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  #1   ^
Old Wed, Sep-22-10, 09:42
Unfinished Unfinished is offline
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Default “Obesity: Often An Infectious Disease”

http://perfecthealthdiet.com/

I've been increasingly impressed with what I've been reading on The Perfect Health blog, and today's article has given me much to think about.

Quote:
In the book we attribute obesity mainly to food toxins and malnutrition. Both are well attested as causes of obesity in animals:

The easiest way to induce obesity in animals is to feed them a carb toxin and a fat toxin – e.g. wheat, fructose, or alcohol with polyunsaturated fats or hydrogenated trans-fats.
Obesity in animals can also be induced by nutrient deficiencies, as in the “methionine-choline deficient diet.”
These causes also seem to be active in humans:

Intake of fructose and polyunsaturated fats is strongly associated with obesity in humans.
Famine studies show that those who experience a period of severe malnourishment are more likely to become obese.
However, in general we attribute diseases to three causes: food toxins, malnutrition, and infections. This suggests we should look also for infectious causes of obesity.

Adenoviruses Can Cause Obesity in Humans
The study of “infectoobesity,” or pathogen-induced obesity, got underway with the discovery of four viruses that could induce obesity in animals. These four viruses — canine distemper virus, Rous-associated virus type 7, Borna disease virus, scrapie agent – were not able to infect humans. However, in chickens, mice, sheep, goat, dogs, rats and hamsters, these viruses infect the central nervous system and induce obesity through effects on the brain and nerves. [1,2]

But then an avian adenovirus, SMAM-1, was found that infects humans and induces obesity in chickens. SMAM-1 works by a different mechanism; it acts directly on fat cells. [2]

Subsequently 3 human adenoviruses, AD-36, AD-37, and AD-5, have been found that act directly on human fat cells and are associated with human obesity. [2] A group led by Dr. Nikhil Dhurandhar of Wayne State University in Michigan showed that AD-36 can induce obesity when given to chickens, mice, and marmosets. [1]

AD-36 Can Spread By Contact
In Dr. Dhurandhar’s chicken experiments, the virus spread fairly easily. Chickens that shared a cage with an infected bird showed signs of the virus in their blood within 12 hours, suggesting that the virus can be spread by nose or mouth secretions. [3]

To Get Really Fat, You Need an Adenovirus Infection
A new study [4] has given us new information about the prevalence and effects of AD-36 in humans. The study found that 22% of obese children (that is, children in the top 5 percentiles of BMI), but only 7% of non-obese, have AD-36 antibodies. Moreover, among the obese children, those who were AD-36-antibody-positive were much fatter than the other obese children. It seems the top 0.1% of children in BMI are probably overwhelmingly made up of AD-36-infected children.

Metabolic Benefits?
It may not be all bad news. AD-36 promotes proliferation of fat cells. Thus, while it promotes obesity, it may also help prevent diabetes. By creating a bigger pool of fat cells to help clear excess glucose from the blood, toxicity from hyperglycemia is reduced, at least for a time.

In Dr. Dhurandhar’s experiments, the extra fat cells showed metabolic effects consistent with enhanced glucose clearance. Infected chickens had lower serum cholesterol and lower triglyceride levels. [3] So infected chickens are fatter, but in some respects healthier.

Pathogens May Be The Source of Disease Diversity
Close readers of our book may have noticed that a combination of carb and fat toxins is, we believe, the most common cause of metabolic syndrome, diabetes, and obesity.

Yet there are thin diabetics and obese non-diabetics. How is it that the same cause can produce different diseases?

One thing the adenovirus work is telling us is that the nature of one’s chronic infections may determine how bad diets translate into disease. Toxic and malnourishing diets make disease inevitable, but which disease depends on which pathogens happen to be around to exploit the bad diet and weakened immunity.

Lessons for the Non-Obese
I certainly wouldn’t avoid contact with obese people for fear of contracting AD-36. These pathogens are everywhere and infection is inevitable. Most elderly probably have hundreds of chronic infections.

The key to health is not avoiding germs, but maintaining a powerful immune system that prevents pathogens from causing disease. That means a healthy diet, good nutrition, and immune-enhancing practices like fasting and ketogenic diet days.

Conclusion
It appears that:

It’s possible to become obese from food toxins and malnutrition alone;
Some – it’s not yet clear what fraction – obese people do become obese from food toxins and malnutrition alone;
But to become really obese, or to become obese really young, you need a viral infection to help the obesity along.
In the book, we focus on elimination of food toxins and malnutrition as weight-loss steps. The Perfect Health Diet, controlled to 2,000 calories per day, is a weight loss diet for the obese as well as a healing diet for the metabolic derangements that underly obesity.

What the evidence for adenoviruses in obesity is telling us is that the obese may need to take another dietary step as well: autophagy-promoting steps like fasting. Autophagy is a primary immune mechanism against viruses, so fasting enhances viral immunity.

As always, we recommend that fasts include substantial amounts of coconut oil to help the liver make ketones and relieve the burden on the liver and the risks of glucose deficiency.

References
[1] van Ginneken V et al. “Infectobesity”: viral infections (especially with human adenovirus-36: Ad-36) may be a cause of obesity. Med Hypotheses. 2009 Apr;72(4):383-8. http://pmid.us/19138827.

[2] Atkinson RL. Viruses as an etiology of obesity. Mayo Clin Proc. 2007 Oct;82(10):1192-8. http://pmid.us/17908526.

[3] Dhurandhar NV et al. Transmissibility of adenovirus-induced adiposity in a chicken model. Int J Obes Relat Metab Disord. 2001 Jul;25(7):990-6. http://pmid.us/11443497.

[4] Gabbert C et al. Adenovirus 36 and Obesity in Children and Adolescents. Pediatrics. 2010 Sep 20. [Epub ahead of print] http://pmid.us/20855385. See also http://ucsdnews.ucsd.edu/newsrel/he...alInfection.asp.


Cheryl
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  #2   ^
Old Thu, Sep-23-10, 04:24
Hutchinson's Avatar
Hutchinson Hutchinson is offline
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Adenovirus 36 DNA in Adipose Tissue of Patient with Unusual Visceral Obesity

Intracellular Infections Enhance Interleukin-6 and Plasminogen Activator Inhibitor 1 Production by Cocultivated Human Adipocytes and THP-1 Monocytes
Both these are free full text papers that bring this story up to date.

Don't forget the role of Vitamin D in maintaining immune function (our innate ability to fight infection) and also as an ANTI-INFLAMMATORY agent.
I'm sure everyone is aware obesity is strongly linked with vitamin D insufficiency status.

Everyone who is overweight needs relatively more vitamin D to correct insufficiency than do normal weight individuals.

1000iu/daily per 25lbs is generally required but 25(OH)D testing after 3 months at that level will indicate if it's sufficient for your body. If you have undershot the target of 60ng/ml (sufficient to provide a stored reserve of D3) increase intake by 1000iu/daily extra for each 10ng/ml under 60ng/ml.
(If, but it's very unlikely, you have overshot 80ng/ml then reduce daily intake by 1000iu/d to reduce 25(OH)D 10ng/ml)
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  #3   ^
Old Thu, Sep-23-10, 04:53
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leemack leemack is offline
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Quote:
Originally Posted by Hutchinson
Everyone who is overweight needs relatively more vitamin D to correct insufficiency than do normal weight individuals.

1000iu/daily per 25lbs is generally required but 25(OH)D testing after 3 months at that level will indicate if it's sufficient for your body. If you have undershot the target of 60ng/ml (sufficient to provide a stored reserve of D3) increase intake by 1000iu/daily extra for each 10ng/ml under 60ng/ml.
(If, but it's very unlikely, you have overshot 80ng/ml then reduce daily intake by 1000iu/d to reduce 25(OH)D 10ng/ml)


So are you saying I should be taking 21000iu of d3?

Lee
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  #4   ^
Old Thu, Sep-23-10, 08:26
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rightnow rightnow is offline
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I find this very interesting from a subjective point of view. When I very rapidly gained 200# in my early 20s, it was after 2 years of crazy life. Chronic sleep deprivation, forced sedentary, eating once a day massive carbs just before sleep, immense personal stress on several levels. It was easily a recipe for how to destroy your health. Obesity may have been the outcome but I think malnutrition, and immune system issues, were the underlying problems. I find it very believable that there may be a viral component to severe obesity. (I am coming to suspect there may be a viral component to a lot of stuff we haven't thought of in that way before.)

PJ
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  #5   ^
Old Thu, Sep-23-10, 08:33
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Water Lily Water Lily is offline
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Makes me wonder. When I was 22, I contracted a very severe case of mono.. I wonder if I had some type of secondary virus along with the mono, because directly after the mono subsided, I contracted every little cold and flu that came along, and German measles, too.

After the mono I started on BCP, and started gaining weight and haven't been able to keep it off. I always attributed the weight gain to the hormones in the Pill. Maybe it was a virus?
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  #6   ^
Old Thu, Sep-23-10, 10:12
maile1 maile1 is offline
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Quote:
Originally Posted by Water Lily
Makes me wonder. When I was 22, I contracted a very severe case of mono.. I wonder if I had some type of secondary virus along with the mono, because directly after the mono subsided, I contracted every little cold and flu that came along, and German measles, too.

After the mono I started on BCP, and started gaining weight and haven't been able to keep it off. I always attributed the weight gain to the hormones in the Pill. Maybe it was a virus?


almost everyone who has Hashimoto's thyroiditis tests positive for EBV or has had mono so there could indeed be a link to weight gain and infection.
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  #7   ^
Old Thu, Sep-23-10, 16:26
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Water Lily Water Lily is offline
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Quote:
Originally Posted by maile1
almost everyone who has Hashimoto's thyroiditis tests positive for EBV or has had mono so there could indeed be a link to weight gain and infection.


Thanks for that. I'll have to do some research.
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  #8   ^
Old Tue, Sep-28-10, 01:24
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Demi Demi is offline
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Quote:
From the Times
London, UK
September 28, 2010

Does a virus trigger obesity?

The cyclic myth that an obesity bug is resposible for expanding waistlines in the Western world rears its head once again

Let’s invent a new disorder: Goldfish Memory Syndrome (GMS), a condition that afflicts harried health journalists. Symptoms involve republishing the same story year after year, no matter how tenuous it is. The latest manifestation is the news in The Independent, Daily Mail and The Daily Telegraph of a virus that “causes obesity”.

The reports highlight research that found a strain of adenovirus (versions of which cause the common cold) in overweight children. From this, one might possibly leap to the conclusion that being overweight is contagious. Thus The Independent warned: “The obesity explosion that has swept the Western world over the past 30 years may have been caused by a virus.”

This may prompt a sense of déjà vu in anyone whose memory span is greater than that of a goldfish. These latest stories about the “obesity bug”, adenovirus 36, were sparked by research reported in the journal Pediatrics. But the news first appeared ten years ago, in The Sun and Daily Mail. It since reappeared across the nationals in 2003, 2006, 2007 and 2009.

This is despite regular criticism of the studies involved, including in an editorial in The Times in 2007. The latest headlines might be merited if there were something excitingly persuasive in the new study. But there isn’t. The study has not tackled the main problem with the “obesity virus” claim: it confuses association with causation. It’s like skidmarks and car crashes: you often find skidmarks at crashes, but that does not necessarily mean that skidmarks cause crashes. Statistically, adenovirus 36 and obesity may well be seen together in notable numbers of children — because the virus is common nowadays, and so is childhood obesity.

The latest research did indeed find the virus in some overweight children. But it was also found in healthily sized children. And the virus was not found in the majority of children studied who were overweight. What we are left with is a tenuous association between some overweight kids and a virus.

On top of that, this latest report covers minuscule numbers: 124 children. Only 19 had the virus. Fifteen of them were overweight. Four were not. With those tiny numbers, the statistics can’t rule out chance. They certainly do not prove that the virus causes obesity.

Nevertheless, these findings have been reported worldwide as “proof”. This has prompted sceptics to suggest that the drug industry is at work, trying to push the case for lucrative new antiviral “cures” for obesity. Well perhaps. But such outbreaks of health-hysteria are usually more to do with cock-up than conspiracy — thanks to global media bouts of Goldfish Memory Syndrome.
http://www.thetimes.co.uk/tto/healt...icle2743036.ece
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  #9   ^
Old Tue, Sep-28-10, 02:03
Hutchinson's Avatar
Hutchinson Hutchinson is offline
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Quote:
Originally Posted by Hutchinson
Ideally you need to take (or acquire from UVB exposure) sufficient D3 daily to raise your 25(OH)D to around 60ng/ml.
From this graph you can see the response to amounts up to 10,000iu is very varied.

If you look at the graph plotting response to 10,000iu/d you see it's entirely possible you will be in the cluster of dots around 40ng/ml and will need to take more than 10,000iu/daily for a while.
Remember it takes at least 40,000iu/daily for many months to raise status to the 200ng/ml above which adverse events may be expected.
Given full body, non burning, midday sun exposure it's probable you skin would create 10,000~20,000iu D3 so using an amount higher than 10,000iu for a short while and while also monitoring the change in 25(OH)D would allow you to work out what is an appropriate amount for your body.
Remember it isn't just Vitamin D3 that fights inflammation, omega 3 and magnesium are equally important and vitamin K2mk 4 is also required to make sure the additional calcium you will be absorbing gets fixed in your bones.

I should point out that 1000iu per 25lbs is a "rule of thumb" that adjusts intake according to bodyweight. We know obese people always have higher inflammatory status than normal weight and lower 25(OH)D levels compared to normal. It is simply a common sense adjustment to account for lower starting point and greater usage of D3, but monitoring of 25(OH)D will show in 3 ~ 6months what a daily intake of 10,000iu/d achieves and if it takes 20,000iu/daily then providing you keep monitoring the situation to see what's actually happening in practice, that's what it takes.
People with Celiac disease often find they need 2000iu/daily to raise status 10ng/ml so even a below average bodyweight celiac may require more than 10,000iu/daily to maintain a 25(OH)D around 60ng/ml. That's why you need to test and adjust intake to achieve your goal.
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  #10   ^
Old Tue, Sep-28-10, 02:22
M Levac M Levac is offline
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Considering that carbs drive insulin drives fat accumulation in a dose response fashion, and considering that carbs suppress the immune system in a dose response fashion as well, it's no surprise to find that the rate of infection will rise with the rate of obesity. Indeed, the rate of pretty much any disease rises with the rate of obesity.
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  #11   ^
Old Tue, Sep-28-10, 06:14
leemack's Avatar
leemack leemack is offline
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Quote:
Originally Posted by Hutchinson
I should point out that 1000iu per 25lbs is a "rule of thumb" that adjusts intake according to bodyweight. We know obese people always have higher inflammatory status than normal weight and lower 25(OH)D levels compared to normal. It is simply a common sense adjustment to account for lower starting point and greater usage of D3, but monitoring of 25(OH)D will show in 3 ~ 6months what a daily intake of 10,000iu/d achieves and if it takes 20,000iu/daily then providing you keep monitoring the situation to see what's actually happening in practice, that's what it takes.
People with Celiac disease often find they need 2000iu/daily to raise status 10ng/ml so even a below average bodyweight celiac may require more than 10,000iu/daily to maintain a 25(OH)D around 60ng/ml. That's why you need to test and adjust intake to achieve your goal.


Thanks for the information, I've raised my intake to 20,000iu and am getting my first level test next week.

Lee
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  #12   ^
Old Tue, Sep-28-10, 08:00
Nancy LC's Avatar
Nancy LC Nancy LC is offline
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Quote:
Originally Posted by leemack
Thanks for the information, I've raised my intake to 20,000iu and am getting my first level test next week.

Lee

The advice I hear is to wait 3 months after you change your dose to get a new D3 test done.
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  #13   ^
Old Tue, Sep-28-10, 09:36
Hutchinson's Avatar
Hutchinson Hutchinson is offline
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Quote:
Originally Posted by Nancy LC
The advice I hear is to wait 3 months after you change your dose to get a new D3 test done.

The case against vitamin D2
This image shows you why.
It takes 15 days for a single 50,000iu dose amount to reach it's maximum response.

After that it starts to decline, so you need to allow time for 25(OH)D to go up, and reach an equilibrium at any particular daily intake level.

The example was from a single 50,000iu intake but you would expect a smaller daily amount to take a while to build up and then settle at a point of equilibrium.
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  #14   ^
Old Tue, Sep-28-10, 10:13
leemack's Avatar
leemack leemack is offline
NEVER GIVING UP!
Posts: 5,030
 
Plan: no sugar/grains LCHF IF
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Progress: 45%
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Quote:
Originally Posted by Nancy LC
The advice I hear is to wait 3 months after you change your dose to get a new D3 test done.


As I've never had my levels tested, my gp was keen to get some levels done once I told her I was supplementing, I'll get more levels done in a few months.

Lee
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