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


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Ancestral DDT Exposure & Trans-generational Obesity

The data and research studies we’ll look at in this post offer evidence that many, many millions of people today who are suffering from obesity may have a problem that, for those with a specific kind of family history of smoking, is totally independent of their diet or other behavior. In other words they aren’t eating or doing anything that can completely explain their obesity, but they are suffering, getting sick and dying of it. They may not be able or choose to eat the best diet, and they may not be able to live in the healthiest environment, but do those factors explain what’s causing their obesity enough that we can say “case closed”?

The newest research (shown and linked-to below) says the case is far from closed. It is linked to hidden endocrine disrupting pesticides including heavy DDT in the tobacco products smoked by women in the 1955-1980 time period. And by the way, knowing that pesticide damage may have been done to your mother or grandmother by constant DDT exposure, and that you were exposed before and maybe after birth, may lead your doctors today toward thinking about new ways of helping you.

So this post and these ideas aren’t just about raining awareness of the terrible things that smoking did to mothers and grandmothers of today’s generations, it’s about how knowing what was done generations ago may, in these new days of genetic science, give us new options to repair the damage.

To begin with, we have a study that shows us, although that was not the researcher’s objective, that people suffering from obesity today had mothers or grandmothers who were exposed. Not exposed by smoking – nobody knew that or even admits it today. But because as we’ll see shortly cigarettes were loaded with DDT in the period 1955-1980, people struggling with obesity today may well be the victims of DDT in the cigarettes their mother or grandmother smoked in 1970. DDT is now classified along with a number other supertoxic pesticides as an Obesogena chemical compound that causes obesity with the right exposure. It was a hidden but heavy contaminant of the tobacco product supply in those days, along with other supertoxic organochlorines including Endrin, Aldrin, Dieldren, Heptachlor, and Chordane.

This means that that people born to mothers who smoked 1955-1980, or to mothers whose own mother smoked 1955-1980, are at higher risk of transgenerational obesity just from that factor, exposure to DDT in the womb, even without any further exposure. In utero DDT exposure at just the wrong point in the unfolding tissues of the fetus, causes specific DNA damage that extends well beyond obesity in the later life of the unborn child  to include multiple kidney, prostate, testicular and ovarian diseases and several specific cancers including breast cancer and childhood leukemia.

Here is a data table from a confidential internal RJ Reynolds Tobacco Company that shows the levels of DDT contamination of their three most popular brands. Virtually any woman smoking an RJ Reynolds brand in those years, and earlier, was inhaling DDT at these levels. If she was pregnant, her child was exposed at precisely the right point to initiate the obesogenic process because even if she didn’t smoke every day of her pregnancy DDT lingers and accumulates in organs and fatty tissues. Her babies would have been exposed, and the transgenerational process initiated.

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

I hope that this information can empower people suffering from obesity or any of the other diseases now associated with transgenerational effects of DDT exposure to seek alternative treatments and therapies that may help in ways not being addressed by Western Allopathic medicine as represented by the US FDA, which actively rejects responsibility for regulating pesticide contamination of tobacco products. FDA simply refuses to so so, and there can only be one reason for that. Only one.

Ancestral dichlorodiphenyltrichloroethane (DDT) exposure promotes epigenetic transgenerational inheritance of obesity

BMC Medicine 2013 11:228

Background

Ancestral environmental exposures to a variety of environmental factors and toxicants have been shown to promote the epigenetic transgenerational inheritance of adult onset disease. The present work examined the potential transgenerational actions of the insecticide dichlorodiphenyltrichloroethane (DDT) on obesity and associated disease.

Conclusions

Observations indicate ancestral exposure to DDT can promote obesity and associated disease transgenerationally. The etiology of disease such as obesity may be in part due to environmentally induced epigenetic transgenerational inheritance.

Here is direct evidence that smokers of at least brands of RJR cigarettes were exposed to DDT with each puff they took before, during and after pregnancy. I have a copy of the original report found in the Tobacco settlement files. Here are the important data.

RJR Confidential June 21, 1972

Project 2358 – Cigarette Development

Notebook Pages: 250701-250719

In 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 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

This level of contamination was universal in 1972, and included many other organochlorines that RJR didn’t test for – at least not in this report. But tobacco products in those days were heavily contaminated with the whole range of OC pesticides including Endrin, Aldrin, Dieldrin, Chlordane, and many others whose impact on human health have never been studied.

This also means that people who themselves smoke or use DDT contaminated tobacco products today are reinforcing the transgenerational effects of DDT exposure by their mother or grandmother. It’s also important to say that the tobacco products with the highest levels of DDT today are those being smoked by poor, marginalized Hispanic, African American and Native American youth.

Obesity is one of the known effects of current DDT exposure, so as long as this synergistic pathway goes unrecognized in our understanding of obesity the opportunities for successful healing will be unnecessarily limited. A good first step would be to remove all tobacco products contaminated by high levels of DDT from the market.

This study of transgenerational effects of exposure to DDT ought to provoke questions about what the tobacco manufacturers knew in 1972, or earlier, or afterwards about organochlorine pesticides in their products.


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Prostate Cancer & Tobacco Pesticides: The Hidden Connection

There doesn’t seem to be any question about the connection between pesticide exposure of agricultural workers and prostate cancer. We know that this kind of exposure leads to prostate cancer, and we know which pesticides are the causal agents.

Through new research that we have just completed, we can also now identify specific pesticides that are known to cause prostate cancer that contaminate specific tobacco products. This means that a whole new connection between smoking and prostate cancer starts to emerge. 

We can see that specific pesticide contaminants of tobacco products are the same pesticides that have been shown to cause prostate cancer in exposed farm workers. (I discuss farm worker exposure vs smoker exposure below.)

Check out this data from lab tests we’ve just finished running on off-the-shelf tobacco products. Notice the totally illegal and banned worldwide DDT. Notice all the Azole fungicides like Penconazole. Check that amazing concentration of Cypermethrin. But really, with 0.816 mg/kg of DDT in every puff, all day every day, what other direct linkages to prostate cancer would you need? How about that 0.843 mg/kg of Carbenzadim, banned in the EU since 2014.

We are sadly confident that the entire tobacco product supply in the US will prove to be similarly heavily contaminated. We plan to test as many brands as possible as soon as funding becomes available. But here’s what we’ve found so far.

Community Tobacco Control Partners Test Results 12/18

Farm workers are exposed heavily to known prostate carcinogens regularly during certain parts of the year, whereas smokers of the brands shown above are inhaling known prostate carcinogens 50-100 times a day and more, year-round. So we are looking at two kinds of exposure – heavy during the season for farm workers, and low-level 7/365 for smokers. Intermittent mid-level exposure vs chronic low-level exposure. Also the farm workers are being exposed to one chemical at a time where the smoker is getting a toxic cocktail. Then of course there are farm workers who smoke the cheap tobacco brands like little cigars because that’s all they can afford. Double or triple whammy there. 

One thing that needs special attention with this new connection is the clear evidence that a smoker with prostate cancer risks that cancer turning very aggressive if it feeds on DDT and other endocrine-disrupting pesticides, which we can now show are just what that aggressive cancer is getting with every puff. Doctors see this happen in relapsing patients and know that it’s connected with their smoking but can’t explain why it’s happening. 

Here’s the message: If you stop feeding that thing in your prostate the chemicals that turn it aggressive maybe it will calm down and maybe you and the docs can get it under control.

So, here are a few key references. There are plenty more – it just depends on how much convincing anyone needs.

Rev Environ Health. 2016 Sep 1;31(3):311-27

Exposure to pesticides and prostate cancer: systematic review of the literature.

Results: The review included 49 studies published between 1993 and 2015. All studies were in English and analyzed exposure to pesticides and/or agricultural activities. Most studies (32 articles) found a positive association between prostate cancer and pesticides or agricultural occupations, with estimates ranging from 1.01 to 14.10.

So, what if tobacco products were loaded with pesticides but nobody knew about that contamination, so even though they knew there was a link between smoking and prostate cancer they didn’t know why? Would that show up in smoking & prostate cancer studies? Well, it seems that it might.

Eur Urol Focus. 2015 Aug;1(1):28-38.

Smoking and Prostate Cancer: A Systematic Review

CONCLUSIONS:

Data from the peer-reviewed literature suggested an association of smoking and aggressive PCa. Although the pathophysiology underlying this association remains unclear, smokers presented higher PCa mortality and worse outcome after treatment. Smoking-cessation counseling should be implemented for patients with PCa, although its effect on PCa progression should be investigated.

OK, but how do we know that the pesticides in tobacco products have anything to do with prostate cancer? Well, first, pesticides used in tobacco are heavily used throughout agriculture. Second, we know that at least two of the contaminants of the little cigar we tested are potent human carcinogens and one acts specifically on human testicles. Now your testicles aren’t your prostate, but that’s getting close enough to merit a second glance if you’re a smoker, don’t you think?

https://pubchem.ncbi.nlm.nih.gov/compound/Carbendazim#section=GHS-Classification

“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.”

Oh, and that other carcinogen – the one that directly impacts your prostate?

Chemico-Biological Interactions

Volume 230, 25 March 2015, Pages 40-49

p,p′-Dichlorodiphenyltrichloroethane (p,p′-DDT) and p,p′-dichlorodiphenyldichloroethylene (p,p′-DDE) repress prostate specific antigen levels in human prostate cancer cell lines

“Thus, we conclude that men who have been exposed to either DDT or DDE may produce a false-negative PSA test when screening for prostate cancer, resulting in an inaccurate clinical diagnosis. More importantly, prolonged exposure to these anti-androgens may mimic androgen ablation therapy in individuals with prostate cancer, thus exacerbating the condition by inadvertently forcing adaptation to this stress early in the disease.”

These are farmers, not smokers, but their prostate didn’t like the DDT exposure and neither will the prostate of anyone who inhales pesticide-contaminated tobacco product smoke (or vapor).

Prostate. 2011 Feb 1;71(2):168-83.

Prostate cancer risk and exposure to pesticides in British Columbia farmers.

“The significant association between prostate cancer risk and exposure to DDT (OR = 1.68; 95% CI: 1.04-2.70 for high exposure), simazine (OR = 1.89; 95% CI: 1.08-3.33 for high exposure), and lindane (OR = 2.02; 95% CI: 1.15-3.55 for high exposure) is in keeping with those previously reported in the literature.

If you keep smoking things just get worse; if you quit after 10 years the risk disappears. But if you are going to keep smoking at least pay attention to the pesticides that you’re inhaling and choose the least contaminated brand possible.

European Urology, December 2015, Volume 68, Issue 6, Pages 949–956

Association of Cigarette Smoking and Smoking Cessation with Biochemical Recurrence of Prostate Cancer in Patients Treated with Radical Prostatectomy

We investigated the effect of smoking on the risk of prostate cancer recurrence in patients with treated with surgery. We found that former smokers and current smokers were at higher risk of cancer recurrence compared to patients who never smoked; the detrimental effect of smoking was mitigated after 10 yr or more of smoking cessation.

I’m not writing this post as a science paper – I’m writing it to point out a connection that is as obvious as it is hidden, and hoping that the message will reach people who can benefit. The message to smokers is that if you are going to smoke, pay close attention to the contaminants in your brand and stop feeding your cancer with banned pesticides. I know this is heresy but – if you’re going to keep smoking than at least smoke American Spirit organic tobacco. Fair disclosure – I invented American Spirit but lost the company to the tobacco industry not long after we started and I have absolutely no connection of any kind to the company. I don’t benefit in any way from anyone choosing American Spirit. Well, actually, the benefit I get is the only one I want, which is knowing that I may have made a contribution to the health and happiness of another person.

 

 


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Prostate Cancer “Speeding Up”? WTF? Pass the CBD!

APCI’m reading an alarming article on the rapidly rising rate of metastatic prostate cancer in US men 55-69, and there is much discussion of things like the role of reduced screening in the explosion of this out-of-control disease.

But what really caught my eye were comments by the doctors conducting the research like:

“The fact that men in 2013 who presented with metastatic disease had much higher PSAs than similar men in 2004 hints that more aggressive disease is on the rise,”

“One hypothesis is the disease has become more aggressive, regardless of the change in screening.”

My reaction here is probably the same as yours – these guys are saying that less aggressive types of cancer can become more aggressive! 

Not just in one person, but as a type of disease.

News flash (2/13/2019) – I’ve just published a post showing the dramatic but totally hidden link between pesticides in tobacco products and prostate cancer in smokers. 

They seem to be saying that types of Cancers evolve, similar to disease-causing bacteria that gradually become resistant to antibiotics. So a type of cancer – in this case Prostate Cancer – that historically has been pretty slow-moving can all of a sudden, nationwide, for no apparent reason, speed up?

Maybe this is old news and I haven’t been listening, but it seems pretty important in the context of the urgency of gaining widespread credibility & acceptance for natural medicines like Cannabis, Coca and Opium, especially since after over 50 years of the miracle cancer medicines created by Pig Pharma we now have the goddamned things speeding up!

Meanwhile people worldwide are telling the internet that they or somebody they love has been cured of Cancer by one Cannabis-based treatment or another – there are very fluid limits to Cannabis as a medicine and I suspect that we’re nowhere near them yet. And we’re not focusing at all in the US on the healing properties of pure Coca Leaf.

There is work to be done, and at least there are a lot of talented people doing it.

Anyone can find out the latest 2016 clinical and streetwise information with some quick searches, and NIH’s “PubMed” website is a great place to look for the clinical side of Cannabis health research.

To get you started here is a good summary of Cannabis Prostate research as of 2012 by the National Institutes of Health “PubMed” (there are later findings, but this is a good place to start if you haven’t been on PubMed yet):

“The Role Of Cannabinoids In Prostate Cancer: Basic Science Perspective And Potential Clinical Applications”

“Prostate cancer is a global public health problem, and it is the most common cancer in American men and the second cause for cancer-related death. Experimental evidence shows that prostate tissue possesses cannabinoid receptors and their stimulation results in anti-androgenic effects. To review currently relevant findings related to effects of cannabinoid receptors in prostate cancer. PubMed search utilizing the terms “cannabis,” “cannabinoids,” “prostate cancer,” and “cancer pain management,” giving preference to most recent publications was done.”

“Articles identified were screened for their relevance to the field of prostate cancer and interest to both urologist and pain specialists.”

“Prostate cancer cells possess increased expression of both cannabinoid 1 and 2 receptors, and stimulation of these results in decrease in cell viability, increased apoptosis, and decreased androgen receptor expression and prostate-specific antigen excretion. It would be of interest to conduct clinical studies utilizing cannabinoids for patients with metastatic prostate cancer, taking advantage not only of its beneficial effects on prostate cancer but also of their analgesic properties for bone metastatic cancer pain.”

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3339795/