The real risks of male infertility and how Cannabis sativa L can reverse the anti-androgen agenda

For more than 100 years now this world has been pushing the agenda that Cannabis causes male infertility. For the past 45 years I have without fail received weekly panic stricken messages from men requesting information on this government perceived threat. I’ve also been using Cannabis for that long to help people to conceive.

From my perspective men that consume Cannabis have been taking the blame for infertility problems while in reality based on my clinical observations and the science the greatest risk is in fact an under developed female Endocannabinoid System (ECS).

What are the risks of male infertility in modern society?

1.      1. A daily dose of Endocrine disruptors, neurotoxins and carcinogenic compounds

The earliest history of endocrine disruptors goes back to the American pig farmers in the 1920’s when they became concerned about low swine fertility.

As far as pesticides go they all contain hormone disruptors and it’s interesting to note that the Sumerians used sulphur compounds to controls pests 4500 years ago according to the tablets. Sulfates are known hormone disruptors and are now even found in bottled water,

About 3200 years ago the Chinese started using mercury and arsenic in their pest control efforts. Today we have pesticides known as’ glyphosate’ and ‘squamiquart’ that also contain toxic hormone disruptors that are also neurotoxic.  It is said that no one on Earth can escape pesticide poisoning, not even on the North Pole where it has been detected.

Heavy metals, also been around since before creation, also known to block hormone receptors and testosterone production.

2.      2. The modern lifestyle is literally destroying the future of humanity

Caffeine and sugar are known hormone disruptors but more than half the population is addicted to both!

Known disruptors of human and animal hormones include but definitely not limited to BPA’s (Bisphenol A found in all plastic products, windows, eyewear, resins, food cans, bottle tops, water supply), caffeine, peanut butter, alcohol, nicotine, cosmetics, laundry detergents, soap, intimate products, toothpaste, Vaseline/petroleum jelly, toys, carpets, sugar and especially sugar substitutes definitely cause hormonal imbalances.

Even some essential oils like tea tree and lavender contain compounds that can affect the sex hormones.

All pharmaceuticals, pesticides, plasticizers and processed foods, including their packaging contain endocrine disruptors including milk, meat, poultry, cheese, yogurt, yellow oils, grains like bread, oats, crackers, pasta, rice, soya beans and cereals,

All of these items and many more can lower testosterone by increasing the activity of an enzyme called Aromatase. This enzyme converts testosterone into estrogen in men.

Also, all of these hormone disruptors are also carcinogenic and are in my opinion the biggest cause of the radical increase in hormonal cancers we are seeing today like womb, prostrate, testicular and breast cancers.

So not only are these human-made toxins able to cause cancer and disrupt hormones they are also all neurotoxic meaning that they also destroy brain cells.

There is no shortage of scientific papers providing evidence that all of these substances and even substances still unknown to us result in reduced testosterone levels in the blood. 

What happens in the womb during pregnancy?

Even more concerning is the effect of endocrine disruptors on the unborn baby.

In Pallotti et al, scientists explored the potential dangers including the disruption of testosterone production and reproductive tract development.

Maternal exposure to endocrine disruptors is a great risk to the unborn male baby and to the future of humanity. Here is a potent quote from this paper that is quite alarming:

“Maternal exposure during fetal life offers the greatest risk to the developing organism: exposure in this phase is associated with disruption of testosterone production and reproductive tract development, as demonstrated by the in vivo and in vitro detection of multiple anti-androgenic EDCs in fetal life.”

This is the phase in which sex is determined, with differentiation of the reproductive tissues, a fundamental step for the future development and maintenance of reproductive function.

In the male fetus, these processes are dependent on the initiation and maintenance of androgen activity. This may be disrupted by EDCs at various levels, including AR antagonization and interference with the synthesis of steroid hormones Disruption of these processes may thus lead to a risk of damage to the reproductive tissues while the fetus is still in the womb, leading to malformations (hypospadias, cryptorchidism, testicular hypertrophy, reduced anogenital distance), impairment of future fertility (altered spermatogenesis, infertility) and/or even the appearance of testicular tumors.”

Dr Pallotti’s  2020 paper had 97 citations as evidence of the potential dangers of endocrine disruptors to testosterone production, and I am just going to share a few here today for those who wish to do their own research and I really do encourage this. [1-6]

So as you can see the very last thing you need to worry about is Cannabis causing male infertility when you have so many other risks of exposure from governments and corporations.

The main pathway for endocrine disruptors to enter the body is through food, breast milk and water. Small children and the developing fetus are far more likely to be affected by these dangerous chemicals than adults.

The issues surrounding so-called safe low-doses remains highly controversial especially in the face of all the evidence that endocrine disruptors are very UNSAFE not only for us but also for future generations that have not even been exposed yet!

What does the science say about Cannabis and male infertility?

We know that the ECS controls the Endocrine system, the hormone system, and we also know that like most hormones, Testosterone actually increases Endocannabinoid tone. [7-8]

But this is not all! Scientists have also realized that testosterone also plays a vital role in the production of Endocannabinoids in the male body and especially 2-AG that is the human version of CBD produced within the body. [9-13]

There are literally hundreds of journal papers on this topic that prove the vital role of the ECS in sperm production and regulation.

People need to know that Endocannabinoids and therefore Cannabis are actually responsible for the production of human sperm. [14]

This means that a man with an underdeveloped Endocannabinoid System (ECS) will struggle with infertility issues.

Men need Cannabis to supplement their ECS and their sperm production with the human companion plant

Not only does human sperm express EC receptors but Anandamide, 2-AG and other Endocannabinoids are also present in human sperm. So clearly Cannabis has a role to play in human reproduction! [15]

 

The science also proves that there is no difference in testosterone levels between users and non-users of Cannabis. Here is a quote from the paper written by Dr Thistle and team for the Andrology Journal. [16]

“…indicating that recency of use, and not duration or frequency, had the strongest relationship with testosterone levels.

Serum testosterone concentrations were higher in men with more recent marijuana use.”

This paper was very interesting because it was a Danish study on American men and the study involved 1577 men. This study revealed increased testosterone levels among Cannabis using men and especially in respect of recency testing.

And here is a very recent study by Dr Janaina da Silva that was published in the World Journal of Men’s Health in 2023.

I’m a huge fan of Dr Janaina’s work because she also has a passion for exploring heavy metal toxicity and I’d love to just share her bio with you as she is doing incredibly important research in the field of Cannabis Medicine.

“Actually, I am researching the impact of cannabinoids used for recreational and therapeutical purposes on the male reproductive biology of mice and humans. Also, I am investigating the mechanisms that heavy metals can lead to repro-toxicity. My current interests also involve: cancer biology and therapy, cardiovascular diseases.”

Here is the punch line from her brilliant scientific paper:

 “Results: The testosterone production and the spatial distribution of Leydig cells did not change upon CBD and/or THC exposure versus controls after 48 hours or 9 days. The overall tissue morphology of the cannabinoids-exposed testis explants was similar to their control upon 24 hours or 9 days of exposure, a finding confirmed by morphometric analyses on short-term cultures. In line, the number of apoptotic cells was not affected by either 48 hours or 9 days of cannabinoids treatment versus mock. Cannabinoids had no impact on the number of proliferating cells nor on mRNA expression of genes encoding proteins involved in sperm cell differentiation, meiosis, or Sertoli and Leydig functions after 24 hours exposure.

Conclusions: Altogether, these findings show an absence of acute direct effects of exposure to cannabis-derived cannabinoids THC and CBD on testicular testosterone production and sperm cells ex vivo. Further studies are warranted to explore an indirect impact of cannabinoids on testis functions through the hypothalamic-pituitary-testis axis, as well as the potential effects of long-term exposures.” [17]

Infertility in general is becoming a worldwide health problem and it’s affecting people’s mental health and happiness. It is one of the many massive lies that has been fed to humanity, that Cannabis lowers testosterone. Please do not be afraid to invite Cannabis into your lives and especially into your bedroom.

Endocannabinoid deficiency is real and people need to know how to heal themselves from all kinds of medical conditions and especially infertility.

The proof is irrefutable that even though Cannabis has been helping people to conceive for thousands of years, It turns out that Cannabis has no direct effect on the incidence and evolution of male infertility.

Please feel free to reach out to me if you or a loved one needs any help to nudge their Endocannabinoid System in the right direction.

CITATIONS

[1] (Pallotti F et al, 2020) “Mechanisms of Testicular Disruption from Exposure to Bisphenol A and Phtalates” Journal of Clinical Medicine Volume 9 Issue 2 page 471, 8 February 2020 PMCID PMC7074154 PMID: 32046352 https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7074154/

[2] (Kortenkamp A, 2020) “Which chemicals should be grouped together for mixture risk assessments of male reproductive disorders?” Journal of Molecular Cellular Endocrinology page Volume 1 Issue 499, https://pubmed.ncbi.nlm.nih.gov/31525431/

[3] (Gaudriault P et al, 2017) “Endocrine disruption in human fetal testis explants by individual and combined exposures to selectd pharmaceuticals, pesticides, and environmental pollutants.” Journal Environmental Health Perspective 2017 Volume 125 Issue 1 page 11, https://pubmed.ncbi.nlm.nih.gov/28796631/

[4] (Conley J.M. et al, 2018) “Mixed “Antiandrogenic” chemicals at low individual doses produce reproductive tract malformations in the male rate.” Journal Toxicology Science 2018 Volume 164 pages 166-178, https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6677127/

[5] (Howdeshell K.L. et al, 2007) “Cumulative effects of dibutyl phthalate and diethylhexyl phthalate on male rat reproductive tract development: Altered fetal steroid hormones and genes.” Journal Toxicology Science 2007 Volume 99 pages 190-202, https://pubmed.ncbi.nlm.nih.gov/17400582/#:~:text=In%20the%20fetal%20male%20rat,critical%20for%20gubernacular%20ligament%20development.

[6] (Howdeshell K.L. et al 2008) “Mechanisms of action of phthalate esters, individually and in combination, to induce abnormal reproductive development in male laboratory rats.” Journal Environmental Research 2008 Volume 108 pages 168-176, https://pubmed.ncbi.nlm.nih.gov/18949836/#:~:text=Mixtures%20of%20phthalate%20esters%20with,during%20sexual%20differentiation%20in%20utero.

[7] (Kristie Conde et al, 2017) “Testosterone Rapidly Augments Retrograde Endocannabinoid Signaling in Proopiomelanocortin Neurons to Suppress Glutamatergic Input from Steroidogenic Factor 1 Neurons via Upregulation of Diacylglycerol Lipase-α” Journal Neuroendocrinology Volume 105 Issue 4, 6 March 2017 PMCID PMC5839320 PMID 27871072 NIHMSID NIHMS852640 https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5839320/

[8] (Borgquist A et al, 2015) “The role of AMP-activated protein kinase in the androgenic potentiation of cannabinoid induced changes in energy homeostasis.” Journal Physiological Endocrinology Metabolism  Volume 308, 2015 https://pubmed.ncbi.nlm.nih.gov/25550281/

[9] (Marzo DI et al, 2001) “Leptin-regulated endocannabinoids are involved in maintaining food intake.” Journal Nature Volume 410 pages 822-825, 2001, https://pubmed.ncbi.nlm.nih.gov/11298451/#:~:text=Leptin%2Dregulated%20endocannabinoids%20are%20involved%20in%20maintaining%20food%20intake

[10] (Malcher-Lopes et al, 2006) “Opposing crosstalk between leptin and glucocorticoids rapidly modulates synaptic excitation via Endocannabinoid release.” Journal Neuroscience Volume 26 pages 6643-6650, https://pubmed.ncbi.nlm.nih.gov/16775153/

[11] (Kola B et al, 2008) “The orexigenic effect of Ghrelin is mediated through central activation of the endogenous cannabinoid system.” Journal PloS One Volume 3 page 1797, https://pubmed.ncbi.nlm.nih.gov/18335063/#:~:text=The%20orexigenic%20effect%20of%20ghrelin,of%20the%20endogenous%20cannabinoid%20system

[12] (Kirkham TC et al, 2002) “Endocannabinoid levels in rat limbic forebrain and hypothalamus in relation to fasting, feeding and satiation: stimulaton of eating by 2-arachidonyl glycerol” British Journal of Pharmacology Volume 136 pages 550-557, https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1573386/#:~:text=Endocannabinoid%20levels%20were%20compared%20to,2%2DAG%20in%20the%20hypothalamus.

[13] (Yoshida T et al, 2006) “Localization of diacylglycerol lipase-α around postsynaptic spine suggests close proximity between production site of an endocannabinoid, 2-arachidonyl-glycerol, and presynaptic cannabinoid CB1 receptor”. Journal of Neuroscience and Journal of Fertility and Sterility, Volume 26 Issue 18 pages 4740-4751, https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6674155/

[14] (Claudia Osycka-Salut et al, 2017) “Anandamide induces sperm release from oviductal epithelia through nitric oxide pathway in bovines” Journal PloS One Volume 7 Issue 2 12 February 2017 PMID 22363468 PMCID: MPC3281848

[15] (M Rossato et al 2005) “Human sperm express cannabinoid receptor Cb1, the activation of which inhibits motility, acrosome reaction, and mitochondrial function” Journal Clinical Endocrinology Volume 90 Issue 2 pages 984-91, February 2005 PMID 15562018 https://pubmed.ncbi.nlm.nih.gov/15562018/

[16 ] (Thistle et al, 2017) “Marijuana use and serum testosterone concentrations among U.S. males” Journal Andrology Volume 5 Issue 4 pages 732-738 PMID 28395129 PMCID PMC5660879 https://pubmed.ncbi.nlm.nih.gov/28395129/

[17] (da Silva J et al, 2023) “The Acute Exposure of Human Adult Testis Tissue to Cannabinoids THC and CBD Does Not Impact Testosterone Production Nor Germ Cell Lineage” World Journal of Men’s Health Volume 41 Issue 4 pages 928-939 PMID 37118951 PMCID: PMC10523127 https://pubmed.ncbi.nlm.nih.gov/37118951/