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Virus Induced Obesity - what the hell!?

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posted on Jan, 9 2006 @ 12:20 PM
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Originally posted by bsl4doc
Did you read the titles of your results?


~MFP


Did you read all your science journals in med school?
careful... i might know better. (just making a point, no need to answer)

As to your speculation of "a few might be from medical reasons"...

I am 6.4" weigh between 185-205 and living proof that genetic metabolism makes all the difference...
I cant gain significant weight... but can gain or loose 5-10 pounds per week, without any effort.

Most of my friends are the same, Perhaps I have a "no gain" virus, that I have blessed my friends with, Or perhaps they also have a good metabolism...

So "WE" can eat anything we want, without the effects that you claim will affect us.

why not the opposite...

Not saying that a good percentage (IMO 45-65%) have no one to blame but their own lifestyle...
but with diabetes, thyroid, this virus, genetic predisposition, and other knowns/unknowns...
can you really confidently say "all but a few cases result from ****")

I really dont think so... if you truly look at all the various factors outside of lifestyle that affect this.




posted on Jan, 9 2006 @ 01:07 PM
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You know, I’m quite fond of ATS, but I never realized so many of the posters were so angry at us overweight people.

This started out as a bit of a wacky thread, but it quickly deteriorated into some posters just putting down others. I'm "over weight" But I’m attractive (for verification please U2U shadowflux) and healthy. And nobody really has the right to call me lazy or make any other hideous generalizations about my life.
I thought this board was for constructive conversation and the sharing of ideas and theories. Plus, isn't our motto "Deny Ignorance"? *claps* good job at upholding it guys.
Last time I checked, I'm (speaking personally) not a drain on your society, I don't require constant medical attention, and I’m not throwing my lifestyle in your face and forcing you to accept it.
I am not saying that there aren't cases where some people truly do not care for their lives, and over indulge to the point of no return. But there are also some people who are not capable of being thin due to metabolism, genetics or simply not having the will power or self esteem to be the best them possible.

So please, keep your generalizations to your self. There's really no need.



posted on Jan, 9 2006 @ 01:42 PM
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Originally posted by decidedlyundecided


This started out as a bit of a wacky thread,


Sorry but I have to disagree here.
Nothing "wacky" about a virus causing obesity, particularly when viruses have been manipulated, changed, modified, over used, abused and all the other 'tweeking' we could never know about...by drug companies and their World Health Org. 'sugar daddy'.

To me this is like the towns big brothel, situated nice and handy to the judges and politicians, but that no one wants to admit is there.

The thread is not about opinions of or by overweight people, but viruses that are identified with a significant percentage of our larger members of society.

Give it some thought, wouldn't some of those who actually suffer from obesity, be pretty angry to find the recent and dramatic viral spread, came out of a lab, maybe even deliberately?



posted on Jan, 9 2006 @ 01:47 PM
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Originally posted by suzy ryan
Give it some thought, wouldn't some of those who actually suffer from obesity, be pretty angry to find the recent and dramatic viral spread, came out of a lab, maybe even deliberately?

That sounds far fetched at first but considering the size of the 'fitness' industry; including diet books, exercize dvds, mags, magic slimming pills etc I guess it's possible.



posted on Jan, 9 2006 @ 02:13 PM
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Originally posted by bsl4doc
Patty, please refrain from personally attacking me simply because you have a difference of opinion, especially when you can't provide any information or sources. Ciao!

~MFP


I apologize , however , I have more experience than you know. I am a female who had a weight problem after giving birth to twin boys. I was able to lose this weight. I have no other credentials than that. However, I am a human being with feelings. I know that and have been on the receiving end of all of these remarks. Your remark about not coddling a cancer patient , but coddling overweight people is what really bothered me. People with cancer ( with the exception of lung cancer) do not get riddliculed or treated with the disdain that obese people do. I am concerned that you also made attacks on American Doctor's as opposed to Euro's . I wondered if you were going to stay in Europe or come here because of your attitude . You actually attacked not only obese people but made a slight about American's there.

As far as the article about the fat virus, I read it and concluded that it is just a subject that indeed needs further studies. THATS ALL.



posted on Jan, 9 2006 @ 02:24 PM
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Originally posted by suzy ryan
Well I still think the virus was created and spread through vaccination (remember how it was 'induced' in critters) and though Australia is suddenly catching up with the US, this didn't coincide with fast food or video games etc. but our increased vaccination rate.

Sorry to end OT, but you folk all really need a laugh!


Thanks, but I got my laugh from the tired "death by vaccine" story. Now if I can just get sofi to link it all to prions,

You know, it's far more likely that an overabundance of corn has a major causal relationship with the fat "epidemic" in the U.S. than some majically undiscovered (except by a bunch of non-medically trained, non-scientifically trained "researchers," and the occasional unpublished, non-peer-reviewed quack) vaccine ailment.

I mean that, by the way. About the corn.

Also, as a final aside, hopefully before going any farther down the vaccine highway (and then making a right turn off topic), it's nice that the "average" person 50 years ago who wasn't exposed to a vaccine was not likely as fat as the "average" person today.

It's probably because he was dead, having an average life expectancy 8.2 years less than today (68.2 in 1950, 76.9 today). Or, he could have just died in his younger years, as mortality in young people (12 months to 24 years) has declined by more than half since the '50's).

As for this virus, I hope they find the cure, and I hope they vaccinate for it. Not to make people more attractive, but to help them live healthier lives. I think almost all of us would like that.

mod edit: removed inappropriate comment

[edit on 10-1-2006 by sanctum]



posted on Jan, 9 2006 @ 03:42 PM
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Hamberglar, you vaccinate against viruses with manipulated viruses, it's very much on topic.

As to life expectancies, westernised and impoverished nations, cut a huge chunk out of the 'average' age. They are dodgy stats folks like you use to sell the, "only man can save save themselves with science lie". I'm damn glad my grand and great grand parents didn't try to live down to them.

Rubbish every researcher in one post if you must, but when their results fit the drug companies own buried studies (thank God for whistleblowers) you just come across as a "company man", with your rude attempt to kill discussion on this topic.



posted on Jan, 9 2006 @ 03:59 PM
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Soficrow, those summaries you gave were of articles that I didn't see listed in your original list of articles, so are you admitting that long list was emrely for shock value and of no real value?

Also, patty, my post as to the educational system in America is totally valid. In Europe, not everyone gets a college degree. I studied for two years as an undergraduate in America, and it was amazing to me the sense of "entitlement" all the students had, as if failing a course were some sort of breach of contract. A professor in a psychology class I took while in the USA said that by the time our class would be 30, the American college degree would be the equivalent of our parents' high school diploma; everyone would have one, and you must achieve something higher to stand out. I agree completely with him. The idea that even half of the population has a degree makes that degree mean less. Obviously, every educational system has it's faults. Some people see some European systems as cold and unfair or simply black and white, which can be true in some cases. But is blocking a few people per year from getting a degree who may have the ability to get one worse than allowing 15,000 people who don't deserve one to get one simply by coddling them and holding their hand throughout the whole process? And yes, I did slight the American medical licensing programs, because honestly, why do you think several licensing ceritification tests are required by EU law for an American to practice here? Sorry to get off topic, but it infuriates me when someone attacks me and doesn't even stop to think outside their ethnocentric world.



posted on Jan, 9 2006 @ 04:07 PM
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I am overweight! I blame McDonalds! and Capitalism...or I could just blame myself. its easier.



posted on Jan, 9 2006 @ 04:07 PM
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Originally posted by suzy ryan
Hamberglar, you vaccinate against viruses with manipulated viruses, it's very much on topic.


Ohh gee whiz, suzy, thanks for teachin' me 'bout how vaccines work. I'sa didn't know dat, boss!


Originally posted by suzy ryanAs to life expectancies, westernised and impoverished nations, cut a huge chunk out of the 'average' age. They are dodgy stats folks like you use to sell the, "only man can save save themselves with science lie".


Care to rephrase so it's intelligible? The only thing I can get from this is that apparently if DOCTORS AND WORLD HEALTH OFFICIALS say something, it must be dodgy. Good reasoning!

And, if you're trying (badly) to suggest that these stats are for the whole world, try again. They're for the U.S. Assuming, of course, that was your point.


Originally posted by suzy ryanI'm damn glad my grand and great grand parents didn't try to live down to them.


Me too, except, being above average people, they probably understood that just because there is an average, doesn't mean that EVERYONE falls in that range. Just ask Robert Wadlow. Don't really, he's dead. But Google him. You should get the point. I guess your anecdotal evidence and his staggering non-averageness have proved once and for all how dodgy these statistics are. Good work. Way to think critically!


Originally posted by suzy ryanRubbish every researcher in one post if you must, but when their results fit the drug companies own buried studies (thank God for whistleblowers) you just come across as a "company man", with your rude attempt to kill discussion on this topic.


Not every researcher, just fakes, frauds, charlatans, quacks, snake-oil salesmen, eccentrics, and mad scientists. True researchers, you know, the ones who go to school for their craft, hone their skills over the years, and subject their work to clinical trials and peer review, are A-Okay with me.

Surprising that they ALL seem to agree that vaccines are safe. I know, that must mean we are all "company men" (which is cool, I always wanted to be a spy as a kid). Or, it could mean that your lack of vaccination allowed you to catch Mumps, causing encephalitis, which deteriorated your ability to discern credible science from fantastic science.

As for killing discussion, I am killing any further discussion from me on vaccination-caused viral obesity and whether "the man" is trying to keep us fat. I'll stick to the topic if I have anything else to add. Meanwhile, start your own vaccine thread if you want to discuss this.



posted on Jan, 9 2006 @ 05:06 PM
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On par with being able to find cures for some types of obesity, some might be interested that we apparently have a 6th taste sensation (other than sweet, salty, bitter etc). The fat taste buds.

Yes they state that we can actually experience a taste sensation of fat (which of course like sweet tasting, sour, bitter, salty etc are all pleasurable in theirown ways), leading perhaps to addiction and you know how the rest goes. Link

Also whats this?Contraversial device claims to "melt away" fat

Oh and this ones obvious...but now they have a direct link which is always good.Metabolism rules weight loss?

Finally i think this may be related to the last one but i havent read it properly. Fat busting jab. the new liposuction?

Well that should keep yall busy for, well a few minutes! ah well....an ats'ers work is never done.



posted on Jan, 9 2006 @ 05:49 PM
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Why are the people with "ham" in their name so rude, insulting, argumentative and belligerent?

If you know vacs. and viruses are mother and daughter, why do you insist you can't discuss a relationship?

I won't go off topic playing the stats. game with you, but poverty, of which America has always had a great deal of, kills people. In that country ALOT of people, and it greatly effects the nations stats.

Could be your life expectancy 'average' went up with more free clinics and welfare during that time, than anything else.

Anyway normal, healthy human life, baring accidents and epidemics, that always ran their course and naturally relented anyway, has always been around that 60-70-80, give or take, range. Bad Governance and living/working conditions have always been the greatest shortner of life. Not a lack drugs, that a healthy body doesn't need.

Take more and different samples, and 'the obesity gene' could be found to be in a greater % of the population. Reguardless, how can they know it isn't a 20% increase from 20, 30 years ago? If there is an increase, what caused it?

Increase in overweight people. Found obesity virus. Has there been a monitoring of the virus in the population over time? Is the virus spreading? If it is spreading, what does the spread correlate with?

Oh and please don't bring up the, 'smallpox in the Americas' disaster, to promote vaccination. It's a whole other issue that doesn't fit post exposure populations, which is pretty much the whole world now.

Something other than 'lifestyle' is making people fatter than ever around the world, and we all don't have the American obsession with corn. We are however, hooked on your drugs.

Oh is that it? Is this news of a fat virus supposed to have us all clamering for another 'possible' problem to vaccinate against? That's my bet, create another 'disease' to sell cures for. There's a good thread on that very topic.



posted on Jan, 9 2006 @ 06:11 PM
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Originally posted by waffleprime
I am overweight! I blame McDonalds! and Capitalism...or I could just blame myself. its easier.


I can set you up with a good lawyer for 15% of your settlement. His name is John Edwards.



posted on Jan, 9 2006 @ 07:27 PM
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Originally posted by bsl4doc
Soficrow, those summaries you gave were of articles that I didn't see listed in your original list of articles, so are you admitting that long list was emrely for shock value and of no real value?



The original list came straight from the National Institutes of Health database - the second list was filtered through Google's science for dummies search engine.



posted on Jan, 9 2006 @ 08:29 PM
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The original list came straight from the National Institutes of Health database - the second list was filtered through Google's science for dummies search engine.


What I was pointing out was that your original list didn't contain any articles relating to obesity and viruses or vaccines, so it was really just a waste of space. Thanks for reading my post though (/sarcasm).

Ciao,
~MFP



posted on Jan, 9 2006 @ 08:38 PM
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Originally posted by bsl4doc

The original list came straight from the National Institutes of Health database - the second list was filtered through Google's science for dummies search engine.


What I was pointing out was that your original list didn't contain any articles relating to obesity and viruses or vaccines, so it was really just a waste of space. Thanks for reading my post though (/sarcasm).



The original list was good - although the word obesity was not in the titles, the research was about viral-obesity links and syndromes as they manifest at the molecular and cellular levels.



posted on Jan, 9 2006 @ 09:15 PM
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Umm..no, they weren't soficrow, sorry. You need to read the titles of the articles again. I can't find any even somewhat related to viral obesity. Let's take a look at some of the titles in your list...



-1: Shan XC, Goodwin PH. Links
Abstract Silencing an ACC oxidase gene affects the susceptible host response of Nicotiana benthamiana to infection by Colletotrichum orbiculare.
Plant Cell Rep. 2006 Jan 6;:1-7 [Epub ahead of print]
PMID: 16397784 [PubMed - as supplied by publisher]

ACC oxidase is a gene found in plants, not humans or mammals or any other organism other than plants. If you look at the citation entry for that article, you'll see this phrase "Plant Cell Rep. 2006 Jan 6;:1-7". That means it's found in the journal Plant Cell Reproduction. This has nothing to do with viral obesity whatsoever.



2: Yang K, Shi H, Qi R, Sun S, Tang Y, Zhang B, Wang C. Links
Free Full Text Hsp90 Regulates Activation of IRF-3 and TBK-1 Stabilization in Sendai Virus-infected Cells.
Mol Biol Cell. 2006 Jan 4; [Epub ahead of print]
PMID: 16394098 [PubMed - as supplied by publisher]

This article is about the immune responses phosphorylation of IRF-3 and TBK-1, intracellular signal molecules, in response to laboratory controlled sendai virus infection. It focuses on the ability of IRF-3 to control dsRNA regulation. Nothing at all about obesity.



4: Gern JE, Brooks GD, Meyer P, Chang A, Shen K, Evans MD, Tisler C, Dasilva D, Roberg KA, Mikus LD, Rosenthal LA, Kirk CJ, Shult PA, Bhattacharya A, Li Z, Gangnon R, Lemanske RF Jr. Links
Abstract Bidirectional interactions between viral respiratory illnesses and cytokine responses in the first year of life.
J Allergy Clin Immunol. 2006 Jan;117(1):72-8. Epub 2005 Nov 28.
PMID: 16387587 [PubMed - in process]

This article is about the development of allergies as a response to cytokines (cellular signal molecules of the immune system) as a result of early life repiratory infections. Nothing mentioned in the journal article in reference to obesity or viral linked obesity.



11: Morrison TE, Whitmore AC, Shabman RS, Lidbury BA, Mahalingam S, Heise MT. Related Articles, Links
Abstract Characterization of ross river virus tropism and virus-induced inflammation in a mouse model of viral arthritis and myositis.
J Virol. 2006 Jan;80(2):737-49.
PMID: 16378976 [PubMed - in process]

This article is about the possible link between viruses and myositis (a swelling of muscles at the joints) and arthritis (a swelling of the joints due to rubbing or wear of cartilage, among other causes). No mention of obesity or viral linked obesity.



17: Haller O, Kochs G, Weber F. Related Articles, Links
Abstract The interferon response circuit: Induction and suppression by pathogenic viruses.
Virology. 2006 Jan 5;344(1):119-30.
PMID: 16364743 [PubMed - in process]

This article is about the role of inteferons (cellular signal molecules specific for certain cells) and their ability to destabilize viral molecules. No mention of obesity or viral linked obesity.

So, basically, your list is a wash. I went through and picked a few I thought would be the most interesting reads for me, personally. If you'd be so kind, could you show me which ones you feel have anything whatsoever to do with obesity in any way?

Ciao,
~MFP



posted on Jan, 9 2006 @ 09:20 PM
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Originally posted by suzy ryan
Why are the people with "ham" in their name so rude, insulting, argumentative and belligerent?”


God help me, 'cause I sure can't help myself. I said I was done with this vaccine talk, and I really want to be. But you just keep bringing up the most absurd things I’ve ever read. Maybe people with “ham” in their name are not rude, but instead are tired of having to rehash the same stuff every time this basura hits a thread.

It’s like you have one key on your keyboard, and it’s marked “drivel.”


Originally posted by suzy ryan
If you know vacs. and viruses are mother and daughter, why do you insist you can't discuss a relationship?


It’s not that we shouldn’t discuss potential vaccines. I just don’t really want to see another interesting thread hijacked by the anti-vaccine coalition (you). Your personal beliefs are at odds with those of modern medicine, and they are not really relevant to this discussion.

If , for example, you wrote that all fat people are actually fat as punishment for sinning against against Jebus, I’d be just as quick to suggest we get back to discussing an actual issue, rather than your paranoid, pseudo-scientific fantasies. If that’s rude, tough. Or maybe you got the “thin-skin virus” and think anything that disagrees with your narrow-minded poppycock is “rude.” I wonder if they can vaccinate for that.


Originally posted by suzy ryan
I won't go off topic playing the stats. game with you, but poverty, of which America has always had a great deal of, kills people. In that country ALOT of people, and it greatly effects the nations stats.


What a load of garbage. I’ll invite you to play the stats game by reading about what “poverty” in America is like.


As a group, America's poor are far from being chronically undernourished. The average consumption of protein, vitamins, and minerals is virtually the same for poor and middle-class children and, in most cases, is well above recommended norms. Poor children actually consume more meat than do higher-income children and have average protein intakes 100 percent above recommended levels. Most poor children today are, in fact, supernourished and grow up to be, on average, one inch taller and 10 pounds heavier that the GIs who stormed the beaches of Normandy in World War II.
Biased source normally, but very well documented this time (footnotes even!)


True poverty is nearly non-existent in this country. Certainly no worse than anything you'd find in Cunnamulla.

Now, I challenge you to take a look at true poverty, and try to say America has a serious poverty problem. Only this time, say it with a straight face. Some of this is graphic. Be careful.

Some not so nice pictures
Just some stuff about poverty in Niger
Here’s what starvation looks like
I’ve never seen THIS in the U.S. Have you?
Find some facts!

In short, “poverty” in the United States does not affect our health in any statistically significant way. No, according to the CDC, decreases in Heart Disease deaths have had a much more significant impact on longevity. Speaking of which…


Originally posted by suzy ryan
Anyway normal, healthy human life, baring accidents and epidemics, that always ran their course and naturally relented anyway, has always been around that 60-70-80, give or take, range. Bad Governance and living/working conditions have always been the greatest shortner of life. Not a lack drugs, that a healthy body doesn't need.


Do you just write whatever pops into your head? Are you actually mentally ill, or just terribly under-informed? Or maybe this came off a Chick Tract somewhere, who knows? I can’t believe your fingers would allow you to type such nonsense. I can’t even believe your computer didn’t just shut down at the utter ridiculousness of this statement.

It is a simple matter to go somewhere like the CDC’s National Center for Heath Statistics to find all sorts of good information.

According to them, average life expectancy in the U.S. in 1900 was 49.24 years.

49.24!!!

You’ll find that on page 29 (great tables, by the way)

So your guesses are not only off, but they are off by a decade in your closest estimate, and that’s just for a century ago. I wonder what I can find out for 250 years ago…


Originally posted by suzy ryan
Something other than 'lifestyle' is making people fatter than ever around the world, and we all don't have the American obsession with corn. We are however, hooked on your drugs.


Uhh, no, it’s not. Not for the 70% without the virus, anyway. I already wrote this, but I’ll try again. Straight from the horse’s mouth:


Mexico probably will surpass the U.S. in obesity rates for the first time next year as the Latin American nation adopts the fast food and sedentary lifestyles of its neighbor to the north.
Read it.


And yes, you are hooked on corn. So is every developed nation. Except our abundance of corn gets transmogrified into high fructose corn syrup. This crap is in EVERYTHING. Look at any five foods in your cupboard. It’s probably in that Vegemite you had for lunch.


Originally posted by suzy ryan
There's a good thread on that very topic.


So go post your hooey there.

I swear to Jebus I’m done with you now. Feel free to wallow in your ignorance. I won’t try to help you anymore.

With warmest regards, your friend,

Yamburglar (this is my new name; hopefully you find yams less threatening than hams)



posted on Jan, 10 2006 @ 05:15 AM
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God this was the first thing i noticed when i visited america, popeyes chicken burgers, soggy in a pool of it, corn syrup infused bagels, dairy queen icecream containing corn syrup, "uh sir, would you lke some corn syrup with that?". They look at you like you've told them their mum is unfaithful with the mailman if you say no.
It is one of THE WORST, habits of modern american society. Im surprised you dont have corn syrup fountains you seem to like it so much. You should put a warning sign on food saying "danger: contains corn syrup". Oh actually no, since it would probably consume the worlds rainforests in a day just to produce enough labels for your food.



posted on Jan, 11 2006 @ 01:02 PM
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Originally posted by bsl4doc
...soficrow, sorry. You need to read the titles of the articles again. I can't find any even somewhat related to viral obesity.


Although the titles do not include the word obesity, the articles are related to induced obesity - as I stated earlier. I did a quick search on the National Institutes of Health PubMed database, as I also said earlier, and my terms were +virus +induced obesity. No, I did not read the articles, nor did I claim to have done. I simply shared the first page of the search results.

You need to know a bit more about 'induced obesity' to see how the articles relate. So here's the poop:

Most infectious obesity does NOT result from a direct cause-and-effect relationship - the disease-causing microbes (pathogens) do NOT head straight for the fat cells (lipids or adipose cells) when they enter the body.

Instead, induced obesity usually occurs later on in a larger disease process that affects numerous body systems - sometimes called "multisystem disease." The systems affected in this disease process include the:
* nerves (neurological);
* hormones (endocrine);
* immune system; and
* metabolism.

Many paths lead to obesity, but generally, obesity does not occur unless and until the multisystem disease reaches the fat or adipose cells. Once the fat cells are 'infected' one of two things happens: a) individual fat cells grow larger, called hypertrophy or hypertrophic; or b) fat cells multiply out of control, called hyperplasia.

More than one virus is linked to obesity; and in addition, many other pathogens present in food and the environment also are known to induce obesity. These other pathogens cause disease by releasing toxins.




[0024] As used herein the term "exposed to a toxin-forming organism" refers to any patient contact with the toxin, such as direct contact with the toxin-producing organism itself, or by contact with the toxin, produced by the microbial organism. Such contact can occur, for example, by ingestion, inhalation, or contact through skin or mucosal membrane. Such toxin-forming dinoflagellates include but are not limited to Pfiesteria, Ciguatera, and Chattonella. Such toxin-forming fungi include but are not limited to Stachybotrys, Penicillium, Aspergillus, Cladosporium, and Fusarium. Such toxin-forming spirochetes include but are not limited to Borrelia, Treponema, Leptospira, and Denticola. Such toxin-forming protozoa include, but are not limited to Babesia and Plasmodium. Such toxin-forming cyanobacteria include but are not limited to Microcystis, Anabaenopsis and Cylindrospermopsis. Such toxin-forming bacteria include but are not limited to Bacillus, Clostridia, and coagulase-negative Staphylococcus.

United States Patent Application: 0030219400
Sorry, there's no direct link. Go to the US Patent Office website, and search under applications for #0030219400, or "Methods for treating or inhibiting neurotoxin-mediated syndromes"

***

* The biphasic change in hypothalamic leptin receptor expression seen during the progression of CDV-induced obesity provides a new paradigm for understanding mechanisms of neuroendocrinological, virus-induced abnormalities.

* ...infection with the obesity-inducing BDV-ob results most likely in neuroendocrine dysregulations leading to the development of an obesity syndrome.

* ...obesity has multiple etiologies

* Viruses can induce progressive neurologic disorders associated with diverse pathological manifestations




Sometimes these pathogens and toxins cause rapidly progressive acute disease that ends quickly, but more often, disease is slowly progressive and occurs as a forme fruste. Traditional western medicine tends to focus on acute disease and ignore the formes fruste. As a result, we now face a worldwide chronic disease epidemic that's kicking everyone in the butt - individually, nationally, socially and economically.

We "catch" these diseases by eating, drinking, breathing, or touching something that is contaminated - and much of our food is contaminated with one or another of the "toxin-forming organisms" outlined above. But people react differently to the same exposures.

The disease process is complicated and involves numerous different factors, so it's multifacto rial. What happens in the individual body results from a complex interplay between pathogen exposure, genetic susceptibility, other environmental influences, and more. Also, the disease process can take a long time, and makes a lot of stops along the way - affecting various enzymes, hormones, and other essential body products. Many disease symptoms like obesity result from a domino effect inside the body, called a cascade.

The research looks at the whole cascade, all its parts, and all the factors, not just the disease-causing microbe and obesity alone - which is why you do not see the word obesity in every title.

Damage-control corporate-politicos say obesity is solely a matter of personal responsibility and blame individuals; their goal is to avoid liability and lawsuits. On the other side, responsible scientists seek the truth, and ways to make the food industry and our world safer. Available research is either funded by industry and tries to disprove the relationship between common pathogens and the larger multisystem disease process, or alternately, tries honestly to understand what's really going on.



Let's take a look at some of the titles in your list...


-1: Shan XC, Goodwin PH. Links
Abstract Silencing an ACC oxidase gene affects the susceptible host response of Nicotiana benthamiana to infection by Colletotrichum orbiculare.
Plant Cell Rep. 2006 Jan 6;:1-7 [Epub ahead of print]
PMID: 16397784 [PubMed - as supplied by publisher]


ACC oxidase is a gene found in plants, not humans or mammals or any other organism other than plants. If you look at the citation entry for that article, you'll see this phrase "Plant Cell Rep. 2006 Jan 6;:1-7". That means it's found in the journal Plant Cell Reproduction. This has nothing to do with viral obesity whatsoever.



ACC oxidase is the gene that makes vine-ripened fruits and vegetables ripen. The ACC oxidase gene is silenced in genetically modified (GM) fruit and vegetables to prevent ripening on the vine, and extend storage life for shipping and sales by delaying ripening off the vine. Ie., see here.

The cited article shows that silencing the ACC oxidase gene makes GM Nicotiana benthamiana more susceptible to infection by a fungus called Colletotrichum orbiculare. Fungi produce poisonous proteins called mycotoxins.
Note to hamburglar. Here it is: The anticipated protein-prion connection. Just don't ask me to connect all the dots for you.


As outlined above, many mycotoxins are neurotoxins, linked to multisystem disorders that can include obesity and obesity syndromes. For example, one thing neurotoxins do to contribute to the larger disease process is muck up the calcium-activated potassium channels.

So - the article speaks to genetically modified (GM) fruits and vegetables, specifically a transgenic gene affecting ACC oxidase, engineered to prevent ripening on the vine and delay ripening in shipping and storage. The research is relevant in considering the connection between obesity and mycotoxins; it suggests that genetically modified (GM) fruits and vegetables play a role in mycotoxin contamination of the food supply.

The researchers show that this particular GM plant is more susceptible to infection by the fungus Colletotrichum orbiculare: "Inoculated NbACO1-silenced plants developed more lesions more quickly as a result of an accelerated switch from the symptomless, biotrophic phase to the symptomatic necrotrophic phase of infection compared to inoculated control plants."

Taken further, research also may prove that all GM fruits and vegetables are more susceptible to all mycotoxin and neurotoxin producing pathogens. If so, we will have learned for example that
GM fruits and vegetables cause obesity.


Self-Defense: For people unwilling to wait until all the i's are dotted and all the t's are crossed.

The Top-10 MYCO-Toxic Foods
Dietary Strategies to Counteract the Effects of Mycotoxins





2: Yang K, Shi H, Qi R, Sun S, Tang Y, Zhang B, Wang C. Links
Free Full Text Hsp90 Regulates Activation of IRF-3 and TBK-1 Stabilization in Sendai Virus-infected Cells.
Mol Biol Cell. 2006 Jan 4; [Epub ahead of print]
PMID: 16394098 [PubMed - as supplied by publisher]


This article is about the immune responses phosphorylation of IRF-3 and TBK-1, intracellular signal molecules, in response to laboratory controlled sendai virus infection. It focuses on the ability of IRF-3 to control dsRNA regulation. Nothing at all about obesity.



The immune system in general is involved in multisystem disease processes that lead to obesity, sometimes by mucking up metabolism. There are many paths to the same place, but IRF3 specifically is involved in metabolism regulation; it causes inflammation, which in turn contributes to causing obesity. This article looks at one way IRF3 gets activated on exposure to viruses: "Our study uncovers an essential role of Hsp90 in the virus-induced activation of IRF3."

Here are a few other articles that mention IRF3. They might help you to understand the very complicated links between viruses, IRF3, inflammation and obesity, and the many different ways IRF3 can be activated:





Obesity, diabetes, and cardiovascular disease are the leading causes of morbidity and mortality in industrialized societies. The common thread that links these disorders is dysregulation of lipid metabolism. With the discovery of nuclear receptors that are activated by lipids, a new paradigm has emerged for the transcriptional regulation of metabolic pathways. Included in this group of receptors are the peroxisome proliferator-activated receptors (PPARa, -g, and -d) and the liver X receptors (LXRa and -b). ...PPAR and LXR Mediate Oxidized Lipid Signaling in Macrophages. ...LXRs Link Metabolic and Immune Functions in Macrophages. ...These observations identify the LXR pathway as a common regulator of lipid metabolic and immune functions in macrophages and suggest that LXR ligands may have utility in the treatment of inflammatory diseases. ...Dissection of the TLR3/4 signaling pathway revealed that inhibition of LXR is mediated by the viral response transcription factor IRF3.

Lipid Signaling Pathways in Physiology and Disease

***

An effective immune system requires rapid and appropriate activation of inflammatory mechanisms but equally rapid and effective resolution of the inflammatory state. A review of the canonical host response to gram-negative bacteria, the lipopolysaccharide-Toll-like receptor 4 signaling cascade, highlights the induction of repressors that act at each step of the activation process. These inflammation suppressor genes are characterized by their induction in response to pathogen, typically late in the macrophage activation program, and include an expanding class of dominant-negative proteins derived from alternate splicing of common signaling components. Despite the expanse of anti-inflammatory mechanisms available to an activated macrophage, the frailty of this system is apparent in the large numbers of genes implicated in chronic inflammatory diseases. This apparent lack of redundancy between inflammation suppressor genes is discussed with regard to evolutionary benefits in generating a heterogeneous population of immune cells and consequential robustness in defense against new and evolving pathogens.

Inflammation suppressor genes: please switch out all the lights. J Leukoc Biol. 2005 Jul;78(1):9-13. Wells CA, Ravasi T, Hume DA. Griffith University, Queensland, Australia. PMID: 15774547

***

Mammalian cells respond to virus infections by eliciting both innate and adaptive immune responses. One of the most effective innate antiviral responses is the production of alpha/beta interferon and the subsequent induction of interferon-stimulated genes (ISGs), whose products collectively limit virus replication and spread. Following viral infection, interferon is produced in a biphasic fashion that involves a number of transcription factors, including the interferon regulatory factors (IRFs) 1, 3, 7, and 9. In addition, virus infection has been shown to directly induce ISGs in the absence of prior interferon production through the activation of IRF3. This process is believed to require virus replication and results in IRF3 hyperphosphorylation, nuclear localization, and proteasome-mediated degradation. Previously, we and others demonstrated that herpes simplex virus type 1 (HSV-1) induces ISGs and an antiviral response in fibroblasts in the absence of both interferon production and virus replication. In this report, we show that the entry of enveloped virus particles from diverse virus families elicits a similar innate response. This process requires IRF3, but not IRF1, IRF7, or IRF9. Following virus replication, the large DNA viruses HSV-1 and vaccinia virus effectively inhibit ISG mRNA accumulation, whereas the small RNA viruses Newcastle disease virus, Sendai virus, and vesicular stomatitis virus do not. In addition, we found that IRF3 hyperphosphorylation and degradation do not correlate with ISG and antiviral state induction but instead serve as a hallmark of productive virus replication, particularly following a high-multiplicity infection. Collectively, these data suggest that virus entry triggers an innate antiviral response mediated by IRF3 and that subsequent virus replication results in posttranslational modification of IRF3, such as hyperphosphorylation, depending on the nature of the incoming virus.

Innate cellular response to virus particle entry requires IRF3 but not virus replication. J Virol. 2004 Feb;78(4):1706-17. Collins SE, Noyce RS, Mossman KL. Department of Pathology and Molecular Medicine, McMaster University, Hamilton, Ontario, Canada L8N 3Z5. PMID: 14747536
Full Text

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Chen and his colleagues were seeking a regulatory molecule that would provide a missing link in the activation of two important triggers of the innate immune system -- NF-eB and IRF3. Somehow, these molecules are activated in response to a receptor molecule, called RIG-I, which detects viral genetic material. RIG-I binds to the RNA of viruses such as the influenza virus, hepatitis C virus, West Nile virus and SARS virus. ...The researchers knew the molecule they were seeking was present in a biochemical pathway somewhere between RIG-I and other "downstream" regulatory molecules. They initiated a search for this missing molecule by searching for proteins in the cell that contain a characteristic molecular domain, called a CARD domain, which mediates interactions between different regulatory proteins. Their search yielded a protein, which they called MAVS for mitochondrial antiviral signaling. ...Their experiments revealed that MAVS activated NF-eB and IRF3 in cell cultures.

Cellular power plants also fend off viruses

***

IKK-i(epsilon) overexpression promotes dimerization and nuclear translocation of interferon regulatory factor 3 (IRF3), induces activation of the DNA-binding protein C/EBPdelta and enhances proinflammatory gene induction by transforming growth factor-beta (TGF-beta).

Meeting on the biology and pathology of NF-kappaB

***

Also see: Mitofusin-2 determines mitochondrial network architecture and mitochondrial metabolism. A novel regulatory mechanism altered in obesity.
Full Text

Cell-line-induced mutation of the rotavirus genome alters expression of an IRF3-interacting protein.
Full Text







4: Gern JE, Brooks GD, Meyer P, Chang A, Shen K, Evans MD, Tisler C, Dasilva D, Roberg KA, Mikus LD, Rosenthal LA, Kirk CJ, Shult PA, Bhattacharya A, Li Z, Gangnon R, Lemanske RF Jr. Links
Abstract Bidirectional interactions between viral respiratory illnesses and cytokine responses in the first year of life.
J Allergy Clin Immunol. 2006 Jan;117(1):72-8. Epub 2005 Nov 28.
PMID: 16387587 [PubMed - in process]


This article is about the development of allergies as a response to cytokines (cellular signal molecules of the immune system) as a result of early life repiratory infections. Nothing mentioned in the journal article in reference to obesity or viral linked obesity.



Viruses cause immune responses that involve inflammation, which involve cytokines. Some allergies develop in response to cytokines and some cause a cytokine response - the article basically says it's a two-way street, and potentially part of a larger cascade.

Elevated levels of pro-inflammatory cytokines cause deficiencies in the melanocyte-stimulating hormone called MSH - and refractory symptoms of MSH deficiency include obesity.



[0048] We have seen that deficiencies in MSH are commonly seen in patients with elevated levels of pro-inflammatory cytokines associated with exposure to environmental sources of biotoxin production, including indoor toxin forming fungi leading to SBS. The pro-opiomelanocortoid pathway (POMC) generates MSH in the hypothalamus. Leptin is an agonist of cytokine receptors that initiate activity of the POMC. Serum leptin can be measured looking for evidence of reduced receptor activity for the leptin agonist, and thus an elevated level of leptin is a marker of impaired MSH production. The inability of the POMC pathway to make MSH is marked by refractory symptoms, such as obesity and leptin resistance.

United States Patent Application: 0030219400
Sorry, there's no direct link. Go to the US Patent Office website, and search under applications for #0030219400, or "Methods for treating or inhibiting neurotoxin-mediated syndromes"







11: Morrison TE, Whitmore AC, Shabman RS, Lidbury BA, Mahalingam S, Heise MT. Related Articles, Links
Abstract Characterization of ross river virus tropism and virus-induced inflammation in a mouse model of viral arthritis and myositis.
J Virol. 2006 Jan;80(2):737-49.
PMID: 16378976 [PubMed - in process]


This article is about the possible link between viruses and myositis (a swelling of muscles at the joints) and arthritis (a swelling of the joints due to rubbing or wear of cartilage, among other causes). No mention of obesity or viral linked obesity.



This research shows that viruses can cause myositis and arthritis by causing inflammation in the infected tissues: "...histological analyses demonstrated that RRV infection resulted in severe inflammation of these tissues." Other research shows that physical trauma like rubbing only causes arthritis or myositis when infection already is present. These researchers say, "...we found that the primary targets of RRV infection are bone, joint, and skeletal muscle tissues," and "Characterization of the inflammatory infiltrate within the skeletal muscle tissue identified inflammatory macrophages, NK cells, and CD4+ and CD8+ T lymphocytes."

Again, as explained above, the disease process involves inflammation and cytokines implicated in a larger, longer disease process that can cause obesity. Here is an article from Arthritis Research and Therapy that might help explain some of the connections:



...both IL-2 and IL-15 act as chemoattractants for T cells. The two cytokines stimulate the proliferation of NK cells and can synergize with IL-12 to facilitate their synthesis of IFN-γ and TNF-α [31]. Both cytokines induce the proliferation and immunoglobulin synthesis by human B cells stimulated with anti-IgM or CD40 ligand [32]. ...mice made JAK3-deficient by homologous recombination manifest an absence of NK cells and abnormalities of T and B cells but do not have disorders in nonimmunological systems [46]. ...our emerging understanding of the IL-15/ IL-15R system, including the definition of the actions that this cytokine manifests – both those that are shared with IL-2 and those that are distinct – is opening new possibilities for the development of more rational immune interventions directed toward IL-15 and IL-15 receptors that may be of value in the treatment of cancer, the prevention of allograft rejection, the therapy of diseases associated with the retrovirus HTLV-I, and the treatment of autoimmune diseases such as RA.

The contrasting roles of IL-2 and IL-15 in the life and death of lymphocytes: implications for the immunotherapy of rheumatological diseases







17: Haller O, Kochs G, Weber F. Related Articles, Links
Abstract The interferon response circuit: Induction and suppression by pathogenic viruses.
Virology. 2006 Jan 5;344(1):119-30.
PMID: 16364743 [PubMed - in process]


This article is about the role of inteferons (cellular signal molecules specific for certain cells) and their ability to destabilize viral molecules. No mention of obesity or viral linked obesity.



Again, this article came up on a search for "induced obesity" because the interferon response circuit is part of the immune system - and is involved in multisystem disease processes and cascades leading to obesity.

The research reported here looks at how one part of the immune system works - and why it doesn't work - to fight viruses and block viral-related disease cascades. As the researchers say, "Viruses, ...have evolved multiple strategies to counter the IFN system which would otherwise stop virus growth early in infection." And again, the focus is on inflammation and cytokines, both implicated in larger disease cascades that can lead to obesity.

This kind of research is geared towards developing vaccines to prevent chronic disease like obesity. Here is an earlier article that outlines the problem a bit more clearly:



Viruses need to multiply extensively in the infected host in order to ensure transmission to new hosts and survival as a population. This is a formidable task, given the powerful innate and adaptive immune responses of the host. In particular, the interferon (IFN) system plays an important role in limiting virus spread at an early stage of infection. It has become increasingly clear that viruses have evolved multiple strategies to escape the IFN system. They either inhibit IFN synthesis, bind and inactivate secreted IFN molecules, block IFN-activated signaling, or disturb the action of IFN-induced antiviral proteins. The molecular mechanisms involved range from a broad shut-off of the host cell metabolism to fine-tuned elimination of key components of the IFN system. Type I (alpha/beta) IFNs are produced in direct response to virus infection and double-stranded RNA (dsRNA) molecules that are sensed as a danger signal by infected cells. IFNs induce the expression of a number of antiviral proteins, some of which are again activated by dsRNA. Therefore, many viruses produce dsRNA-binding proteins to sequester the danger signal or express virulence genes that target specific components of the IFN system, such as members of the IFN regulatory factor (IRF) family or components of the JAK-STAT signaling pathway. Finally, some viruses have adopted means to directly suppress the very antiviral effector proteins of the IFN-induced antiviral state directed against them. Evidently, viruses and their host's innate immune responses have coevolved, leading to a subtle balance between virus-promoting and virus-inhibiting factors. A better understanding of virus-host interactions is now emerging with great implications for vaccine development and drug design.

Inverse interference: how viruses fight the interferon system. Viral Immunol. 2004;17(4):498-515. Weber F, Kochs G, Haller O. Abteilung Virologie, Institut fur Medizinische Mikrobiologie und Hygiene, Universitat Freiburg, Freiburg, Germany. PMID: 15671747





So, basically, your list is a wash.


Not at all. Quite illuminating, IMO.



I went through and picked a few I thought would be the most interesting reads for me, personally.


Good choices.




If you'd be so kind, could you show me which ones you feel have anything whatsoever to do with obesity in any way?


Done. And I hope it helps. But pulling this stuff together and writing simple explanations is time-consuming hard work. So when I say, "Done," I mean it. I have other interests. Honest. You have to do your own research now.



If you're really interested in the very many pathogens in our food, air and water that can cause obesity, and how all the different factors work together - here are a few search terms that will help:
Obesity Pathogenesis Brown Fat/metabolism Membrane Transport Proteins/biosynthesis Energy Metabolism/physiology Fatty Acids, Nonesterified/blood Hypothalamus/metabolism Hypothalamus/physiopathology Neuropeptides/metabolism Neuropeptides/physiology Obesity/physiopathology Mycotoxins/pathogenesis Neurotoxins/pathogenesis


Enjoy.





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