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Obesity: Why are we getting fat? :epizza:


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The pop theory of Obesity is that it is caused by eating too much and exercising too little.

While this is no doubt true it oversimplifies the issue.

What I have been trying to show in these many, many, posts is that there are many, many, reasons for obesity

Unless we address them all we will not control the world wide epidemic or intelligently come to grips with the problem.

it is unfair to stigmatize people who may just suffer from a super efficient digestive and/or immune system

 

paigetheoracle one way a human body has of dealing with chemicals that it cannot break down (so many of our new man made 'plasticy' ones that the human organism has never encounted in its evolution) is to wrap them in fat and store them away.

When someone diets they often get sick due to the release of toxins as the fat breaks down.

In some mammals these can lead to all sorts of problems

Seals contaminated with agricultural chemicals live off fat when birthing. The chemicals released in them can then lead to deadly confusion of the mothering instinct.

 

One wonders if this storage of chemicals is also partly responsible for the epidemic of breast cancer. A recent European study found over 400 man made foreign chemicals in mothers milk. They only found 400 because that was all they could afford to analyze and detect!

 

We know chemicals act synergistically but in reality have no way of proving a scientific link between illness and the countless thousands of environmental contaminants. You would think that common sense would be enough, but no, we continue to go on poisoning our planet and our bodies with impunity as if we were supermen. IMHO This costs us more in health costs than the money saved by using the chemicals, let alone the human costs.

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After six weeks, peripheral insulin sensitivity significantly improved in 18 patients who received feces from lean donors compared with those who received an autologous transplant (P<0.05), said Anne Vrieze, MD, of the Academic Medical Center in Amsterdam, and colleagues.

http://natmednews.po...ulin-resistance

 

 

"It is tempting to think that if you wanted to treat human obesity, that you could do fecal transplants with the microbiota from lean individuals," Rawls said. But it may be somewhat premature to proceed, he cautioned — "if we don't understand the rules that govern the establishment and maintenance of those microbial communities in the gut, the effects of other people's transplants could potentially be short-lived or even deleterious." <br style="margin-top: 0px; margin-right: 0px; margin-bottom: 0px; margin-left: 0px; padding-top: 0px; padding-right: 0px; padding-bottom: 0px; padding-left: 0px; "><br style="margin-top: 0px; margin-right: 0px; margin-bottom: 0px; margin-left: 0px; padding-top: 0px; padding-right: 0px; padding-bottom: 0px; padding-left: 0px; ">Read more: Same poop, different gut - The Scientist - Magazine of the Life Sciences http://www.the-scien.../#ixzz157VW1F6B

http://www.the-scien.../display/57795/

 

 

 

 

Gut Microbiota and Its Possible Relationship With Obesity

 

http://mayoclinicpro...t/83/4/460.full

 

the definition

http://www.nejm.org/...200206273462617

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If you were a UK Health Secretary faced with soaring rates of obesity, alcohol misuse, and diet-related diseases, what would you do? Were you to take an evidence-based approach, you might consider minimum pricing per unit of alcohol and restrictions on its availability. You might look at toughening the regulation of how the least healthy foods are marketed to children. You could even demand that manufacturers reformulate their least healthy products to meet minimum nutritional standards. Or you could, if your name was Andrew Lansley, dismiss all of the above and instead invite representatives of McDonald's, PepsiCo, and the drinks giant Diageo among others, to submit their policy suggestions on how best to deal with the UK's public-health crises for a forthcoming governmental white paper.After the initial surprise, it can still take a while for the bizarre reality to sink in—that the companies who have profited the most from the epidemics of obesity and alcohol misuse should now be responsible for setting the agenda on public health simply beggars belief.

http://www.thelancet.com/journals/lancet/article/PIIS0140-6736(10)62150-2/fulltext

 

There's no question that humans have been getting bigger and bigger, and now it seems that animals living near us are coming along for the ride. A new study of 12 distinct populations of eight different mammals -- including feral rats, lab animals and domestic pets -- shows that they, too, have been gaining weight over the last several decades.

. . .Allison pointed out at least three potential contributions to this and the other observations: endocrine disrupting chemicals, pathogens such as a virus, and/or changes in temperature where the animals are kept.

 

There is evidence to support a role for each of these in obesity. The endocrine-disrupting chemical tributyltin, for instance, which is added to marine paints to prevent growth of aquatic life on ship hulls and other places, has been shown to make mice fatter, Allison said.

 

Meanwhile, several types of animals have been shown to gain weight when injected with a virus known as adenovirus-36, indicating that pathogens may play a role in some cases of obesity.

 

As for temperature, Allison pointed out that hog farmers know that it's easier to fatten pigs if you keep the temperature just right:

http://news.discovery.com/animals/fat-pets-obesity-weight.html

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Back in the 1970-80's jogging and fitness were the craze. The ideal of fitness became the fad and most people were trim. The fashions, especially in the summer were very skimpy such that people felt the need to be trim, since so many people were. This was also before the personal computer which didn't become wide spread until the mid-1990's, such that there wasn't the option to sit in front of the computer surfing the web.

 

I am not sure of the exact date, but some PC irrationality appeared which tried to protect the minority of over weight people from feeling peer pressure. Science went along with their cue and came out with empirical studies that showed thin was not always optimum, and that some people were meant to be heavier. Not much later the trend toward being overweight started to emerge. Does this historical data mean anything?

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http://www.scienceda...01122172002.htm

Excess Fructose May Play Role in Diabetes, Obesity and Other Health Conditions

ScienceDaily (Nov. 23, 2010) — More and more people have become aware of the dangers of excessive fructose in diet. A new review on fructose in an upcoming issue of the Journal of the American Society of Nephrology (JASN) indicates just how dangerous this simple sugar may be.

</h1>http://www.scienceda...00707212127.htm

Inactivity 'No Contributor' to Childhood Obesity Epidemic, New Report Suggests

ScienceDaily (July 8, 2010) — A new report from the EarlyBird Diabetes Study suggests that physical activity has little if any role to play in the obesity epidemic among children.

http://www.scienceda...00520112347.htm

Reducing Niacin Intake Can Prevent Obesity, Study Suggests

ScienceDaily (May 21, 2010) — Dietary factors have long been known to play a major role in the development of obesity. The global increasing prevalence of obesity suggests that there should be some common changes in diet worldwide. In fact, a significant, yet, often neglected worldwide change in dietary factors in the past few decades is the food fortification-induced marked increase in the content of niacin. However, the effect of long-term exposure to excess niacin on human health remains to be unclear.

 

 

Stress Hormone, Depression Trigger Obesity in Girls, Study Finds

ScienceDaily (Feb. 24, 2010) — Depression raises stress hormone levels in adolescent boys and girls but may lead to obesity only in girls, according to researchers. Early treatment of depression could help reduce stress and control obesity -- a major health issue.

 

http://www.scienceda...00223154342.htm

Obesity Epidemic Taking Root in Africa

ScienceDaily (Jan. 1, 2010) — The urban poor in sub-Saharan Africa are the latest victims of the obesity epidemic. Researchers writing in the open access journal BMC Public Health claim that overweight and obesity are on the increase among this group

 

.http://www.scienceda...91214201003.htm

Antibiotic growth promotants and pig performance

Considering data collected from 1978 to 1985, Zimmerman (1986) reported an average improvement in daily gain of 15 percent in nursery pigs and 3.6 percent in finishing pigs when antibiotics were included in the feed

 

. . .

Zinc and copper. Both zinc and copper have antibacterial properties and have been shown to improve performance of pigs

. . .

Plasma protein and egg yolk specific antibody. Spray-dried plasma protein is typically included in young pig diets because of its known stimulatory effect on feed intake and, subsequently, increased growth.

 

</h3>http://www.thepoultrysite.com/articles/1564/probiotics-in-poultry-and-pig-nutrition-basics-and-benefits

<h3 style="font-weight: bold; font-family: arial, verdana, sans-serif; font-size: medium; color: rgb(86, 43, 0); text-shadow: rgb(170, 170, 170) 1px 1px 3px; line-height: 18px; ">Effects of Probiotics on Poultry Performance

Addition of probiotics has shown beneficial effects on growth performance of poultry. In broilers supplementation of a control diet with probiotics based on Bacillus cereus orSaccharomyces boulardii improved feed conversion rate by 12 and 11 per cent, respectively (Gil de los Santos et al., 2005). Moreover, after 47 days, average live weight was significantly higher (16 and 7 per cent, respectively) in birds fed the two types of probiotics in comparison to the control group. The effect on growth performance of the same probiotic preparation was investigated in a study with 200 day-old broilers (Mohnl et al., 2006). Administration of the multi-strain probiotic (PoultryStar) in the drinking water significantly improved live weight (4 per cent) and daily weight gain (4 per cent) (Figure 2) and numerically reduced mortality rate (48 per cent) in comparison with a negative control.

 

Figure 2. Effect of probiotic preparation PoultryStar on performance parameters in broilers

a.b Significant difference between treatments (P<0.05)

 

 

 

 

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. . .

The endocannabinoid system mediates signaling in the brain and peripheral tissues involved in the regulation of energy balance, is highly active in obese patients, and represents a strong candidate pathway to examine for genetic association with body mass index (BMI).

...

The set of rare variants in the FAAH promoter associated with BMI is also associated with increased level of FAAH substrate anandamide, further implicating a functional role in obesity.

http://genomebiology.com/2010/11/11/R118/abstract

Genome Biology 2010, 11:R118 doi:10.1186/gb-2010-11-11-r118

 

Published: 30 November 2010

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Animals are getting fatter, too

 

Is something in the environment making everyone -- animals and humans -- gain weight?

 

http://www.the-scien.../display/57821/

>Read more: Animals are getting fatter, too - The Scientist - Magazine of the Life Sciences http://www.the-scien.../#ixzz16rTvFbxG

 

. . .scientists, including many at UAB, are beginning to look at alternative reasons for obesity beyond the usual suspects of increases in food intake, provoked mainly by availability, and decreases in activity level, provoked mainly by labor-saving devices. Here are several candidates for the lineup:

 

  • Light. Studies have shown that subtle changes in the amount of time spent in light or dark environments changes eating habits. Allison wonders if increased light pollution in our industrial society may play a role. <br style="clear: both; ">
  • Viruses. Infection with adenovirus-36 is associated with obesity, and the presence of antibodies to AD36 correlates to obesity in humans. Could AD36 or other infectious agents be contributing to obesity in populations? <br style="clear: both; ">
  • Epigenetics. Genetic modifications brought about by any number of environmental cues such as stress, resource availability, release from predation or climate change.

The bottom line, say the authors, is that obesity is a problem that most likely has many causes and will need many solutions.

http://www.physorg.c...us-culprit.html
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It's simple. When leaders demonstrate greed and economic gluttony, followers unknowingly emulate this in the most easily available way: eating.

 

There are other problems with the emulation of the gluttonous rich by the poor, besides weight related health issues: credit issues, economic meltdown, worldwide depression increase, etc.

 

The epidemic is a symptom of having leaders who lack the discipline to regulate their own gluttony, causing a spiral of misery which weakens the whole world physically, economically, socially, and mentally. The only way out of this is to put those with self discipline in charge: those who will not allow gluttony (economic or otherwise), but still allow joyful freedoms to be experienced IN MODERATION.

 

The problem isn't a virus, although it is viral in a memetic sense.... and one of the hard to deal with issues is that those who are sick cannot be allowed to have an influence on decision making (in a democratic society), or they will perpetuate their sickness by electing the infected (or those who cater to the infected) to power.

 

It is a tremendous problem rooted in the freedoms that the infected demand, but should not be granted. They need external moderation, yet will not willingly accept it, and will continue to erode and destroy the fabric of society if left unchecked.

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I still like to go back to an energy balance. If food energy input = 0 it is impossible to gain get fat or become obese, since that would violate the conservation of energy. As we add energy input, if one burns as much energy as they added, the net energy = 0, making it impossible to gain fat or become obese without violating conservation of energy. All the viral and genetic arguments are moot, when the energy balance =0. These arguments are all contingent on an energy imbalance. If we factor that out an energy balance and/or place it low on the scale of explanations, all the rest appear more than they are.

 

I used a little historical perspective, when thin was in. All the same chemical and biological obese arguments should still have applied back then, unless the DNA changed overnight and the magic virus suddenly appeared out of nowhere. The difference then and now was the energy balance was more favorable then, due to the extra activity and dieting resulting from the social push to look fit. People did their own energy balance. If you didn't like to exercise, you would diet. If you liked to eat, you ran an extra mile or two. The goal was to look good. There was no excuse, just lazy or compulsive. This was more of a masculine approach.

 

Today we have personal computers, internet, cell phones and video games. These can make one feel tired without burning many calories. It is more of a mental and emotional activity/fatigue which is different than physical fatigue which will better alter the energy balance. One needs to se large muscles and not just finger muscles. Back then one could not use the modern excuses, since most of these had not been make up yet. But today we have so many excuses, one can pick and choose and forget about the simple energy balance which can be violated with genetic perpetual motion. It appears to be more feminine.

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I still like to go back to an energy balance. If food energy input = 0 it is impossible to gain get fat or become obese, since that would violate the conservation of energy. As we add energy input, if one burns as much energy as they added, the net energy = 0, making it impossible to gain fat or become obese without violating conservation of energy. All the viral and genetic arguments are moot, when the energy balance =0. These arguments are all contingent on an energy imbalance. If we factor that out an energy balance and/or place it low on the scale of explanations, all the rest appear more than they are.

 

I used a little historical perspective, when thin was in. All the same chemical and biological obese arguments should still have applied back then, unless the DNA changed overnight and the magic virus suddenly appeared out of nowhere. The difference then and now was the energy balance was more favorable then, due to the extra activity and dieting resulting from the social push to look fit. People did their own energy balance. If you didn't like to exercise, you would diet. If you liked to eat, you ran an extra mile or two. The goal was to look good. There was no excuse, just lazy or compulsive. This was more of a masculine approach.

 

Today we have personal computers, internet, cell phones and video games. These can make one feel tired without burning many calories. It is more of a mental and emotional activity/fatigue which is different than physical fatigue which will better alter the energy balance. One needs to se large muscles and not just finger muscles. Back then one could not use the modern excuses, since most of these had not been make up yet. But today we have so many excuses, one can pick and choose and forget about the simple energy balance which can be violated with genetic perpetual motion. It appears to be more feminine.

I agree with you whole heartedly. Although I made the same arguments a while ago in this thread and was told that I was "oversimplifying" and lacked an understanding for the nuances of weight gain and loss.

 

I think that in a lot of ways obesity research has been perverted and people grasp at it for a "not my fault" answer. If obese individuals can tell themselves that there is a genetic, viral, or specific food responsible for their weight gain, then they don't have to feel responsible for their own misery, and also don't have to put in the effort to fix it. As long as they can take some science out of context and make it fit their chosen reality then it makes them feel better. A study may say that XYZ gene has been shown to be related to obesity people can tell themselves that "it's not my fault, I must have that gene and I'm just destined to be fat". When in reality XYZ gene may actually mean that individuals with that gene have a lower BMR and therefore do not need to eat as many Calories to satisfy their daily Calorie needs.

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Functional food targeting the regulation of obesity-induced inflammatory responses and pathologies.

http://docs.google.com/viewer?a=v&q=cache:J_3aUilB8rQJ:downloads.hindawi.com/journals/mi/2010/367838.pdf+Functional+food+targeting+the+regulation+of+obesity-induced+inflammatory+responses+and+pathologies.&hl=en&gl=au&pid=bl&srcid=ADGEESiuCw6MZwpKOyBa7o44yJBUqVxKMyHF8o-jkCjJ8wjstpeMpTcBSSOXhvpSBtktOLezdbVUM9DpmmVsE-mA90e9eYFaymYGTppkdMmGq6-05fD5P_M-hzGYVraI3tWGrV_fOYji&sig=AHIEtbSayfaWQVv-4WoMx6lM_ZBZIP6Npw

Posted:

 

Related ArticlesFunctional food targeting the regulation of obesity-induced inflammatory responses and pathologies.

 

Mediators Inflamm. 2010;2010:367838

 

Authors: Hirai S, Takahashi N, Goto T, Lin S, Uemura T, Yu R, Kawada T

 

Obesity is associated with a low-grade systemic chronic inflammatory state, characterized by the abnormal production of pro- and anti-inflammatory adipocytokines. It has been found that immune cells such as macrophages can infiltrate adipose tissue and are responsible for the majority of inflammatory cytokine production. Obesity-induced inflammation is considered a potential mechanism linking obesity to its related pathologies, such as insulin resistance, cardiovascular diseases, type-2 diabetes, and some immune disorders. Therefore, targeting obesity-related inflammatory components may be a useful strategy to prevent or ameliorate the development of such obesity-related diseases. It has been shown that several food components can modulate inflammatory responses in adipose tissue via various mechanisms, some of which are dependent on peroxisome proliferator-activated receptor gamma (PPARgamma), whereas others are independent on PPARgamma, by attenuating signals of nuclear factor-kappaB (NF-kappaB) and/or c-Jun amino-terminal kinase (JNK). In this review, we introduce the beneficial effects of anti-inflammatory phytochemicals that can help prevent obesity-induced inflammatory responses and pathologies.

 

PMID: 20508825 [PubMed - indexed for MEDLINE]

 

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Hungry Neurons = Hungry Person

 

Starving neurons of the hypothalamus appear to take a two-pronged approach to nutrient shortages: eat themselves in a process called autophagy as a short-term fix, and set off a cascade to make the organism crave more food, . . .

 

Many people who try to diet simply can’t stick with the program, often driven by strong cravings for junk foods high in fat. Previous studies have demonstrated that increased levels of fatty acids floating extracellularly in the hypothalamus, a region of the brain that monitors nutritional status, triggers cravings. But the mechanisms that controlled the levels of these fatty molecules inside brain cells were unknown.

 

Molecular biologist Susmita Kaushik and her colleagues at the Albert Einstein College of Medicine in the Bronx, New York, decided to investigate one variety of hypothalamic neuron, the agouti-related peptide neuron (AgRP), whose production of the AgRP molecule has been linked to increased food intake.

 

By removing nutrients supplies from the neurons in vitro and keeping food from mice, the researchers discovered that starvation activates autophagy—a common process involving the breakdown of a cell’s organelles and proteins. In essence, both in vitro and in the mice, AgRP neurons began to eat themselves, breaking down bits of fat droplets stored within their organelles and cytoplasm.

 

 

http://the-scientist.com/2011/08/02/hungry-neurons-hungry-person/

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Repeated Exposure to Severely Limited Sleep Results in Distinctive and Persistent Physiological Imbalances in Rats

Chronic sleep disruption in laboratory rats leads to increased energy expenditure, connective tissue abnormalities, and increased weights of major organs relative to body weight.

Here we report on expanded findings and the extent to which abnormalities become long-lasting, potentially permanent changes to health status after apparent recuperation from chronic sleep disruption

For example, obesity is considered an adaptation (e.g., [7]) that possesses a distinct survival benefit during starvation [8], [9], but also has numerous medical implications.

 

results from human studies that have pointed to glucose intolerance and insulin insensitivity as consequences of sleep restriction that would promote obesity and pose a risk for type II diabetes

http://www.plosone.o...al.pone.0022987

/////////////////////////////////////////////////////////////////////////////////////////

 

Alter taste buds to curb obesityDEAKIN UNIVERSITY TUESDAY, 16 AUGUST 2011Overconsumption of fatty foods could lead to a decreased sensitivity to fat in foods.<br style="line-height: 1.5em; ">

Image: lisegagne/iStockphoto

Training our taste buds sensitivity to fat is a potential way to reduce overweight and obesity, Deakin University nutrition experts have found.<br style="line-height: 1.5em; "><br style="line-height: 1.5em; ">Associate Professor Russell Keast, Dr Jessica Stewart and PhD student Lisa Newman have found that eating a high fat diet can desensitise a person’s ability to taste fat in foods which may lead to overeating of fatty foods and subsequent weight gain.

 

http://www.scienceal...test+Stories%29

 

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