cancer history did not explain the findings.

DDT and Breast Cancer: Prospective Study of Induction Time and Susceptibility Windows . Journal of the National Cancer Institute, 13 February 2019

“Considering the patterns we observed, working backward to determine when a woman first came into contact with the chemical could help inform early detection and treatment of DDT-associated breast cancer.”

Women who were born roughly between 1955-1980 to mothers who smoked (or dipped or chewed) any of the popular tobacco brands of the times were heavily exposed to DDT and other organochlorines in the womb and probably throughout early childhood as Mommy smoked to get rid of all that pregnancy weight and then kept on smoking, maybe in secret, just a little, because it calmed her nerves.

A confidential industry study done in 1972 that I located in the Tobacco Settlement files reported an average of almost 6 mg/kg total DDT over all the brands they tested anonymously. The report ended with a hope that DDT concentrations would be dropping in the future (it had just been banned worldwide for the first time in 1972), and a warning that the data must be kept secret.

But when you look at what we found in tobacco products in 2018 you can see how little progress has been made. While there is only one instance of DDT contamination here it is extreme, and as you can see there are several rather extreme concentrations of other hazardous endocrine disrupting pesticide residues here even in this small sample. There are also residues of pesticides for which no data exist – their effects are unknown. It’s a crap shoot with human lives rolling snake eyes.

Community Tobacco Control Partners Test Results 12/18

If my interpretation of how our new tobacco pesticide residue data applies to the breast cancer research on endocrine disrupting chemicals is right, and it seems pretty straightforward, women in 2019 with medical history that includes parental and especially maternal smoking during birth years 1955-1980 are at severely heightened risk that requires close attention. I am NOT saying that the threat ended in 1980 – it changed, and it got worse. As you can see from the data above, female babies born today to young mothers who smoke Swisher Sweets, or who live in a household where they are smoked, are continually exposed to heavy doses of DDT. What does that say about their risk for breast cancer in 2050?

But in this post I am talking only about DDT and organochlorine exposure of women who were born to smoking mothers 1955-1980.

Know thy unknowns: why we need to widen our view on endocrine disruptors, Journal of Epidemiology and Community Health, 71:3, 2016 (209-212)

These compounds ‘interfere with any aspect of hormone action’, and by doing so can adversely affect physiology and development and thus increase the risk of metabolic and reproductive disorders as well as hormone-sensitive carcinogenesis and impaired neurodevelopment

So keeping with the theme, here are a few more things you may want to review.

Environmental chemicals and breast cancer: An updated review of epidemiological literature informed by biological mechanisms, Environmental Research, 160, (152-182)

Organochlorine concentrations in adipose tissue and survival in postmenopausal, Danish breast cancer patients, Environmental Research, 163,(237-248)

Receptor activities of persistent pollutant serum mixtures and breast cancer riskEndocrine-Related Cancer, 10.1530/ERC-17-036625:3, (201-215),

 Evidence of the Possible Harm of Endocrine-Disrupting Chemicals in Humans: Ongoing Debates and Key IssuesEndocrinology and Metabolism10.3803/EnM.2018.33.1.4433:1, (44), 

 Changes in the total effective xenoestrogen burden (TEXB) of breast cancer patients during an 18-month post-surgical follow-upReproductive Toxicology10.1016/j.reprotox.2017.03.007, 69, (212-220),

A Ternary Mixture of Common Chemicals Perturbs Benign Human Breast Epithelial Cells More Than the Same Chemicals Do IndividuallyToxicological Sciences10.1093/toxsci/kfy126

Finally, as you look at this last reference, note the “higher girl’s BMI” factor, and consider the role of EDC in obesity. What if the EDC’s in the mother’s tobacco products contribute in utero and during childhood to the child’s obesity which in turn adds to her potential for breast cancer development? If so, we know for sure harmful pre-natal EDC exposure is going on today and is not just something that happened 1955-1980. 

Prenatal smoking and age at menarche: influence of the prenatal environment on the timing of puberty  Human Reproduction, Volume 30, Issue 4, 1 April 2015, Pages 957–962

We find that older maternal AAM (hazards ratio (HR): 0.75, confidence interval (CI) (95%): 0.71–0.79) and higher birthweight (HR: 0.86, CI (95%): 0.75–0.97) lower the chance of earlier menarche; while higher girls’ BMI at 8–9 years (HR: 1.12, CI (95%): 1.10–1.15), and maternal cigarette smoking on ‘most days’ during gestation (HR: 1.40, CI (95%): 1.10–1.79 with ‘no smoking’ as the reference level) increased the chance of earlier menarche. All factors were statistically significant at P = 0.05.