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Selenium and Diabetes:


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#1 doug123

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Posted 12 July 2007 - 07:30 AM


An rather interesting editorial was published in Annals of Internal Medicine; it's called Selenium and Diabetes: More Bad News for Supplements.

Let me please provide some introductory information regarding the primary source, The Annals of Internal Medicine

This information is provided by MedicineNet.com:

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Definition of Annals of Internal Medicine

Annals of Internal Medicine, the: A medical journal especially concerned with information in the field of internal medicine (adult medicine). Designed to be read largely by internists, the Annals states it is "is the leading journal for studies in internal medicine." (Such claims aside, the Annals is without question one of the leading journals in medicine today. It is widely read and well respected. --Editor.)

Established in 1927 by the American College of Physicians (ACP), the Annals now serves as the official journal of the ACP and the American Society of Internal Medicine (ASIM).


According to the Annals, "The purpose of the journal - to promote excellence in the clinical practice of internal medicine - is supported by presentation of a wide variety of experimental and clinical subject matter in the Article, Brief Communication, Update, and Review formats. And to support the belief that physicians should also be well-informed citizens of both the medical community and society at large, Annals offers background and discussion of issues that influence both physicians and patients. This information is primarily carried in the Perspective, In the Balance, and Editorial formats. In addition, the journal presents personal narratives in the On Being a Doctor and the On Being a Patient formats that convey the feeling and the art of medicine."

"Over the years, both ACP (now ACP-ASIM) and Annals have grown. The College is the largest specialty organization in the country, continuing to work to enhance health care by fostering professionalism as prescribed in its mission statement. And the journal has expanded in circulation, improved in impact factor score, and adopted useful new features. A few of these features are peer review of articles (1960), the use of the structured abstract (1987), and the twice-monthly distribution of the journal (1988). As ACP-ASIM and Annals continue to grow, the central values of the art and science of medicine will continue to steer policy and practice."


Click here to read: Selenium and Diabetes: More Bad News for Supplements:

Here's an extract from the text:

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EDITORIAL
Selenium and Diabetes: More Bad News for Supplements
Joachim Bleys, MD, MPH; Ana Navas-Acien, MD, PhD; and Eliseo Guallar, MD, DrPH

21 August 2007 | Volume 147 Issue 4

In this issue, Stranges and colleagues (1) report findings from the Nutritional Prevention of Cancer (NPC) trial that show an increased risk for diabetes among participants randomly assigned to receive supplements with 200 µg of selenium daily for 7.7 years compared with placebo. This effect was largely limited to participants in the top tertile of plasma selenium level at baseline (>121.6 ng/mL). In this group, the hazard ratio for incident diabetes in persons using selenium supplements compared with placebo was 2.70 (95% CI, 1.30 to 5.61). The NPC trial is the largest and longest available experimental study of selenium supplements compared with placebo. Although diabetes was not a primary end point of the trial and the investigators used self-report and medical records to assign the diagnosis, the results have credibility because of the randomized, double-blind design; the monitoring of baseline and follow-up plasma selenium levels; and other methodological strengths. The public health implications of these findings are substantial: More than 1% of the U.S. population take selenium supplements, and more than 35% take multivitamin and multimineral supplements (2) that often contain selenium.

...

Although obesity and lack of physical activity are the major factors responsible for the diabetes epidemic, environmental exposures may also be important. High selenium levels (12) or use of selenium supplements by persons with adequate selenium status (1) may contribute to this problem, although the extent of the role of these factors is unknown. Furthermore, the potential harmful effects of selenium supplementation in persons with high-normal selenium levels could extend beyond diabetes. A secondary analysis of the NPC trial identified some benefit of selenium supplementation for cancer prevention among participants with baseline plasma selenium levels less than 121.6 ng/mL but a possible small increase in total cancer risk among participants with higher levels (hazard ratio, 1.20 [CI, 0.77 to 1.86]) (18).

In the past decade, randomized, controlled clinical trials have shown that ß-carotene and vitamin E supplements, which were widely believed to be safe, increase mortality and morbidity (19, 20). No dietary supplement, including selenium, has proven useful so far for the prevention of cardiovascular disease or cancer in the general U.S. population. The balance of the potential benefits and harms of selenium supplementation depends on the dietary selenium intake in different countries. However, the U.S. public needs to know that most people in this country receive adequate selenium from their diet. By taking selenium supplements on top of an adequate dietary intake, people may increase their risk for diabetes.

Author and Article Information 
From Welch Center for Prevention, Epidemiology and Clinical Research, Johns Hopkins University Bloomberg School of Public Health, Baltimore, MD 21205.

Potential Financial Conflicts of Interest: None disclosed.

Requests for Single Reprints: Eliseo Guallar, MD, DrPH, Department of Epidemiology, Welch Center for Prevention, Epidemiology and Clinical Research, Johns Hopkins University Bloomberg School of Public Health, 2024 East Monument Street, Room 2-639, Baltimore, MD 21205; e-mail, eguallar@jhsph.edu.

Current Author Addresses: Drs. Bleys and Guallar: Department of Epidemiology, Welch Center for Prevention, Epidemiology and Clinical Research, Johns Hopkins University Bloomberg School of Public Health, 2024 East Monument Street, Suite 2-600, Baltimore, MD 21205.

Dr. Navas-Acien: Department of Environmental Health Sciences, Johns Hopkins University Bloomberg School of Public Health, 615 North Wolfe Street, Room W7033B, Baltimore, MD 21205.


Here's something Annals released that's kind of cool for mainstream folks:

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SUMMARIES FOR PATIENTS
Long-Term Use of Selenium Supplements and Risk for Type 2 Diabetes
21 August 2007 | Volume 147 Issue 4

Summaries for Patients are a service provided by Annals to help patients better understand the complicated and often mystifying language of modern medicine.

Summaries for Patients are presented for informational purposes only. These summaries are not a substitute for advice from your own medical provider. If you have questions about this material, or need medical advice about your own health or situation, please contact your physician. The summaries may be reproduced for not-for-profit educational purposes only. Any other uses must be approved by the American College of Physicians.


The full report is titled "Effects of Long-Term Selenium Supplementation on the Incidence of Type 2 Diabetes. A Randomized Trial." It is in the 21 August 2007 issue of Annals of Internal Medicine (volume 147). The authors are S. Stranges, J.R. Marshall, R. Natarajan, R.P. Donahue, M. Trevisan, G.F. Combs, F.P. Cappuccio, A. Ceriello, and M.E. Reid.

What is the problem and what is known about it so far?

Selenium is a mineral that is required in very low doses for the body to function normally. It is an antioxidant, meaning that it prevents damage to cells by oxygen.

Although most people get enough selenium in their diet, selenium is included in many multivitamins and is sold as a supplement itself. Many people take selenium supplements to stay healthy. Some research suggests that selenium supplements can improve the way the body handles sugar and might prevent some of the complications of diabetes. However, other research suggests that selenium supplementation has no effect on diabetes or health.

Why did the researchers do this particular study?

To see whether taking selenium supplements prevents diabetes.

Who was studied?

1, 202 people with skin cancer other than melanoma who were seen in dermatology clinics in areas of the United States where people tend to have low blood levels of selenium. None of the participants had diabetes.

How was the study done?

The researchers measured participants' blood selenium levels. They then randomly assigned the participants to take selenium supplements (200 micrograms) or placebo pills. They followed the participants over an average of 7 years to see who developed diabetes. They then compared the number of people with diabetes in the 2 groups.

What did the researchers find?

More people who took selenium developed diabetes compared with those who took placebo pills. The risk of developing diabetes seemed to be higher in people who had higher blood selenium levels at the start of the study.

What were the limitations of the study?

The researchers relied on participants' reports that they developed diabetes and did not confirm those reports with measures of blood sugar. The findings apply to the specific dose of selenium used in the study. Participants tended to be older and white, so the findings might not apply to younger people and those of other races.

What are the implications of the study?

Selenium supplements appear to increase the risk for diabetes. Although the findings need to be confirmed, long-term selenium supplementation should not be viewed as harmless and a possibly healthy way to prevent illness.


Thoughts or comments?

Take care.

#2 Mixter

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Posted 12 July 2007 - 07:50 PM

I don't have time to research them, but I'm not very sure of those studies.

One thing, what the pharma is researching a lot about is *correlations* of metabolic factors to existing diabetes or risk of diabetes. Increased gluthatione peroxidase activity definitely is correlated. So are other factors, e.g. high amount of carnitine metabolites (having to do with PPARs). Correlation would of course NOT have to mean that they causes diabetes or the risk thereof. I am not sure if I can find it in their study that they established this link -- IMO they only refer to selenium<->gluthatione peroxidase<->diabetes and similar *correlations*.

In any case, the study is not representative, more research is needed. Especially, it was not done with healthy probands, but cancer cases. Cancer victims, for example, have altered glucose metabolism, and often have developed cancer also due to prior high-sugar/high-carb diet. Which would cause increased diabetes risk independently of antioxidant intake. It may also be that the combination high-carb diet AND specific antioxidants is indeed a risk factor.

And in any case, if I judge only by the excerpts and what I can google/pubmed on diabetes and gluthatione peroxidase, there is IMO NO proof of a direct cause in the general population...

PS: OUCH... and it looks too biased to take it very serious. Not even HBA1c measured. I think non-diabetics can even turn up diabetic in single blood tests and vice versa.

What were the limitations of the study?

The researchers relied on participants' reports that they developed diabetes and did not confirm those reports with measures of blood sugar. The findings apply to the specific dose of selenium used in the study. Participants tended to be older and white, so the findings might not apply to younger people and those of other races.



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#3 Matt

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Posted 12 July 2007 - 08:26 PM

My selenium intake is in the UPPER range of normal from diet and supplements... and by the way, my glucose has decreased to 4.3 (77mg/dl). So thats what I care about, my OWN experience in this case...

#4 quicksilver

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Posted 15 July 2007 - 09:31 PM

An rather interesting editorial was published in Annals of Internal Medicine; it's called Selenium and Diabetes: More Bad News for Supplements.

Thoughts or comments?

Take care.


Worthless study using a poor form of selenium. Bad news for bad research more like it.

#5 EmbraceUnity

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Posted 15 July 2007 - 10:43 PM

I think it is highly likely that fat people just eat more selenium... correlation solved

#6 Brainbox

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Posted 15 July 2007 - 10:46 PM

Worthless study using a poor form of selenium. Bad news for bad research more like it.


Yep. But the "general public" is not aware of that... Manipulation seems evident... [angry]

Or am I to negative?

#7 krillin

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Posted 15 July 2007 - 11:57 PM

One thing bothered me at first: only those with the highest plasma selenium (pre-supplementation) were negatively affected. They already had more than enough to maximize GPX, so how could GPX be to blame? It turns out that when the RDA-setters talk about maximizing GPX, they mean GPX3: the extracellular GPX in plasma.

http://books.nap.edu...d=9810&page=284

GPX1, the one being blamed here, is a storage form, so supplementation can cause it to increase. (Without limit?)

http://books.nap.edu...d=9810&page=286

Here's some human results on GPX1 and insulin resistance. They don't say GPX1 explicitly, but they measured GPX in erythrocytes, so that would be the form.

http://jcem.endojour...e658d333e5d4e22

#8 doug123

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Posted 16 July 2007 - 02:54 AM

Dear quicksilver,

Thank you for commenting.

Here are the references cited:

1. Stranges S, Marshall J, Donahue R, Trevisan T, Natarajan R, Cappuccio F,
et al. Effects of long-term selenium supplementation on the incidence of type 2
diabetes. A randomized trial. Ann Intern Med. 2007;147:217-223.
2. Radimer K, Bindewald B, Hughes J, Ervin B, Swanson C, Picciano MF.
Dietary supplement use by US adults: data from the National Health and Nutrition
Examination Survey, 1999-2000. Am J Epidemiol. 2004;160:339-49.
[PMID: 15286019]
3. Rotruck JT, Pope AL, Ganther HE, Swanson AB, Hafeman DG, Hoekstra
WG. Selenium: biochemical role as a component of glutathione peroxidase. Science.
1973;179:588-90. [PMID: 4686466]
4. Schwarz K, Calvin F. Selenium as an integral part of factor 3 against dietary
necrotic liver degeneration. J Am Chem Soc. 1957;79:3292-3.
5. U.S. Department of Health and Human Services. Toxicological Profile for
Selenium. Atlanta, GA: U.S. Department of Health and Human Services, Public
Health Service; 2003.
6. Papp LV, Lu J, Holmgren A, Khanna KK. From selenium to selenoproteins:
synthesis, identity, and their role in human health. Antioxid Redox Signal. 2007;
9:775-806. [PMID: 17508906]
7. Rayman MP. The importance of selenium to human health. Lancet. 2000;
356:233-41. [PMID: 10963212]
8. Burk RF. Selenium, an antioxidant nutrient. Nutr Clin Care. 2002;5:75-9.
[PMID: 12134713]
9. Food and Nutrition Board, Institute of Medicine. Dietary Reference Intakes
for Vitamin C, Vitamin E, Selenium, and Carotenoids. A Report of the Panel on
Dietary Antioxidants and Related Compounds, Subcommittees on Upper Reference
Levels of Nutrients and Interpretation and Uses of Dietary Reference Intakes,
and the Standing Committee on the Scientific Evaluation of Dietary Reference
Intakes. Washington, DC: National Academy Pr; 2000.
10. Drake EN. Cancer chemoprevention: selenium as a prooxidant, not an antioxidant.
Med Hypotheses. 2006;67:318-22. [PMID: 16574336]
11. Fridlyand LE, Philipson LH. Oxidative reactive species in cell injury: mechanisms
in diabetes mellitus and therapeutic approaches. Ann N Y Acad Sci.
2005;1066:136-51. [PMID: 16533924]
12. Bleys J, Navas-Acien A, Guallar E. Serum selenium and diabetes in U.S.
adults. Diabetes Care. 2007;30:829-34. [PMID: 17392543]
13. Czernichow S, Couthouis A, Bertrais S, Vergnaud AC, Dauchet L, Galan
P, et al. Antioxidant supplementation does not affect fasting plasma glucose in
the Supplementation with Antioxidant Vitamins and Minerals (SU.VI.MAX)
study in France: association with dietary intake and plasma concentrations. Am J
Clin Nutr. 2006;84:395-9. [PMID: 16895889]
14. Rajpathak S, Rimm E, Morris JS, Hu F. Toenail selenium and cardiovascular
disease in men with diabetes. J Am Coll Nutr. 2005;24:250-6. [PMID:
16093402]
15. Hughes K, Choo M, Kuperan P, Ong CN, Aw TC. Cardiovascular risk
factors in non-insulin-dependent diabetics compared to non-diabetic controls: a
population-based survey among Asians in Singapore. Atherosclerosis. 1998;136:
25-31. [PMID: 9544728]
16. Lippman SM, Goodman PJ, Klein EA, Parnes HL, Thompson IM Jr,
Kristal AR, et al. Designing the Selenium and Vitamin E Cancer Prevention
Trial (SELECT). J Natl Cancer Inst. 2005;97:94-102. [PMID: 15657339]
17. Marshall JR, Sakr W, Wood D, Berry D, Tangen C, Parker F, et al. Design
and progress of a trial of selenium to prevent prostate cancer among men with
high-grade prostatic intraepithelial neoplasia. Cancer Epidemiol Biomarkers Prev.
2006;15:1479-84. [PMID: 16896036]
18. Duffield-Lillico AJ, Reid ME, Turnbull BW, Combs GF Jr, Slate EH,
Fischbach LA, et al. Baseline characteristics and the effect of selenium supplementation
on cancer incidence in a randomized clinical trial: a summary report of
the Nutritional Prevention of Cancer Trial. Cancer Epidemiol Biomarkers Prev.
2002;11:630-9. [PMID: 12101110]
19. Miller ER 3rd, Pastor-Barriuso R, Dalal D, Riemersma RA, Appel LJ,
Guallar E. Meta-analysis: high-dosage vitamin E supplementation may increase all-cause mortality. Ann Intern Med. 2005;142:37-46. [PMID: 15537682]
20. Bjelakovic G, Nikolova D, Gluud LL, Simonetti RG, Gluud C. Mortality in
randomized trials of antioxidant supplements for primary and secondary prevention:
systematic review and meta-analysis. JAMA. 2007;297:842-57. [PMID:
17327526]


Your claim is:

Worthless study using a poor form of selenium. Bad news for bad research more like it.


Can you please support your statements with evidence?

This meta analysis appears to be superb in all respects and studies included for meta-analysis appear to be the same form used in most dietary supplements.

Please attempt to demonstrate otherwise; please at least provide us with at least one counterexample to demonstrate; namely, can you please show us "another" form of selenium and supporting evidence that this "other" form does not have the same characteristics that may increase the incidence of diabetes? That would be great. ;)

Thank you.

Take care.

Edited by adam_kamil, 16 July 2007 - 03:04 AM.


#9 mediumspiny

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Posted 16 July 2007 - 11:40 AM

One thing, what the pharma is researching  -snip-

This is not, as far as I can see, research sponsored by a pharmaceutical company, but an international academic study with researchers from "...the State University of New York at Buffalo and Cancer Prevention and Population Sciences, Roswell Park Cancer Institute, Buffalo, New York; Clinical Sciences Research Institute, Warwick Medical School, Coventry, United Kingdom; and U.S. Department of Agriculture Human Nutrition Research Center, Grand Forks, North Dakota."

-snip- In any case, the study is not representative, more research is needed. Especially, it was not done with healthy probands, but cancer cases. -snip-

The subjects were attendees at a dermatology clinic and are described thus:

"Persons were eligible if they had a confirmed history of nonmelanoma skin cancer in the year before randomization, had an estimated life expectancy of 5 years, and had no reported internal cancer in the previous 5 years. Participants with a history of clinically important liver or kidney disorders were excluded."

Nonmelanoma skin cancer is most likely basal cell carcinoma, a relatively benign condition, also known as rodent ulcers and pretty common in the over 70s. It does not affect your potential lifespan and, AFAIK, has no metabolic implications.

-snip- PS: OUCH... and it looks too biased to take it very serious. Not even HBA1c measured. I think non-diabetics can even turn up diabetic in single blood tests and vice versa. -snip-

From the methods section of the study: "Participants who had a new diagnosis of type 2 diabetes during the blinded phase of the trial (15 September 1983 to 1 February 1996) were noted. The initial report of diabetes came from 3 sources: self-report during the clinical interview, reported use of drugs for diabetes, and reports in medical record documents. Medical record requests were then sent to the primary physicians for every patient with a report. This process of requesting and reviewing documentation was done in a blinded manner. About 92% of these reports, regardless of source, were corroborated with medical record documentation, as determined by registered nurse reviewers."

So diagnosis of diabetes was not based on a single blood test. I fail to see where the bias that you refer to is.

#10 mike250

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Posted 16 July 2007 - 12:10 PM

so is there any reason why didn't they measure HBA1c? and chose to rely on the other methods?

#11 mediumspiny

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Posted 16 July 2007 - 12:49 PM

so is there any reason why didn't they measure HBA1c? and chose to rely on the other methods?

I think they were not looking for diabetes. The finding was incidental and they consider the documentation provided by 3rd party doctors to be sufficient evidence of type II diabetes.

As they say in the discussion:

Our study has limitations. First, the incidence of diabetes was not a primary end point of the NPC trial. Our findings must be interpreted cautiously because they result from exploratory analyses, albeit from the largest completed randomized clinical trial in which selenium alone was the intervention.

Second, diagnosis of type 2 diabetes was self-reported, which may have led to some misclassification (underdiagnosis) at baseline or during the trial. However, given the randomized design, blinding, and documentation of the diagnosis by using medical records in our study, differential misclassification according to treatment assignment is unlikely. The effect of nondifferential misclassification would probably be to underestimate the true relative risk and decrease the statistical power of our study (37). However, the incidence rates that we observed are similar to national figures in the United States (38).


They also have some other points about limitations:

Third, although the incidence estimates were adjusted for potential confounders, such as age, sex, smoking status, and BMI, detailed information on unmeasured risk factors at baseline, such as family history of diabetes, body fat distribution, and physical activity, are lacking. However, randomization should have minimized the likelihood of confounding by these factors, as shown by the lack of significant differences in the evaluated baseline characteristics between treatment groups.

Fourth, the NPC sample consisted of elderly individuals (mean age, 63.2 years) from low-selenium areas in the eastern United States who had a history of nonmelanoma skin cancer. The generalizability of our findings to other groups may therefore be limited.

Finally, we cannot rule out the role of chance in our findings. The exposure–response gradient across tertiles of baseline plasma selenium levels seems to indicate that the observed associations are unlikely to be due to chance. However, a few more cases of diabetes in the placebo group would attenuate the main effect of selenium treatment and produce null findings.


Basically, although the study was quite large, 1200 non-diabetic participants at the start, the number developing diabetes (97) was quite low over a period of 7.7 years.

Of the 97 new cases of type 2 diabetes, 58 developed in the selenium group and 39 developed in the placebo group

So the statistical power of their analysis is not overwhelming; but it is significant.

#12 mike250

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Posted 16 July 2007 - 12:57 PM

thanks for clearing that out. the study looks very credible indeed. the question remains how do you know you're getting enough selenium?. is there any way to test for selenium levels in the body?

#13 krillin

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Posted 16 July 2007 - 07:53 PM

I'm going nuts trying to figure out an optimal selenium intake. Looking at the selenium cancer study (PMID: 12101110), it's best to get more than from diet, since the lowest baseline tertile plus 200 mcg was best, followed by middle tertile plus 200 mcg, followed by highest tertile plus placebo. So we want more than 121.6 ng/ml in the plasma, but don't want to overdo it. No more than what 105.2 ng/ml + a 200 mcg supplement would give you.

Correlating plasma selenium increases with selenium intake is tough once you get beyond 70-90 ng/ml, but here's my best guess. SU.VI.MAX gave 100 mcg and raised selenium in men from 89 ng/ml to 130 ng/ml. (PMIDs 16115341 and 11718454) So let's say a 200 mcg supplement will give you an increase of 80 ng/ml. Thus, we want a maximum of 185.2 ng/ml.

NHANES III found that Americans ate an average of 106 mcg and had an average of 124 ng/ml in plasma.

http://books.nap.edu...d=9810&page=309
http://books.nap.edu...d=9810&page=310

Increasing that to a maximum of 185.2 ng/ml means adding no more than 153 mcg selenium (assuming +80 ng/ml for every 200 mcg eaten), for a total of no more than 259 mcg.

So maybe we should be taking 100 mcg selenium supplements? And definitely in the form of SeMC.

http://jnci.oxfordjo...rint/90/16/1219 estimated that the lowest risk came from 159 mcg/day, based on toenail clipping data. (And contrary to what the National Academies Press book cited above said, the subjects didn't get 200 mcg supplements and it was published in 1998, not 1999.) So maybe 50 mcg supplements are a better idea?

#14 superpooper

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Posted 27 July 2007 - 11:06 AM

so is there any reason why didn't they measure HBA1c? and chose to rely on the other methods?

I think they were not looking for diabetes. The finding was incidental and they consider the documentation provided by 3rd party doctors to be sufficient evidence of type II diabetes.

As they say in the discussion:

Our study has limitations. First, the incidence of diabetes was not a primary end point of the NPC trial. Our findings must be interpreted cautiously because they result from exploratory analyses, albeit from the largest completed randomized clinical trial in which selenium alone was the intervention.

Second, diagnosis of type 2 diabetes was self-reported, which may have led to some misclassification (underdiagnosis) at baseline or during the trial. However, given the randomized design, blinding, and documentation of the diagnosis by using medical records in our study, differential misclassification according to treatment assignment is unlikely. The effect of nondifferential misclassification would probably be to underestimate the true relative risk and decrease the statistical power of our study (37). However, the incidence rates that we observed are similar to national figures in the United States (38).


They also have some other points about limitations:

Third, although the incidence estimates were adjusted for potential confounders, such as age, sex, smoking status, and BMI, detailed information on unmeasured risk factors at baseline, such as family history of diabetes, body fat distribution, and physical activity, are lacking. However, randomization should have minimized the likelihood of confounding by these factors, as shown by the lack of significant differences in the evaluated baseline characteristics between treatment groups.

Fourth, the NPC sample consisted of elderly individuals (mean age, 63.2 years) from low-selenium areas in the eastern United States who had a history of nonmelanoma skin cancer. The generalizability of our findings to other groups may therefore be limited.

Finally, we cannot rule out the role of chance in our findings. The exposure–response gradient across tertiles of baseline plasma selenium levels seems to indicate that the observed associations are unlikely to be due to chance. However, a few more cases of diabetes in the placebo group would attenuate the main effect of selenium treatment and produce null findings.


Basically, although the study was quite large, 1200 non-diabetic participants at the start, the number developing diabetes (97) was quite low over a period of 7.7 years.

Of the 97 new cases of type 2 diabetes, 58 developed in the selenium group and 39 developed in the placebo group

So the statistical power of their analysis is not overwhelming; but it is significant.


You argue like a 5 year old. You have no proof amalgam fillings are safe. You have know proof those statistical studies are legit science.

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#15 markymark

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Posted 27 July 2007 - 11:51 AM

If the ongoing SELECT Trial, which prospectively investigates, whether selenium (200 µg) and or vitamin E 400 IE (unfortnately only alpha-toc) eventually lead to lower prostate cancer numbers, has - as a byproduct - the same result, i.. e. more new diabetes type two cases, this would indeed mean something, (duck an cover for selenium).
But I am of the opinion , that such an underpowered, or at least borderline-powered study like the one in question here, induces more intellectual entrophy, rather than it produces clarity.
I really wonder, how the reviewers of the Annals have letting it pass..

MM 43 Y

Edited by markymark, 27 July 2007 - 12:01 PM.





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