Obesity: Why are we getting fat? :epizza:

[Michaelangelica]

A new perspective about the infectious aetiology of obesity would stimulate research to assess the contribution of infectious agents to obesity and possibly to prevent or treat obesity of infectious origin.

A recently published review article sets out to do just that (Infectobesity: obesity of infectious origin. Adv Food Nutr Res. 2007 52: 61-102)

 

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The first obesity-promoting pathogen to be reported was canine distemper virus, a paramyxovirus which infects dogs. . .

. . .

In 1983, Rous-associated virus-7 (RAV-7) was the second pathogen reported to cause obesity. RAV-7 is an avian retrovirus Retroviruses found in domesticated poultry (Rous-associated virus type 7 induces a syndrome in chickens characterized by stunting and obesity. Infect Immun. 1983 39: 410-422). In this case, a decrease in thyroid hormone levels is the major metabolic change that may explain the obesity observed.

 

Chlamydia pneumoniae is the first bacterium reported to be associated with increased body mass index (BMI) in humans.

A number of epidemiological studies have linked infection with this organism to increased weight, although other studies have failed to find any connection. Unlike the organisms previously mentioned, experimental inoculation of animals with this organism to study the effect on body weight has not been reported, and so the link remains somewhat uncertain.

Scrapie is a neurodegenerative prion disease of sheep and goats.

Much of the work with scrapie has been performed using mice as a model, and scrapie has been reported to cause obesity in mice.

Unlike other biological properties of scrapie, this effect is not dependent on the strain involved, although it is dependent on the route of inoculation.

Scrapie-induced obesity is related to changes in the central nervous system (CNS) and neuroendocrine dysfunction in infected mice. Although a number of human prion diseases are known, the relevance of these findings in rodents to obesity in humans has not been established.

Borna disease virus (BDV) is an enveloped, nonsegmented, negative-stranded RNA virus belonging to the Mononegavirales. Infection with BDV causes psychological as well as physical symptoms.

BDV can cause obesity in experimentally infected rats, although only certain strains of the virus seem to do this. In this case, weight gain may be due to inflammatory lesions due to virus antigen expression in brain, especially in the hypothalamus, which is known to regulate body weight and food intake.

Finally, four strains of adenovirus have been reported to be adipogenic pathogens. Avian adenovirus SMAM-1 causes fat deposition (adiposity) in chickens, but also shows a serological association with human obesity (Association of adenovirus infection with human obesity. Obes Res. 1997 5: 464-9).

 

This was the first virus to be linked with human obesity. It has been suggested that SMAM-1 infection could impair normal liver function, causing fatty liver and decreasing cholesterol and triglyceride levels in the blood. Subsequently, adenovirus types 5, 36 and 37 have also been shown cause obesity in animals.

 

Of these, Ad-36 is the best studied. Sero-epidemiological studies show association between Ad-36 antibodies and human obesity, although the exact mechanism of adipogenic action in vivo remains unknown. Of the 50 known serotypes of human adenovirus, only these three seem to cause obesity.

Infectobesity: the bugs that make you fat « MicrobiologyBytes

 

Despite all this research we are focusing only on food

Why?

Body of evidence

Article from: Herald-Sun

ditorialune 22, 2007 12:00am

 

AT first glance obesity might seem an odd subject for an in-depth review by Auditor-General Des Pearson.

 

But the depressing statistics in Mr Pearson's report cannot fail to have a massive impact on Victoria's economy and government health spending for decades to come.

 

Too many Victorians are too fat and the health implications are devastating.

 

Mr Pearson revealed a 77 per cent increase in diabetes cases from 2001 to 2006 and he warned the annual health cost of diabetes would exceed $1 billion by 2015.

 

He predicted the rate of obesity in children would be the same as adults within 30 years - about 60 per cent.

 

The Auditor-General says these statistics show that taxpayer-funded health campaigns are failing to stem the epidemic of obesity, particularly in poorer areas.

 

No one suggests this is an easy problem to solve.

 

Health minister Bronwyn Pike correctly stated that the government should not become the "food police".

 

But a greater effort must be put into innovative public education campaigns, particularly targeted at the young.

 

Without that greater effort Victorian taxpayers will end up the biggest losers

.

Body of evidence | Herald Sun

[Michaelangelica]

Gene Deficiency Is A Protective Barrier To Obesity

 

Science Daily —

A search for the molecular clues of longevity has taken Mayo Clinic researchers down another path that could explain why some people who consume excessive calories don't gain weight.

 

The study, which was done in laboratory mouse models, points to the absence of a gene called CD38. When absent, the gene prevented mice on high-fat diets from gaining weight, but when present, the mice became obese.

 

"Obesity is a complex problem compounded by multiple factors, one of which is our genes

ScienceDaily: Gene Deficiency Is A Protective Barrier To Obesity

[charles brough]

You are well informed on the subject of gaining weight. How about telling me how I can gain weight. I am about 10 lb. underweight and totally unable to gain it back. . . . !

 

charles, HOME PAGE

[palmtreepathos]

Some one told me "if you drink a beer a day you will gain 10 pounds in a couple weeks" so I tried it. At the end of the first week I noticed that the happy little buzz that helped me clean house after work was no longer there. At the end of 2 weeks every time I got thirsty I wanted a beer. Then I found myself daydreaming about going to get a beer while I was working. I cleaned all wine and beer from the fridge that night! DO NOT use this method! :doh: B)

[Michaelangelica]

Some one told me "if you drink a beer a day you will gain 10 pounds in a couple weeks"

At that rate Australians would have taken over all of the planet!

 

I guess this is nothing new to those that have been following this thread; but it is interesting how scientific knowledge slowly percolates though society

As a Doc friend said "It takes 50 years for a good idea to be accepted by medicine and 100 years for a bad idea to be thrown out"

 

Gut microbes may make you fat

News in Science - Gut microbes may make you fat - 21/12/2006

Gut bugs may have lived in deep sea

News in Science - Gut bugs may have lived in deep sea - 03/07/2007

 

This is just for fun

Fart-free beans

News in Science - Fart-free beans - 26/04/2006

[maikeru]

Michaelangelica, very good links on gut microbes. I've always wondered if gut microbes might play a role in obesity, and I know this is stepping out on thin ice--but I think they do. Just as important in my mind, I think the food we eat, kinds and quantity, influences the composition and health of gut microbes, and in turn, influences our digestion and metabolism. The types of foods we eat and how they influence our gut ecology is fairly well known in nutrition and medicine, for you'll always hear doctors recommending to some to eat yoghurt, fibery foods, etc. Yoghurt populates the digestive system with lactobacillus and other friendly bacteria. Many fruits and vegetables, for example, contain chemicals which show antimicrobial properties to some microbes and pro-microbial properties for others. Even common chemicals like tannins in fruits and vegetables are metabolised and changed by microbes and gut juices (enzymes, acid, etc.), conjugating some molecules and breaking down others. Some of these chemicals are absorbed, others not at all.

 

It is a complex process, and probably one which we need to understand better to understand why food and health are intimately intertwined.

[Monomer]

Gut microbes may make you fat

News in Science - Gut microbes may make you fat - 21/12/2006

 

That's an interesting article because Bacteroides aren't generally seen as a desirable bacteria to have residing in your gut. There has been a lot of research on probiotics and where I work we're looking at diets that increase lactobacilli and bifidobacteria populations. So it will be interesting to see the implications of an increased number of bacteroides; you might be lean, but what about your overall gut health...?

 

 

Bacteroides thetaiotaomicron, for example -- the most populous member of the bacterial community -- produces 240 carbohydrate-busting enzymes that enable it to break down a massive range of plant fibers. Humans, by comparison, have a much more limited toolbox, with fewer than 100 of these enzymes. This ''microbial nation," Gordon explained, allows humans to digest food that evolution hasn't enabled them to digest on their own.

 

'Gut bugs' studied as a cause of obesity - The Boston Globe

[Monomer]

The ever increasing variety of fattening food...

 

Junk Food Blog: Jimmy Dean Chocolate Chip Pancakes & Sausage on a Stick

[Michaelangelica]

The ever increasing variety of fattening food...

 

Junk Food Blog: Jimmy Dean Chocolate Chip Pancakes & Sausage on a Stick

"so just nukem and pukem."

 

?

The Ancient Romans would have been proud.

[Michaelangelica]

Health Report - 9July2007 - The obesity epidemic

Insulin and leptin in obsity

 

9 July 2007

The obesity epidemic

 

Listen Now - 09072007 |Download Audio - 09072007

 

A researcher in the United States claims that the reason for the obesity epidemic is more than just the calories we eat and the lack of exercise. It's a substance that food manufacturers are widely using.

Robert Lustig: That's right, it's produced by fat cells, it circulates in the bloodstream, binds to specific receptors in the hypothalamus, the area of the brain that controls energy balance and it's supposed to turn eating off. In addition it also raises the tone of an area of your brain called the sympathetic nervous system which is designed to actually help you burn energy. So by reducing food intake and by increasing the burning of energy you're supposed to stay in balance -- but clearly these kids are not in balance.

 

So the question is, could insulin actually be interfering with that leptin signal, and that's what we've ultimately shown by actually suppressing insulin with a drug.

EgS

Norman Swan: Dr Robert Lustig who's Professor of Pediatric Endocrinology at the University of California, San Francisco. And you're listening to a Health Report special here on ABC Radio National on how food manufacturers by adding fructose to our foods, either from corn syrup as in the United States or added sucrose as in Australia, may actually be making the obesity epidemic even worse, starting with damage to our liver cells, the hepatocytes.

So we see these children with brain tumours who can't see their leptin and we asked the question -- could we somehow influence this disastrous feedback cycle?

What we did is we gave a drug called Octreotide and we knocked down their insulin levels with this medicine and all of a sudden, not only did these kids stop eating, they started exercising spontaneously, they just did it. Two kids started lifting weights at home, one kid became a competitive swimmer, one kid became a manager of his high school basketball team, running around collecting all the basket balls.

 

Robert Lustig: Exactly, in fact exercise is the best treatment. The question is why does exercise work in obesity? Because it burns calories? That's ridiculous. Twenty minutes of jogging is one chocolate chip cookie, I mean you can't do it. One Big Mac requires three hours of vigorous exercise to work that off, that's not the reason that exercise is important, exercise is important for three reasons exclusive of the fact that it burns calories.

And the answer is very simple -- it's called fructose, because fructose is really not a carbohydrate. If you look at the metabolism, the liver metabolism of fructose it is just like a fat, it doesn't stimulate insulin, just like fat. It causes all this de novo lipogenesis.

Nutritional Examination Survey in America which actually shows that the most obese hypertensive kids are making more uric acid and have an increased percentage of their calories coming from fructose.

Robert Lustig: The first thing it does is it increases the phosphate depletion of the hepatocyte which ultimately causes an increase in uric acid. Uric acid is an inhibitor of nitric oxide, nitric oxide is your naturally occurring blood pressure lowerer. And so fructose is famous for causing hypertension.

[Monomer]

I read an article which suggests that obesity may be spread from person to person:

 

Since diverse phenomena can spread within social networks, we conducted a study to determine whether obesity might also spread from person to person, possibly contributing to the epidemic, and if so, how the spread might occur.

 

We evaluated a network of 12,067 people who underwent repeated measurements over a period of 32 years.

 

Ego: The person whose behavior is being analyzed.

Alter: A person connected to the ego who may influence the behavior of the ego.

 

If an ego stated that an alter was his or her friend, the ego’s chances of becoming obese appeared to increase by 57% (95% confidence interval

[CI], 6 to 123) if the alter became obese. However, the type of friendship appeared to be important. Between mutual friends, the ego’s risk of obesity increased by 171% (95% CI, 59 to 326) if an alter became obese. In contrast, there was no statistically meaningful relationship when the

friendship was perceived by the alter but not the ego (P = 0.70). Thus, influence in friendship ties appeared to be directional.

 

 

http://jhfowler.ucsd.edu/spread_of_obesity.pdf

[Michaelangelica]

I read an article which suggests that obesity may be spread from person to person]

The New England journal of medicine has just agreed with you(or are you one of the authors?)

ABSTRACT

 

Background The prevalence of obesity has increased substantially over the past 30 years. We performed a quantitative analysis of the nature and extent of the person-to-person spread of obesity as a possible factor contributing to the obesity epidemic.

. . .

A person's chances of becoming obese increased by 57% (95% confidence interval [CI], 6 to 123) if he or she had a friend who became obese in a given interval.

. . .

If one spouse became obese, the likelihood that the other spouse would become obese increased by 37%

 

I am not sure what this means-

. Whereas increasing social distance appeared to decrease the effect of an alter on an ego, increasing geographic distance did not

.NEJM -- The Spread of Obesity in a Large Social Network over 32 Years

 

So does not this strongly suggest an infective factor -bacteria or virus??

 

 

charles brough

Want to put on weight? Eat lots of fructose- figs, fruit juice etc (Dukes Data Base will give you a list)

Take St. Mary's Thistle extract or just the seed, to stop fructose buggering your liver.

[InfiniteNow]

So does not this strongly suggest an infective factor -bacteria or virus??

While I maintain that an infective factor is possible, I do not believe this study necessarily supports or suggests that notion. They mention that the effect works in reverse, as well. So, if your friend/loved one LOSES weight, you are more likely to lose weight as well.

 

It would be odd for an infective factor to sometimes increase weight, and sometimes decrease it. :doh:

[maikeru]

Health Report - 9July2007 - The obesity epidemic

Insulin and leptin in obsity

 

 

 

EgS

 

I thought the link between fructose and obesity--its possible role as a signal to encourage fat creation and deposition--was a very good point.

 

I've read the same on a few websites, and I had one bookmarked a while back where a doctor went into quite a bit of molecular biology about how fructose, he thought, maybe was a major suspect in the obesity epidemic. The gist of it, as I understand it, is that large amounts of fructose encourage the body to start laying down a lot of fat. This could be evolution's way of helping people and animals stay in touch with the seasons and food availability, telling the body to store extra energy as fat during times of abundance. Fructose is of course found in fruits and some other foods, and when they ripen or are ready to be eaten, that would be a good time to enjoy the fruits of your labour. Using a key chemical like fructose as a signal makes good sense in this case, at least in my mind. But one thing we should note that even though fructose is abundant in fruit, its make up of total sugars in natural foods is usually very small. I'm pretty sure the amount of fructose in an apple or banana would be tiny compared to a soda, which is a concentrated source of fructose and glucose (HFCS). This scarcity and specificity makes it a good signal in natural foods and an overpowering and monstrous one in processed foods. (Also note that I'm not advocating natural, organic, or raw foods here or talking about them specifically as healthier or superior foods. Food is food, so long as it's edible. Whether it's good food or not is another matter.)

 

Another point which I've thought about is that fructose enters the cell's energetics by skipping a step, which would normally require the rearrangement of glucose, the cleavage of ATPs, and other chemical reactions. These actions all have energy costs. A bit of energy is lost in every step of glycolysis. Every step skipped in glycolysis is energy saved...energy spent by your cells to get certain types of chemical energy into more useful forms (ATP, the cell's favorite energy carrier). When your cells can save more, their "energy bank accounts" get bigger. You could put on a bit more weight because of that energy they save and lessened need to draw on reserves. More energy might be saved when larger amounts of sugars and carbohydrates can bypass those energy-consuming steps in glycolysis. If it does indeed act on the cell's genes and alters energy metabolism within cells and across the body, by say encouraging fat cells to lay down more fat and grow, this could be a disaster if not regulated properly.

 

I'll admit this is speculation. Unless I get up to date with my cell biology and biochemistry, do more research reading articles and thinking about the evidence, I can't back it up with much more than what I learned in textbooks and connecting the dots with news stories and websites.

[charles brough]

Maikeru seems to have the physiology down rather well. We not only consume a lot of glucose, but a lot of it is in the form of corn syrup. That is, we are digesting our starches for us in the manufacturing process. That saves us energy and allows more of it to be stored as fat. I notice on food labels that many products list sugar as the second (hence next to the biggest) ingredient. Then lower down, we find corn syrup listed, then high-fructose corn syrup. All that is basically the same sugar except that a little fructose has been added to the glucose. So, sugar is actually the product's main ingredient.

 

However, we should not overlook that the problem of obesity is not new and an abundance of sugar was not the cause in the past. For example, during the Period of Church Decedence in the 14th and 15th Century Europe, obesity was so common among the clergy that the fat monk holding up his glass of wine came to stand for the whole Church. Can we really doubt but what many of the wealthy people of Ancient Rome were obese? When people center their lives around getting material and sensual pleasure, eating becomes an important one. When a society loses its goals, what else is there to seek?

[InfiniteNow]

Can we really doubt but what many of the wealthy people of Ancient Rome were obese? When people center their lives around getting material and sensual pleasure, eating becomes an important one. When a society loses its goals, what else is there to seek?

High quality single-malt scotch. :)

[paigetheoracle]

laziness and diet.. our society is making things to easy for people and our food is getting worse.

 

Of course - It's like that graffitti "My mother made me a homosexual - If I gave her the wool, would she make me one too?' Or the criminal who murdered his parents and whose lawyer asked for leniency because he was an orphan.

 

It's always somebody elses fault that we're the way we are: Criminals, homosexual, fat, black, women etc. Society made me do it or made me the way I am. It could be a reaction to all the pollution in the food. It could be environmental (fat storage reaction gene in preparation for extreme cold conditions). Could this explain why two people from the same background go off in opposite directions - one to become a lawyer, the other a gangster?