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Repeatedly drinking half-pints of hot water (as hot as possible) continually kills the bacteria responsible for the continued presence of cold symptoms. This does NOT mean to do it as you always have, where you take five or six, maybe even eight sips of hot liquid, and then drink the rest of it warm. That has limited benefit - limited, of course, to the benefits produced by a few sips of hot tea, versus the benefits of sipping a cup of tea.Instead, use this excellent shortcut, wherein the shortcut is successful no less than ninety percent of the time, works hugely and instantly, provided you include the foundation of you drinking more hot tea.You don't even need to increase the number of cups of tea!! It DOES mean sipping more of the cups of tea that you DO have. It means some two hundred or more hot sips or mouthfuls of piping hot liquid within those first 24 hours.If the water is warm or tepid, it's not doing its primary job of killing the bacteria. Must be hot, must be repeated, again and again and again. In between cups or bowls of hot liquid, cool fresh water maintains the flushing function. Pints of clean fresh water help accomplish the primary task, flushing out the body.Depending on what you like or dislike, you can flavor the hot water, such as with soup, tea, etc., as long as "serious" food is mostly avoided for just 12 to 18 hours. As you may remember from school, the digestion of food demands a great deal of the body's resources when it's not food from the ground.Considering what most of us put into our bodies regularly, it's far, far more effective to allow the body to focus on getting rid of the cold and clearing up the systems quickly, rather than being distracted by the enormity of digestion and its attendant and ancillary functions.
Get better Neil ![8D]BTW , my Microbiology teacher says that for rhinoviruses the best cure is to inhale hot air from your range (i`m not sure for this word, I looked in the vocabulary, It`s the place where you cook coffee etc. ) Optimal temperature for them to multuply is 33 C, which is the temperature in your upper respiratory pathways. Thay don`t feel comfortable on 37 C , though.
...with a little help from Rhinology and viruses:4xC = Cardiff Common Cold Centre... How neat!...sorry, you cannot view external links. To see them, please
REGISTER or LOGINAcute cooling of the body surface and the common cold.Eccles R.Common Cold Centre, Cardiff School of Biosciences, Cardiff University, United Kingdom. There is a widely held belief that acute viral respiratory infections are the result of a "chill" and that the onset of a respiratory infection such as the common cold is often associated with acute cooling of the body surface, especially as the result of wet clothes and hair. However, experiments involving inoculation of common cold viruses into the nose, and periods of cold exposure, have failed to demonstrate any effect of cold exposure on susceptibility to infection with common cold viruses.Present scientific opinion dismisses any cause-and-effect relationship between acute cooling of the body surface and common cold.This review proposes a hypothesis; that acute cooling of the body surface causes reflex vasoconstriction in the nose and upper airways, and that this vasoconstrictor response may inhibit respiratory defence and cause the onset of common cold symptoms by converting an asymptomatic subclinical viral infection into a symptomatic clinical infection.Rhinology. 2002 Sep;40(3):109-14.
...Holmes and colleagues conducted a trial of cod-liver oil among industrial workers in a factory in the American midwest....sorry, you cannot view external links. To see them, please
REGISTER or LOGINmarburg.jpgCutting edge: vitamin D-mediated human antimicrobial activity against Mycobacterium tuberculosis is dependent on the induction of cathelicidin.Liu PT, Stenger S, Tang DH, Modlin RL.Division of Dermatology, Department of Medicine, David Geffen School of Medicine, University of California, Los Angeles, CA 90095, USA.Host defense against intracellular pathogens depends upon innate and adaptive antimicrobial effector pathways. TLR2/1-activation of monocytes leads to the vitamin D-dependent production of cathelicidin and, at the same time, an antimicrobial activity against intracellular Mycobacterium tuberculosis. To determine whether induction of cathelicidin was required for the vitamin D-triggered antimicrobial activity, the human monocytic cell line THP-1 was infected with M. tuberculosis H37Ra and then activated with the active vitamin D hormone 1,25-dihydroxyvitamin D(3) (1,25D(3)). 1,25D(3) stimulation resulted in antimicrobial activity against intracellular M. tuberculosis and expression of cathelicidin mRNA and protein. Using small interfering RNA (siRNA) specific for cathelicidin, 1,25D(3)-induced cathelicidin mRNA and protein expressions were efficiently knocked down, whereas a nonspecific siRNA control had little effect. Finally, 1,25D(3)-induced antimicrobial activity was completely inhibited in the presence of siRNA against cathelicidin, instead leading to enhanced intracellular growth of mycobacteria. These data demonstrate that cathelicidin is required for the 1,25D(3)-triggered antimicrobial activity against intracellular M. tuberculosis.J Immunol. 2007 Aug 15;179(4):2060-3.