Dow Chemicals Invoking NAFTA to Block 2,4-D Ban in Canada Cosmetic Pesticide Ban Mar. 29th, 2009 at 3:01 PM. Jorma Jyrkkanen

Dow Chemicals Invoking NAFTA to Block 2,4-D Ban in Canada Cosmetic Pesticide Ban Mar. 29th, 2009 at 3:01 PM. Jorma Jyrkkanen

29 March 2009 An American chemical company is trying to use NAFTA to block Canada from regulating its own pesticide health and safety through made in Canada anti-cosmetic use pesticide laws. This is economic subversion of our democratic rights to health and safety and protection of the people of Canada by the Government of Canada. Dow chemicals is demonstrating economic imperialism and the complete and utter evil that it is. Not only should 2,4-D be banned as along with all cosmetic pesticides, we need to scrap NAFTA. It blocks Progress in health and safety regulation development and interferes in national autonomy in protection of citiz

My Introductory String Theory Course Summary, Princeton University December 28, 2013.. Jorma Jyrkkanen

Summary of my Thoughts on Finishing Susskinds 10 Lecture String Theory. jjyrkkanen76@outlook.com 28 Dec 2013 Finished the String Theory course put on by Leonard Susskind at Princeton. Whew. Beauty. Wish I could just blurt out what I Iearned. It was a whole pile of pretty insightful physics. Maybe I will find time one day to translate some of the high points. Rooted in least action principles, Lagrangians and Hamiltonians, it links to energy, momentum, proper time and relativity and quantum mechanics and is solid. So is the fact that the four forces are unifiable under string theory, a result Einstein spent his post dissertation life searching for incidentally discovered theoretically by Schwartz and Green. It provides an explanation for relativity, Dn-Branes and QED, QCD, hadrons, photons, electrons, positrons, gravitons, gluons and that whole family and is simply beautiful as a theory being invariant under transformations. From Dn-Branes comes the surprising discovery that Feynman diagrams can arise naturally and easily from string theory. Compactification of dimensions is lovely to watch infold explained beautifully by conformal mapping. String Theory does generate a monopole, a very exciting development for physics. Branes which arose naturally from string theory are now the best way to study QCD. Two open strings comer together in space time moving to the right and are mapped by conformal mapping onto a sphere. The four foci on the sphere are the four momenta at the infinity ends of the strings in purple. I call this the butterfly. In our course students called it the sports bandage.

2DOpenStModel

Image Where string theory needs attention is in xplaining the masses of the particles and the best hope for this in my view is from the winding and conjugal progeny of transition through Calabi-Yau manifolds of which there are probably 10^500 and likely there exist as many universes. Also the graviton may be hitch hiking along on massive strings and I suspect are there creating hybrid angular momenta which might be diagnostic. The finding of Higgs field explained a good deal of the mass and virtual particles explained more and dark matter explained the remainder. Tags:Jorma Jyrkkanen, physics, QM, relativity, String Theory, Supersymmetry, Susskind, TOE

Terrible News. Beer and Coffee. Many Will Consider Suicide as a Viable Option.

Beer Causes Cancer jjyrkkanen76@outlook.com May 15, 2009 May. 12th, 2009 at 3:56 PM.

Methanol in Beer Metabolizes in the Body to Formaldehyde, a Carcinogen. Methanol is known to break down into formaldehyde and formic acid. Formaldehyde has now been found to be a carcinogen increasing risk of pharyngeal cancers, blood cancers, lymphatic cancers, leukemia and Hodgkins disease. It is therefore reasonable to conclude that beer is a carcinogen leading to increased risk of these cancers. Because of the high exposure levels, a large number of cancers may be due to this cause. The solution is simple, evaporate the methanol out of beer. Jormawankenobe jorma60@gmail.com Copyright 2009 Jorma Jyrkkanen. All rights reserved. Tags: methanol, beer, formaldehyde, carcinogen, blood cancers, pharyngeal cancers, lymphatic cancers, Hodgkins disease Coffee Causes Cancer STATE OF CALIFORNIA ENVIRONMENTAL PROTECTION AGENCY OFFICE OF ENVIRONMENTAL HEALTH HAZARD ASSESSMENT SAFE DRINKING WATER AND TOXIC ENFORCEMENT ACT OF 1986 CHEMICALS KNOWN TO THE STATE TO CAUSE CANCER OR REPRODUCTIVE TOXICITY March 19, 2021 The Safe Drinking Water and Toxic Enforcement Act of 1986 requires that the Governor revise and republish at least once per year the list of chemicals known to the State to cause cancer or reproductive toxicity. The identification number indicated in the following list is the Chemical Abstracts Service (CAS) Registry Number. No CAS number is given when several substances are presented as a single listing. The date refers to the initial appearance of the chemical on the list. For easy reference, chemicals which are shown underlined are newly added. Chemicals or endpoints shown in strikeout were placed on the Proposition 65 list on the date noted, and have subsequently been removed. Home Proposition 65 Chemicals Considered or Listed Under Proposition 65 Caffeic Acid Caffeic Acid More information about Caffeic Acid Caffeic Acid Chemical Status Cancer: Currently listed Chemical Listing Details Cancer Listed as causing: Cancer Date of Listing: 10/01/1994 Basis for Listing: AB-IARC Sobering Findings.

Found. The Cause of Cancer and why Black Bears are Black. April 2009. Jorma Jyrkkanen

I am a lifelong nature lover and environmental researcher who has found the meaning of life! I dedicate this site to the Prevention of Cancer and Preservation of Planet Earth’s Creatures and to the Seekers of Truth and Sustainable Ecological Equilibrium ie. Conservation Biology and Ecology and Total Global Health. As an Eco Sleuth, I can get pretty excited when I get onto the trail of a hot one. After discussions with Dr. David Monroe, USA Toxicologist, I analysed and discovered 350 ppm of carcinogenic 1,4-dioxane a few years back, in Vision herbicide, after the Feds and Monsanto said it was safe! I also found that the surfactant was polyoxyethyleneamine (POEA), a probable human carcinogen. These smoking pistols with Monsanto fingerprints all over them has resulted in a few changes in ‘Inert’ management and increased toxin contaminant disclosure in the US but not in Canada. The Feds subsequently and reluctantly admitted that they had corroboration on the dioxane contamination. My third most important observation, ‘Given Infinite Time and Space and Random Turns, the most Improbable Event Becomes Certitude'(JJ, 1974). Translated, this implies that quantum mechanics rules the universe and serendipity is our friend besides being the occassional pain in the butt. For a great example of salmon habitat enhancement involving kids and fish and education click ‘Salmon Habitat’. One of my goals is to expand my conservation studies and to continue this work for many years for nature. These investigations could be used as material in a university course in environmental toxicology. There are certainly many opportunities for a digression into researching numerous topics suggested by my review materials themselves. PHd’s lurk there. Another hobby of mine is making huge predictions, for example I predict that human caused global warming will cause post-glacial rebound and increased plate tectonic movements due to mass shifts over the plates with resulting increases in earthquakes, tsunamis and volcanism, possibly the first time an organism has ever done so on such a scale. If it leads to eruption of the Yellowstone volcano, it may also be our self induced undoing as a species My friends are all wonderful unique individuals who excel at some fantastic thing they do. I believe I have discovered why Black bears are black. For answer, contact me. I have a gift from my 18 years in Northwestern BC and my years with the F&W Branch. I know where every good steelhead fishing hole in the country is and what gear to use to catch em. Same for chinook. I may write it up into a book one day. I believe that I have also discovered the main causes of cancer through my studies. The P’s that cause cancer. Pollution, Profit and Prevention-lack thereof. Look no further than smoking to see how true this is. I believe that cancers are for the most part preventable if the political will were to exist to eliminate carcinogens, mutagens, endocrine disruptors, immune system damaging chemicals and cancer promoters. The Stockholm Accord is a step in the right direction but it is far too narrow in scope. The CNA Nurses resolution is a strong step in the right direction but with a limited voice. The Earth Charter goes a long way towards environmental protection. But collectively, we can wield the biggest club with our pocketbook in the marketplace and in the stock exchange. For example, buy chlorine free food packaging. The individual can take preventative steps by life-style choices like organic foods, anti-cancer diets, avoiding carcinogen exposure and living in healthy environments though these are getting hard to find. The Cancer Orgs completely misallocate the monies donated to them. They should give ten percent to molecular geneticists and the rest to organizations dedicated to prevention. We could eliminate probably 60% of all cancers in short order by this more realistic focus on the cause instead of the wasteful quest for the magic bullet which just feeds the cancer industry. There are of course cancers that are contagious like those obtained via specific Herpes strains, Epstein-Barr virus, hepatitis virus, HIV, SV40, JC polyomaviruses, certain papillomas or other possible viruses like CMV which has been associated with colon and glioma cancers and these are possibly preventable by hygienic prophylaxis or possibly development of immunization anitsera or through understanding and controlling the mechanisms of contagion. Good news November 18th, 2002..My prediction has come true. A vaccine has been developed for HPV 16 which is completely effective against cervical cancer in preliminary trials. This was confirmed again in a large study done in 2005. Immunization can prevent contagious cancers. The common stomach ulcers bacteria has been implicated as a cause of gastric cancer and parasitic flukes, both and liver have been nailed as agents that cause cancer. Aspergillis mould fungi are also cancer causing. Breast cancer is mostly explainable by persistent organic pesticides and vinyl chloride and related pollutants that harm the genes through the endocrine system. Just like hormone therapy increases breast cancer incidence, so too do these chemicals that disrupt the endocrine systems. To prevent breast cancer, once again, fight pollution. For more info and prevention, check out my references in ‘Archives’. I believe that there are two major flaws in human civilization. In my personal opinion, which I express without malice, our philosophical underpinnings are irrational and the other is that our socio-economic policy founded on population growth and economic growth is ultimately unsustainable by the environment. We have had insufficient information to understand reality and insufficient distribution of intelligence to make sense of it regardless during the early course of our evolution and sadly this will continue for a long time. These imaginary solutions evolved quite naturally not only into the marvellous cultural diversity which we should celebrate, but also into the ethnic and religious arrogances we have seen warring amongst each other which now threaten global security and the environment. Security concerns arising from religion-based differences for example, have misappropriated vast vital financial and infrastructure resources which should go towards environmental repair and protection. Half of all wars are fought over religion which puts a huge burden of blame for global suffering on its practioners. It is valid to ask if a way of being which kills over 50 million people is a good thing. Science today is still fighting a rear-guard action for Darwin and modern cosmic and biological evolution theory against the primitive notion that the universe was created by magic because it has become commonly accepted that one can believe anything whether it is the truth or not, a perhaps highly dangerous and potentially suicidal notion. There can be only one truth in reality in one place and at one time. All the others must therefore be something else. Antagonistic groups have put themselves in boxes that differ from each other in only minute details in their thoughts yet they kill people in other boxes because of these minute differences. These groups have yet to open Darwin’s book and smell the aroma of scientific evolutionary coffee which would enable them to progress to a whole new reality unimaginable to our ignorant fore-bearers and unenlightened contemporaries. The AIDS pandemic, the drought and massive starvation in Africa and elsewhere, CJD, CWD, superbugs, pest epidemics, genocide, fisheries collapses, wars against Islamic ers, flood and fires, are reminders that Headmaster Darwin is ringing his bell on the steps of his school, calling the evolution non-believers to class to read his book and to understand our place. They are Nature, the driver of the horses of evolution, the mother of life, the creator of life, the sustainor of life, pulling the reins back, saying to humanity, ‘whoa boy, slow down and pull your goats back from my overgrazed land and stop your rampant carbon combustion and stop breeding like rabbits and wake up to the undeniable truth of evolution’. They are a natural result of ignoring nature, the health of ecosystems, overpopulation and limiting factors and of human society hitting the wall of continued unmitigated growth. They are the result of globalization of probably the most dangerous notion that ever existed, that prosperity requires population growth and that unrestrained growth of humanity is the best goal and that it can be fudged into sustainability. How dare we pack more people in while we squander so much of the existing humanity we have already produced while destroying ecosystems. Sustainability is notwithstanding a wonderful aspiration and part of any harmonizing concept but it alone will not stop habitat destruction and alienation and extinction because selfishness and dire necessity will prevent its full implementation. The infidels on this planet are not Professor Hashem Aghajari or Rushdi or the Jews or Atheists or Pagans or myself, but all those who destroy nature and deny evolution. This leads me to my first and most important observation. It was we humans who created all the gods, not the other way round. Evolution, a physical and organic process, is the creator. Humanity does not have dominion over nature but is rather a part of it and totally dependent upon it. You see my friends, nature operating through evolution, is both our planets life Creator and the Creation and to see her working we need just turn around and listen to her progeny singing in the springtime or blowing in the wind or spinning webs in the shadows or laughing in the playground. The time has come to put our inherited religious ideas into a folder called traditional mythologies and undergo collective cultural evolution for we now know that they were incorrect and move on to the verifiable pure truths of scientific evolution and a cosmologically scientifically consistent philosophy. Our socio-economic policy is rooted in the ancient primate hoarding instinct, our primal need for a peck-order and territorial tribalism, primitive hard-wired primate instincts we cannot escape but must try to control by rational over-sight. Clearly, our mischievous greedy, territorial, racist, promiscuous, warring little monkey genes still direct our cultural evolution and behaviour and may ultimately be our undoing. Don’t believe me. Check the human genome project and chimp DNA hybridization research projects (ex. Wildman et al Genomics studied 73104 DNA bases and found 99.01% similarity between chimps and humans) and keep an eye on nightly news covering human behaviour! It appears from our behaviour and our genetic similarities that we are in fact still monkeys. More profoundly, genetic researchers studying phylogeny, have found that our genes still share 500 genes in common with the earliest forms of life on earth, the Archaea, 5000 genes in common with fish, and identical eye genes in common with ocean flatworms and mice, providing support for the idea that we are related to all living things. My second best prediction back in the early 1970’s was that humanity was poised for an epidemic by a delayed lethal disease pathogen and AIDS came along. My follow-up prediction is that there is a still worse epidemic of an even more aggressive pathogen brewing. I also predict on this day, 7 May 2006, that MS is caused by Dioxin. It causes degenerative disease in every other species, why not human. The collapse of so many fisheries worldwide are the planet’s miners’ canaries going silent? Will we heed their message? Clearly we need to move to that new paradigm and I suggest rather than ‘Sustainable Development’, we pursue ‘Ecological Harmonization’. My first most important observation is that evolution is the creator, both noun and verb; physical inorganic evolution created the universe and organic biological evolution created life and we humans created the gods in our imagination. I am so convinced of my observations that they amount to a belief which is open to contrary evidence. It is this: My Creed: I believe that inorganic evolution creates and destroys universes; organic evolution creates life and all species. Energy is eternal and links everything everywhere. We are monkies made by evolution struggling in vain against our genetic inheritance to be something else. Evolution is the creator ergo God but its a process like cheese and doesn't give a dam if we pray to it. Only asks one question. Are we fit .

Democracy Would be Utopia if Only ...Posted 2010 Jorma Jyrkkanen

Democracy Would be Utopia But March 4, 2010 Democracy would Be Utopia 4 March 2010

Enhancing Bighorn sheep habitat, West Kelowna. Democracy would be Utopia but for the liars, crooks, bullies, con artists, druggies, plagiarers, slanderers, lazy asses, cold hearted lovers, barking dogs and the extinctions and disease they cause by pollution. Then there is the problem of the majority getting its way all the time pissing on the minority. Yes it could be such a wonderful thing. The trouble with Utopia is the human beings. If we could just get rid of them. © 2010 Jorma Jyrkkanen. All rights reserved. Tags: Democracy, Utopia, human beings, Jorma Jyrkkanen

Warning to the People of Cuba; Capitalism is not Democracy, its an Inequity Parasite. Orig 2014 Jorma Jyrkkanen (My Blog)

Warning to the People of Cuba; Capitalism is not Democracy, its an Inequity Parasite I am warning you that you will lose your country if your not careful. Capitalism is not a friend but a disease.

I have analyzed long and hard what it is that is wrong with the world and with the body politic and it is this. The free licence of the greed genes in the belief of its greater good is a global delusion leading to destruction of our planet, loss of the commons to the commoners, loss of agricultural and forested lands to corporations and the creation of a culture of drugs and hopelessness where whole generations have no future but as menial servants of the rich kleptocrats who also take over the governments. It is possession and control by the Inequity Parasite. In Canada and in America the governments are under the control of the business class and kleptocrats have puppets installed in the highest places who serve corporations and not the masses. Agricultural land has been usurped for dirty businesses or become so chemically dependent they cannot live without them and everyone is forced to eat GMO or be sued by corporations. Many pesticides also influence gender. The resulting foods and lifestyles are unhealthy leading to obesity, diabetes, heart disease and cancers and to growing autoimmune disorders. Capitalism is a kleptocracy inequity parasite and you will lose your lands and homes to rich Americans and Canadians and become homeless or barrio dwellers and like in the Yucatan, be denied access to the very beaches you once owned and shared with visitors and rich people will have big beautiful homes on your once humble residential properties and there will be gated communities into which you will not have access. Your future will have enormous unemployment because that is what most of you will eventually become as the plutocrats cut costs by reducing labour. This will lead to a police state more insidious than what you have now with every imaginable spy device tracking everyones every word and movement. It will be secretly more totalitarian than communism in its first incarnation in the spying and treachery that is invoked to control the masses and it will be ruled by Corporations just like your country. You are buying into the Corporate Rule of Cuba. Your deluded appetite for the glossy stuff Ad Pushers educate you to want will lead you to this fate and to sell trinkets on the street. The shift you are embarking upon is from benevolent socialism to kleptocratic corporatocracy and rule by Inequity Parasites. In Canada we no longer elect caring socialists to run the country but instead business pandering scoundrels who despise having to share corporate wealth with the majority. They the worst forms of back stabbers, liars and cut throats. Wealth flows to the richest from all the rest. The rich write their own tax laws. They also own the media and by that the message and the brain washing system. Your jails will fill up with the poor and your police will be busy dealing with vast numbers of lost souls who no longer have a stake in your beautiful nation and your beggars cemeteries will fill with those hopeless unfortunates lost in space who commit suicide. Education is free in Cuba. Don’t ever lose that. Never. Protect your core values in any deals and beware of smiling rich people bearing gifts of money. They are there to screw you out of your rights and properties and freedoms and nature rich Island homes. Capitalism is unsustainable and free licence of the greed gene is a delusion leading to inequity and loss of your natural treasures. Protect your farm land and forests and sea and their ecosystems in perpetuity no matter what happens and public ownership of them. They alone will sustain your people in perpetuity when Capitalism crashes at the end of oil and in the ecological climate disaster unfolding due to cancerous global capitalism. Free trade is a sneaky device used to undermine all your rights and freedoms and make you and your governments Serfs of Corporate Lords and Masters. Use alternate energy only. Do not be suckered into gasoline dependence. It is one of the greets evils on the planet. The French revolution over-threw the arrogant pompous bastards that were the royal ruling classes hiding their disgusting lives behind castle walls who were steeped in privilege and rolled in the wealth stolen from the masses. They have all been replaced by Kleptocratic Corporations who now rule the world. Know this and do the right thing. Make laws to ensure in never happens on your soil. Copyright 2014 Jorma Jyrkkanen. All rights reserved.

Antibiotics Impact on Mitochondria Result in Potential Contributions to Carcinogenesis, Coronary pathology, other Medical Conditions and Ecosystem Risks June 29, 2021 Jorma Jyrkkanen jormabio@hotmail.com ph:1-250-859-5330

Antibiotics Impact on Mitochondria Result in Potential Contributions to Carcinogenesis, Coronary pathology, other Medical Conditions and Ecosystem Risks June 29, 2021 Jorma Jyrkkanen 29 June 2021 ph:1-250-859-5330 jjyrkkanen76@outlook.com Abstract With the discovery by Calghatgi (2013) that three common antibiotics (Abs) increased mitochondrial reactive oxygen (ROS) and lipid peroxide (LP) and depleted their natural absorbant glutathione led me to investigate further the potential impacts of these genotoxic substances on carcinogenesis. The range of impacts on mitochondria and cellular DNA varied by antibiotic to those consistent with known prior contributions to carcinogenesis. Specific cancers probably increased by these changes were HCC, RCC (KCC), CRC, cancer of the esophagus. Tumour suppressor gene mutations resulting from LP were noteworthy in this regard and mutations induced in CRC were consistent with those found in carcinogenesis of CRC. In addition depression of short chain fatty acids in microbiomes were found which depress the immune system increasing risk of all cancers. Many cancers were increased according to epidemiological studies linking Abs with elevated odds ratios, with one concern in particular, fatal breast cancer. The impact of loss of functionality of the mitochondria was also linked to depression of the citric acid cycle and therefore ATP which deflected metabolism to glycolysis, the Warburg mechanism, also increasing risk of all cancers, favoured by cancer cells. In conclusion, some portion of many cancer types are probably increased in likelihood by number, type and frequency of Abs treatment and chronic residue exposure which varies from individual to individual. This led me to propose a three pronged carcinogenesis mechanism for Abs. 1. Cancer critical mutations 2. Immune depression 3. loss of mitochondrial functionality leading to Warburg effects. Damage to mitochondria were also noted by common pesticides tested in China and more recently by covid spike protein ( Keshav K. Singh et al July 2020) and cancer associations were also found for many pesticides suggesting a similar contributory mitochondrial etiology. Heart health concerns were raised by these findings because of the myriad mitochondria in the heart and because of long term reliability needs. Studies suggesting hearts were affected by Abs and pesticide exposure were presented. Because of their geographical ubiquitousness and the huge range of diseases associated with mitochondrial dysfunction, antibiotics and pesticides and bacteriocidal biocides are of concern for biodiversity and life in general. I propose research steps to evaluate antibiotic safety and suggest directions for further research and make suggestions on ways to ameliorate Abs toxicity. Key Words antibiotic, mitochondria, DNA damage, P53 tumor suppressor gene, mutp53, ROS, lipid peroxide, cell perforation, cell rupture, oxidative phosphorylation, cancer, carcinogenesis, glycolysis, Warburg effect, microbiome, dysbiosis, immune suppression, pesticides, mechanism, clastogenic, epigenetic silencing, microRNA, DNA, heart Introduction Antibiotics kill or slow the growth of bacteria or interfere in their reproduction. The mitochondria, an ancient alpha-proteobacteria [Rickettseae] that has become an endosymbiont in higher life forms with critical functions, response to them has been found to be a decrease of beneficial antioxidant glutathione, increased reactive oxygen, increased harmful lipid peroxide, possible DNA damage and mutations in tumour suppressor genes increasing cancer risk, possible inability to reproduce, possible cell perforation and or rupture. Some antibiotics have been shown in the past to be clastogenic. These types of responses have broad biochemical and health implications. They could lead to carcinogenisis, microbiome dysbiosis with resulting immune system depression and or loss of oxidative phosphorylation (OP) favouring glycolysis metabolism which is also the favoured method for cancer cells. Changes could enhance the Warburg effect favouring cancers. P53 genes may be turned off epigenetically at the DNA. Defective mitochondria have been implicated in over 200 medical conditions. In addition a big unknown is the relationship between which biocides may epigenetically shut down critical genes found with each particular kind of cancer. Clinical and epidemiological evidence supports the conclusion that some antibiotics are carcinogens, others promote cancers and cancer risk increases with frequency and type. Microbiome dysbiosis and immune depression risk is increased. While exposure may not complete all the steps to cancer it may contribute important mutations along the way. Other life time exposures can can complete the process. Chinese researchers recently found that a high proportion of common pesticides ruptured mitochondria like some antibiotics. Individuals who were exposed to pesticides were more than twice as likely overall to have conditions like heart disease, heart failure or an irregular rapid heartbeat known as atrial fibrillation (Lisa Rapaport, 2019). It can be inferred that ruptured mitochondria from antibiotics would lead to similar coronary pathologies. There is reason to suspect that all Eukaryotes are subject to pathological impacts. The mitochondria enabled multicellular evolution to higher forms of life and is now under attack worldwide by anthropogenic biocide pollution. More research is needed to determine which of all biocides is mitochondria friendly, enables them to be fully functional without mutations, prior to regulatory approvals. I propose an antibiotic mitochondria carcinogenesis mechanism. For a general overview of impacts of antibiotics on total general physiology and health of ecosystems including plants see Wang, Xu et al. (2015 Sept 8). A criticism of some findings is that people with cancer are more prone to infections and this can account for much of the association of antibiotics with cancer (Hui Zhang, Luis A. García Rodríguez and Sonia Hernández-Díaz, June 2008). However the finding of immune compromise is consistent with antibiotic induced microbiome associated dysbiosis. Mitochondrial Job and Creation of Toxic Mix by Antibiotic Mitochondria, a primitive endosymbiotic bacteria, related to extant SARII marine bacteria and Rickettsias, in eukaryotes is responsible for OP resulting in ATP and NAD production for energy. When exposed to clinically equivalent doses of antibiotics that target bacteria (cipromycin, ampicillin, kanamycin), exhibited a decline in glutathione titre, an increase in reactive oxygen (ROS) and an increase in lipid peroxide with damage to DNA and potential mitochondrial rupture (Calghatgi et al. 2013). Tetracyclines used for humans and livestock have also been linked to mitochondrial genetic damage (Granados-Chinchilla et al. 2017). Some antibiotics have been found to be break chromosomes (Nersessian, A. K. et al. 1991). Others are known to prevent their replacement for example these FDA-approved antibiotics inhibit mitochondrial biogenesis; the erythromycins, the tetracyclines, the glycylcyclines, an anti-parasitic drug, and chloramphenicol (Rebecca Lamb et al. 2015). Without mitochondria, oxidative phosphorylation stops and Warburg glycolysis kicks in favouring cancer growth and proliferation and also the mitochondrially dependent heart would cease to function normally. Mitochondria play key roles in activating apoptosis in mammalian cells. Bcl-2 family members regulate the release of proteins from the space between the mitochondrial inner and outer membrane that, once in the cytosol, activate caspase proteases that dismantle cells and signal efficient phagocytosis of cell corpses. Loss of this function or alteration of it can have dire consequences leading to cancer and immune disorders (Chukxin Wang et al. 2016). Modes of Action of Antibiotics on Mitochondria and Microbiome 1. quinolones- commonly prescribed antibacterial organofluorine compounds which act by inhibition of bacterial DNA synthesis and result in rapid cell death (Aldrid, Katie J. et al. 2014). This group contains ofloxacin, norfloxacin (noroxin), ciprofloxacin (Cipro), moxyfloxacin (Avelox). Expectation is to obstruct mitochondrial replication. Norfloxacin demonstrated a linear antibiotic-DNA mutation rate, compromised DNA oxidative damage repair and post replicative mismatch repair (Hongan Long et al. 2016). They could be expected to do similar collateral damage to mitochondria and to members of the human microbiome. 2. aminoglycosides-ex gentamicin, amicasin which create holes in the outer cell wall of bacteria suggesting mitochondria and the microbiome might be at risk of similar damage (Loui S Gonzalez III and Jianne P. Spencer, 1998). Damage to lipid membranes can be expected. Lipid membranes have wide distribution in both microbes and other animals including humans. 3. β-lactams or penicillin derivatives such as cephalosporins, monobactams, carbapenems, carbacephems inhibit cell wall synthesis in bacteria and by inference inhibit cell wall synthesis in mitochondria during division and repair and microbiomes thereby obstructing microbial reproduction. Penicillamine is listed as a ‘developmental’ in California Proposition 65. 4. Tetracyclines-used on cattle and humans and possibly acquired secondarily as dietary residues may affect mitochondria because they specifically target Rickettsias a probable evolutionary ancestor (Emelyanov, V. V. (2001) of mitochondria (Moullan, Norman et al. 2015; Xu W. et al. (2015)). 5. Anthracyclines-result in clastogenicity (Nerssessian, A. K. et al. 1991) Harmful Impact of Liberated Substances on DNA, P53 Tumour Suppressor gene, Mutagenicity and Known effects in Other Cancers Glutathione is an antioxidant that soaks up ROS and is essential for many neurological and other body functions. Glutathione is capable of preventing damage to important cellular components caused by reactive oxygen species such as free radicals, peroxides, lipid peroxides, and heavy metals. Genomic instability occurs in myeloid malignancies with increased reactive oxygen species ROS, DNA double strand breaks (DSBs) and error-prone repair (Annahita Sallmyr et al. 2008) . ROS Linked to many Cancers by oxidative DNA Damage “numerous studies have shown generation of reactive oxygen species (ROS) that can cause oxidative damage of DNA. This is a well-known mechanism in carcinogenesis for many agents” (Lennart Hardell and Michael Carlberg 2015). Excessive levels of ROS accumulation due to altered equilibrium between ROS and antioxidants may lead to different kinds of diseases such as atherosclerosis, diabetes, neurodegeneration, and cancer including CRC. It is widely known that ROS-induced DNA damages and genetic mutations are critical causes of cancers including CRC. The main intracellular DNA lesions caused by ROS are single and double strand DNA breaks, and the common genetic mutations include p53, KRAS, APC, and BRAF mutations often seen in CRC’s. For example, a direct relation among oxidative stress, DNA damage and elevated frequency of p53 mutation in CRC has been observed. Most extensively studied endogenous DNA damage by ROS is the formation of 8-oxo-7,8-dihydro-2′-deoxyguanosine (8-oxodG). As the biomarker of oxidative stress, 8-oxodG level is higher in colorectal tumors than in normal mucosa. Mitochondrial DNA is particularly prone to be oxidatively damaged and is more meaningful in colorectal carcinogenesis (Liu H et al. 2017). I would expect antibiotic induced drop in antioxidant glutathione to contribute to such an altered equilibrium and assay for 8-oxodG post antibiotic treatment might be a good indicator of antibiotic carcinogenic potential as well as looking for deficits of ATP, an indicator that metabolism has switched to cancer cell loving glycolysis from pyruvate metabolism. Lipid Peroxide Associated Cancers Besides being generated by mitochondria exposed to antibiotics, lipid peroxide is also increased with analgesics like aspirin (though some studies show it reduces LP) and NSAIDS naproxin, indomethacin and diclofenac, being male, among hypertensives, diabetics, smokers, oophorectomized and pregnant women especially with eclampsia and pre-eclampsia (Manuela Gago-Dominguez and J. Esteban Castelao, 17 Oct 2005). Ochratoxin a mycotoxin found in cereals and grains also increases LP. These mutiple sources need assaying when making links to antibiotics impact on mitochondria. Lipid peroxide has been linked to esophageal carcinogenesis (Mufti, Siraj I. 1997) and to red meat and treated meat colon carcinogenesis (Marten et al. 2018). The major lipid peroxidation product, trans-4-hydroxy-2-nonenal, preferentially forms DNA adducts at codon 249 of human p53 gene, a unique mutational hotspot in hepatocellular carcinoma (Wenwei Hu et al. 2002). In a seemingly unrelated exposure from afltoxin researchers report an increased frequency of loss of the Hae III allele and base G mutation on p53 gene at codon 249 where it is mutated to C (Zhuo-Lin Deng and Yun May 1998, Feb 15). Why this matters is because this same P53 gene locus is linked to HPV cervical cancers from a study done on Kenyan women (Jiangjun Zhiang et al. 2 Sept 2019). HPV cancers are associated with genital, anal and oral tissues. Antibiotics production of lipid peroxide and its metabolites can also mutate this gene locus and that is found with HCC. Lipid peroxidation has been proposed as a mechanism for renal cell carcinoma RCC (Manuela Gago-Dominguez and J. Esteban Castelao, 17 Oct 2005). Based on their work I added my comments. Lipid peroxide (LP) degrades into mutagens that target tumor suppressor gene p53 and may alter functionality of other tumor suppressor genes like VHL specifically linked to hereditary RCC and is postulated by me and the latter authors to be a carcinogen linked to renal cell carcinoma. I phrase this as a question. Lipid peroxide is generated by antibiotics attacking mitochondria which then release it into the tissue environment and may even rupture cells in the process. I recommend an investigation to study additionally antibiotic history in regards to VHL depressed kidney cancer. The placenta is the main source of LP in pregnant women. Look also at Aspergillis and ochratoxin A as a mutagen for the TSG genes involved. The following article hints at LP causality. Fumonisims, a fungus in corn and other grains is linked to kidney cancer and is possibly acting through mutation of the p53 gene. P53 overexpression has been correlated with increased RCC. Inactivation of the VHL TSG is responsible for polycystic kidney disease and for renal cell carcinoma of the hereditary VHL cancer syndrome and for the majority of sporadic renal cell carcinomas. Protectively, polyphenolics in red wine are postulated to soak up the lipid peroxides and reduce RCC risk. Estrogens especially 2-hydroxyestradiol, mannitol, SOD and vitamin E are all LP sponges along with the mitochondrial glutathione. This suggests antibiotics are a cofactor in carcinogenesis of several if not multiple cancers via this same p53 locus 249 mutation’s contribution or by lipid peroxide contribution and ROS contributions to reduce TSG DNA repair and function. Lipid peroxide metabolite hydroxy-2-nonenal is also found in red meat and treated meat carcinogenesis. It is safe to conclude that antibiotics are one cause of or major contributing factor to hepatocelluar carcinoma and are also potentially involved in colon carcinogenesis. In CRC, the commonest lipid peroxidation products are MDA and HNE, the levels of which in the CRC tissue are significantly increased with clinical staging (Skrzydlewska E et al. 2005). CRC and RCC are likely to be cancers potentially associated with antibiotic mitochondrial disruption. P53 Changes Associated with Warburg Effect Possible P53 gene upregulation (PUMA->WTP53) may lead to the Warburg effect favouring cancer (Kim et al. 2019). Proximicins A, B, and C—antitumor furan analogues of netropsin from the Marine Actinomycete verrucosispora induce upregulation of p53 though I am not certain this is the same effect as PUMA (Schneider et al. 2008). Mutated P53 actually becomes the mutP53 guardian of cancer cells (Mantovani et al. 2019). Normal function of p53 blocked by loss of mitochondria through damage or rupture. Tumor suppressor p53 plays a central role in tumor prevention. As a transcription factor, p53 mainly exerts its function in tumor suppression through its transcriptional regulation of its target genes to initiate various cellular responses. Cell cycle arrest, apoptosis and senescence are most well-understood functions of p53,and are traditionally accepted as the major mechanisms for p53 in tumor suppression. Recent studies have revealed a novel function of p53 in regulation of cellular metabolism. p53 regulates mitochondrial oxidative phosphorylation, glycolysis, glutamine metabolism, lipid metabolism, and antioxidant defense. Through the regulation of these metabolic processes, p53 maintains the homeostasis of cellular metabolism and redox balance in cells, which contributes significantly to the role of p53 as a tumor suppressor (Liang et al. 2013). P53 Cell guardianship and critical OP obviously cannot happen if the mitochondria is ruptured or defective or if the p53 gene has been mutated, silenced or sequestered to assist cancer cells. With diminished OP, Warburg effects will increase and cancer cells will be given a boost. This might well be a serious collateral impact of antibiotics. Antibiotics Render the Immune system Less Effective in Infection Researchers reporting in Frontiers in Microbiology found that short chain fatty acids (SCFA) from resident bacteria were important in protecting the immune system, and inflammation control. Both of these side effects have important ramifications for prevention of cancer initiation. Antibiotics diminished resident bacteria carrying out this role and supplemental SCFA were not effective in ameliorating the effect. Dysbiosis of resident microbes is unequivocally associated with immune-related disorders and opportunistic and pathogenic infections which can themselves set the stage for cancer (Natarajan Pashkaran et al. 2018). If potentially carcinogenic microbes Helicobacter pylori, Streptococcus bovis, Salmonella typhae, Fusobacterium, Chlamydophyla, Bartonella or Caries bacteria or any carcinogenic viruses such as EBV, HPV, alpha-HPV, beta-HPV, HHV, HBV, HVC, KSHV and possibly retroviruses or Schistosomes and liver flukes facilitated by (See IARC, 2009) depressed immune systems proliferate as a consequence this can lead to increased incidence of cancers especially the viral cancers which do not respond to antibiotics but will take advantage of a depressed immune system. Along this line there has been an increase in oropharyngeal HPV cancers in Canadian men (Habbous S 2017) . The depressed immune system may also lessen the bodies ability to kill cancerous cells regardless of their etiological origins. Another of the consequences of antibiotic use is development of antibiotic resistance. One of the carcinogenic bacteria, H. Pylori is an example (Megraud F. 2004) the consequence of which may lead to an increase in stomach cancers in developed countries unless we can come up with new more effective mitochondria friendly antibiotics. Dysbiosis may be countered by restoration of the microbiome (El Hage R et al. 2019) The Evidence of Carcinogenesis from Population Research Seeing that these changes were consistent with steps found in carcinogenesis (Kohanski, MA et al. 2016) I asked the question, what is the clinical and epidemiological evidence that antibiotics increase the risk of cancer? It appears others have also addressed this question (Ben Boursi, et.al. 2015; Annamari Kilkkinen et al. 2008, [antibiotic use predicts an increase in the risk of cancer]; I reproduce Kilkkinen’s results because they speak to the range of cancers brought under suspicion. “The use of antibiotics was associated with an increased risk of cancer; for categories of increasing antibiotic use (0–1, 2–5 and#6prescriptions), RRs (95% CIs) were 1.0 (reference), 1.27 (1.26–1.29) and 1.37 (1.34–1.40) (Table I). The association was found both in men (RR for comparison of lowest and highest exposure group 1.47, 95% CI 1.42–1.53) and women (RR 1.31, 95% CI 1.28–1.35). The most common cancers i.e. prostate, breast, lung and colon comprised half of all cancer cases; RR (95% CI) was 1.39 (1.31–1.48) for prostate, 1.14 (1.09–1.20) for breast, 1.79 (1.67–1.92) for lung, and 1.15 (1.04–1.26) for colon cancer. RRs for other primary sites varied between 0.90 (0.76–1.05) for ovary and 2.60 (1.60–4.20) for endocrine gland cancers. In addition to endocrine gland and liver cancers, the risk of non-melanoma skin, duodenum, pancreas, kidney, bladder, male genitals (excluding prostate) and thyroid cancers as well as myeloma and leukemia was more than 1.5 times higher among participants with 6 or more antibiotic prescriptions compared with the lowest exposure group. Restricting analyses to participants with 5 or more years follow-up did not produce significantly different results from those covering the entire study population (RR for the comparison of lowest and highest exposure group 1.37, 95% CI 1.34–1.40). Similar results were obtained when the data were stratified according to age (data not shown). We also observed an increased risk of death due to cancer with use of antibiotics (RR 1.33, 95% CI 1.28–1.38). There was a similar tendency for an increased cancer risk with annual antibiotic use (table is available from authors by request). Compared with non-users of antibiotics, RRs (95% CI) for 1 year,2 and 3 years of use were 1.33 (95% CI 1.32–1.35), 1.40 (1.38–1.42) and 1.46 (1.43–1.49), respectively. RRs (95% CI) for 3 years of use for different primary sites varied from 0.99 (0.86–1.14) for ovary to 1.81 (95% CI 1.62–2.02) for non-melanoma skin cancers and was 1.21 (1.15–1.26) for breast and 1.57 (1.49–1.66) for prostate cancers.” Tim Newman 2017 [antibiotics may increase the risk of bowel cancer]; Millipore-Sigma 516104. [penicillin/streptomycin/amphotericin-harmful, teratogenic and carcinogenic]). Velicer et al. (2004) found prolonged use of antibiotic increased risk of fatal breast cancer. This has broad global ramifications because of the chronic long term exposure of antibiotic residues in diet from treated foods such as beef, pork, poultry and farmed fish and sea food products. In a new epidemiological study ‘intakes of dairy calories and dairy milk were associated with BC hazard ratios (HRs) of 1.22 [95% confidence interval (CI): 1.05–1.40] and 1.50 (95% CI 1.22–1.84)’ (Gary E. Fraser et al. 2020). Petrelli F. et al. (2019) found Overall, antibiotic use was an independent risk factor for cancer occurrence (OR 1.18, 95%CI 1.12–1.24, p < 0.001). The risk was especially increased for lung cancer (OR 1.29, 95%CI 1.03–1.61, p = 0.02), lymphomas (OR 1.31, 95%CI 1.13–1.51, p < 0.001), pancreatic cancer (OR 1.28, 95%CI 1.04–1.57, p = 0.019), renal cell carcinoma (OR 1.28, 95%CI 1.1–1.5, p = 0.001), and multiple myeloma (OR 1.36, 95%CI 1.18–1.56, p < 0.001). There is moderate evidence that excessive or prolonged use of antibiotics during a person’s life is associated with slight increased risk of various cancers. This is strong support for my finding. These results are deeply troubling despite any experimental difficulties because they almost unanimously point in the same direction to increasing carcinogenicity and the huge global populations exposed to residues. Zhang et al. (June 2008) offered criticisms of association studies and the reader is encouraged to weigh them against the evidence presented here. My rebuttle is that the above findings are also consistent with reactive oxygen DNA adduct mutations’ range of cancers, defective tumor suppressor genes and Warburg effects from mitochondrial OP knockdown and antibiotic induced dysbiosis induced immune compromise. IARC Anomaly Discussion The problem in developed countries is that use a lot of antibiotics is that infection related cancers are lower than in the Third World [cf.7.4% versus 22.9%] showing that they are protective for these but overall reported in 2019 in Canada for example is that cancer incidence reported is 50% (IARC 2008). This suggests carcinogen and life style related cancers (see Proposition 65 list) and perhaps population of age classes contribute to the high rate. This anomaly suggests cumulative mutations and other mechanisms such as I am investigating and exposures are setting the stage for later cancer illness. That we have long insidious exposure to mutation inducing carcinogens and endocrine disruptors is confirmed by my review of pesticide and chemical carcinogens in mothers breast milk (Jyrkkanen J. 3 Nov 2010). CRC Cancers Increasing in Canada How safe and contributory to cancer are antibiotics? This can be addressed considerably by the experiments I propose at the end of this article. Colorectal cancers (CRC) are very informative in this story. CRC incidence increased exclusively in young adults in nine high-income countries spanning three continents, potentially signalling changes in early-life exposures that influence large bowel carcinogenesis (Siegel et al. 5 Sept 2019) and a fail for antibiotics for this cancer and microbiome dysbiosis may play a pivotal role. Another intriguing possibility is inherited epigenetic markers from parental exposures. Alcohol and obesity are confounding factors for CRC etiology with interaction effects (Zhao, J et al. 2012). Downregulation of tumor suppressor gene TUSC3 facilitates proliferation of colon cancer CRC. Its absence or dysfunction of expression after exposure to chemicals and drugs can give a prognosis of chemicals safety (see Taniue K et al. 2020). Antibiotics Change Tissue Environment to Favour Cancer Metabolism by the Warburg Effect With the loss or reduction of OP from ROS and LP damaged cells and genomes we can expect that the default respiration glycolysis increases dominance. This is called the Warburg Effect which cancer cells have been shown to prefer in which they employ glycolysis instead of OP for their energy and this may aggravated by from defects in mitochondria. (see https://en.wikipedia.org/wiki/Warburg_effect_(oncology)). It can be expected that this ideal environment for glycolysis favouring cancer cells will be the norm whenever and wherever mitochondria are damaged or ruptured as they are with these antibiotics tested and with common pesticides. Increasing mitochondrial reproduction should reverse this process by restoring OP, replacing the Warburg effect, and that is exactly what is found (Wang, Xiao et al. 2011). This finding is strong confirmation of the carcinogenic effect of losing mitochondria and their function. Aerobic exercise suggests itself to me as a way to build up mitochondria and fight carcinogenesis via this mechanism an others I discuss below. My Proposed Antibiotic Mitochondrial Carcinogenicity Mechanism AMCM Requirements for Carcinogenesis Contribution Induce mitochondrial malfunction, damage or rupture-YES; prevent mitochondria from faithful reproduction in quality and quantity-Probable; cause mutations and genetic material damage-YES; interfere with tumour suppressor genes-YES; create microbiome dysbiosis-YES; harm the immune system-YES; increase the Warburg effect-YES; statistically significant associations-Probable.' AMCM 1. Reactive oxygen linked to oxidative mutations of DNA found in many cancers and Lipid peroxide induces P53 mutations and mutated P53 no longer repairs DNA and may in fact assist cancer cells and probably the primary cause of some portion of hepatocelluar carcinomas 2. Glutathione deficiency increases toxicity of many metabolites it normally neutralizes 3. Obstruct mitochondrial and microbiome lipid membrane integrity and mitochondrial replication leading to OP reduction and increasing microbiome dysbiosis 4. Reduction of OP and mutant P53 increase Warburg Effect favouring cancer cells glycolysis providing an advantage to cancer cells 5. Antibiotic induced microbiome dysbiosis immune compromise decreasing efficacy of subjects cancer immune defense mechanisms Further research suggested by these studies includes testing all antibiotics for their mitochondrial impacts. Related Mitochondrial Stressors and Potential Ramifications These findings also raise the question are there pesticides with similar consequences? There are intriguing findings in China. 9 Common pesticides tested induce morphological changes of mitochondria at low concentrations. Paraquat, rotenone, chlorpyrifos, pendimethalin, endosulfan, fenpyroximate and tebufenpyrad induced mitochondria fragmentation. Furthermore, some of them (paraquat, rotenone, chlorpyrifos, fenpyroximate and tebufenpyrad) caused a significant dose-dependent decrease of intracellular ATP suggesting increased risk of Warburg syndrome because ATP is a proxy for OP integrity. Interestingly, these pesticides which induce mitochondria dysfunction also inhibit 26S and 20S proteasome activity (Chen et al. 2017) which suggests to me we should be looking at antibiotics and proteasome homeostasis because of its required integrity for health. These results in turn raise the obvious question, are the consequences similar in terms of potential long term carcinogenicity? The answer is yes (Michael C.R. Alavanja, Dr. P.H., Senior Investigator and Matthew R. Bonner, Ph.D., Assistant Professor, 2018) in which they state that “Chemicals in every major functional class of pesticides including insecticides, herbicide, fungicides, and fumigants have been observed to have significant associations with an array of cancer sites”. Biocide-Mitochondrial Effects on Heart Function Another interesting question. The heart muscle is full of mitochondria. Do antibiotics and pesticides affect the hearts mitochondria and if so in what way and for how long? I would expect this heart loss of OP combined with ROS and increased peroxides to lead to a condition like chronic fatigue and possibly compromised coronary function. Azithromycin induced increased deaths in patients with prior coronary issues according to study authors Wayne A. Ray, Ph.D. and C. Michael Stein, M.B., Ch.B., and Dan May 17 May 2012. John R. Giudicessi et al. 2013 also found increased risk of sudden death from Azithromycin. Azithromycin is a macrolide which prevents bacteria from growing by interfering with their protein synthesis. How this might be linked to mitochondrial protein production needs to be examined. A UBC study found a 2.4 X increased risk of mitral valve regurgitation in fluoroquinolone users (UBC, 2019). This is an area needing more research and review. FDA (Sara Fox 20 Dec 2018 ) issued a warning that some antibiotics used for URI’s and urinary infections can cause aortic rupture and prescriptions to people at risk is contraindicated. Lifetime Cumulative Augmentation Cumulative antibiotic for clinical treatment exposures are unwittingly augmented by chronic low level residues of other antibiotics from dietary sources like poultry, beef, farmed fish and pork and may not immediately cause a cancer but may contribute to the conditions for one to occur at a later date by facilitating entry of carcinogenic infectious agents. Other mutagens and carcinogen residues (See California Proposition 65 List), radiation, chemical and pesticide residues and immune decline with age can complete the cancer induction. Calghatgi (1973) suggests that deleterious effects of bactericidal antibiotics were alleviated in cell culture and in mice by the administration of the antioxidant N-acetyl-l-cysteine or prevented by preferential use of bacteriostatic antibiotics. Is this sufficient to eliminate the microbiome dysbiosis immune depression effects and does it work for all antibiotics including tetracycline which specifically targets relatives of mitochondria in humans? This needs critical examination because of the enormous populations exposed. An Evolution Approach Enables these Extrapolations These findings in normal mitochondria of their stress response to antibiotic biocides is consistent with their evolutionary origin from Rickettseae alpha-proteobacteria and are linked to biochemical pathways already shown linked to carcinogenesis and confirmed in the literature. Another probably most definitive path to investigate the carcinogenicity of antibiotics is to run epigenetic profiles on them to determine of they are able to turnoff genes found turned off in DNA and microRNA in cancers (Pere Llinas-Arias and Manuel Esteller (2017), Wang et al. (2017)). Each antibiotic and mitochondria rupturing pesticide should be put through trials to look for P53 upregulation, mutation (mutP53) and epigenetic silencing in mice and rats at ppb resolutions. Calghatgi tests should be included on all antibiotics and pesticides that rupture mitochondria at ppb resolutions as well as testing for missense mutations, characteristic of p53 mutations associated with carcinogenesis (Rivlin, N. et al. 2011) and of course the CRC risk indicator assay pre and post antibiotic treatment for [8-oxodG] titre. A simple test to determine Warburg potential would be to compare pre and post antibiotic treatment intracellular ATP titre. Uncontacted Tribes with infection linked cancers might also be good controls for p53 mutations, p53 upregulations, p53 epigenetic silencings but some of them would of course have been exposed to plants that have traditional medical effects (Cadernos de Saude 2019) and their sample size would be small. Another potential cell guardian to assess for antibiotic related mutations, epigenetic silencing is the suspected tumor suppressor trichoplein/mitostatin (TpMs) which inhibits mitofusin-2 and hence mitochondrial associated membrane formation, but is downregulated or mutated in a number of types of cancer (Arun Raturi and Thomas Simmen, 2013). Challange to My Fundamental Thesis, Wallace 2012 Wallace opens with cancer needs functional mitochondria to prosper. This seems to imply disaster for my above hypothesis. However in further reading I find his conclusions strongly supportive. My response to his work is this. How do his findings speak to my antibiotic-mitochondrial knockdown-cancer hypothesis? The glutathione, ROS, lipid peroxide DNA mutagenicity, microbiome dysbiosis are part of my answer. He also [supportively] states “mitochondrial reactive oxygen species (ROS)…….altering the activities of transcription factors such as HIF1α and FOS–JUN to change gene expression and stimulate cancer cell proliferation.” Moreover he adds “Cancer cell ROS production inactivates caveolin 1 in adjacent stromal fibroblasts. This increases mitophagy, reduces mitochondrial function and increases lactate production in these fibroblasts. Secreted stromal cell lactate then fuels cancer cell oxidative metabolism, which drives tumour growth and proliferation. This is known as the ‘reverse Warburg effect’. Its clear that one analysis needed to determine antibiotic/biocide/selected pesticide carcinogenicity is to measure the cancer cells mitochondrial ROS and lipid peroxide output in response to biocide use. I expect cancer cell mitochondria to respond the same as normal cellular mitochondria with low glutathione, increased ROS and lipid peroxide. This is an easy test. A careful read shows his work is supportive of my hypothesis. Follow Up Research To resolve the safety of antibiotics (Abs) regarding their potential impact on mitochondrial impacts, I have arrived a number of research questions which can help steer our understanding and antibiotic futures. Independent academic institutional involvement is preferred so that vested interests don’t cloud the results. 1. How large and persistent is the glutathione decrease, ROS and lipid peroxide increase post antibiotic treatment for each antibiotic if any? 2. What effect do Abs have on future reproduction, integrity and populations of mitochondria in heart muscle. 3. Need to survey and list genetic mutations and epigenetic alteration of cancer gene expression and especially cancer gene silencing post Abs treatment in DNA and microRNA. 4. Assess dysbiosis linked impacts on immune system post Abs treatment and duration of the effect. 5. Do a full analysis of coronary function and mitochondrial health post Abs for each Abs. 6. Broad survey of Abs clastogenicity with complete description. 7. Which Abs rupture mitochondria and or cells and at what concentrations? 8. Assay 8-oxodG post Abs treatment to determine potential carcinogenicity? 9. Do any Abs impact on promotion of hepatocellular carcinoma and CRC? 10. Assay tumor suppressor epigenetic gene up-regulation, down-regulation, silencings and mutations and their loci for P53 and TUSC and TpMs. 11. Conduct a population study for Abs usage and Breast Cancer with proper controls and examine BC associated genes (Joseph S Baxter et al. 12 March 2018) for mutations or epigenetic silencings post Abs treatments and relationship to exposure history. 12. Assess OP and glycolysis potential of each Abs to determine potential for Warburg effect. 13. Abs history study of HPV oropharyngeal cancers in men in developed countries. 14. Abs impact on proteasome activity. 15. Assay Abs for reverse Warburg activity for H1F(alpha) and FOS-JUN which stimulate cancer cell proliferation. 16. Assay Abs treatment for caveolin 1 in adjacent stromal fibroblasts which increase mitophagy and lactate in fibroblasts driving tumor growth and proliferation. 17. Routine clinical assay for interstitial ATP titre recovery once antibiotic use is discontinued to see if the Warburg effect if initiated on application has been neutralized. I think this would clarify the scale and degree of impact of antibiotics and point to areas needing remedies. Many other diseases are linked to mitochondrial alterations. The reader is referred to Salvatore diMauro and Darryl C De Vivo book Diseases of Mitochondrial Metabolism. Basic Neurochemistry: Molecular, Cellular and Medical Aspects. 6th edition. Siegel GJ, Agranoff BW, Albers RW, et al., editors. Philadelphia: Lippincott-Raven; 1999. Salvatore diMauro and Darryl C De Vivo. Clinical Strategies Worth Investigating for Mitigating Loss of Mitochondrial Function and Mitochondrial Restoration Rosiglitazone (and metformin diabetic drugs for type 2 increased mitogenesis and may be a potential therapy for antibiotically damaged mitochondria and combined with vitamin C (absorbs ROS) D (reduces cancer risk of damaged mitochondria) and vitamin E (absorbs Lipid Peroxide) and N-acetyl-l-cysteine antioxidant (Calghatgi 2013) provides a tool kit to experiment with in the case of antibiotic induced glutathione deficiency. Anti-inflammatories like myrrh, frankinsence, curcumin and commercially available glutathione oral spray may also be helpful to reduce carcinogenic and cardiopathology potential. Its questionable whether antibiotics should be given to covid patients because of Covid’s propensity to rupture mitocondria. It creates a double hit on the mitochondria. Periodic fasting with protein deficiency helps boost mitochondrial replacement and phagocytosis of damaged potentially cancer contributing mitochondria (Dr. Jason Fung. 2020) and a 3 day fast helps reset the immune system with potential benefits for mitochondrial deficits and cancer prevention. Fasting triggers stem cell regeneration of damaged, old immune system by shutting down the PKA gene. The most urgent issue in the light of growing antibiotic resistance are these two critical health questions, ie mitochondrial health relative to heart health and carcinogenicity contributions. There is an interesting similar cancer and heart presentation from arsenic exposure to that observed in antibiotic exposure and it is very worthwhile to assess whether the subject has any history of such exposure. This would lead to a different clinical approach and prognosis. Mitochondria attempt to compensate for arsenic poisoning (Tchounwou PB et al. 2004). 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