Your iPhone Gives You Cancer – But Protects You From Malaria!
*** Warning – irony below! ***
Do you have an iPhone? Beware: according to new studies, having an iPhone increases your risk for breast and prostate cancer!
However, your iPhone will protect you from infectious diseases like tuberculosis, malaria and HIV. Hence, you don’t need to take malaria prophylaxis when traveling with your iPhone.
The above has been proven in many new scientific studies on cell phone habits among millions of people around the world. The map above is one example. Areas with many cell phones show an increased risk for cancer, while areas with few cell phones show an increased risk for malaria and certain other infections.
Paradoxes?
South Africa is tragically hard hit by HIV, despite many cell phones. This is the “South African Paradox”. Researchers speculate that perhaps wine drinking offers protection.
Statistical correlations don’t prove causation
NOTE: The above is of course pure nonsense. This kind of statistics can’t prove that the iPhone causes cancer or protects against malaria.
Unfortunately, many “experts” in the health debate lean on such statistics. The difference is that they express themselves in such a way that people take them seriously.
The most common type of studies on lifestyle and health is almost as unreliable: it’s only statistics based on questionnaires.
If you see a health alert in the tabloids based on “researchers followed X thousand people during X years” please remember: this is speculation based on statistics, not evidence.
Previously
Eggs, Smoking and Silly Health Scares
Meat, Pseudoscience and Why People Who Eat Their Placebo Are Healthier
Do Unhealthy Meat Eaters Live Shorter Lives?
Stunning: Saturated Fat and the European Paradox
How about some basic reading on anti-viral and antibacterial effects of medium chain fatty acids, such as lauric, capric, caproic, which constitute 70% of coconut oil.
(Next time before you make worn-out, sweeping statement, pause for a moment and consider that people on this blog don't just make comments out of boredom.)
J Gen Virol. 1994 Feb;75 ( Pt 2):353-61.
Lauric acid inhibits the maturation of vesicular stomatitis virus.
Hornung B, Amtmann E, Sauer G.
Source
German Cancer Research Centre, Department of Molecular Biology of DNA Tumour Viruses, Heidelberg.
Abstract
In the presence of lauric acid (C12), the production of infectious vesicular stomatitis virus (VSV) was inhibited in a dose-dependent manner. The inhibitory effect was reversible; after removal of C12 the antiviral effect disappeared. In addition, the chain length of the monocarboxylic acids proved to be crucial, as those with shorter or longer chains were less effective or had no antiviral activity. Concomitant with the C12-induced inhibition was the stimulation of triacylglycerol synthesis, increasing the amount up to ninefold. Analysis of the antiviral mechanism of C12 revealed that the correct assembly of the viral components was disturbed, but viral RNA and protein synthesis remained unimpaired. By cell fractionation and Western blot analysis the amount of viral M protein located in the plasma membrane was found to be markedly reduced after treatment with C12, whereas in the cytoplasm the quantity of M protein was similar to that in untreated cells. C12 did not influence M protein synthesis, but prevented the binding of M protein to the host cell membrane, where the protein plays an essential role in virus assembly. Thus, treatment of VSV-infected cells with C12 resulted in inhibition of virus release. It is suggested that the newly synthesized triacylglycerols might interact with the host cell plasma membrane and interfere with virus maturation.
Nature. 2009 Apr 23;458(7241):1034-8. doi: 10.1038/nature07831. Epub 2009 Mar 4.
Glycerol monolaurate prevents mucosal SIV transmission.
Li Q, Estes JD, Schlievert PM, Duan L, Brosnahan AJ, Southern PJ, Reilly CS, Peterson ML, Schultz-Darken N, Brunner KG, Nephew KR, Pambuccian S, Lifson JD, Carlis JV, Haase AT.
Source
Department of Microbiology, Medical School, University of Minnesota, MMC 196, 420 Delaware Street S.E., Minneapolis, Minnesota 55455, USA.
Abstract
Although there has been great progress in treating human immunodeficiency virus 1 (HIV-1) infection, preventing transmission has thus far proven an elusive goal. Indeed, recent trials of a candidate vaccine and microbicide have been disappointing, both for want of efficacy and concerns about increased rates of transmission. Nonetheless, studies of vaginal transmission in the simian immunodeficiency virus (SIV)-rhesus macaque (Macacca mulatta) model point to opportunities at the earliest stages of infection in which a vaccine or microbicide might be protective, by limiting the expansion of infected founder populations at the portal of entry. Here we show in this SIV-macaque model, that an outside-in endocervical mucosal signalling system, involving MIP-3alpha (also known as CCL20), plasmacytoid dendritic cells and CCR5(+ )cell-attracting chemokines produced by these cells, in combination with the innate immune and inflammatory responses to infection in both cervix and vagina, recruits CD4(+) T cells to fuel this obligate expansion. We then show that glycerol monolaurate-a widely used antimicrobial compound with inhibitory activity against the production of MIP-3alpha and other proinflammatory cytokines-can inhibit mucosal signalling and the innate and inflammatory response to HIV-1 and SIV in vitro, and in vivo it can protect rhesus macaques from acute infection despite repeated intra-vaginal exposure to high doses of SIV. This new approach, plausibly linked to interfering with innate host responses that recruit the target cells necessary to establish systemic infection, opens a promising new avenue for the development of effective interventions to block HIV-1 mucosal transmission.