lack of SUNSHINE has a lot to do with influenza epidemics--chemtrails, anyone?

Author Topic: lack of SUNSHINE has a lot to do with influenza epidemics--chemtrails, anyone?  (Read 2275 times)

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Virology Journal


The epidemiology of influenza swarms with incongruities, incongruities exhaustively detailed by the late British epidemiologist, Edgar Hope-Simpson. He was the first to propose a parsimonious theory explaining why influenza is, as Gregg said, "seemingly unmindful of traditional infectious disease behavioral patterns." Recent discoveries indicate vitamin D upregulates the endogenous antibiotics of innate immunity and suggest that the incongruities explored by Hope-Simpson may be secondary to the epidemiology of vitamin D deficiency. We identify and attempt to explain nine influenza conundrums: (1) Why is influenza both seasonal and ubiquitous and where is the virus between epidemics? (2) Why are the epidemics so explosive? (3) Why do they end so abruptly? (4) What explains the frequent coincidental timing of epidemics in countries of similar latitude? (5) Why is the serial interval obscure? (6) Why is the secondary attack rate so low? (7) Why did epidemics in previous ages spread so rapidly, despite the lack of modern transport? (8) Why does experimental inoculation of seronegative humans fail to cause illness in all the volunteers? (9) Why has influenza mortality of the aged not declined as their vaccination rates increased? We review recent discoveries about vitamin D's effects on innate immunity, human studies attempting sick-to-well transmission, naturalistic reports of human transmission, studies of serial interval, secondary attack rates, and relevant animal studies. We hypothesize that two factors explain the nine conundrums: vitamin D's seasonal and population effects on innate immunity, and the presence of a subpopulation of "good infectors." If true, our revision of Edgar Hope-Simpson's theory has profound implications for the prevention of influenza.

It is useful, at times, to question our assumptions. Arguably, the most universally accepted assumption about influenza is that it is a highly infectious virus spread by the sick. Edgar Hope-Simpson not only questioned that assumption, he went much further. Realizing that solar radiation has profound effects on influenza, he added an unidentified "seasonal stimulus" to the heart of his radical epidemiological model [1]. Unfortunately, the mechanism of action of the "seasonal stimulus" eluded him in life and his theory languished. Nevertheless, he parsimoniously used latent asymptomatic infectors and an unidentified "season stimulus" to fully or partially explain seven epidemiological conundrums [2].

1. Why is influenza both seasonal and ubiquitous and where is the virus between epidemics?

2. Why are the epidemics so explosive?

3. Why do epidemics end so abruptly?

4. What explains the frequent coincidental timing of epidemics in countries of similar latitudes?

5. Why is the serial interval obscure?

6. Why is the secondary attack rate so low?

7. Why did epidemics in previous ages spread so rapidly, despite the lack of modern transport?

An eighth conundrum one not addressed by Hope-Simpson is the surprising percentage of seronegative volunteers who either escape infection or develop only minor illness after being experimentally inoculated with a novel influenza virus. The percentage of subjects sickened by iatrogenic aerosol inoculation of influenza virus is less than 50% [3], although such experiments depend on the dose of virus used. Only three of eight subjects without pre-existing antibodies developed illness after aerosol inhalation of A2/Bethesda/10/63 [4]. Intranasal administration of various wild viruses to sero-negative volunteers only resulted in constitutional symptoms 60% of the time; inoculation with Fort Dix Swine virus (H1N1) a virus thought to be similar to the 1918 virus in six sero-negative volunteers failed to produce any serious illness, with one volunteer suffering moderate illness, three mild, one very mild, and one no illness at all [5]. Similar studies by Beare et al on other H1N1 viruses found 46 of 55 directly inoculated volunteers failed to develop constitutional symptoms [6]. If influenza is highly infectious, why doesn't direct inoculation of a novel virus cause universal illness in seronegative volunteers?

A ninth conundrum evident only recently is that epidemiological studies question vaccine effectiveness, contrary to randomized controlled trials, which show vaccines to be effective. For example, influenza mortality and hospitalization rates for older Americans significantly increased in the 80's and 90's, during the same time that influenza vaccination rates for elderly Americans dramatically increased [7,8]. Even when aging of the population is accounted for, death rates of the most immunized age group did not decline [9]. Rizzo et al studying Italian elderly, concluded, "We found no evidence of reduction in influenza-related mortality in the last 15 years, despite the concomitant increase of influenza vaccination coverage from ~10% to ~60%" [10]. Given that influenza vaccinations increase adaptive immunity, why don't epidemiological studies show increasing vaccination rates are translating into decreasing illness?

After confronting influenza's conundrums, Hope-Simpson concluded that the epidemiology of influenza was not consistent with a highly infectious disease sustained by an endless chain of sick-to-well transmissions [2]. Two of the three most recent reviews about the epidemiology of influenza state it is "generally accepted" that influenza is highly infectious and repeatedly transmitted from the sick to the well, but none give references documenting such transmission [11-13]. Gregg, in an earlier review, also reiterated this "generally accepted" theory but warned:

"Some fundamental aspects of the epidemiology of influenza remain obscure and controversial. Such broad questions as what specific forces direct the appearance and disappearance of epidemics still challenge virologists and epidemiologists alike. Moreover, at the most basic community, school, or family levels of observation, even the simple dynamics of virus introduction, appearance, dissemination, and particularly transmission vary from epidemic to epidemic, locale to locale, seemingly unmindful of traditional infectious disease behavioral patterns." [14] (p. 46)

Questioning a generally accepted assumption means asking anew, "What does the evidence actually show? Thus, we asked, are there any controlled human studies that attempted sick-to-well influenza transmission? Do naturalistic studies of outbreaks in confined spaces prove sick-to-well transmission or are they compatible with another mode of dissemination? Is there an easily measurable serial interval (the median time between the index case and the secondary cases), so crucial to establishing sick-to-well transmission? Are measured secondary attack rates in families (the percentage of family members sickened after a primary case) suggestive of a highly infectious virus? What do animal models of influenza tell us?
(Well, let's see--they've told us in the last 3 months that if your corporations name is Baxter Pharmaceuticals,  if you mix live avian flu + a seasonal flu virus+NEGLECT IN RADIATING THEM= a buttload of almost-instantly-dead ferrets, THAT'S what it tells us. And also that pigs DO make the best recombination hosts (Btw, thanks, all relevant Canadian and U.S. earth-worshiping, human-hating, biology department scum for their various levels of involvement in the development, planning, and implementation (not cover-up, though--the nwo's killed WAAAY too many microbiologists and it's totally obvious) of one of the most diabolically evil plans in human history ; although if you listen to that slimeball wench Laurie Garret, CFR member that was on The Colbert Report, everything I just talked about is apparently "antisemitic" for some reason. ::))

Do current theories explain the explosive onset and then abrupt disappearance of epidemics, epidemics that cease despite a wealth of potential victims lacking adaptive immunity [15]? Why have epidemic patterns in Great Britain not altered in four centuries, centuries that have seen great increases in the speed of human transport [16]? If each successive epidemic increases herd immunity and children born since the last epidemic are non-immune, why doesn't the average age of persons infected in successive epidemics become progressively lower[17]? Why did the peak of 25 consecutive epidemics in France and the USA occur within a mean of four days of each other [18]?

Review of Jordan's sobering monograph of the 1918 pandemic leaves little room to doubt that close human interaction propagates influenza [19]. Furthermore, laboratory evidence leaves no doubt that droplets or aerosols can transmit influenza; droplets containing a high dose of virus, or aerosols containing a much lower dose, both can result in iatrogenic human infection [20].
(If he's saying what I THINK he's saying, Barium and Aluminum are the LEAST of our worries when it comes to chemtrails)

Subjects that sicken do so two to four days after being iatrogenically infected; that is, the incubation period is about three days. However, it is crucial to remember that the incubation period only tells us what the serial interval should be, not what it is. Furthermore, induction of human infection in the laboratory only tells us such infection is possible; it does not tell us who is infecting the well in nature.

The obvious candidate is the sick. However, Edgar Hope-Simpson contended that the extant literature on serial interval, secondary attack rates, and other epidemiological aspects of influenza are not compatible with sick-to-well transmission as the usual mode of contagion. In his 1992 book, after considering all known epidemiological factors, he presented a comprehensive, parsimonious and radically different model for the transmission of influenza, one heavily dependent on a profound, even controlling, effect of solar radiation. Furthermore, while agreeing the sick could infect the well, Hope-Simpson's principal hypothesis was that epidemic influenza often propagates itself by a series of transmissions from a small number of highly infectious but generally symptomless latent carriers, briefly called into contagiousness by the "seasonal stimulus."

In contrast, Kilbourne's 1987 text without mentioning serial interval or secondary attack rates in his chapter on epidemiology concluded, "Any doubt about the communicability of influenza from those ill with the disease is dispelled by studies in crowded, confined, or isolated populations" [21]. (p. 269) As discussed below, the naturalistic studies Kilbourne refers to certainly indicate human interaction facilitates transmission of influenza. However, these naturalistic studies simply assume that the first person with identified illness is the index case. Obviously, A preceding B does not prove A causes B.
Vitamin D, innate immunity, and influenza

Hope-Simpson's model theorized that an unidentified "seasonal stimulus," inextricably bound to solar radiation, substantially controlled the seasonality of influenza. Recent evidence suggests the "seasonal stimulus" may be seasonal impairments of the antimicrobial peptide (AMPs) systems crucial to innate immunity [22], impairments caused by dramatic seasonal fluctuations in 25-hydroxy-vitamin D [25(OH)D] levels [23]. (Figure 1) The evidence that vitamin D has profound effects on innate immunity is rapidly growing [24].

thumbnailFigure 1. Geometric mean monthly variations in serum 25-hydroxyvitamin D [25)OH)D] concentration in men (dark shade, n = 3723) and women (light shade, n = 3712) in a 1958 British birth cohort at age 45. 25(OH)D levels are in ng/ml; to convert to nmol/L, multiply by 2.5. Adapted from: Hypponen E, Power C: Hypovitaminosis D in British adults at age 45 y: nationwide cohort study of dietary and lifestyle predictors. Am J Clin Nutr 2007, 85: 860868. Reproduced with kind permission of the American Society for Nutrition.

In fact, Aloia and Li-Ng presented evidence of a dramatic vitamin D preventative effect from a randomized controlled trial (RCT) [25]. In a post-hoc analysis of the side effect questions of their original three-year RCT, they discovered 104 post-menopausal African American women given vitamin D were three times less likely to report cold and flu symptoms than 104 placebo controls. A low dose (800 IU/day) not only reduced reported incidence, it abolished the seasonality of reported colds and flu. A higher dose (2000 IU/day), given during the last year of their trial, virtually eradicated all reports of colds or flu. (Figure 2) Recent discoveries about vitamin D's mechanism of action in combating infections [26] led Science News to suggest that vitamin D is the "antibiotic vitamin" [27] due primarily to its robust effects on innate immunity.

thumbnailFigure 2. Incidence of reported cold/influenza symptoms according to season. The 104 subjects in the placebo group (light shade) reported cold and flu symptoms year around with the most symptoms in the winter. While on 800 IU per day (intermediate shade) the 104 test subjects were as likely to get sick in the summer as the winter. Only one of the 104 test subjects had cold/influenza symptoms during the final year of the trial, when they took 2,000 IU of vitamin D per day (dark shading). Adapted from: Aloia JF, Li-Ng M: Epidemic influenza and vitamin D. Epidemiol Infect 2007; 135: 10951096. (Reproduced with permission, Cambridge University Press).

Unlike adaptive immunity, innate immunity is that branch of host defense that is "hard-wired" to respond rapidly to microorganisms using genetically encoded effectors that are ready for activation by an antigen before the body has ever encountered that antigen. Activators include intact microbes, Pathogen Associated Molecular Patterns (PAMPS), and host cellular constituents released during tissue injury. Of the effectors, the best studied are the antimicrobial peptides (AMPs) [28].

Both epithelial tissues and phagocytic blood cells produce AMPs; they exhibit rapid and broad-spectrum antimicrobial activity against bacteria, fungi, and viruses [29]. In general, they act by rapidly and irreversibly damaging the lipoprotein membranes of microbial targets, including enveloped viruses, like influenza [30]. Other AMPs, such as human beta-defensin 3, inhibit influenza haemagglutinin A mediated fusion by binding to haemagglutinin A associated carbohydrates via a lectin-like interaction [31].

AMPs protect mucosal epithelial surfaces by creating a hostile antimicrobial shield. The epithelia secrete them constitutively into the thin layer of fluid that lies above the apical surface of the epithelium but below the viscous mucous layer. To effectively access the epithelium a microbe, such as influenza, must penetrate the mucous barrier and then survive damage inflicted by the AMPs present in the fluid that is in immediate contact with the epithelial surface. Should this constitutive barrier be breached, the binding of microbes to the epithelium and/or local tissue injury rapidly provokes the expression of high concentrations of specific inducible AMPs such as human beta-defensin 2 and cathelicidin, that provide a "back-up" antimicrobial shield. These inducible AMPs also act as chemo-attractants for macrophages and neutrophils that are present in the immediate vicinity of the site of the microbial breach [28-30]. In addition, cathelicidin plays a role in epithelial repair by triggering epithelial growth and angiogenesis [32].

The crucial role of vitamin D in the innate immune system was discovered only very recently [33,34]. Both epithelial cells and macrophages increase expression of the antimicrobial cathelicidin upon exposure to microbes, an expression that is dependent upon the presence of vitamin D. Pathogenic microbes, much like the commensals that inhabit the upper airway, stimulate the production of a hydroxylase that converts 25(OH)D to 1,25(OH)2D, a seco-steroid hormone. This in turn rapidly activates a suite of genes involved in defense [35].

In the macrophage, the presence of vitamin D also appears to suppress the pro-inflammatory cytokines, Interferon γ, TNFα, and IL12, and down regulate the cellular expression of several PAMP receptors. In the epidermis, vitamin D induces additional PAMP receptors, enabling keratinocytes to recognize and respond to microbes [36]. Thus, vitamin D appears to both enhance the local capacity of the epithelium to produce endogenous antibiotics and at the same time dampen certain arms of the adaptive immune response, especially those responsible for the signs and symptoms of acute inflammation, such as the cytokine storms operative when influenza kills quickly.

Of particular note is that not all animals appear to depend on vitamin D for their innate immune circuitry. The cathelicidin genes of mouse, rat, and dog, lack a vitamin D receptor-binding site, and do not require vitamin D for expression [34]. Therefore, one cannot extrapolate the role vitamin D plays in human infections from studies of such animals.

Plasma levels of vitamin 25(OH)D in African Americans, known to be lower than white skinned individuals, are inadequate to fully stimulate the vitamin D dependent antimicrobial circuits operative within the innate immune system.However, the addition of 25(OH)D restored the dependent circuits and greatly enhanced expression of AMPs [37].  High concentrations of melanin in dark-skinned individuals shield the keratinocytes from the ultraviolet radiation required to generate vitamin D in skin [38]. In addition, the production of vitamin D in skin diminishes with aging [39]. Therefore, relative but easily correctable deficiencies in innate immunity probably exist in many dark-skinned and aged individuals, especially during the winter.

Because humans obtain most vitamin D from sun exposure and not from diet, a varying percentage of the population is vitamin D deficient, at any time, during any season, at any latitude, although the percentage is higher in the winter, in the aged, in the obese, in the sun-deprived, in the dark-skinned, and in more poleward populations [40,41]. However, seasonal variation of vitamin D levels even occur around the equator [42] and widespread vitamin D deficiency can occur at equatorial latitudes [43], probably due to sun avoidance [44], rainy seasons [45], and air pollution [46]. For example, a study of Hong Kong infants showed about half had 25(OH)D levels less than 20 ng/ml in the winter [47]. Even in the summer, few of the infants had levels higher than 30 ng/ml, which many experts now think are below the lower limit of the optimal range [40,41,48,49]. As 25(OH)D levels affect innate immunity, then a varying percentage of most populations even equatorial ones will have impaired innate immunity at any given time, together with distinct seasonal variations in that percentage. The effects such impairments have on influenza transmission are unknown.
(I wonder if THIS is why mexico got hit first? remember the hydrocarbon atmospheric program? Well, apparently from this picture from their site, guess who's listed in their top 5 as far as high levels of hydrocarbon aerosols that are BLOCKING OUT THE SUN-- this be an intentional use of vitamin d deprivation to make mexico deficient right before releasing H1N1 swine/human flu? )
Human studies attempting sick-to-well human transmission

Offline pizzedoff

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They have been working all year almost daily here Alberta.
I've seen planes with no "contrails" suddenly just magically appear, and no elevation changes were involved.
Do not judge by appearances; a rich heart may be under a poor coat.- Scottish Proverb

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