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Letter from Dr Cannell: "Vitamin D is incredibly protective against H1N1"-- New Evidence, 9/17/09 -x

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tiptoe Donating Member (1000+ posts) Send PM | Profile | Ignore Thu Sep-17-09 04:53 PM
Original message
Letter from Dr Cannell: "Vitamin D is incredibly protective against H1N1"-- New Evidence, 9/17/09 -x
Edited on Thu Sep-17-09 05:50 PM by tiptoe

see:   Letter from Dr J Cannell: "Vitamin D is incredibly protective against H1N1" -- New Evidence, 9/17/09
"Editor's note: The following was received in two emails from Dr. John Cannell, a vitamin D expert who is President of Vitamin D Council. Please forward this page to as many friends as you can because this information can help all people particularly children who are most susceptible to the H1N1 virus or swine flu infection. It may save their lives !!!"

Latest research on Toxicity
One of the least toxic substances to humans, overdose of vitamin D3 doesn't occur until more than 100 times (approximately one bottle of vitamin D3 tablets) the daily RDA has been taken daily for several months. Acute, one-time overdoses require over 50 mg (10,000 times the RDA).

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notadmblnd Donating Member (1000+ posts) Send PM | Profile | Ignore Thu Sep-17-09 04:59 PM
Response to Original message
1. Got Milk?
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tabatha Donating Member (1000+ posts) Send PM | Profile | Ignore Thu Sep-17-09 05:01 PM
Response to Reply #1
2. Got sunshine?
Edited on Thu Sep-17-09 05:04 PM by tabatha
Concentrated food sources of vitamin D include salmon, sardines, shrimp, milk, cod, and eggs.
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DavidDvorkin Donating Member (1000+ posts) Send PM | Profile | Ignore Sat Oct-24-09 11:38 AM
Response to Reply #2
32. Got skin cancer
Have learned to avoid the sun.
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Dappleganger Donating Member (1000+ posts) Send PM | Profile | Ignore Sat May-15-10 04:20 PM
Response to Reply #32
50. 15 minutes a day does the body good.
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Sukie Donating Member (563 posts) Send PM | Profile | Ignore Thu Sep-17-09 05:20 PM
Response to Original message
3. I have been taking vitamin D-3 for about half a year now.
I read that women especially needed it to feel well and to maintain weight. Hopefully that is a nice added benefit.
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jbnow Donating Member (1000+ posts) Send PM | Profile | Ignore Thu Sep-17-09 05:56 PM
Response to Reply #3
6. I get sunshine, love milk and still had very low D levels. Taken
2,000 mg D3 a day and have still not gotten up to normal but it is closer. (My doctor monitors)

Vitamin D has crazy good benefits
It helps in preventing and managing glucose intolerance and diabetes. It's an immune system modulator,both boosting your immunity and inhibiting autoimmune disease. Studies have shown reductions in some cancers, osteoporosis, heart disease and it helps regulates blood pressure. And more.
There has been more and more studies on it in recent years and more and more doctors are monitoring it now. Seven out of 10 US kids have vitamin D levels that are too low. Considering it's many actions in the body that's disturbing.

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MichaelHarris Donating Member (1000+ posts) Send PM | Profile | Ignore Thu Sep-17-09 05:45 PM
Response to Original message
4. Got nuts?
Edited on Thu Sep-17-09 05:59 PM by MichaelHarris
We had this same thing closed last night. Vitamin D can be dangerous, not one mention in the OP about that.

Vitamin D toxicity (hypervitaminosis D) induces abnormally high serum calcium levels (hypercalcemia), which could result in bone loss, kidney stones, and calcification of organs like the heart and kidneys if untreated over a long period of time. Hypercalcemia has been observed following daily doses of greater than 50,000 IU of vitamin D (38). When the Food and Nutrition Board of the Institute of Medicine established the tolerable upper intake level (UL) for vitamin D, published studies that adequately documented the lowest intake levels of vitamin D that induced hypercalcemia were very limited. Because the consequences of hypercalcemia are severe, the Food and Nutrition Board established a very conservative UL of 2,000 IU/day (50 mcg/day) for children and adults (see table below) (30). Research published since 1997 suggests that the UL for adults is likely overly conservative and that vitamin D toxicity is very unlikely in healthy people at intake levels lower than 10,000 IU/day (39, 97, 98). Vitamin D toxicity has not been observed to result from sun exposure (38). Certain medical conditions can increase the risk of hypercalcemia in response to vitamin D, including primary hyperparathyroidism, sarcoidosis, tuberculosis, and lymphoma (39). People with these conditions may develop hypercalcemia in response to any increase in vitamin D nutrition and should thus consult a qualified health care provider regarding any increase in vitamin D intake. /

Do the right thing, if you're going to poison people at least give them a chance. Do you know the medical conditions of anyone on DU? Do any of them have any of the mentioned pre-existing conditions? You guys doing this voodoo diagnosing may kill someone yet. SEE A DOCTOR, DON'T PROMOTE MEDICAL CURES OVER THE GOD-DAMNED INTERNET!
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Why Syzygy Donating Member (1000+ posts) Send PM | Profile | Ignore Thu Sep-17-09 07:19 PM
Response to Reply #4
8. I saw you in the other thread.
Edited on Thu Sep-17-09 07:21 PM by Why Syzygy
and am glad there is a chance to respond to you now. No doubt you were invited by your alert partner.

No one here is giving "medical advice". It's against the rules, and threads get locked for crossing the line. This is for informational purposes. Furthermore, the OP presents letters from MEDICAL DOCTORS. And you're really going to need to get a grip if you expect to invade the Health forum with guns blazing.

Here's some information on your scare tactic:

Decreased appetite (anorexia)


Stop taking vitamin D. Consult your physician. In severe cases, other treatment may be necessary.

An excess of vitamin D causes abnormally high levels of calcium in the blood, which can eventually severely damage the bones, soft tissues, and kidneys. It is almost always caused by forms of vitamin D that require a doctor's prescription.

A.D.A.M. creates health content for consumers that is physician-reviewed by experts in their field. 1997-2009 A.D.A.M., Inc. Any unauthorized duplication or distribution of the information contained herein is strictly prohibited.

A.D.A.M., Inc. is accredited by URAC, also known as the American Accreditation HealthCare Commission ( ). URAC's accreditation program is an independent audit to verify that A.D.A.M. follows rigorous standards of quality and accountability. A.D.A.M. is among the first to achieve this important distinction for online health information and services. Learn more about A.D.A.M.'s editorial process. A.D.A.M. is also a founding member of Hi-Ethics and subscribes to the principles of the Health on the Net Foundation ( ).


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MichaelHarris Donating Member (1000+ posts) Send PM | Profile | Ignore Thu Sep-17-09 07:39 PM
Response to Reply #8
9. Your
MD is from where? Also where did you do Nutritional research at? No scare tactic at all, just a very well trained person who knows about this subject. You? Other than Google searches?
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Why Syzygy Donating Member (1000+ posts) Send PM | Profile | Ignore Thu Sep-17-09 07:45 PM
Response to Reply #9
10. If you are one of those
Edited on Thu Sep-17-09 07:47 PM by Why Syzygy
partisan posters who have absolute faith in (some) medical doctors and the government, we've seen it before.

I've studied nutrition for more than 30 years, if it's any of your business. I don't care about your credentials, so don't bother.

Partisans get very frustrated in the Health forum. You're already there, right?
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MichaelHarris Donating Member (1000+ posts) Send PM | Profile | Ignore Thu Sep-17-09 07:59 PM
Response to Reply #10
11. really?
We must know each other, where did you do your work and who under? My work was under Earl B. Dawson at the University of Texas Medical Branch in Galveston, I'm sure I've read your work :sarcasm:
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Why Syzygy Donating Member (1000+ posts) Send PM | Profile | Ignore Thu Sep-17-09 08:01 PM
Response to Reply #11
12. I'm sure you will
be highly respected. In the skeptic's group. Maybe someone will toss you a line.

There are plenty of experts who post here. Watch it, your halo is slipping.
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MichaelHarris Donating Member (1000+ posts) Send PM | Profile | Ignore Thu Sep-17-09 08:13 PM
Response to Reply #12
13. silence
on your "real" qualifications. Keep preaching pseudo-medicine,hopefully you won't see some of the damage I've seen when people choose alternative medicines without proper education. As I mentioned in the closed thread, I've seen a child die because of Vitamin D toxicity, I've seen metal toxicity from vitamin abuse, I watched a friends mom die at the hands of such quackery. By all means though, you keep preaching Readers Digest medicine over the internet, it's faceless, you won't even know who you're hurting.
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Why Syzygy Donating Member (1000+ posts) Send PM | Profile | Ignore Thu Sep-17-09 09:21 PM
Response to Reply #13
15. I don't need you to certify my qualifications!
Edited on Thu Sep-17-09 09:23 PM by Why Syzygy
I'm sure my research has helped more people than yours has! :hi:

I'll carry on. Surely you are not naive enough to think some partisan poster is going to change my 30+ years of experience.
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omega minimo Donating Member (1000+ posts) Send PM | Profile | Ignore Thu Sep-17-09 09:36 PM
Response to Reply #15
18. No, it's just a distraction.
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MichaelHarris Donating Member (1000+ posts) Send PM | Profile | Ignore Thu Sep-17-09 10:30 PM
Response to Reply #15
19. hahahahahahah
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tiptoe Donating Member (1000+ posts) Send PM | Profile | Ignore Fri Sep-18-09 12:15 AM
Response to Reply #13
21. "As I mentioned in the closed thread, I've seen a child die because of Vitamin D toxicity". No, you
Edited on Fri Sep-18-09 12:32 AM by tiptoe

actually said on that thread (emphasis mine):

I've seen children die from Vit D toxicity.

Right. Your "report" -- and perspective from John Cannell's article "The Truth About Vitamin D Toxicity" -- lead me to concur with DeschutesRiver from the same thread:

66. ...your response gives me an idea of how much weight I should attach to your opinions on this subject, so thanks for the input which allowed me to reach a conclusion with respect to the opinion you've expressed in your posts. It is not persuasive any longer. ...

The Truth About Vitamin D Toxicity

It seems clear that restoring physiological serum levels of 25(OH)D will help many more patients that it will hurt. In fact, living in America today while worrying about vitamin D toxicity is like dying of thirst in the desert while worrying about drowning.

Vitamin D Toxicity Fears Unwarranted

Is vitamin D toxic? Not if we take the same amount nature intended when we go out in the sun.1 Vieth attempted to dispel unwarranted fears in medical community of physiological doses of vitamin D in 1999 with his exhaustive and well-written review.

His conclusions: fear of vitamin D toxicity is unwarranted, and such unwarranted fear, bordering on hysteria, is rampant in the medical profession.2 Even Ian Monroe, the chair of the relevant IOM committee, wrote to the Journal to compliment Vieth's work and to promise his findings will be considered at the time of a future Institute of Medicine review.3 That was more than two years ago.

In 1999, Vieth indirectly asked the medical community to produce any evidence 10,000 units of vitamin D a day was toxic, saying "Throughout my preparation of this review, I was amazed at the lack of evidence supporting statements about the toxicity of moderate doses of vitamin D." He added: "If there is published evidence of toxicity in adults from an intake of 250 ug (10,000 IU) per day, and that is verified by the 25(OH)D concentration, I have yet to find it."4

Like most medication, cholecalciferol is certainly toxic in excess, and, like Coumadin, is used as a rodent poison for this purpose. Animal data indicates signs of toxicity can occur with ingestion of 0.5 mg/kg (20,000 IU/kg ), while the oral LD50 (the dose it takes to kill half the animals) for cholecalciferol in dogs is about 88 mg/kg, or 3,520,000 IU/kg. An Overview of Cholecalciferol Toxicosis. The American Board of Veterinary Toxicology (ABVT). This would be equivalent to a 110-pound adult taking 176,000,000 IU or 440,000 of the 400 unit cholecalciferol capsules. Vieth reports human toxicity probably begins to occur after chronic daily consumption of approximately 40,000 IU/day (100 of the 400 IU capsules).5 Heavy sun exposure when combined with excessive supplement use is a theoretical risk for vitamin D toxicity, but if such a case has been reported, I am not aware of it. Physician ignorance about vitamin D toxicity is widespread. A case report of four patients appeared in the 1997 Annals of Internal Medicine, accompanied by an editorial warning about vitamin D toxicity.6,7 However, careful examination of the patients reveals that both papers are a testimony to the fact that incompetence about vitamin D toxicity can reach the highest levels of academia.8,9 See worst science for a full critique.

Cholecalciferol, Not Ergocalciferol, Is Safe

Although there are documented cases of pharmacological overdoses from ergocalciferol, the only documented case of pharmacologicalnot industrialtoxicity from cholecalciferol we could find in the literature was intoxication from an over-the-counter supplement called Prolongevity.10 On closer inspection, it seemed more like an industrial accident but it was interesting because it gave us some idea of the safety of cholecalciferol. The capsules consumed contained up to 430 times the amount of cholecalciferol contained on the label (2,000 IU). The man had been taking between 156,0002,604,000 IU of cholecalciferol a day (equivalent to between 3906,500 of the 400 unit capsules) for two years. He recovered uneventfully after proper diagnosis, treatment with steroids, and sunscreen.

It is true that a few people may have problems with high calcium due to undiagnosed vitamin D hypersensitivity syndromes such as primary hyperparathyroidism, granulomatous disease, or occult cancers, but a blood calcium level, PTH, 25(OH)D, and calcitriol level should help clarify the cause of the hypersensitivity. Although D can be toxic in excess, the same can be said for water.

Therapeutic Index

As a physician, I know that psychotic patients should drink about 8 glasses of water a day. However, many would hurt themselves by regularly drinking 40 glasses a day (called compulsive water intoxication). So you could say that water has a therapeutic index of 5 (40/8).

Heaney's recent research indicates that healthy humans utilize about 4,000 units of vitamin D a day (from all sources).11 However, 40,000 units a day, over several years, will hurt them.12 Therefore, vitamin D has a therapeutic index of 10 (40,000/4,000)twice as safe as water. We are not saying vitamin D is as safe as water, we are saying vitamin D is safe when used in the doses nature uses.

Sun Supplies 10,000 Units Of Vitamin D

The single most important fact anyone needs to know about vitamin D is how much nature supplies if we behave naturally, e.g., go into the sun. Humans make at least 10,000 units of vitamin D within 30 minutes of full body exposure to the sun, what is called a minimal erythemal dose.13 Vitamin D production in the skin occurs within minutes and is already maximized before your skin turns pink.

Fear of the fatal form of skin cancer, malignant melanoma, keeps many people out of the sun. The problem with the theory is that the incidence of melanoma continues to increase dramatically although many people have been completely avoiding the sun for years.14 We are not saying sunburns are safe, they are not. We are saying that brief, full-body sun exposure (minimal erythemal doses) may slightly increase your risk of skin cancer but it is a much smarter thing to do than dying of vitamin D deficiency.

Hypersensitivity, Not Toxicity

Vitamin D hypersensitivity syndromes are often mistaken for vitamin D toxicity, as they cause hypercalcemia. The most common is primary hyperparathyroidism although some cases of "primary" hyperparathyroidism are actually secondary to Vitamin D deficiency. Patients with hyperparathyroidism should only take vitamin D under the care of a knowledgeable endocrinologist. Granulomatous diseases such as sarcoidosis, granulomatous TB, and some cancers can also cause Vitamin D hypersensitivity, as the granuloma or the tumor may make excessive amounts of activated Vitamin D, thus raising serum calcium. These patients should not take vitamin D except when under the care of a knowledgeable physician.

Other syndromes occur when abnormal tissue subverts the kidney's normal regulation of endocrine calcitriol production. Aberrant tissues, usually granulomatous, convert 25(OH)D into calcitriol causing high blood calcium. The most common such conditions are sarcoidosis, oat cell carcinoma of the lung, and non-Hodgkin's lymphoma but other illnesses can cause the syndrome and they can occur while the patient's 25(OH)D levels are normal, or even low. For that reason, while rare, it is advisable to seek a knowledgeable physician's care when repleting your vitamin D system, especially if you are older, have sarcoidosis, cancer, or other granulomatous diseases. In such high-risk patients, periodic monitoring of 25(OH)D levels and serum calcium will alert the physician to the need to do more testssuch as calcitriol or PTHand take further action.

It seems clear that restoring physiological serum levels of 25(OH)D will help many more patients that it will hurt. In fact, living in America today while worrying about vitamin D toxicity is like dying of thirst in the desert while worrying about drowning.

John Jacob Cannell MD
Executive Director
updated 2009.06.20

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Why Syzygy Donating Member (1000+ posts) Send PM | Profile | Ignore Fri Sep-18-09 09:25 AM
Response to Reply #21
23. Perspective
(1996): "Each year, use of NSAIDs (Non-Steroidal Anti-Inflammatory Drugs) accounts for an estimated 7,600 deaths and 76,000 hospitalizations in the United States." (NSAIDs include aspirin, ibuprofen, naproxen, diclofenac, ketoprofen, and tiaprofenic acid.)

Although normal food and pill vitamin D concentration levels are far too low to be toxic in adults, people taking multiples of the normal dose of codliver oil may reach toxic levels of vitamin A, not vitamin D, <44> if taken in an attempt to increase the levels of vitamin D. Most officially-recorded historical cases of vitamin D overdose have occurred due to manufacturing and industrial accidents.<43> In the United States, overdose exposure of vitamin D was reported by 284 individuals in 2004, leading to 1 death.<45>

Deaths from several common cancers could be cut by half within five years if the majority of people took a vitamin D supplement, saving billions of pounds a year in medical costs, according to scientists.

A report from researchers in America claims that instead of hunting for the different reasons for various cancers, “a new era of public health” could be brought in by simply giving people 2,000 units of vitamin D per day.

People with low blood levels of vitamin D are more than twice as likely to die from cardiovascular disease as those with high levels, suggests a new study.

Higher blood levels of the vitamin, measured as 25- hydroxyvitamin D and 1,25-dihydroxyvitamin D (1,25(OH)2D), were associated with both lower overall death rates deaths from cardiovascular causes among 3,258 participants in the prospective cohort study, published in the Archives of Internal Medicine.

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MichaelHarris Donating Member (1000+ posts) Send PM | Profile | Ignore Fri Sep-18-09 10:31 PM
Response to Reply #21
26. someone really needs to stop
your drug shilling
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tiptoe Donating Member (1000+ posts) Send PM | Profile | Ignore Fri Nov-13-09 04:04 PM
Response to Reply #26
39. and someone really needs to stop
Edited on Fri Nov-13-09 04:53 PM by tiptoe

their cheap fear-mongering about vitamin D by bringing up off-topic vitamin A (no less, thereby, also implicitly, recklessly confounding relative safety issues of directly taking raw substrate beta-carotene vs the active form, retinol) and their "attacking the messenger" instead of addressing the latest studies of the numerous, credentialed research scientists, including findings on the safety of vitamin D3 and The Truth About Vitamin D Toxicity.

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truedelphi Donating Member (1000+ posts) Send PM | Profile | Ignore Fri Sep-18-09 02:02 AM
Response to Reply #9
22. Look, people share information all the time.
Edited on Fri Sep-18-09 02:03 AM by truedelphi
I combatted several conditions I suffered by sharing info I gleaned through Internet searches with my doctors, as the nasty HMO corporation my health insurance premiums were tied to felt that the doctors should advise me of off the wall protocols, one of which involved bathing my internal organs in a warm H20 solution. (That protocol wouldn't be effective, though it would have been cheaper than what I really needed done. I needed surgery and/or one or two other procedures. All of which were more expensive than the "Warm water baths.")

The internet has been a boon to people researching information about our health information. If someone has made a Google search or two, or discussed a matter with their physician whom they have confidence in, there is no law on the books that says that the information cannot be shared.

If you watch TV, you'll note that every other commmercial is for some type of drug. Or do you click away from those commercials so that your mind is not polluted by that?

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laughingliberal Donating Member (1000+ posts) Send PM | Profile | Ignore Sat Nov-14-09 03:31 PM
Response to Reply #9
40. Here's what Mayo Clinic has to say:
Vitamin D toxicity: What if you get too much?
What is vitamin D toxicity, and should I worry about it since I take supplements?

from Katherine Zeratsky, R.D., L.D.
Vitamin D toxicity, also called hypervitaminosis D, is a potentially serious but treatable medical condition that occurs when you get too much vitamin D.

Vitamin D toxicity usually results from taking an excessive amount of vitamin D supplements not from your diet or too much sun exposure. That's because your body produces only a limited amount of vitamin D from sun exposure, and even fortified foods don't contain large amounts of vitamin D. Although vitamin D toxicity is rare even among people who take supplements, you may be at greater risk if you have health problems, such as liver or kidney conditions, or if you take thiazide-type diuretics.<snip>

<snip> Vitamin D is an essential nutrient. The Institute of Medicine recommends that children and adults up to age 50 get 200 international units (IU) of vitamin D daily. The recommendation for adults over age 50 is 400 to 600 IU daily. However, many health experts consider these recommendations to be too low. The American Academy of Pediatrics, for instance, now recommends that children and adolescents get 400 IU of vitamin D daily. Many experts now "unofficially" recommend that adults get as much as 1,000 to 2,000 IU of vitamin D daily. In addition, it's likely that the vitamin D guidelines will be revised upward.

Supplements can be a reasonable way to meet recommended levels as long as you pay attention to how much you take. And be sure to tell your doctor about any supplements you take.
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Sinistrous Donating Member (1000+ posts) Send PM | Profile | Ignore Thu Sep-17-09 09:32 PM
Response to Reply #4
16. Thank you for confirming how safe Vitamin D really is.
Vitamin D toxicity (hypervitaminosis D) induces abnormally high serum calcium levels (hypercalcemia), which could result in bone loss, kidney stones, and calcification of organs like the heart and kidneys if untreated over a long period of time. Hypercalcemia has been observed following daily doses of greater than 50,000 IU of vitamin D (38). When the Food and Nutrition Board of the Institute of Medicine established the tolerable upper intake level (UL) for vitamin D, published studies that adequately documented the lowest intake levels of vitamin D that induced hypercalcemia were very limited. Because the consequences of hypercalcemia are severe, the Food and Nutrition Board established a very conservative UL of 2,000 IU/day (50 mcg/day) for children and adults (see table below) (30). Research published since 1997 suggests that the UL for adults is likely overly conservative and that vitamin D toxicity is very unlikely in healthy people at intake levels lower than 10,000 IU/day (39, 97, 98). Vitamin D toxicity has not been observed to result from sun exposure (38). Certain medical conditions can increase the risk of hypercalcemia in response to vitamin D, including primary hyperparathyroidism, sarcoidosis, tuberculosis, and lymphoma (39). People with these conditions may develop hypercalcemia in response to any increase in vitamin D nutrition and should thus consult a qualified health care provider regarding any increase in vitamin D intake.

Wouldn't taking 25 times the recommended dose of almost anything on a daily basis be toxic?

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Celebration Donating Member (1000+ posts) Send PM | Profile | Ignore Thu Sep-17-09 09:35 PM
Response to Reply #4
17. not sure why you are upset?
I would assume that people here have enough sense not to go overdosing themselves on Vitamin D. These non profit Vitamin D groups, who have board members that are scientists and MDs doing research on the vitamin, are simply raising awareness. Additionally, they offer discounted testing so that people actually know their vitamin D levels. They aren't making money off it. They passionately feel that enough evidence is in that people should get their vitamin D levels tested, and maintain optimal levels, which are generally higher than the lab normals.

And none of them go so far as to recommend 10,000 units per day. Plus they feel that Vitamin D levels should continue to be monitored to optimize the Vitamin D dosage.

Saying things like seventy percent of children have vitamin D levels are too low is NOT diagnosing on the internet. Obviously thirty percent of children have okay vitamin D levels. How could anyone possibly know which was which without having their Vitamin D levels checked? I just don't see the controversy here.
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MichaelHarris Donating Member (1000+ posts) Send PM | Profile | Ignore Thu Sep-17-09 05:55 PM
Response to Original message
5. Vitamin A and D
are two of the most toxic, dammit you guys are going to kill someone with this crap.
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Why Syzygy Donating Member (1000+ posts) Send PM | Profile | Ignore Thu Sep-17-09 10:38 PM
Response to Reply #5
20. Maybe YOU are...
Edited on Thu Sep-17-09 11:17 PM by Why Syzygy
if anyone listens to you. Just because it's printed on the Internet, doesn't make it False.
You, in fact, are the only one who has offered medical advice.

The first San Diego speaker was Dr. William Grant. Since leaving NASA to begin a full-time career as a vitamin D researcher, Bill has published dozens of studies and has another dozen in the works. Using ecological studies (from Greek oikos, house + German -logie, study or studying your own house) of UVB irradiance and cancer, Bill reported that 15 cancers (colon, esophageal, gallbladder, gastric, pancreatic, rectal, small intestinal, bladder, kidney, prostate, breast, endometrial, ovarian, Hodgkin's lymphoma, and non-Hodgkin's lymphoma) are associated with lower UVB light. He concluded that 257,000 cancer deaths in 2007 in the USA were accounted for by inadequate vitamin D levels.


The next speaker was Professor Bruce Hollis. He reviewed basic physiology of vitamin D and emphasized that the entire system is designed to deal with an excess not with an insufficiency of vitamin D. Numerous mechanisms are available in your body to prevent vitamin D toxicity but few are available to deal with insufficiency. Then he briefly mentioned one of the most important discoveries about vitamin D in the last few years, one where Professor Neil Binkley of the University of Wisconsin was senior author. (In the last four years, Professor Binkley has become a prolific vitamin D expert and I hope Carol Baggerly is able to get him to speak at some of the upcoming conferences she hopes to sponsor.) As I have pointed out before, Hollis and Binkley's crucial discovery was that the body doesn't start storing the parent compound, cholecalciferol, until 25(OH)D levels reach about 50 ng/ml. They showed, using basic steroid pharmacology, that 50 ng/ml should be considered the lower limit of adequate 25(OH)D levels.

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NickB79 Donating Member (1000+ posts) Send PM | Profile | Ignore Fri Sep-18-09 08:20 PM
Response to Reply #20
24. Dr. William Grant worked at NASA in their Atmospheric Science division
As far as I can figure, he as no formal education in any health-related fields.

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Why Syzygy Donating Member (1000+ posts) Send PM | Profile | Ignore Fri Sep-18-09 09:00 PM
Response to Reply #24
25. He has published research papers.
Grant WB. An estimate of premature cancer mortality in the U.S. due to inadequate doses of solar ultraviolet-B radiation. Cancer. 2002 Mar 15;94(6):1867-75.

Grant WB. Hypothesis--ultraviolet-B irradiance and vitamin D reduce the risk of viral infections and thus their sequelae, including autoimmune diseases and some cancers. Photochem Photobiol. 2008 Mar-Apr;84(2):356-65.

Grant WB, Garland CF. A critical review of studies on vitamin D in relation to colorectal cancer. Nutr Cancer. 2004;48(2):115-23.

Grant WB, Garland CF, Holick, MF. Comparisons of estimated economic burdens due to insufficient solar ultraviolet irradiance and vitamin D and excess solar UV irradiance for the United States. Photochem Photobiol. 2005;81:1276-86.

Grant WB, Garland CF. The association of solar ultraviolet B (UVB) with reducing risk of cancer: multifactorial ecologic analysis of geographic variation in age-adjusted cancer mortality rates. Anticancer Res. 2006 Jul-Aug;26(4A):2687-99
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tiptoe Donating Member (1000+ posts) Send PM | Profile | Ignore Fri Sep-18-09 10:42 PM
Response to Reply #24
27. William B Grant-Ph.D. Physics, UC Berkeley- Published first paper linking diet + Alzheimer's disease

March 13, 2004

Name:  William B. Grant

Degree:  Ph.D. in Physics, U.C. Berkeley

Professional Career:
Worked at the level of senior research scientist in the fields of optical and laser remote sensing of the atmosphere and atmospheric sciences at SRI International, the Jet Propulsion Laboratory, and the NASA Langley Research Center. This career included doing pioneering laser remote sensing instrument development, while the latter half included participating on many NASA-led airborne atmospheric chemistry field missions to the far corners of the world, as well as writing a number of papers on the observations. Author or coauthor of over 60 articles in the peer-reviewed journals, edited 2 books of reprints, and contributed half a dozen chapters to other books. Elected Fellow of the Optical Society of America in 1992.

Current Position:
Director, Sunlight, Nutrition and Health Research Center, an entity devoted to research, education, and advocacy relating to the prevention of chronic disease through changes in diet and lifestyle.

Key contributions in the field of nutrition and ultraviolet radiation research, health and disease:
Published the first paper linking diet to Alzheimer's disease and identifying the major dietary components that are risk and risk reduction factors.
Presented strong evidence that sweeteners are an important risk factor for coronary heart disease for pre-menopausal women.
Extended the list of internal cancers for which vitamin D reduces the risk from 5 to 16 in an ecologic study including solar ultraviolet-B (UVB) irradiance, degree of urbanization, lung cancer mortality rates, alcohol consumption, fraction of white Americans with Hispanic heritage, and fraction of the population living below the poverty level (submitted).
Confirmed a recent finding from Scandinavia that men with moderate serum 25(OH)D levels have lower risk for prostate cancer than those with lower or higher levels. An ecologic study of prostate cancer mortality rates in the U.S. was used.
Confirmed allium family vegetables (onions, garlic, etc.) as important risk reduction factors for prostate cancer.
Confirmed that animal products are important risk factors for breast, colon, and prostate cancer.
Performed a critical review of papers reporting findings on vitamin D and colorectal cancer, concluding that at the population level, dietary vitamin D amounts are insufficient at present to significantly reduce the risk; only total ingested vitamin D (diet plus supplements) plus solar or artificial UVB can raise serum 25(OH)D3 levels to protective levels.
Summarized the evidence on UVB and vitamin D in reducing the risk of non-calcemic diseases for a National Institutes of Health vitamin D conference (submitted).

Current health-related research activities:
Making the case that autism is, to some extent, a maternal vitamin D-deficient disease.
Extending studies on solar UVB and vitamin D in reducing the risk of cancer.
Extending studies on dietary links to cancer and other chronic diseases.
Investigating dietary, lifestyle, smoking, and UV links to melanoma and non-melanoma skin cancer.
Investigating the health aspects of solar and artificial UVA and UVB.
Working to restore the ecologic approach to a position of respect among the health research community.
Researching whether autism is, to some extent, a maternal vitamin D-deficient disease, and the role that infant vaccinations may play.

Key publications:
Grant WB. Dietary links to Alzheimer's disease, Alz Dis Rev 1997;2:42-55 (55 Institute of Scientific Information (ISI) citations, 4 book citations)

Grant WB. Milk and other dietary influences on coronary heart disease, Altern Med Rev, 1998;3:281-94 (5 ISI citations, 1 book citation)

Grant WB. An ecologic study of dietary and solar UV-B links to breast carcinoma mortality rates, Cancer. 2002;94:272-81. (16 ISI citations)

Grant WB. An estimate of premature cancer mortality in the United States due to inadequate doses of solar ultraviolet-B radiation, Cancer. 2002;94:1867-75. (26 ISI citations) (note - this puts the paper in the top 1 percentile of clinical medicine papers published in 2002)

Grant WB. A multicountry ecologic study of risk and risk reduction factors for prostate cancer mortality, Eur Urol. 2004;45:371-9.

Grant WB, Garland CF. A critical review of studies on vitamin D in relation to colorectal cancer, Nutr Cancer. 2004;48(2):115-23. in press (accepted mid-February 2004).

Grant WB. Geographic variation of prostate cancer mortality rates in the U.S.A.; implications for prostate cancer risk related to vitamin D; Int J Cancer. 2004 Sep 1;111(3):470-1; author reply 472. (accepted Feb. 12, 2004)

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MichaelHarris Donating Member (1000+ posts) Send PM | Profile | Ignore Thu Sep-17-09 05:57 PM
Response to Original message
7. You do know
you're getting your information from a site with this: Your tax-deductable gift will help us to be more effective in our mission to end the worldwide epidemic of vitamin D deficiency.

Why not try this site with actual research:
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Celebration Donating Member (1000+ posts) Send PM | Profile | Ignore Thu Sep-17-09 09:10 PM
Response to Reply #7
14. from Linus Pauling Institute
"Growing awareness that vitamin D insufficiency has serious health consequences beyond rickets and osteomalacia highlights the need for accurate assessment of vitamin D nutritional status. Although there is general agreement that serum 25(OH)D level is the best indicator of vitamin D deficiency and sufficiency, the cutoff values have not been clearly defined (18). While laboratory reference ranges for serum 25(OH)D levels are often based on average values from populations of healthy individuals, recent research suggests that health-based cutoff values aimed at preventing secondary hyperparathyroidism and bone loss should be considerably higher. In general, serum 25(OH)D values less than 20-25 nmol/L (8-10 ng/mL) indicate severe deficiency associated with rickets and osteomalacia (17, 19). Although 50 nmol/L (20 ng/mL) has been suggested as the low end of the normal range (33), more recent research suggests that PTH levels (34, 35) and calcium absorption (36) are not optimized until serum 25(OH)D levels reach approximately 80 nmol/L (32 ng/mL). Thus, at least one vitamin D expert has argued that serum 25(OH)D values less than 80 nmol/L should be considered deficient (17), while another suggests that a healthy serum 25(OH)D value is between 75 nmol/L and 125 nmol/L (30 ng/mL and 50 ng/mL) (37). With this latter cutoff value for insufficiency (i.e., 75 nmol/L or 30 ng/mL), it is estimated that one billion people in the world are currently vitamin D deficient (38). Data from supplementation studies indicate that vitamin D intakes of at least 800-1,000 IU/day are required by adults living in temperate latitudes to achieve serum 25(OH)D levels of at least 80 nmol/L (39, 40)."
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laughingliberal Donating Member (1000+ posts) Send PM | Profile | Ignore Mon Oct-26-09 07:06 PM
Response to Reply #7
34. Well, people get information from a site that says this:
Is my gift tax-deductible?
St. Jude Childrens Research Hospital is exempt from federal income taxes under Section 501(C)(3) of the Internal Revenue Code, therefore your gift is tax-deductible to the full extent provided by law. St. Jude is a nonprofit charity operating since 1962. Our federal tax identification number is 62-0646012. You should consult your financial planner or tax adviser to determine the exact tax advantages of any gift you are considering. We provide a receipt for all online gifts that can be used to claim a tax deduction. If you need a copy of the receipt or need a receipt for your annual giving please call 1-800-822-6344.

A very reliable source that is the 2nd largest fund raising organization in the world and a former employer of mine :)
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Sinistrous Donating Member (1000+ posts) Send PM | Profile | Ignore Fri Sep-18-09 11:11 PM
Response to Original message
28. K
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snagglepuss Donating Member (1000+ posts) Send PM | Profile | Ignore Mon Sep-28-09 08:11 PM
Response to Original message
29. The researcher that Dr Cannell consults is Dr Rienhold Vieth at U of Toronto.
Vieth is considered one of the world's preeminent Vitamin D experts. In a 1999 study published in the American Journal of Clinical Nutrition he addresses the safety of large doses of Vitamin D. This is a must read for anyone concerned about Vit D safety.

Vieth has been a tireless crusader for increasing over the counter Vitamin D. His 135 published studies cited in countless scientific publications can be read at PubMed.

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mzmolly Donating Member (1000+ posts) Send PM | Profile | Ignore Mon Sep-28-09 08:53 PM
Response to Original message
30. I did not see how much vitamin D to take? In english
anyway. ;)
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fanofvan Donating Member (2 posts) Send PM | Profile | Ignore Sat Oct-24-09 03:39 AM
Response to Reply #30
31. How much should one take?
I have skin issues so I currently take 10,000IU A with 400 IU D a day. I don't have a chance to get out in the sun.

I don't see where anyone said to take an overdose.
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HysteryDiagnosis Donating Member (1000+ posts) Send PM | Profile | Ignore Sat Oct-24-09 01:37 PM
Response to Reply #31
33. Until you put some on ignore?.... quite a bit apparrently. Welcome
to DU, hope your stay is a pleasant one.
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tiptoe Donating Member (1000+ posts) Send PM | Profile | Ignore Fri May-14-10 12:57 PM
Response to Reply #31
42. Vitamin A as retinol (pre-formed, active A) or beta-carotene (pro-formed, substrate A)?
Vitamin D, Vitamin A and Cancer

So it is not just autistic children that are being harmed by vitamin A. Avoid cod liver oil like the poison it is and check your multivitamins. Life Extension Foundation just reformulated their multivitamin to contain only 500 IU of preformed retinol. And, I am happy to report that Purity Products, which markets my vitamin D, has no preformed retinol at all in any of their multivitamins, only beta-carotene. Purity has also stopped selling cod liver oil. Now, if only Carlson, Solgar, Nature's Way, and other companies would stop selling cod liver oil and stop selling their concentrated vitamin A supplements to a country whose problem is widespread sub-clinical vitamin A toxicity, I'd be a happier agitator.

Vitamin A Toxicity
The crux of the problem is that a form of vitamin A, retinoic acid, weakly activates the vitamin D response element on the gene and perhaps blocks vitamin D's more robust activation. In fact, the authors of a 1993 study state "there is a profound inhibition of vitamin D-activated...gene expression by retinoic acid."

The key is having the proper ratio of vitamin D to vitamin A in your body. To obtain this proper D/A ratio, you must make a choice. (1) Either obtain the D/A ratio Nature intendedthat is, the ratio the human genome evolved onor (2) assume one knows better and intervene in a closed system, bypass the controls in the intestine, and inject active A directly into your blood by taking vitamin A or cod liver oil. Vitamin A production is tightly controlled in the body, the source (substrate) being carotenoids from vegetables in your intestine. The body uses these carotenoid substrates to make exactly the right amount of retinol for your body. That is, it is a closed, tightly regulated, system, one designed to perfection by Nature. When you take vitamin A as retinol, such as in cod liver oil, you intervene in this closed system and bypass the controls. Proceed at your peril.

Vitamin D is also a closed, controlled system and I don't recommend intervening in that system either. Vitamin D cholecalciferol is a substrate like carotenoids, it is not the active substance. Taking vitamin A as retinol is like taking activated vitamin D (calcitriol). Doing so bypasses controls and I have never recommended anyone take activated vitamin D except patients with renal failure under the care of a nephrologist. As long as your vitamin D (cholecalciferol) dose is not excessive, you are not intervening in a closed system, you are simply providing the vitamin D substrate. The body, if and when it has enough vitamin D substrate, will use what it needs and dispose of, or store, the rest.

Thus the goal is to provide all the vitamin A and vitamin D substrate the body would have obtained in a natural state, so the body can regulate both systems naturally. This is best done by eating colorful vegetables and by exposing your naked skin to equatorial sun every day. Since most of us can't do the later, and won't do the former, we have to take the same amount of vitamin D substrate we would have obtained living 100,000 years agoand may want to take beta-carotene substrate in a multivitamin. As far as I know, low doses of beta-carotene (1,0002,000 IU per day) will not do too much harm. The best way to get vitamin D substrate, as far as I can tell, is to take at least 5,000 IU of vitamin D3 per day in the winter and stop all vitamin D in the summer and sunbathe. Alternatively, use a tanning bed when the sun is too low on the horizon to sunbathe. Remember, when you are outside, if your shadow is longer than you are, you are not making any vitamin D.

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tiptoe Donating Member (1000+ posts) Send PM | Profile | Ignore Mon Nov-02-09 06:18 PM
Response to Reply #30
37. see below
Edited on Mon Nov-02-09 07:17 PM by tiptoe

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xchrom Donating Member (1000+ posts) Send PM | Profile | Ignore Mon Oct-26-09 08:51 PM
Response to Original message
35. ...
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Fire_Medic_Dave Donating Member (1000+ posts) Send PM | Profile | Ignore Mon Oct-26-09 09:24 PM
Response to Original message
36. The Vitamin D Council. Are you serious?
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tiptoe Donating Member (1000+ posts) Send PM | Profile | Ignore Tue Apr-20-10 07:06 AM
Response to Reply #36
41. are you...oh...never mind nt
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tiptoe Donating Member (1000+ posts) Send PM | Profile | Ignore Mon Nov-02-09 07:19 PM
Response to Original message
38. "How Much Vitamin D Do I Take?" (Safety and MD general recommendations) - x
Edited on Mon Nov-02-09 08:17 PM by tiptoe

for maintaining wellness, see  Safety & two MD general recommendations: "How Much Vitamin D Should I Take?"
(for an understanding and appreciation of the researched safety and efficacy of various dosages of vitamin D3, wrt 'Disease Incidence Prevention')

re treating H1N1 w vitamin D3, Dr. John Cannell writes:
3. Stock your home's pharmacy with several fresh bottles of 50,000 IU capsules of Vitamin D3 (a medicine at this dosage, not a supplement) and if you get this flu, take 2,000 IU per kg of body weight per day for a week. ..."

also, Treating Disease With Vitamin D
We predict that treatment with physiological doses of vitamin D3 (between 4,00010,000 IU/day from all sources, including sun, food and supplements) along with periodic monitoring of blood calcidiol and calcium levels will become routine.1,2  Research indicates it will help several vitamin D deficiency-associated diseases such as: autism, autoimmune illness, cancer, chronic pain, depression, diabetes, heart disease, hyperparathyroidism, hypertension, influenza, myopathy (neuromuscular disorders), and osteoporosis.

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EvolveOrConvolve Donating Member (1000+ posts) Send PM | Profile | Ignore Fri May-14-10 04:42 PM
Response to Reply #38
43. I've asked this before:
Why do all your links lead eventually to the Vitamin D Council? Even your links to your other DU posts lead to links back to the Vitamin D Council. Which, as I noted in another thread, is listed as a questionable organization by Quackwatch. The Vitamin D Council is funded by organizations that sell vitamin D. Just like pro-smoking lobbyists are funded by tobacco companies and energy "reform" laws are promoted by groups funded by oil companies.

John Cannell himself has good credentials, but some questionable practices and recommendations. The fact that he has weighed in with a quack-worthy hypothesis regarding autism (surprise, surprise, it includes consuming more vitamin D, which he is paid to promote) leads me to question his motives.

Look, vitamin D has benefits, and maybe the RDA is even too low, but you're promoting vitamin D as a potential cure for "autism, autoimmune illness, cancer, chronic pain, depression, diabetes, heart disease, hyperparathyroidism, hypertension, influenza, myopathy (neuromuscular disorders), and osteoporosis" at levels that are potentially dangerous. That's irresponsible.
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tiptoe Donating Member (1000+ posts) Send PM | Profile | Ignore Fri May-14-10 10:56 PM
Response to Reply #43
45. "John Cannell has good credentials, but some questionable practices and recommendations"
Edited on Fri May-14-10 11:51 PM by tiptoe

"At levels that are potentially dangerous"

Explain both statements and be specific, so readers can assess

1) Cannell and his "questionable practices and recommendations" and latest research on toxicity.
2) you and/or whatever you'll hopefully be clarifying.

Latest Research articles on all those topics you listed are updated on Cannell's site.
Is that irresponsible? (I find it helpful.)

I find it curious for Quackwatch (or any "watchdog") to publicize an organization as "questionable" without a basis given for readers to reflect upon. "Guilty" before "proven" innocent? Is that the standard of "responsible" that you respect? If John Cannell's credentials are "good", then his opinions presumably are based on science and are "professional." If not, please explain your basis...wait, you've already apparently accepted Quackwatch's standard of "no need to explain." Or do you just not like the implications of the Vitamin D findings?? If so, which implications and why?

Some "Panacea":
Vitamin D-Deficient Fathers

That is, toxin ingestion by Vitamin D deficient men causes oxidative damage leading to genetic mutations in sperm. The authors' suggestion is to give Vitamin D to men, before they go around impregnating, to prevent genetic damage by toxins and thus prevent autism. While I certainly agree men should take Vitamin D before they impregnate anyone (and I suspect they will be more successful in their mission if they do), I doubt healthy men will take Vitamin D any time soon.

Even if the new Food and Nutrition Board recommends 5,000 IU/day for healthy adultsand they won'thealthy men will ignore any new FNB recommendation because most men will not take supplements,
unless they think it prevents hair loss,
increases sexual abilities, or
improves athletic performance

(Vitamin D has no effect on the first two but certainly improves athletic performance).

John Cannell, MD

"The public health implications of vitamin D deficiency are as stunning as they are vast. No one is proposing that vitamin D is a panacea, however it seems to provide part of the sturdy framework for our physical and mental well being."

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EvolveOrConvolve Donating Member (1000+ posts) Send PM | Profile | Ignore Fri May-14-10 11:50 PM
Response to Reply #45
46. Um, I provided links to information on that
And, you responded with..... drum roll please..... MORE links to the Vitamin D Council.
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tiptoe Donating Member (1000+ posts) Send PM | Profile | Ignore Fri May-14-10 11:55 PM
Response to Reply #46
47. "but you're promoting vitamin D as a potential cure for..." Passing along findings of scientists. nt
Edited on Sat May-15-10 12:01 AM by tiptoe
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tiptoe Donating Member (1000+ posts) Send PM | Profile | Ignore Sat May-15-10 12:24 AM
Response to Reply #43
48. "quack-worthy hypothesis regarding autism" Again, without your specifics, isn't that irresponsible?
Edited on Sat May-15-10 01:24 AM by tiptoe

The scientists at Harvard probably receive theories about everything under the sun.

I'm going to go out on a limb and surmise that "quackworthy" theories would be among the ones the five scientists at Harvard would reject -- based on success at falsifying -- not the ones they accept and publicize as doing do, because they couldn't (yet) falsify -- like Cannell's Vitamin D Theory if Autism. (That's obvious, right?)

Cannell's theory re autism will continue to be subjected to scientitifc scrutiny, even after the Harvard scientists' acceptance. Cannell claims he hasn't found a major facet of autism that his theory cannot explain. Attempts will continue to falsify it (even by Cannell himself). That's how science proceeds.

Meanwhile, the CDC, AMA, AAP, NIH, Kaiser et al mainstream-science, standards-setting "non-quacks" will continue along their respective presumably non-$$$-conflicted practices and recommendations...

If Cannell's theory is correct, however, the "non-quacks" are responsible for the epidemic of autism.

At least Kaiser is measuring and recording vitamin d status of its patients (and showing the actual D-value to the patient, I believe...not sure, though), which is good, for reasons Warpy points out. Hopefully, Kaiser will be sharing its scientific findings on rates of autism in its health plan members' children. What would they have to lose? If testing shows a comparative, statistically-significant higher rate of autism in Kaiser members' children, Kaiser's business interest in cutting operational costs would be reflected in any new posture towards the current "non-quack" AAP 1999 advisements.
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EvolveOrConvolve Donating Member (1000+ posts) Send PM | Profile | Ignore Sat May-15-10 08:43 AM
Response to Reply #48
49. Nice, a link to something other than the Vitamin D Council
You're making some nice headway!
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tiptoe Donating Member (1000+ posts) Send PM | Profile | Ignore Fri Aug-06-10 09:45 PM
Response to Reply #49
52. a few more links at #51
Edited on Fri Aug-06-10 10:18 PM by tiptoe

...for the elderly to make some headway against the vaccine(-only) industry shills.

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tiptoe Donating Member (1000+ posts) Send PM | Profile | Ignore Sun Aug-08-10 04:53 PM
Response to Reply #43
53. Five 'quacks' @ Harvard University accept the Vitamin D Theory of Autism - x

5 Harvard researchers accept the Vitamin D theory of autism

Kinney DK, Barch DH, Chayka B, Napoleon S, Munir KM

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HuckleB Donating Member (1000+ posts) Send PM | Profile | Ignore Fri May-14-10 04:53 PM
Response to Original message
44. More Flu Woo For You, Boo Boo
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tiptoe Donating Member (1000+ posts) Send PM | Profile | Ignore Mon May-17-10 03:18 PM
Response to Original message
51. On the Epidemiology of Influenza -- JJCannell, MZasloff, CFGarland, RScragg, EGiovannucci
Edited on Mon May-17-10 03:59 PM by tiptoe

On the Epidemiology of Influenza

John J Cannell,  Michael Zasloff,  Cedric F Garland,  Robert Scragg  &  Edward Giovannucci

author addresses and corresponding & author emails

Virology Journal 2008, 5:29 doi:10.1186/1743-422X-5-29

The electronic version of this article is the complete one and can be found online at:
Published: 25 February 2008

2008 Cannell et al; licensee BioMed Central Ltd.
This is an Open Access article distributed under the terms of the Creative Commons Attribution License ( ), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.



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?

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.

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.

Figure 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.

Figure 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-ϒ, 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.

Human studies attempting sick-to-well human transmission

In 2003, Bridges et al reviewed influenza transmission and found "no human experimental studies published in the English-language literature delineating person-to-person transmission of influenza. This stands in contrast to several elegant human studies of rhinovirus and RSV transmission ..." 50. (p. 1097)

However, according to Jordan's frightening monograph on the 1918 pandemic, there were five attempts to demonstrate sick-to-well influenza transmission in the desperate days following the pandemic and all were "singularly fruitless" 19. (p. 441) Jordan reports that all five studies failed to support sick-to-well transmission, in spite of having numerous acutely ill influenza patients, in various stages of their illness, carefully cough, spit, and breathe on a combined total of >150 well patients 51-55.

Rosenau's work was the largest of the studies, illustrative of the attempts, and remarkable for the courageousness of the volunteers 52. In 1919 in a series of experiments he and six colleagues at the U.S. Public Health Service attempted to infect 100 "volunteers obtained from the Navy." He reports all volunteers were "of the most susceptible age," and none reported influenza symptoms in 1918. That is, "from the most careful histories that we could elicit, they gave no account of a febrile attack of any kind," during the previous year. The authors then selected influenza donors from patients in a "distinct focus or outbreak of influenza, sometimes an epidemic in a school with 100 cases, from which we would select typical cases, in order to prevent mistakes in diagnosis of influenza." Rosenau made every attempt to get donors who were early in their illness, "A few of the donors were in the first day of the disease. Others were in the second or third day of the disease."

"Then we proceeded to transfer the virus obtained from cases of the disease; that is, we collected the material and mucous secretions of the mouth and nose and bronchi from (19) cases of the disease and transferred this to our volunteers. We always obtained the material in the following way: The patients with fever, in bed, has a large, shallow, traylike arrangement before him or her, and we washed out one nostril with some sterile salt solution, using perhaps 5 c.c., which is allowed to run into this tray; and that nostril is blown vigorously into the tray. That is repeated with the other nostril. The patient then gargles the solution. Next we obtain some bronchial mucous through coughing, and then we swab the mucous surface of each nares and also the mucous membranes of the throat."

Then they mixed all the "stuff" together and sprayed 1 cc of the mixture in each of the nostrils of 10 volunteers, and "into the throat, while inspiring, and on the eye" and waited 10 days for the volunteers to fall ill. However, "none of them took sick in any way." Undaunted, Rosenau conducted another experiment in which ten acutely ill influenza patients coughed directly into the faces of each ten well volunteers. Again, "none of them took sick in any way."

Perhaps Rosenau's and similar experiments failed because all the well volunteers had contracted infections in 1918 and were immune from further infection. While possible, none of the volunteers reported symptoms in 1918, even a fever. Furthermore, adaptive immunity to influenza is relative to the immune response that infection generates and to the time since infection; it is seldom absolute and abiding.

Another explanation is that all of the influenza patients had passed their time of infectivity although Rosenau obtained donors in the first, second, or third day of their illnesses. As no laboratory confirmation was possible, perhaps the ill did not have influenza, but we doubt U.S. Public Health Service physicians had much trouble making accurate clinical diagnosis of influenza in 1919. Furthermore, all the donors were symptomatic; peak viral shedding occurs 2472 hours after infection, and the amount of virus shed is associated with symptoms 56. Perhaps peak viral shedding is not associated with peak infectivity. Perhaps although Rosenau does not report the date or season of the experiments all the naval volunteers had adequate innate immunity from sun exposure. Obviously, another explanation is that sick-to-well transmission is not the usual mode of contagion.

Naturalistic reports of sick-to-well transmission

A number of naturalistic studies suggest influenza is transmitted from the sick to the well 57-59. They all assume the first case was the index case. The best-known case is an airliner in Alaska, where an extensive outbreak of influenza occurred after an infected patient appeared among well, and the airliner subsequently malfunctioned, causing a four-hour delay in which passengers breathed re-circulated air 60.

Although her influenza culture was negative, the authors hypothesized their "index case" infected 37 well passengers within a mean of 38 hours after she boarded the plane. However, 30 other passengers boarded the Alaskan plane at the same time as the sick passenger, and other passengers were already onboard, any of whom could have been the common source. The airline study, like other naturalistic studies, is very suggestive of a common source and aerosol transmission, but offers no proof that the common source was the suspected index case, other than the logic that if A preceded B then A must have caused B.

Experts frequently cite an experience at an "irradiated" Livermore, California, VA hospital during the 195758 influenza epidemic as naturalistic evidence of sick-to-well aerosol influenza transmission. McLean (as part of a general discussion in a paper by Jordan) 61 reported an entire hospital building unit, housing approximately 150 patients with chronic pulmonary disease, was "totally radiated" in an attempt to reduce TB contagion through the air. There remained, nonradiated, another 250 control patients. He reported a two percent influenza attack rate for the "radiated patients" compared to a 19 percent attack rate for the "nonradiated patients." (p. 37).

However, Maclean's description of the Livermore hospital's irradiation procedures is inadequate to know if patients were being directly irradiated, thus triggering vitamin D production in their skin. However, careful inspection of another 1957 publication about a similarly irradiated Baltimore VA hospital co-authored by McLean is illuminating 62. The Baltimore hospital wing apparently used a similar irradiation set-up with "standard ultraviolet light fixtures." (p. 421) Illustrations clearly show despite text stating that only upper air was irradiated that the rooms and hallways were all equipped with UV lights that either shone directly or indirectly on patients, apparently 24 hours per day, seven days a week (see pp. 422423 for illustrations). If the irradiation processes were similar in Livermore and Baltimore hospitals, they would have significantly raised the 25(OH)D levels of the irradiated, and relatively influenza-free, patients.

Furthermore, if irradiation of the air destroyed viral aerosols and was responsible for the lower attack rate, such results should be reproducible. In a carefully controlled trial, Gelperin et al directly investigated the possibility of transmission of viral respiratory illness by aerosols 63. For four months during the height of the flu season, the authors carefully irradiated only the upper air in half the classrooms in eight New Haven schools with ultraviolet light, and, unlike the Livermore VA hospital, the researchers took great care not to irradiate the students, either directly or indirectly. When they compared absenteeism in irradiated classrooms to non-irradiated control schools, they found no effect from upper air irradiation. Two other large field studies in schools likewise showed no effect from UV air irradiation on viral diseases transmitted via the respiratory tract 64,65.

These last three studies do not disprove aerosol transmission. Such transmission could have occurred at lower room levels and the schoolchildren were free to contract infections outside of the classroom. However, one might have expected some decrease in infection rates. Furthermore, their negative results stand in stark contrast to the dramatic effects seen in the irradiated patients in Livermore, leading us conclude the irradiated Livermore patients were the beneficiaries of more than just cleaner air.

What is the serial interval for influenza?

The generally accepted theory of sick-to-well transmission demands direct epidemiological measurement (not calculation from the incubation period) of a serial interval between causal and resultant cases (time between successive cases in a chain of transmission) as has been amply demonstrated for other respiratory infectious diseases. In families, where the virus infects one member outside the home and that member then infects others inside the family, a serial interval should be easy to demonstrate if the virus is propagating itself via sick-to-well transmission. Unfortunately, when the World Health Organization Writing Group reported that "the serial interval ... is 2 4 days" (p. 83) for influenza, they failed to give a reference and apparently meant the incubation period is 2 4 days 56. While the incubation period of influenza is well documented, if anyone has successfully documented a serial interval for influenza in families, we have yet to locate their work.

In contrast, Hope-Simpson, using viral isolates obtained over 8 years, found low attack rates within households, a high proportion of affected households with only one influenza case (70%), and no demonstrable serial interval 66. A five-year serological surveillance study found that 73% of family members who get influenza get it on the first day and are apparent index cases 67. They could not identify a serial interval. Jordan et al followed 60 families during the Asian epidemic of 1957, isolating the virus from 86% of the families 68. They found no evidence of a serial interval. Jordan later reviewed similar studies and reported, "No peak occurred at the expected incubation period when secondary cases in families were plotted by intervals from the index case" 61. (p. 32).

Viboud et al did not say so, but they apparently could not demonstrate a serial interval in families, as secondary cases did not peak at any particular interval after the first case in the family 69. Remarkably, in 116 families, two family members developed symptoms simultaneously. Of the 131 family members who developed a flu-like illness within five days of the 543 serologically confirmed first cases, it appears that 38 of 131 occurred on day one, 40 on day two, 30 on day three, 28 on day four, and nine on day five.

If influenza is highly contagious, a serial interval should be evident easily observed and directly measured as sick family members infect the well. The large percentage of family members that sicken on the first day and the lack of a demonstrable serial interval, despite numerous attempts to measure one, seems more consistent with a limited number of infectors, usually outside the family, than with all the sick being infectors.

What is the secondary attack rate for influenza?

The reproductive number, R0, an estimation of the average number of new cases of influenza produced by each infectious case in a fully susceptible population, has replaced secondary attack rates in most epidemiological models. However, the R0 for influenza has been "notoriously hard to estimate" 70 (p. 11146). While the estimated R0 remains obscure, epidemiologists have directly measured its father, secondary attack rates, for more than 5 decades. For a highly infectious virus, secondary attack rates for influenza are surprisingly low.

Secondary attack rates for influenza cannot be accurately determined without knowing the serial interval and are thus actually subsequent attack rates. Subsequent attack rates inflate the rate because they include all co-primary, tertiary, and later cases as secondaries. The subsequent attack rate for rhinovirus among non-immune family members is 58% 71. The rate for unvaccinated household contacts is 70% for measles 72 and 71% for varicella 73. If influenza is highly contagious and spread by the sick, then secondary attack rates should reflect that contagiousness.

However, 80% of household members with an infected family member escaped the first outbreak of Hong Kong influenza in Great Britain despite it being a new antigenic variant in a non-immune population 74. Thus, even if one assumes all subsequent cases were secondaries, the secondary attack rate was only 20%. Neuzil et al found that 22% of household members became ill within three days of a child in the family being absent from school due to illness but did not report how many family members became ill on the same day as the child 75. Using a specific clinical definition in secondary cases, Viboud et al found a subsequent attack rate of 18% 69.

Longini et al analyzed data from four large family studies, reporting the apparent secondary attack rates varied from 13 to 30% 76. After taking the community infection rate into account, they concluded the actual secondary attack rate among family members was 15%. Later, Longini et al estimated the secondary attack rate for adults and children with low levels of preexisting viral specific antibodies was 18 percent and 37%, respectively, while the secondary attack rate in adults and children with high levels of such antibodies was 1.6% and 3.4%, respectively 77.

For a review of all studies on subsequent attack rates up to 1986, see Thacker 78. Of the eight household studies he analyzed, four showed a subsequent attack rate in the teens (14%, 15%, 15%, 17%), two in the twenties (21% and 27%), one was 31%, while one was 58% (H3N2 in New Zealand in 1973). The weighted mean of subsequent attack rates in all 870 households was 22%.

A recent review combining the data from four controlled household studies of antiviral effectiveness in the control households found a combined subsequent attack rate of 13% for symptomatic laboratory confirmed infections (136 of 1061 contacts) and 23% for any laboratory confirmed infections (246 of 1061 contacts) 79.

Such low subsequent attack rates in families seem inconsistent with a highly infectious virus sustaining itself by sick-to-well transmission. They seem more consistent with large intrafamilial variations in immunity and family members contracting the infection, usually outside the home, from a common source.

Animal studies

Ironically, the strongest evidence for sick-to-well transmission in man comes from studies of ferrets. Unlike human studies, studies show infected ferrets readily transmit influenza to well animals and those newly sickened animals readily infect a third animal and so on 80. Recently, similar experiments with guinea pigs were able to sustain a chain of eight successive transmissions but the animals do not become ill (written communication with Lowen A., Palese Laboratory). Likewise, hamsters can transmit influenza but apparently do not become ill 81. Schulman and Kilbourne were able to infect about 50% of secondary mice after caging them with a two experimentally infected animals 82. However, they were unable to get the newly sickened mice to transmit, that is, instigate a chain of transmission from sick to well mice.

Schulman and Kilbourne did demonstrate that some infector mice are "good transmitters" while other mice will not transmit the virus, it spite of inoculation with the same dose of virus. That is, for unknown reasons, some infected mice readily transmit the disease to their littermates and some will not. As all infector mice received an identical inoculum of virus, it is reasonable to hypothesize that good transmitters have an unidentified inadequacy in innate immunity that facilitate their ability to transmit the virus.

It is worth noting that one animal study indicated vitamin D, when added to the diet of rats, prevented influenza but a subsequent paper reported it did not 83,84. Young et al also reported that a Japanese researcher, Midzuno, was able to reproduce influenza in rats simply by maintaining them on diets deficient in vitamin D, apparently part of Japan's World War II biological weapons research. (The American CIA confiscated Midzuno's papers after the war.) As vitamin D does not upregulate AMPs in murine mammals, it is unclear what these studies mean. If researchers can identify an influenza susceptible species in which vitamin D increases expression of AMPs, it would be useful to know if vitamin D deficiency promotes the pathology of influenza.


After a 20 year search for parsimony, Hope-Simpson hypothesized that influenza is mainly transmitted by a limited number of highly infectious latent carriers carriers infected the prior season who are called into infectivity by a "seasonal stimulus" inextricably bound to sunlight and who remain highly infective for brief periods, thus explaining the waves of influenza that abruptly end despite a wealth of non-immune potential victims 2. Nevertheless, to our knowledge, researchers have never demonstrated latency for influenza, as expected with a constantly replicating RNA virus.

However, significant seasonal and population variations in innate immunity make it unnecessary to postulate latency to explain the bizarre epidemiology of influenza. While any theory of influenza must take into account four factors: transmissibility, virulence, adaptive immunity, and innate immunity, it has been easy to ignore innate immunity as it lacked demonstrable seasonal variations, population variations, and a mechanism of action.

To make sense of influenza's epidemiology, we revise Hope-Simpson theory, hypothesizing marked variation in the infectivity of the infected (the good infectors demonstrated in rats by Schulman and Kilbourne in 1963) and that vitamin D deficiency is Hope-Simpson's seasonal stimulus. Adding these two factors to transmissibility, virulence, and adaptive immunity, solves a number of influenza's mysteries.

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

    If influenza were surviving in an endless chain of transmissions from good transmitters to the well the good transmitters being generally asymptomatic during times of enhanced innate immunity the disease would be widely seeded in the population, explaining its ubiquity. Seasonal impairments in innate immunity would allow seasonal epidemics in temperate latitudes and less predictable epidemics in tropical zones, depending on viral novelty, transmissibility, virulence, and the innate immunity of the population. Non-seasonal isolated outbreaks would usually only appear in nursing homes 85 or prisons 86 where lack of sunlight impaired innate immunity; such isolated outbreaks would seldom lead to community outbreaks. More extensive out-of-season outbreaks, as occurred in 1918, would arise when novel antigenic viruses with significantly greater infectivity and virulence overwhelm innate immunity.

  2. Why are influenza epidemics so explosive?

    Predictable fall and winter impairments in innate immunity in temperate latitudes and less predictable recurrent impairments in subequatorial and equatorial latitudes would cause a percentage of the non-immune population to become suddenly susceptible to background influenza virus. The size of that susceptible subpopulation would vary, not only by the size of their impairments in innate immunity, but with the transmissibility and virulence of the virus, and the percentage of the population with competent adaptive immunity. Abrupt deficiencies in innate immunity, especially when large segments of the population also have inadequate adaptive immunity, would allow quiescent influenza to erupt.

  3. Why do epidemics end so abruptly?

    The rapid depletion of the population with both impaired innate and inadequate adaptive immunity may explain the abrupt disappearance of influenza. Impairments in innate immunity may also increase transmission, in effect, turning more infectors, symptomatic or not, into good transmitters. Furthermore, if only a small population of good transmitters and not all the sick usually spread the virus, and their transmission period is limited, the epidemic would end shortly after the good transmitters lose their infectivity.

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

    Simultaneous impairments of innate immunity at similar latitudes due to seasonal sunlight deprivation explain the almost simultaneous eruption of influenza at sites of different longitude but similar latitude. If the virus had already imbedded itself in a population and a subgroup of the infected became good transmitters when their innate immunity declines to a critical threshold, such transmitters would coincidentally infect populations at similar latitudes made susceptible by those same impairments in innate immunity.

  5. Why is the serial interval obscure?

    Good transmitters explain the difficulty identifying influenza's serial interval especially since influenza's incubation period is well known. If only subpopulations of infected persons are good transmitters, and if their infectious period is limited, then the serial interval would remain obscure until we identified the good transmitters. Vitamin D induced variations in natural immunity may also affect influenza's incubation period, further obfuscating the serial interval.

  6. Why is the secondary attack rate so low?

    The studies we identified found a secondary attack rate of around 20%, impossibly low for a highly infectious virus spread from the sick to the well. If only a subpopulation of the infected, the good transmitters, are infective, this would explain the surprisingly low secondary attack rates. Current estimates of secondary attack rates assume the first case in the family is the index case and is spreading the disease. However, if only a subpopulation of infected persons transmit the disease, the true secondary attack rate could not be accurately determined until we identify the good infectors.

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

    If influenza were embedded in the population, only to erupt when impairments in innate immunity create a susceptible subpopulation, the disease would only give the appearance of spreading. Instead, it would appear in large segments of the population seasonally, and almost simultaneously, as long as good transmitters were available. Furthermore, as good transmitters traveled, populations with neither adequate innate immunity nor competent adaptive immunity may succumb. That is, the disease would actually spread, as good transmitters traveled and subsequently infected well subpopulations with impaired immunity.

  8. Why does experimental inoculation of seronegative humans fail to cause consistent illness?

    If influenza is highly infectious, one would expect most, if not all, human volunteers iatrogenically inoculated with a novel virus to fall ill. Although the rate of illness depends on the virus used and the dose of the inoculum, variations in the innate immunity of the volunteers also explain such variable illness response. We propose individual variations in 25(OH)D levels explain some degree of the variations in illness response.

  9. Over the last 20 years, why has influenza mortality in the aged not declined with increasing vaccination rates?

Given that influenza vaccines effectively improve adaptive immunity, the most likely explanation is that the innate immunity of the aged declined over the last 20 years due to medical and governmental warnings to avoid the sun. While the young usually ignore such advice, the elderly often follow it 87,88. We suggest that improvements in adaptive immunity from increased vaccination of the aged are inadequate to compensate for declines in innate immunity the aged suffered over that same time.


Kilbourne once wrote the "student of influenza is constantly looking back over his shoulder and asking 'what happened?' in the hope that understanding of past events will alert him to the catastrophes of the future" 89. That is all we are attempting.

Certainly, without factoring in the effects of innate immunity, we must contort our logic to make sense of influenza's bewildering epidemiological contradictions. When seasonal and population variations in innate immunity are considered in context with the novelty, transmissibility, and virulence of the attacking virus, the conundrums are fewer. A subpopulation of good transmitters among the infected further clarifies influenza's confusing epidemiology. The addition of both variables would improve current epidemiological models of influenza.

Compelling epidemiological evidence indicates vitamin D deficiency is the "seasonal stimulus" 22. Furthermore, recent evidence confirms that lower respiratory tract infections are more frequent, sometimes dramatically so, in those with low 25(OH)D levels 90-92. Very recently, articles in mainstream medical journals have emphasized the compelling reasons to promptly diagnose and adequately treat vitamin D deficiency, deficiencies that may be the rule, rather than the exception, at least during flu season 40,41. Regardless of vitamin D's effects on innate immunity, activated vitamin D is a pluripotent pleiotropic seco-steroid with as many mechanisms of action as the 1,000 human genes it regulates 93. Evidence continues to accumulate of vitamin D's involvement in a breathtaking array of human disease and death. 40,41

In 1992, Hope-Simpson predicted that, "understanding the mechanism (of the seasonal stimulus) may be of critical value in designing prophylaxis against the disease." Twenty-five years later, Aloia and Li-Ng found 2,000 IU of vitamin D per day abolished the seasonality of influenza and dramatically reduced its self-reported incidence 25. (Figure 2) Hence, we propose this modification of Hope-Simpson's theory. We do not expect our revisions to prove invincible, nor do we delude ourselves that influenza is now comprehensible. Rather, we build on Hope-Simpson's theory so that it "may be corroborated, corrected, or disproved." (Hope-Simpson, 1992, p. 191)

AMPs: antimicrobial peptides; RCT: randomized controlled
trial; Pathogen Associated Molecular Patterns: PAMPS

Competing interests
Dr. Cannell heads the non-profit educational group, 'The Vitamin D Council'.

Authors contributions
JJC conceived of the project, consulted with EG, and wrote each new draft.
MZ added material on innate immunity.
CFG and RS revised the first and subsequent drafts and expanded the article's scope.
EG revised and reviewed all drafts and added additional material to each draft.
All authors read and approved the final manuscript.

The authors wish to thank Dr. Brian Mahy of the Centers for Disease Control
and Dr. Cecile Viboud of the National Institutes of Health

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