Life Extension Federal Government-Funded Study Fails to Recognize Value of Vitamin D

Life Extension

A brutal war is being waged whose outcome will determine how long humans live and whether our health care system economically collapses. On one side are the earnings projections of the entrenched medical establishment. These profits are contingent on large numbers of aging Americans contracting cancers, heart attacks, strokes, viral infections and other ailments. On the other side are irrefutable scientific findings showing the incidence of these deadly diseases can be slashed if Americans increase their intake of vitamin D. If too many Americans optimize their vitamin D blood status, the medical establishment will sustain huge economic losses as incident rates of degenerative disease rapidly plummet. In order to protect their outlandish profits, the medical establishment will do whatever it takes to mislead and frighten the public away from higher supplemental vitamin D usage. The medical establishment has a stranglehold over our federal government, academia, and a large segment of the media. As a result, what you are led to believe is tightly controlled by those whose financial interests are dependent on millions of Americans each year contracting degenerative diseases. In response to overwhelming documentation that higher levels of vitamin D protect against virtually every disease, the federal government commissioned the Institute of Medicine to assemble a committee of experts to formally evaluate the data. The experts on this panel have ties in one way or another to the vested interests of the entrenched medical establishment. On November 30, 2010, the Institute of Medicine (IOM) issued a 1,016 page report that concludes that most people in the U.S. and Canada — from age 1 to age 70 — need to consume no more than 600 international units (IU) of vitamin D a day to maintain health. The IOM report mandated those levels as the « recommended dietary allowance » for vitamin D. This new recommendation is triple the previous recommended daily amount of 200 IU that the Institute of Medicine established in 1997. Just as the 200 IU dose of vitamin D was woefully inadequate based on data existing in 1997, so is the ridiculous new recommended daily amount of only 600 IU of vitamin D. How do we know this? The Life Extension Foundation conducted the largest analysis of vitamin D blood tests ever on a group of dedicated supplement users. The typical doses of vitamin D that these individuals used were between 800 IU and 2600 IU a day. The findings showed that 85% of these supplement users had insufficient vitamin D, defined as less than 50 ng/mL of 25-hydroxyvitamin D. Virtually all who follow the recommendations of the federal government-funded IOM study (to take only 600 IU a day of vitamin D) will have insufficient or deficient vitamin D blood levels. The IOM report recognizes this and comes to an even more absurd conclusion that most Americans need to maintain blood 25-hydroxyvitamin D levels of a paltry 20 ng/mL. Those who rely on this horribly flawed IOM report are condemned to suffer horrifically high rates of virtually every known disease, thus ensuring the rosy profit projections of the entrenched medical establishment. The IOM’s recommendations are far below the 5,000–8,000 IU per day (and higher) of supplemental vitamin D required to generate 25-hydroxyvitamin D blood levels in the range of 50–80 ng/ml, shown to be optimal based upon a variety of peer-reviewed, published scientific studies.1-2 Furthermore, the IOM recommends 4,000 IU daily of vitamin D as an upper threshold level for safety despite the fact that in their report the lowest dose of vitamin D cited as being toxic for adults is 30,000–60,000 IU daily for up to 7.5 years,1 and the lowest blood level of 25-hydroxyvitamin D cited as being toxic for adults in their report is 145 ng/mL.2 Despite the plethora of evidence highlighting the association between low 25-hydroxy vitamin D levels and various diseases including multiple types of cancer,3,4,5 cardiovascular disease,6,7 diabetes,8 and depression,9 the IOM failed to acknowledge the important role of vitamin D in areas other than bone health in their report. The alarming lack of comprehension exhibited by the IOM in considering the extra-skeletal actions of vitamin D is exemplified by the concluding remarks of the November 30th report: * “At this time, the scientific data available indicate a key role for calcium and vitamin D in skeletal health and provide a sound basis for [the newly established] DRIs. The data do not, however, provide compelling evidence…related to extra-skeletal health outcomes or that intakes greater than those established in the DRI process have benefits for health.” The Life Extension Foundation has undertaken a thorough review and analysis of the Institute of Medicine report as well as the existing peer-reviewed literature on vitamin D. The findings of this comprehensive evaluation immediately follow. Flawed Studies Mislead Public about Pancreatic Cancer and Vitamin D Pancreatic cancer is ranked fifth among cancer-related deaths worldwide with a 5-year survival rate of less than 5%. Currently, surgery is the only effective therapy. However, most patients are diagnosed in the late stage and are not suitable for receiving curative surgery. Moreover, pancreatic cancer doesn’t respond well to traditional chemotherapy and radiotherapy, leaving little effective treatment for advanced pancreatic cancer cases. The biologically active form of vitamin D was originally identified during studies of calcium and bone metabolism though it is now recognized that it exerts biological effects in almost every tissue in the body. Abundant evidence has shown that biologically active vitamin D has anti-proliferative, apoptotic, pro-differentiation and anti-angiogensis effects in many types of cancer cells in vivo and in vitro, including breast, prostate, and colon. Similarly, the anti-tumor growth effect of activated vitamin D on pancreatic cells has been demonstrated.10 The IOM report, however, questions whether higher vitamin D blood levels increase pancreatic cancer rates. One study IOM relied on was of Finnish male cigarette smokers. The study showed that those with 25-hydroxyvitamin D levels above 26.2 ng/mL sixteen years prior to diagnosis were three times more likely to contract pancreatic cancer than those with 25-hydroxyvitamin D below 12.8 ng/mL. One problem with this analysis is that neither of these levels comes close to achieving the blood levels of 25-hydroxyvitamin D (greater than 50 ng/mL) required to provide cancer protection. A more serious problem is the testing methodology used in this study to measure 25-hydroxyvitamin blood levels was later found to be unreliable and is no longer being used. So no one knows what the 25-hydroxyvitamin blood levels really were in this group. The IOM panel members would not have known that the testing methodologies used in this study were recently discredited. We at Life Extension did because the largest blood testing lab in the U.S. (Quest) had been using it and later switched to the LabCorp methodology to avoid the issue of unreliable results. (More on this later.) An epidemiology meta-analysis [a population-based statistical evaluation of ten different studies from the United States, Finland, and China called the Cohort Consortium Vitamin D Pooling Project of Rarer Cancers (VDPP)] examined the associations between circulating 25-hydroxyvitamin D concentrations and the risk of rarer types of cancers like pancreatic cancer. This study used a flawed statistical method to arrive at this conclusion, but the most obvious error was that it stated that those with 25-hydroxyvitamin D levels over 40 ng/mL of 25-hydroxyvitamin D were at the highest risk. Life Extension knows from its own analysis that it takes around 5,000 IU of supplemental vitamin D to achieve blood levels greater than 40 (ng/mL), and that probably NONE of the study participants evaluated ever supplemented with this much vitamin D (or took any supplements at all for that matter). Consider that individuals in Finland have minimal (or no) sun exposure, and over the majority of the time period evaluated (1974–2006), virtually no one was taking more than 200–400 IU of supplemental vitamin D a day (or none at all). Life Extension knows from our own internal analysis that 800–1600 IU daily of vitamin D3 does not yield >40 ng/mL 25-hydroxyvitamin D levels in the blood. (Young individuals in the summertime typically have 25-hydroxyvitamin D levels of >60 ng/mL, but older individuals do not efficiently synthesize vitamin D from sunlight.) We also highly suspect this high blood level of 25-hydroxyvitamin D (>40 ng/mL) was a false reading based on faulty blood test methodologies. Not all of the blood samples were assayed in a central laboratory using a direct, competitive chemiluminescence immunoassay on the DiaSorin LIAISON platform (DiaSorin, Inc., Stillwater, Minnesota) used by LabCorp. This is a critical fact because other types of vitamin D assays, such as the HPLC dual mass spec assay used by Quest, have potential to generate inaccurate results. Scientific data must always be interpreted in the context of the wider literature as a whole. In fact, a review of the literature strongly indicates inconsistency of the results obtained by this flawed epidemiology meta-analysis. Specifically, the vast majority of the data indicates a protective role for vitamin D and pancreatic cancer. Greater sun exposure and vitamin D production in the skin have been associated with lower death rates for pancreatic cancer in studies in Caucasians11,12, Japanese13,14, and African American15 populations. These studies show that changes are attributable to variations in sun exposure by geographic latitude with individuals at lower latitudes having higher vitamin D status and less cancer. Other published data clearly show that risk factors for pancreatic cancer such as age, obesity, and African American ethnicity, are all associated with reduced vitamin D status.16 Two prospective clinical studies conducted in the Health Professionals Follow-up Study (HPFS) and Nurses’ Health Study (NHS) indicate that vitamin D offers protective benefit for pancreatic cancer. These massive, prospective studies evaluated cohorts of 46,771 men ages 40 to 75 years as of 1986 (the Health Professionals Follow-up Study), and 75,427 women ages 38 to 65 years as of 1984 (the Nurses’ Health Study). The first showed that a higher predicted 25(OH) vitamin D status score was associated with a lower total cancer incidence and mortality including 51% reduced risk of pancreatic cancer (pancreatic cancer n=170, RR=0.49, 95% confidence interval (CI), 0.28–0.86 for incremental plasma 25-hydroxy vitamin D status).17 The second was a pooled analysis of the HPFS and NHS that observed higher total vitamin D intake was associated with a 41% reduced pancreatic cancer risk (n=365 cases, diet and supplemental vitamin D, ≥ 600 IU compared to < 150 IU, RR=0.59, 95% CI 0.40–0.88, p-trend=0.01).18 Greater than 90% of the men and women in the ≥ 600 IU category reported multivitamin use. In analyses stratified by cohort, significant associations for total vitamin D status were evident in the HPFS (n=178 cases, ≥ 600 IU compared to < 150 IU, RR=0.49, 95% CI 0.29–0.82, p-trend= 0.01). Of interest, no associations were observed for vitamin D intake from foods in this second study, supporting the powerful benefits of vitamin D supplementation in helping to achieve these impressive, protective benefits for pancreatic cancer. Another biased, methodologically flawed study published in November 2010 that received widespread mainstream media coverage concluded that dietary intake of vitamin D (≥450 IU/d vs. <150 IU/d) was associated with an increased risk of pancreatic cancer in men.19 However, careful review reveals several important facts not discussed by the media. In this study, patients diagnosed with pancreatic cancer between 1995 and 1999 (n=532), were administered a questionnaire and asked to recall their dietary intake prior to their diagnosis of pancreatic cancer. The accuracy of the food questionnaire that was used to determine total vitamin D intake (a 131-item semi-quantitative food frequency questionnaire) depends on the ability of the subject to recall, down to the portion size, the meals he or she ate prior to pancreatic cancer diagnosis, and further that a computer software program then generates an estimated nutrient intake. The key point is that vitamin D intake or blood levels were not directly measured in this study. As expected, the validity of food frequency questionnaires has been questioned.20 Investigators in this study also stated that their results indicated that greater vitamin D intake (≥450 IU daily vs. <150 IU daily) was associated with increased risk for pancreatic cancer in men, but not in women, yet the researchers in this study failed to fully investigate their findings, contributing to the media’s headlines proclaiming that more than 450 IU of vitamin D daily might increase pancreatic cancer risk. A closer look at the data that these researchers gathered reveals that as estimated vitamin D intake increased greater than 800 IU daily, pancreatic cancer risk was actually decreased.Although only a small number of samples were available for vitamin D intakes exceeding 800 IU daily (with an associated risk reduction of 19%), the researchers did offer the following statements in their conclusion. * “Increased risk associated with total vitamin D (vitamin D supplements and food) was limited to men with low to moderate levels of intake and was diminished in the highest [>800 IU daily] category of intake.” * “The results from [other] studies showed a decreased risk [of pancreatic cancer] with increased vitamin D intake [>800 IU daily] similar to our results…” A third study that received widespread media attention also generated unfounded concerns regarding vitamin D and pancreatic cancer.21 The authors of this highly questionable study proclaimed that a single pre-diagnostic measurement of vitamin D blood levels in male smokers was independently associated with pancreatic cancer development up to 16 years later. However, a closer look at their data reveals the true lack of predictive value of their study. This study population consisted of 600 subjects (n = 200 for pancreatic cancer cases and n = 400 for cancer free controls) from Finland, all of whom were current smokers. Researchers assessed 25-hydroxyvitamin D blood levels between 1985 and 1988. As expected in subjects living in Finland, where exposure to sunlight is minimal during the winter months and far less pronounced during other periods of the year due to the relatively extreme northern latitude, the study subjects had, on average, extremely low levels of vitamin D (mean 20 ng/mL for cases and 18 ng/mL for controls). Furthermore, the “highest” stratified 25-hydroxyvitamin D level was identified as >26 ng/mL, woefully insufficient. Furthermore, given that the steady state half-life of vitamin D in the blood is about three weeks and is highly susceptible to seasonal variations22, it is astonishing that these researchers felt it was acceptable to assume that vitamin D blood levels remained constant for 16 years until the patients were diagnosed with pancreatic cancer. To assume that a single 25-hydroxy vitamin D blood level measurement in people who smoke and live in an area where sun exposure is extremely limited has anything to do with the development of pancreatic cancer 16 years later defies scientific, rational logic. However, setting aside the obvious methodological limitations with this study, higher pre-diagnostic 25-hydroxyvitamin D levels may be observed in pancreatic patients. In fact, using advanced techniques like immunohistochemistry, studies show that 1-alpha(OH)ase (a critical enzyme that helps generate activated vitamin D in tissue) is highly expressed in both normal and malignant pancreatic tissue. Expression of this enzyme and enzymatic activity has been detected in pancreatic tumor cell lines. Data indicate that 25-hydroxyvitamin D3 inhibits the growth of pancreatic cell lines in a manner that correlates with the level of induction of the cyclin-dependent kinase inhibitors p21 and p27 and with the induction of cell cycle arrest at the G(1)/S checkpoint. The growth of pancreatic cancer cell lines indicates that activating Ki-Ras mutations, which occur in almost 90% of pancreatic adenocarcinomas, does not interfere with the growth-inhibitory effects of 25-hydroxy vitamin D3. The expression of 1-alpha(OH)ase in normal and malignant pancreatic tissue and the anti-proliferative effects of the prohormone in these cells indicates that 25-hydroxy vitamin D3 may offer potential therapeutic and chemopreventive options for pancreatic cancer.23 What this also means is that since pancreatic cells produce 25-hydroxyvitamin D, when someone is diagnosed with pancreatic cancer they have a large number of rapidly proliferating pancreatic cells secreting higher levels of 25-hydroxyvitamin D. So compared to healthy controls, a group of pancreatic cancer patients may as whole have higher 25-hydroxyvitamin D because they have more rapidly proliferating (malignant) pancreatic cells releasing it into the bloodstream.

Vitamin D Toxicity

Scientific ignorance of past findings often has dire consequences for the present.

In 1934, the Journal of the American Medical Association published a study on vitamin D overdose.24

The authors reported on 300 patients given high doses of vitamin D2 (ergocalciferol) for asthma and hay fever. The authors reported that each unit dose of vitamin D contained 900,000 IU. One patient received 3 cc per day for five days (total dose: 13.5 million IU) without clinical damage.

In their study summary, the researchers concluded:

  • “There need be little apprehension about the administration of amounts ranging up to 150,000 international units daily for indefinite periods. Larger amounts had better be limited to periods of a few months at most, depending on the therapeutic effects desired.”

Also in 1934, researchers at the University of Illinois studied the effects of vitamin D on asthma and hay fever in 212 patients. The authors reported that 82% of the hay fever patients and 96% of the asthma patients experienced definitive significant relief. The authors concluded that the “optimum dose” of vitamin D was 60,000 to 300,000 IU per day.25

In 1935, researchers at the University of Illinois School of Medicine published their findings on 700 patients treated with “massive” doses of vitamin D for up to two years.26

The authors reported that vitamin D had remarkable treatment effects on both osteoarthritis as well as rheumatoid arthritis. Their report indicated that 67 arthritic patients treated with 200,000 IU of vitamin D (either D3 or D2) daily generated a remarkable 75% response rate.

The authors reported:

  • “If there was no improvement and no evidence of sensitivity, the daily dose was increased by 50,000 units each week until there was some improvement or evidence of overdosage. In some stubborn cases, it was found necessary to increase to 600,000 or even 1,000,000 units for a few days and then reduce to 200,000 to 500,000 units. Most of our results have been obtained with daily doses of 300,000 to 500,000 units.”

The authors report that 63 of the 700 patients on this dosage became clinically toxic. Therefore, approximately 10% of the patients over a 2-year period taking massive doses of vitamin D daily (200,000 IU) became toxic.

In 1946, two case reports of fatal vitamin D toxicity in adults (the authors report five previous fatal cases in children) appeared in the medical literature.27,28 Another case report of a fatal dose of vitamin D in adults appeared in 1947. This death was associated with vitamin D2 at a dose of 150,000 IU daily for 18 months, with characteristic foot lesions associated with vitamin D toxicity.29

By 1948, a clinical case series documented symptomatic effects of vitamin D intoxication to include weight loss and fatigue, which occurred before anorexia (poor appetite) and vomiting.30 All of these patients suffered from kidney damage and anemia. Virtually all of the patients had a characteristic eye lesion associated with vitamin D toxicity (calcium deposition in the sclera and cornea, just beneath the conjunctival basement membrane). All patients had high blood calcium, ranging from 12.4 to 15.1 mg per 100 cc. Dosages of vitamin D ranged from the lowest at 150,000 IU/day for 4 months (serum calcium 13.9) to the highest at 500,000 IU/day for 18 months (serum calcium 14.3). The researchers reported on another patient who developed hypercalcemia after taking 300,000 IU of vitamin D2 for only 2 weeks; she also had eye lesions evident on ophthalmologic exam. No patients died but some suffered permanent renal damage from the massive doses of vitamin D. The treatment the authors used for vitamin D toxicity was discontinuation of vitamin D, 4,000 cc of fluid hydration daily, and a low-calcium diet. Improvement occurred within 2–8 weeks when symptoms resolved. Blood calcium decreased in all patients by one month but continued to be elevated for as long as a year in one patient.

Recent studies indicate that supplementation with doses of vitamin D far exceeding the IOM’s newly established DRI have not produced signs of toxicity.

In a study conducted in 40 breast cancer patients, 10,000 IU of vitamin D3 daily for four months was shown to be effective in reducing elevated parathyroid hormone levels and demonstrated no toxicity. The authors of this study concluded:

  • Daily doses of 10,000 IU vitamin D(3) for 4 months appear safe in patients without comorbid conditions causing hypersensitivity to vitamin D. Treatment reduced inappropriately elevated parathyroid hormone levels…”31

Another study monitored 59 patients who received 50,000 IU of vitamin D3 daily for 10 days. The investigators noted that the high-dose vitamin D effectively boosted patients’ 25-hydroxy vitamin D blood levels without elevated calcium levels or renal (kidney) toxicity:

  • No patient developed hypercalcaemia (corrected calcium > 2.6 mmol/L), vitamin D toxicity (25(OH)D > 200 nmol/L) or nephrolithiasis during the study.32

In a separate study, researchers administered 4,000 IU vitamin D daily for three months to mothers one month postpartum. The authors of this study concluded:

  • High-dose vitamin D was effective in increasing 25(OH)D levels in fully breastfeeding mothers to optimal levels without evidence of toxicity. No mother or infant experienced vitamin D-related adverse events, and all laboratory parameters remained in the normal range.”33

A randomized, controlled trial assessed the effect of daily 1,800 IU of vitamin D in 73 elderly individuals over an 11-week period. The authors noted the safety of vitamin D in their conclusion: “The safety indicators, serum Ca, creatinine, and calcidiol, did not indicate any group or individual side effect.”34

Professor Reinhold Vieth of the University of Toronto is a world-renowned expert in vitamin D. His objective 1999 review paper on vitamin D toxicity revealed a fact either ignored or unknown to the authors of the current Institute of Medicine report:

  • « 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-hydroxy vitamin D concentration, I have yet to find it. »35

Professor Vieth reported that human toxicity probably begins to occur after chronic daily consumption of approximately 40,000 IU/day , more than ten-times the current threshold limit endorsed by the Institute of Medicine’ s current report.

John Cannell, MD, is executive director of the Vitamin D Council (, a not-for-profit educational organization. Dr. Cannell is an expert on vitamin D and has extensively reviewed past medical research on vitamin D with a keen eye towards dose range and toxicity.36

Dr. Cannell offers a critically important point concerning vitamin D dosing and evolutionary physiology:

  • “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.37 Vitamin D production in the skin occurs within minutes and is already maximized before your skin turns pink.

Vitamin D Health Benefits

Vitamin D has far-reaching implications that extend far beyond promoting bone health, which were either overlooked or ignored by the IOM committee.

Peer-reviewed scientific research clearly supports profound health benefits associated with vitamin D:

  • Blood pressure: Individuals deficient in vitamin D are much more likely to have elevated blood pressure.38,39 Treatment with vitamin D and calcium significantly lowers systolic blood pressure.26 Vitamin D likely exerts this effect by suppressing the expression of the blood pressure hormone renin.40
  • Inflammation: Vitamin D appears to have a potent effect on reducing inflammation through C-reactive protein (CRP).41
  • Metabolic effects: Diabetes is more prevalent in individuals with low serum vitamin D levels.42 Vitamin D administration reduces blood sugar, increases sensitivity to insulin, and may decrease the risk of developing full-blown diabetes.43
  • Chemoprevention: Vitamin D has demonstrated potent cancer-preventive effects in experimental and animal preparations and in humans.44 A recent study showed that supplementing with vitamin D and calcium reduced the incidence of all types of cancer in postmenopausal women.45
  • Osteoporosis prevention: Women are routinely prescribed expensive prescription drugs costing hundreds of dollars per month yet are deficient in vitamin D, a crucial factor in bone health. Replacement to healthy vitamin D levels substantially increases bone density more effectively than calcium supplementation alone. Intestinal absorption of calcium is magnified considerably when sufficient vitamin D is present.46,47
  • Prevention of stress fractures: Young men with an average age of 19 were shown to experience more stress fractures when blood levels of 25-hydroxyvitamin D were low.48
  • Prevention of multiple sclerosis: Vitamin D deficiency has been linked to an increased likelihood of developing this debilitating neurological disorder in Caucasians; the correlation between poor vitamin D status and multiple sclerosis did not hold true in African American or Hispanic populations.49 Scientists believe that the active form of vitamin D helps avert multiple sclerosis — which is considered an autoimmune disease — by selectively regulating the immune system.
  • Immune Enhancement: Noting that influenza epidemics are more common in the winter months, scientists have proposed that low levels of vitamin D may predispose individuals to succumbing to these potentially dangerous respiratory infections.50

Optimal 25-Hydroxy Vitamin D Blood Levels

When blood is tested to assess vitamin D status, the 25-hydroxyvitamin D form of the vitamin in the serum is measured.

Based on published studies, Life Extension’s optimal target range is 50–80 ng/mL of 25-hydroxy vitamin D. This level represents 25-hydroxy vitamin D concentrations seen in healthy young individuals getting plenty of direct sun exposure.51 One group of researchers assessed vitamin D status in healthy young adults aged 18–25 years. They found that in the summer months, vitamin D levels reached an average (mean) of 52.9 ng/mL and, accounting for statistical standard deviation (SD), as high as 86.6 ng/mL. The authors of this study went on to conclude:

  • Vitamin D sufficiency is a reality with a combination of young skin and optimal and effective sunshine exposure.52

Moreover, experts in the field of vitamin D research including Bruce Hollis, Robert Heaney and Neil Binkley agree that an optimal range of 25-hydroxy vitamin D is 50–80 ng/mL.

John Cannell, MD, the executive director of the Vitamin D Council, a non-profit organization dedicated to the science of vitamin D, indicates:

  • In a recent study, Heaney, et al, expanded on Bruce Hollis’s seminal work by analyzing five studies in which both the parent compound (cholecalciferol) and 25(OH)D levels were measured. They found that the body does not reliably begin storing cholecalciferol in fat and muscle tissue until 25(OH)D levels get above 50 ng/ml. The average person starts to store cholecalciferol at 40 ng/ml, but at 50 ng/ml (125 nmol/L) virtually everyone begins to store it for future use. That is, at levels below 50 ng/ml, the body uses up vitamin D as fast as you can make it, or take it, indicating chronic substrate starvation — not a good thing. 25(OH)D levels should be between 50–80 ng/ml (125–200 nmol/L), year-round.”53

A startling 36% of the general population has 25-hydroxyvitamin D levels below 20 ng/mL, which may represent the world’s leading cause of unnecessary disease and death.54

How Much Vitamin D Do You Really Need to Take?

Dr. Cannell has identified multiple peer-reviewed references55,56,57,58,59,60,61 42-48 in support of optimal vitamin D doses for adults between 4,600 and 10,000 IU, and further advises that the vast majority of adults (97.5%) need to take 5,000 IU a day of vitamin D to generate blood levels above the critical 50 ng/mL level.62

Fears of vitamin D toxicity have caused health-conscious people to limit their vitamin D3 intake to less than 800 IU a day. This amount is woefully inadequate and will not generate an optimal blood level of 25-hydroxy vitamin D.

It is important to monitor your blood level of 25-hydroxy vitamin D to ensure that you are getting adequate vitamin D to achieve blood levels of 50–80 ng/mL.

Those with a rare disorder called sarcoidosis, severe renal impairment, primary hyperparathyroidism, or any condition resulting in an elevated calcium level in the blood should consult with their physician before taking vitamin D supplements. A low-cost blood chemistry test easily rules out elevated blood calcium.

Conflict of Interest Among IOM Committee Members

IOM committee member Glenville Jones is a co-founder of a for-profit, publicly traded company called Cytochroma, which is in the process of developing a drug, currently identified as “CTAP101,” to treat vitamin D insufficiency.

IOM committee member Clifford Rosen has admitted to receiving financial support from pharmaceutical industry giants Eli Lilly and Novartis, and has served on the speaker’s bureau for Procter & Gamble. Procter & Gamble markets the controversial bisphosphonate osteoporosis drug Actonel®.63

IOM committee member J. Christopher Gallagher has disclosed financial relationships with GlaxoSmithKline, which recently received approval from the FDA for the drug Sorilux®, a patented vitamin D3 analog.


The recent Institute of Medicine’s recommendations for vitamin D intake are completely inadequate and ignore fundamental facts from the peer-reviewed literature on vitamin D safety and health benefits. The vast majority of health-conscious adults who do not routinely sunbathe require about 5,000 IU of vitamin D3 daily in order to achieve the low end of the target range (50–80 ng/mL) of 25-hydroxy vitamin D for optimal health.

To determine your individual requirements for vitamin D as well as your current 25-hydroxy vitamin D blood level, contact Life Extension’s Health Advisors toll-free (1-800-226-2370) and inquire about our inexpensive 25-hydroxy vitamin D blood test.


1. Bone. 1994 Mar-Apr;15(2):193-8.

2. Postgrad Med J. 1979 Dec;55(654):897-902.

3. BMJ. 2010 Jan 21;340:b5500.

4. Am J Clin Nutr. 2007 Jun;85(6):1586-91.

5. Br J Cancer. 2010 Apr 27;102(9):1422-7.

6. Am J Clin Nutr. 2009 May;89(5):1321-7.

7. Diabet Med. 2008 Mar;25(3):320-5.

8. Br J Nutr. 2010 Feb;103(4):549-55.

9. Am Heart J. 2010 Jun;159(6):1037-43.

10. World J Gastroenterol. 2009 Jul 21;15(27):3349-54.

11. Int J Cancer. 2007;120(5):1123–1128.

12. BMC Cancer. 2006;(6):264.

13. Health Phys. 2004;87(5):532–538.

14. Int J Health Geogr. 2007;(6):34.

15. Cancer. 2002;94(6):1867–1875.

16. Nutr Rev. 2003;61(7):227–238.

17. J Natl Cancer Inst. 2006;98(7):451–459

18. Cancer Epidemiol Biomarkers Prev. 2006;15(9):1688–1695.

19. Cancer Causes Control. 2010 Nov 12.

20. J Am Diet Assoc. 2006 Oct;106(10):1541-2.

21. Cancer Res. 2006 Oct 15;66(20):10213-9.

22. J Nutr. 1990;120 Suppl 11:1464–9.

23. Carcinogenesis. 2004 Jun;25(6):1015-26.

24. JAMA. 1934;102:1745-1748.

25. J. of Allergy. 1934;5:541-553.

26. Archives of Physical Therapy. 1935;16:537-43.

27. Am J Pathol. 1946 Nov;22(6):1293-1305.

28. JAMA. 1946;130:1208-1215

29. Am J Pathol. 1947 May;23(3):367-387.

30. J. Clin. Endocrinology. 1948;8(11);895-910.

31. Cancer. 2010 Jan 15;116(2):284-91.

32. Med J Aust. 2010 Jun 21;192(12):686-9.

33. Breastfeed Med. 2006 Spring;1(1):27-35.

34. J Am Geriatr Soc. 1990 Aug;38(8):862-6.

35. Am J Clin Nutr. 1999 May;69(5):842-56.

37. Am J Clin Nutr. 1995 Mar;61(3 Suppl):638S–645S.

38. J Clin Endocrinol Metab. 2001 Apr;86(4):1633-7.

39. Am J Hypertens. 1995 Sep;8(9):894-901.

40. J Cell Biochem. 2003 Feb 1;88(2):327-31.

41. QJM. 2002 Dec;95(12):787-96.

42. Arch Intern Med. 2007 Jun 11;167(11):1159-65.

43. Prog Biophys Mol Biol. 2006 Sep;92(1):39-48.

44. Am.J Clin Nutr. 1999 May;69(5):842-56.

45. Am J Clin Nutr. 2007 Jun;85(6):1586-91.

46. Curr Osteoporos Rep. 2006 Sep;4(3):96-102.

47. J Steroid Biochem Mol Biol. 2007 Mar;103(3-5):614-9.

48. J Bone Miner Res. 2006 Sep;21(9):1483-8.

49. Proc Soc Exp Biol Med. 1997 Oct;216(1):21-7.

50. Epidemiol Infect. 2006 Dec;134(6):1129-40.

51. J Clin Endocrinol Metab. 2007 Jun;92(6):2130-5.

52. Endocr Pract. 2010 Sep 14:1-26.

54. Life Extension Magazine. January, 2010

55. J Bone Miner Res. 2007 Dec;22 Suppl 2V64-8.

56. J Nutr. 2005 Feb;135(2):317-22.

57. Am J Clin Nutr. 2001 Feb;73(2):288-94.

58. Am J Clin Nutr. 2007 Jan;85(1):6-18.

59. N Engl J Med. 2007 Jul 19;357(3):266-81.

60. Am J Clin Nutr. 2003 Jan;77(1):204-10.

61. J Steroid Biochem Mol Biol. 2007 Mar;103(3-5):204-5.

63. J Bon Min Res. Vol. 23 Number 8, 2008 Letter to the Editor Optimal Thresholds, linear or nonlinear relationships of fracture risk reduction with therapy

Laisser un commentaire

Entrez vos coordonnées ci-dessous ou cliquez sur une icône pour vous connecter:


Vous commentez à l'aide de votre compte Déconnexion / Changer )

Image Twitter

Vous commentez à l'aide de votre compte Twitter. Déconnexion / Changer )

Photo Facebook

Vous commentez à l'aide de votre compte Facebook. Déconnexion / Changer )

Photo Google+

Vous commentez à l'aide de votre compte Google+. Déconnexion / Changer )

Connexion à %s