Environment Gene Interactions

Epigenetic references

dasevolutionvongott — Tue, 24 Jan 2012 18:26:19 +0000

http://gazette.jhu.edu/2011/11/14/combo-‘epigenetic’-therapy-may-restore-anti-cancer-gene-activity/

http://www.sciencedaily.com/releases/2012/01/120122152540.htmhttp://www.nejm.org/doi/full/10.1056/NEJMra072067

http://www.ncbi.nlm.nih.gov/pubmed/18370850

http://epigenome.eu/en/1,36,0

http://ndt.oxfordjournals.org/content/24/4/1088.full

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1184044/

http://find.lifetechnologies.com/epigenetics/gps?s_kwcid=TC|15586|epigenetics%20and%20cancer||S|b|14645916954

http://learn.genetics.utah.edu/content/epigenetics/inheritance/

http://www.epigeneticsandchromatin.com/

Tags: epigenetics, diabetes, cancer, drugs, journal, jorma jyrkkanen

Preventable Viral, Bacterial, Parasite Induced Cancers

dasevolutionvongott — Fri, 20 Jan 2012 10:11:19 +0000

Pathogens as Causes of Cancer, Jorma Jyrkkanen’s Tweets
20 January 2012

These tweets point to the importance of cancer prevention as a very desirable direction for society.

High risk HPV known to cause cancers of the penis, vagina and vulva. http://1.usa.gov/ztS0H6 I suspect more. EBV, an occasional B-cell mutagen, linked to Hodgkin’s lymphoma, stomach and nasal cancers. Vaccine being sought. HMTV is sometimes associated with Human breast cancers. ncbi.nlm.nih.gov/pubmed/20503403
Kaposi’s Sarcoma Associated Herpesvirus=>Human herpesvirus 8 are Probable 2A Carcinogenic viruses (KSHV/HHV8). JC Polyoma virus probably cause colon and colorectal cancers. HTLV-1 can cause cancer. IARC Vol67, 1996. HIV-2, Lav-2 cell line can cause Acute lymphocytic leukemia. The human Herpes virus 31 and 33 can cause cervical cancers, p testicular cancers and possibly oropharyngeal cancers and possibly more. The HIV Aids virus can cause Kapozi’s sarcoma. The hepatitis B bacteria can cause liver cancer. The gut bacteria Helicobacter pylori can cause stomach cancer. The blood parasite Schistosoma haematobium can cause bladder cancer.

There is also an interaction between pathogens and chemicals which may play a role in cancer causality that needs to be investigated. Other pathogens than those ones I mentioned may also play a role in cancers by immune suppression, synergisms and cancer promotion. I believe that the pathogen vector route as a cause of cancer I have defined is just the tip of the iceberg. I therefore concluded in 2001 an important cause of human cancers are pathogens that can be transmitted. Gardacil demonstrated a cure.

What do I know for sure. Pathogens, chemicals, mutagens can all cause cancers in humans. Where should we focus research? Prevention? PreventablePathogenCancers-penis vagina vulva Hodgkin’s stomach nasal breast colon colorectal cervical sarcoma liver stomach bladder acute lymphocytic leukemia.

Tags: pathogens, viruses, bacteria, parasites, carcinogenic, Jorma Jyrkkanen

Pulp Mills and Cancer Association

dasevolutionvongott — Wed, 03 Mar 2010 12:55:14 +0000

Experimental Determination of Excess Lung Cancers in Pulp Mill School Districts Versus Control No Mill Districts

By: Jorma Jyrkkanen. Sept 1990.

I addressed the simple null (Ho) hypothesis that living in a pulp mill town would have no impact on the incidence of lung cancer (LC) mortality. The research hypothesis (Hi) is that yes there is an effect air pollutants and that it would be elevated leading me to select a one-tailed test.

Major assumptions are that the populations being drawn upon are similar in demographics and life-styles, and that sampling is random, and that there are no other major sources of lung carcinogens. These assumptions are unexplored and should be examined in greater depth if one wishes to improve certitude.

I therefore decided to use the parametric Students t-test with alpha=.05 (the risk that chance alone could cause the observed effect in 5% of cases) and 1-tailed, unequal sample size model. Data (Tables 1, 2) were obtained from Gallagher et. al. 1986. Occupational mortality in BC.. Health and Welfare Canada. BC Research.

Table 1. LC DEATHS AMONG MALES AND FEMALES AMONG TOTAL DEATHS WHERE THERE ARE NO PULP MILLS IN THE SCHOOL DISTRICT

No Mills in School District	Male LC deaths	Total Male deaths	Female LC deaths	Total Female deaths

Nelson	112	2882	33	1938
QCI	15	445	4	234
Merrit	38	922	9	535
Smithers	29	797	7	448
Terrace	56	2530	8	1049
Stikine	5	246	0	122
Keremeos	21	551	2	260
Summerland	46	981	15	688
Central Okanag.	326	6702	89	4415
Vernon	168	3957	49	2693
Penticton	147	3259	40	2153
Delta	164	2871	64	2133
Mission	86	2016	25	1183

N=13

Table 2. LC DEATHS AMONG MALES AND FEMALES AMONG TOTAL DEATHS WHERE THERE ARE PULP MILLS IN THE SCHOOL DISTRICT

Yes Mills in School District	Male LC deaths	Total Male deaths	Female LC deaths	Total Female deaths

Prince George	230	4874	63	2226
Castlegar	47	1126	9	744
Prince Rupert	74	2164	12	1091
Campbell River	98	1836	37	999
Kamloops	250	5669	68	3090
Port Alberni	119	2959	21	1718
Harmac	359	6327	105	4313
Powell River	110	1919	31	1214
Howe Sound	50	862	16	443

N=9

Analysis

Table 3. Statistical comparisons of percentage Lung Cancer mortality between mill school districts and non-mills school districts for males.

MALE LC MORTALITY

N	No Mills LC%	Mills LC%
	X2	X1
1	3.88619	4.781917
2	3.370787	4.174067
3	4.121475	3.419593
4	3.638645	5.337691
5	2.213439	4.409949
6	2.03252	4.021629
7	3.811252	5.674095
8	4.689093	5.732152
9	4.86422	5.800464
10	4.245641
11	4.510586
12	5.712295
13	4.265873

Mean	3.950924	4.80984
SE	0.27927	0.28829
Median	4.121475	4.718917
SD	1.006922	0.864871
Var	1.013891	.748
CL	0.688477	0.665

The results of the Student’s-t test appear in Table 4 below.

Table 4. Results of Student’s-t test

Students t-test assuming Var1=Var2	(Using Microsoft Software in Excel)

Mean	3.956319	4.80984
Var	1.105651	0.85656
Pooled Variance	1.007604
Hypothetical mean diff	0
Calculated t-statistic	1.88771	Significant
P(T<=t), one-tailed	0.037648
t-critical, one-tailed	1.734063
P(T<=t), two-tailed	0.075296
t-critical, two-tailed	2.100924

Conclusion

Since the calculated t 1.88771 falls within the region of rejection, exceeding the critical tabular value 1.734063 (Table 4.), the null hypothesis must be rejected, that is Ho is rejected and therefore the research hypothesis (Hi) must be accepted, implying that there is an elevated lung cancer mortality amongst males in the Mill school districts (.025

<.05).

To conclude, the Mill districts exhibited statistically significantly higher lung cancers in males (4.81% Lung Cancer mortality) compared to No Mill districts (3.95%LC mort) (P(T<=t), one-tailed = 0.037648) as I had predicted. This test alone is not proof however of causality but is highly suggestive. This is especially so when considered along with the other evidence I have examined (see Fenni-excerpts in jormabio/archives).

When the analysis was conducted for females, the same pattern was found for females though the magnitude of the effect was about half.

Warning! When I did this cursory analysis for BONE CANCER, I found that it was very highly linked to pulp mill school districts and should be investigated for specific causal agent.

Tags: cancer, pulp mills, males, females, British Columbia

Beer and wine carcinogenic due to formaldehyde formation from ingesting methanol

dasevolutionvongott — Thu, 04 Jun 2009 17:44:54 +0000

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.

The role of genes in diabetes.

dasevolutionvongott — Mon, 20 Apr 2009 21:37:09 +0000

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

dasevolutionvongott — Fri, 10 Apr 2009 09:46:19 +0000

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

The healthy immune system a function of genes and environment

dasevolutionvongott — Thu, 09 Apr 2009 10:37:20 +0000

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.

Can dietary glutamate ingestion lead to future dementia?

dasevolutionvongott — Tue, 07 Apr 2009 17:08:29 +0000

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

Tags: glutamate hippocampus epigenetic
Tags:
glutamate dementia ApoE4 genes

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

dasevolutionvongott — Tue, 07 Apr 2009 08:27:25 +0000

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.

Gene expression management and suicide prevention

dasevolutionvongott — Mon, 06 Apr 2009 15:33:39 +0000

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/