Sunday, July 12, 2009

(NaturalNews) The fact that nearly two-thirds of U.S. adults are clinically obese is worrisome for a whole new reason: Evidence emerging from a hospital in Michigan (and published by the CDC) appears to indicate that obese patients may be very easily killed by swine flu.

In the Centers for Disease Control and Prevention's report on death and disease, researchers documented the case of ten swine flu patients at a Michigan hospital who became so ill they were put on ventilators. Three of the patients ultimately died from the infection. The kicker? Nine of the ten were obese, and two of the three who died were severely obese.

As reported by Reuters, CDC virologist Dr. Tim Uyeki said, "What this suggests is that there can be severe complications associated with this virus infection, especially in severely obese patients."

Notably, five of the patients showed evidence of blood clots in their lungs, indicating severe cellular trauma in the lungs. Nine of the patients suffered from multiple organ failure, and six experienced kidney failure.

Link to CDC article (Thanks, frankly.)

Bo

No big surprise here. The obese are often very low in blood levels of vitamin D as well. Vitamin D plays a very important role in cold and flu fighting.

In the LPGA, half the field is Korean. Chances are, the next winner will also be Korean. In the US, 1/3 of adults are obese. Chances are, the next to die will also be obese.

For anyone who doesn't feel like clicking through to Bo's dodgy site and helping make money for Mike Adams, here's a direct link to the CDC article, it's a little dry and scientific - but at least you won't be blindsided by SPAM: CDC link

Someone hasn't been bothering to read the threads she's commenting on Wifezilla.
Effect of vitamin D deficiency and replacement on endothelial function in asymptomatic subjects

Vitamin D supplements will raise leptin. Their higher leptin level is the reason why swine flu kills obese people; higher leptin levels tend to lead to a firestorm of inflammation.Fight the flab to fend off swine flu


.

Oh good lord.

"Getting plenty of vitamin D — more than diet can offer — appears to provide potent protection against colds, flu and even pneumonia, a new study reports. Although the amount of protection varies by season, the trend is solid: As the amount of vitamin D circulating in blood climbs, risk of upper respiratory tract infections falls.

Though that’s not too surprising (SN: 11/11/06, p. 312), the researchers found one unexpected trend: “In people with preexisting lung disease, such as asthma and chronic obstructive pulmonary disease — or COPD, low levels of vitamin D act like an effect modifier,” says Adit Ginde, an emergency room physician at the University of Colorado Denver School of Medicine in Aurora who led the study. The findings appear in the Feb. 23 Archives of Internal Medicine. In people with lung disease, he says, low levels of the sunshine vitamin “magnify many-fold” the apparent vulnerability to infection seen in people with healthy lungs."
http://www.sciencenews.org/view/gen...k_of_colds,_flu

I have come to the conclusion that there is a contingency of cave dwelling mutants who have decided to trash vitamin D at every possibly opportunity. No doubt it is a recruitment effort to get more people to join the mutant horde.

Vitamin D mutants are an interesting subject

Vitamin D and aging.
Taken together, aging shows a U-shaped dependency on hormonal forms of vitamin D suggesting that there is an optimal concentration of vitamin D in delaying aging phenomena. Our recent study shows that calcidiol is an active hormone. Since serum calcidiol but not calcitriol is fluctuating in physiological situations, calcidiol might determine the biological output of vitamin D action. Due to its high serum concentration and better uptake of calcidiol-DBP by the target cells through the cubilin-megalin system, calcidiol seems to be an important circulating hormone. Therefore, serum calcidiol might be associated with an increased risk of aging-related chronic diseases more directly than calcitriol. Aging and cancer seem to be tightly associated phenomena. Accumulation of damage on DNA and telomeres cause both aging and cancer, moreover the signalling pathways seem to converge on tumour suppressor protein, p53, which seems to be regulated by vitamin D. Also, the insulin-like growth factor signalling pathway (IGF-1, IGFBPs, IGFR) and fibroblast growth factor-23 (FGF-23) regulate growth, aging and cancer. Vitamin D can regulate these signalling pathways, too. Also NF-kappaB and telomerase reverse transcriptase (TERT) might be molecular mechanisms mediating vitamin D action in aging and cancer. Calcidiol serum concentrations show a U-shaped risk of prostate cancer suggesting an optimal serum concentration of 40-60 nmol/L for the lowest cancer risk.

Premature aging in vitamin D receptor mutant mice Overall, VDR KO mice showed several aging related phenotypes, including poorer survival, early alopecia, thickened skin, enlarged sebaceous glands and development of epidermal cysts[...]Unlike the wildtype controls, VDR KO mice lose their ability to swim after 6 months of age. Expression of all the genes was lower in old VDR KO mice, but only NF-kappaB, Fgf-23, p53 and IGF1R were significantly lower. Since the phenotype of aged VDR knockout mice is similar to mouse models with hypervitaminosis D(3), our study suggests that VDR genetic ablation promotes premature aging in mice, and that vitamin D(3) homeostasis regulates physiological aging.

So the mutant cave is full of mice too?

This explains EVERYTHING!!!

Moles are also an interesting subject

Effect of oral cholecalciferol supplementation at physiological and supraphysiological doses in naturally vitamin D3-deficient subterranean damara mole rats

Maybe you think a naturally vitamin D3-deficient animal would be short lived, in fact naked mole rats are the longest lived of all rodents.
Prolonged longevity in naked mole-rats: age-related changes in metabolism, body composition and gastrointestinal function


researchers found those with more than 100 moles had longer telomeres than those with fewer than 25
No it's not due to UV exposure , associations like that are notoriously difficult to interpret, and we know that boosting vitamin D levels is more likely to shorten telomeres.

And this has to do with swine flu allegedly affecting obese people more severely than others, just how exactly?

It is thought swine flu 'affects' obese people more severely because of their higher leptin levels and when someone implied vitamin D supplements would be beneficial in helping fat people fight swine flu I thought it pertinent to point out (again) that as D raises leptin levels this is not a good idea.

My last link 'has to do with' me trying to show that my opinions are not just off the top of my head; I have read a lot on this subject and can give references. It was a bit tangental, but responding in kind to talk of 'cave dwelling mutants' and 'mole men ' is not my way.

My purpose of posting the vitamin D information was to point out that fat people often have low levels of vitamin D. The effects of low vitamin D and flu are well documented, though apparently mole people take issue with that data.

http://www.scientificamerican.com/b...more-2009-02-23

So now I'm super confused. Do I take my CLO come fall, or not!?