Beer and wine carcinogenic due to formaldehyde formation from ingesting methanol

Carcinogenic formaldehyde decomposition product of methanol ingestion in humans

Jun. 4th, 2009 at 8:10 AM

Beer and Wine Probable Carcinogens by Metabolic Breakdown of Methanol to Formaldehyde.

4 May 2009

Here is the key reference that is of utmost concern to those who drink beer or use windshield washer that leaks into the air conditioning system.

http://www.pubmedcentral.nih.gov/picrender.fcgi?artid=1243424&blobtype=pdf

This coupled to the recent finding confirming the carcinogenicity of formaldehyde seal the story on whether or not beer is a carcinogen. Because beer is not distilled and the methanol is not removed, it is ingested by drinkers leading to the formation of formaldehyde in the body.

The story gets even more insidious. Here is an article showing how methanol increases in chronic drinkers.

http://www.ncbi.nlm.nih.gov/pubmed/19348158?ordinalpos=5&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_DefaultReportPanel.Pubmed_RVDocSum

I therefore conclude that beer and probably wine which is likewise not distilled are both probable carcinogens due to the methanol and its metabolic decomposition byproduct, formaldehyde.

Copyright 2009 Jorma Jyrkkanen. All rights reserved.
Tags:
beer, carcinogens, methanol, wine

The role of genes in diabetes.

Gene mutation and expression in diabetes. Nov. 7th, 2008 at 6:15 AM The role of genes in diabetes. 7 Nov. 2008 Type 2 diabetes often runs in families and is a good candidate for gene mutation or perhaps even gene expression causality. Many genes are involved in controlling fuel intake and production in the body so the location of the problem may be different in different people. Because life style and type 2 diabetes are related, it is apparent to me that gene expression may also have a role through epigenetic gene methylation and research needs to direct some energy in this direction. The beta3-adrenergic receptor gene is one well studied gene that has been implicated in this type of diabetes. It makes a protein in fat cells which affects how much fuel the body burns. A mutation called TRP64ARG in this gene substitutes the amino acid arginine in the 64 position instead of the normal tryptophan and this slows down fat burning and people tend to become obese. It is more common in certain Mexican, Indian and African peoples. People with two copies of the mutation have a slower metabolism than those without. There are now 9 genes known to be involved in type 2 diabetes. Some have influence through a person’s weight and others have influence thorugh controlling the insulin producing pancreatic beta cells are made and work. There is confusion presently about whether the beta cell effects is due to the numbers of cells or their function. My interest in all of this is the fact that pollutants can both cause mutations in genes and also control their expression through epigenetic methylation. Jormawankenobe © 2008 J. Jyrkkanen. All rights reserved. Tags: health diabetes

The great toxicity testing scam

Should toxicity testing be done in the real world experience of end use subjects of singly in rats?

Apr. 10th, 2009 at 2:40 AM

Toxicology testing massive fraud being committed
Related Tags : pollution, fashion, cancer, society, health

Are the protocols used to determine the health of human society adequate?

10 April 2009

If I add a soldier to a platoon with a secret new weapon, do I test the soldier by himself to see what impact he will have on the war, or do I test the platoon he is now a part of? Does the enemy experience a soldier or a platoon?

It has to be the platoon. Would I test these soldiers fighting a war against rats or humans? It has to be humans. Rats are not humans.

So it is with chemical testing. We are not exposed to chemicals in isolation. We are exposed to them in every conceivable mix and combination and at any time of our lives from the sperm and egg to old and crippled. And so they must be tested in combinations, like we test them with our bodies and through our milk secretions, our children’s bodies.

Suppose you want to add hypothetical AGENTGRINGOBAN (AGGB) to the crops of Latin America and Africa. Should AGGB be tested by itself on rats for carcinogencity, mutagenicity, teratogenecity, immunotoxicity? No. It should be tested in conjunction with all the pesticides and pollutants found in our foods and in the human body and in human foods and drinks and in mothers milk because that is who will be testing it as a consumer and that will be our life’s experience.

It needs to be added to the soup of chemicals that is made up of all cancer causing chemicals, mutagens, teratogens, immunotoxins and now by my analysis, methylagenic and acetylagenic chemicals to boot. How many ingredients in the soup we encounter in our lives?

I know the figure is somewhere between 10,000 and 10 million. A starting point might be all chemicals listed with IARC AND WITH EPA. And will rats tell the story of what it will do to humans. No. Only part of the story. What test could tell what it will do to humans?

Use it commercially for years and then find out. Well, we have been doing this soup experiment with humans for years. What has happened to cancer? The nearest I can find any evidence for and this is from very old recall is that cancer formed 5%-7% of the mortality of prechemical society from old data in Sri Lanka. It is now around 33% worldwide.

So lets add AGGB to the soup and see what it we can bump this 33% to. You see, we and all our fellow creatures are the experiment, and none of the controls are alive anymore. There is no place to run and no place to hide from industrial chemicals. They are found in fish in Canada’s most remote lakes, transported there by global air circulation and precipitated out in the rain.

Pesticides used in China on cotton are found in Canadian lakes and the Arctic and in people who eat those fish and in eagles and ospreys, and otter and mink and in bears and belugas and Orcas and seals.

We call it the good life. But how good is it really?

Jormawankenobe

Copyright 2009 J. Jyrkkanen. All rights reserved.
Tags:
pesticides carcinogens mutagens immunoto

The healthy immune system a function of genes and environment

The healthy immune system throughout life
Apr. 9th, 2009 at 2:48 AM.

Health of the immune system is a matter of serendipity and environment.

8 April 2009. http://jorma-jyrkkanen.livejournal.com/95320.html

Serendipity predetermines what genes a child gets, where and when they are born, what parents a child gets and what antibodies and antigens they will be exposed to, and quality of nutrition, care and education, and social environment and cultural taboos all of which impact immunity, survival and longevity.

The genes are very important for we know that children who are born with immune deficiencies are very likely to die earlier from diseases. Having a full set of functional operating genes for immunity is critical. Then there is the colostrum. This first milk primes the immune system of infants and it is very important for an infant to have that feed.

Mothers milk also transfers antibodies from the mother that the infant doesn’t yet have from mother to offspring. This breast feeding time is important, and excess hygiene can make it deficient. Gorillas for example will eat baby poo when the infant is sick and the mothers next milk will have antibodies for the child for the antigen in the poo.

Clearly the priming of the immune system continues during adolescence and all through life. Antigens passed over the intestinal wall will go on to produce antibodies. This is why babies stick everything into their mouths. They are picking up antigens to make antibodies against for life. Scratches in the skin serve the same function.

Nutrition is critical. We know that a well balanced diet is crucial for health. Sailors of old died of scurvy for lack of vitamin C is just one example of how important. The full complement of vitamins and minerals and micronutrients is essential throughout life. Mountain goats on selenium deficient diets suffer white muscle disease and can die from shock of handling. Sheep on micronutrient deficient ranges died. Vitamin D prevents cancers and on and on. Sunlight creates D in human skin. We need sunlight. UVB is another matter and may harm the immune system though I haven’t seen the mechanism explained.

Chemical exposure can dampen or harm the immune system and cause disease. Examples abound. Exposure to benzene compounds can cause lukemia. Friend and Friend and Friend and Trainer did studies with ducks where they exposed them to hepatitis virus with and without pesticides and found that lethality of the virus was dramatically increased in the presence of pesticide residues. Multichemical synergisms, like bad drug interactions, are a strong suspect in my books of depressing and harming the immune system in many ways. Just look at the literature in chemical immunotoxicity. Because residues are so widespread and common throughout the developed world and also carried by air, water and exported foods and drinks and products to the undeveloped world, we will never know what the background control level of non-exposed is. Chemicals can mutate genes leading to disease or interfere in physiogical pathways or operate epigenetically to affect which gene sets will be operative.

Then there are habits like washing with clean water and hygiene around eating and personal habits and sexual habits. AIDS is the biggest and clearest example of how habits, disease, the immune system are related. Need I say more. Socializing can expose people to diseases but may also lead to adaptive immunity. Hands, fingers, nose, mouth are germs best friends for infecting us with diseases.

Love is so so important and I cannot stress this too much. a baby rat not licked by its mother becomes unthrifty and dies. We need touching. Children need good touching for health. Adults need touching for health. Old people need touching for health. Social acceptance and the love of a partner and friends is part of a healthy body. Lone wolves die young due to diseases and poor nutrition. A healthy sex life will prolong your life and if a woman wants to kill her husband all she need do is have a headache every time he wants sex. Its murder pure and complex. This is why its not only ok to fool around but essential for survival. Exercise and stress reduction are also important for health of the immune system.

These are the thoughts I have on the subject and whole courses can be studied on each sub topic. Our knowledge is always growing in this area.

Copyright 2009 J. Jyrkkanen. all rights reserved. jorma60@gmail.com
Tags:
• immune system genes environment luck

Can dietary glutamate ingestion lead to future dementia?

British researchers find a variant of ApoE4 gene increasing risk of future dementia

Apr. 7th, 2009 at 9:36 AM

A genetic variant of ApoE4 increases activity in the hippocampus leading to burnout and future dementia.

7 April 2009

British researchers have found that the greater the prevalence of this variation of the genome, the greater the risk of future dementia.

It was known that carrying a rogue version of a gene called ApoE4 raised the risk of dementia but didn’t explain all of the risk. The thinking is that there is an environmental component to risk as well which may account for the majority of risk.

This leads me to the epigenetic theories I have been postulating for environmental mimetic analogues like acetylagenomimetics and methylagenomimetic pollutants along with potential agonists and antagonists which are capable of altering gene expression.

Burnout of the hippocampus sounds like an interesting hypothesis. The hippocampus is involved in long term memory and spatial orientation. It is known to be damaged by oxygen deficiency, encephaplitis and median temporal lobe epilepsy.

It is especially damaged by Clostridium perfringens, a common soil, intestinal and food poisoning bacteria, which produces epsilon-toxin which leads to excessive release of glutamate which causes the actual tissue damage (Osamu Miyamoto et al, 1998) [The neurotoxicity of epsilon-toxin, one of the major lethal toxins produced by Clostridium perfringens type B (Infect Immun, June 1998, p. 2501-2508, Vol. 66, No. 6
0019-9567].

Glutamate is produced as a byproduct of the Krebs cycle in the brain and is also found in oriental foods but I don’t know if it is unchanged in metabolism and whether or not ingestion would have any effect. These various factors impacting the brain suggests that other toxins are out there that have potential to impact dementia as well and need to be screened.

I am led immediately to the suspicion that excess glutamate is a serious suspect in the elevated environmental risks of dementia, particularly Alzheimers disease but this operates by frank toxicity rather than epigenetic means.

Jormabio

Copyright 2009 Jorma Jyrkkanen. All rights reserved.

Tags: glutamate hippocampus epigenetic
Tags:
glutamate dementia ApoE4 genes

New Words for Websters Dictionary, acetylagenic substances, acetylagens, acetylagenic activity

Chemicals capable of histone actylation can shut down specific genes or groups of genes and therefore act as epigenetic stop switches. In a reversal of the process, histone acetyltransferase removes the acetyl block and permits the genes to be expressed.

Pollutants with this capability need to be screened by EPA and IARC to determine which ones are able to do these things either act as stop or go analogues, and then profiled to determine which genes and gene complexes are acted upon.

It is quite likely that a lot of diseases and freaks of nature are due to epigenetic action of pollutants as well as the better understood genetic mutations we are more familiar with.

An understanding of epigenetic action of methylagens, acetylagens and micrRNA agonists and antagonists, and analogues is vital to a full understanding of gene environment interaction.

I hereby define the science of acetylagenics as I did previously methylagenics.

Copyright 2009 Jorma Jyrkkanen. All rights reserved. jorma60@gmail.com

Gene expression management and suicide prevention

• Oct. 29th, 2008 at 10:04 AM

Epigenetics being seen as a way to go forward on many mystery diseases.
29 October 2008

Adding methyl (-CH3) groups and taking methyl groups away from DNA is how the body causes cells to specialize their function. From generalized embryonic what are called pluripotent cells capable of anything to special tissue specific only functioning cells involves clumping methyl groups around gene sections on the DNA.

This process is called epigenetics because it doesn’t change the genes, only their expression. The methyl groups shut down unwanted genes for any given tissue. Epigenetics is very interesting for those in the health field because it is the link between cell environment, diet, pollution, hormone action and gene behavior.

Well guess what. Drs Michael Poulter and Hymie Anisman and their associates have found ten percent higher methylation in suicide victims than in normal brain tissue. Furthermore the methylation shuts down an essential neurotransmitter receptor that governs behavior. 

What this means for depression is in these cases at least, suicide is probably an epigenetic process, and perhaps it can be treated with drugs that affect gene specific methylation. This neurotransmitter can also be increased by drug therapies targeted specifically to increase receptor function.

This is very exciting news in the treatment of depression for it offers lasting hope of effective treatment. It might be possible to try implanting phages with activated receptors. We know that drugs affect behavior and now the possibility that they work by methylation is added to the clinical bag of goodies.

It also opens the door to the study of pollution’s impact on behavior. How for example does mercury cause insanity? Well, it turns out we have a fabulous hint. Benzopyrene affects methylation strongly and it is present in cigarettes. This is a strong hint suggesting pollution can affect behaviour by epigenetic alteration of normal mythlation of DNA. 

This discovery is proof of the brains malleability throughout life and also provides an link between environment and behavior and probably many other mystery diseases.

How for example, is the immune system primed to target specific antigens? Is it also epigenetic and if so then aberrant targeting where the immune system attacks normal healthy tissue may be reversible. Wonderful discovery! Good work guys. For more information on epigenetics see this site:
http://www.epigeneticstation.com/

Jormawankenobe
© 2008 J. Jyrkkanen

Tags:

• suicide methylation pollution epigenetic

Pollutant induced epigenetic and mutation induced carcinogensis.

• Oct. 29th, 2008 at 9:52 AM

The importance of normal methyl distribution in cell function and carcinogenesis prevention.

29 October 2008

Global under methylation and localized over methylation at CpG islands are the most common finding in tumor DNA.

Hypomethylation can result in chromosome instability and oncogene activation.

The hypermethylation results in the deactivation of numerous important genes that influence cancer prevention.

These include tumor suppressor genes, cell cycle related genes, DNA mismatch repair genes, hormone receptors and tissue or cell adhesion molecules.

For example, tumor-specific deficiency of expression of the DNA repair genes MLH1 and MGMT and the tumor suppressors, p16. Without these babies working, the cell division is going to go nuts.

What I am interested in is how does pollution and which pollutants specifically affect distribution of methylation of DNA?

Turns out acute benzopyrene exposure is associated with alteration of methylation patterns (Sadikovic B. et al. 2004. Breast Cancer Res.)in breast cancer showing a clear environmental-methylation gene expression alteration link to cancer.

I have now demostrated a genetic mutation caused by pollution, hydrogen sulfite from pulp mills, causing the p53 gene to change, leading to small cell lung cancer and it has been shown that benzopyrene, a common hydrocarbon found in cigarettes and the petroleum industry, by affecting epigenetic methylation, can cause breast cancer and in all likelihood, some lung cancers as well.

http://www.geocities.com/jormabio/archive/lungcancer_bisulfite.html

Environmental pollution causes cancer.

What then must we do to prevent cancer? You get a free attaboy from Jormawankenobe if you can figure it out.

Duh! What have us environmentalists been saying all along. All you had to do was look at smokers and ask the simple question, is that pollution going into their lungs?

Jormawankenobe.

2008 J. Jyrkkanen

Tags:

• pollution cancer

Asthma caused by genes and environment, mutants and pollutants.

• Mar. 16th, 2009 at 7:37 PM

U of T Prof finds Asthma genes in Tristan De Cunha Islanders

Added : Monday, March 16th 2009 by quarksandgenes
Related Tags : health, science, medicine, genetic, pollution

Mutant genes is the nature link while pollutants are the nurture link.

16 March 2009

There is a gene that creates a higher incidence of asthma in people on this South Atlantic Island when it is present. But it doesn’t account fo all of the cases of asthma and Dutch researchers have found an air pollution link.

I am going to leap into this battle and suggest that an epigenetic pollutant changes the genetic profile of people and harms the immune system by blocking healing genes and allowing expression of deleterious genes.

When I learned that P(a)H’s are able to change the expression profile of genes, I knew this would be the crack in the door to an enormous scientific field where pollutants can regulate genese expression changing our health forever. 

Epigenetics and its response to pollutants is one environmental link that doesn’t require frank gene mutations, deletions or insertions or changes in genes.

Jormawankenobe

Copyright 2009 Jorma Jyrkkanen. All rights reserved.

Tags:

• genes pollutants epigenetic antigens all

Clinical therapies for MS suggested by extrinsic DNA methylation findings

Clinical therapies for MS suggested by extrinsic DNA methylation findings. Epigenetic Methylation is linked to increased MS Risk and has Potential Clinical Applications

29 Oct 2008

Multiple sclerosis (MS) is a complex trait in which alleles at or near the class II loci HLA-DRB1 and HLA-DQB1contribute significantly to genetic risk. The MHC class II transactivator (MHC2TA) is the master controller of expression of class II genes, and methylation of the promoter of this gene has been previously been shown to alter its function. (Citing from Sreeram V. Ramagopala, et al. 2008. BMC Medical Genetics 2008, 9:63). Major histocompatability complex genes (MHC) encode cell surface glycoproteins that bind short peptides and present them to T-cells which then use the information to discriminate self/non-self apart in targeting fight infectious diseases. There is a broad polymorphism of MHC loci to accommodate the enormous challenges this job entails (Wedekind and Penn.15(9). 1269….NDP). Thus, epigenetic methylation which can be induced by environmental factors such as BAP can concievably increase risk of MS. Secondarily and with potential clinical applications, epigenetic therapies targeting this specific promoter methylation loci may be tested for ability to reverse those risks or the altered expression in MS genes.

Jormawaneknobe

Copyright 2008 J. Jyrkkanen Tags: multiple sclerosis ms methylation clinic