Vitamin D3-5

The Vitamin D Newsletter
More Vitamin D Studies of Interest
March 14, 2010

The mainstream American press is ignoring much of the recent Vitamin D
scientific literature. I suspect newspaper editors have decided that too
many favorable Vitamin D stories run the risk of repeating the folic acid,
beta-carotene and vitamin E affairs, when early epidemiological research was
not routinely substantiated by later randomized controlled trials. If the
press has made that decision, then this newsletter is your best source of
information on new Vitamin D science.

*Genetics, as well as dose, determine response to vitamin D supplements.*

Your vitamin D blood level depends entirely on how much you take or how
often you sunbathe, right? Wrong. Prior studies of identical twins show that
about 25 -50% of the variation of Vitamin D levels depends on genetics. In
July, researchers at the University of Toronto discovered the heritability
of 25(OH)D is probably mediated through the Vitamin D binding protein

Fu L, Yun F, Oczak M, Wong BY, Vieth R, Cole DE. Common genetic variants of
the vitamin D binding protein (DBP) predict differences in response of serum
25-hydroxyvitamin D [25(OH)D] to vitamin D supplementation. Clin Biochem.
2009 Jul;42(10-11):1174-7.<>

One of the common emails I get (and I’m sorry I can’t answer individual
emails) is “I am taking 5,000 IU per day but my blood level is only 35
ng/ml.” What should I do? This study helps answer such questions. You
probably inherited a tendency to not respond to higher doses of Vitamin D.
Simply take a little more and get your blood tested again in 3-4 months.

Also, don’t forget your weight. Does it make sense that if you weigh 300
pounds, you need more vitamin D than a 3 pound baby? If that makes sense to
you, congratulations, it has not made sense to any of the five Food and
Nutrition Boards (FNB) that have convened and issued recommendations to
Americans over the last 60 years; they have all recommended the same 200
IU/day dose for infants and young adults, no matter how much the adults

*More researchers actually recommend that people take Vitamin D and not just
give more money to scientists.*

Researchers from Austria concluded their review paper on vitamin D and high
blood pressure by stating: “In view of the multiple health benefits of
vitamin D and the high prevalence of vitamin D deficiency, as well as the
easy, safe, and inexpensive ways in which vitamin D can be supplemented, we
believe that the implementation of public health strategies for maintaining
a sufficient vitamin D status of the general population is warranted.”

Pilz S, Tomaschitz A, Ritz E, Pieber TR; Medscape. Vitamin D status and
arterial hypertension: a systematic review. Nat Rev Cardiol. 2009

Good for Austria! By the way, while vitamin D may improve hypertension, it
is not the be all and end all of hypertensive disease. If your doctor can
stop your high blood pressure medication after you start taking vitamin D,
great, but I doubt that will happen. Most people will have to continue
taking their antihypertensive medication even after adequate vitamin D
supplementation, albeit sometimes at a lower dose.

While I am on the subject, remember, that vitamin D will not prevent all
cancer or heart disease or respiratory infections. True, evidence is
accumulating that it will help, but you can still develop cancer, heart
disease and respiratory infections with adequate blood levels of vitamin D.
That’s why I believe in complimentary, not alternative, medicine.

*Professor Michael Holick keeps increasing the amount of vitamin D he

As readers know, Professor Holick is one of the world’s foremost authorities
on vitamin D. However, after being on the 1997 Food and Nutrition Board
(FNB), he stuck with the FNB’s 200 IU/day recommendation well into the next
century. Then he slowly went to 400 IU, then 800 IU, then 1,000 IU and now
he is at 2,000 IU/day. Professor Holick is going in the right direction and
is almost there.

Cynthia K. Buccini Sunny Dispositions vitamin D deficiency may be the most
common medical problem in the world. BU Today, March 8,

*Professor Robert Heaney of Creighton University just discovered that if you
take 2,200 IU of vitamin D every day, you only have about 12 days supply of
vitamin D in your body.*

I love Robert Heaney’s papers. In a previous paper, Dr. Heaney discovered
that at blood levels of 35 ng/ml, 50% of people are using up their vitamin D
as quickly as they take it, that is, they are not storing any for future use
and suffer from chronic substrate starvation. Obviously, one wants to take
enough so the body has all it can use, which is why I recommend 25(OH)D
levels of at least 50 ng/ml. At that level, no one should have chronic
substrate starvation.

In the paper below, Dr. Heaney collaborated with two other Creighton
scientists, Dr. Diane Cullen and Dr. Laura Armas, as well as one of the
premier experts in measuring vitamin D in the world, Dr. Ron Horst of
Heartland Assays. Ron runs tens of thousands of vitamin D samples a year as
Heartland Assays performs vitamin D testing for most of the big studies and
Dr. Horst is one of the few people in the world who can accurately measure
cholecalciferol, and not just 25(OH)D.

Heaney RP, Horst RL, Cullen DM, Armas LA. Vitamin D3 distribution and status
in the body. J Am Coll Nutr. 2009

Anyway, in his latest paper, Dr. Heaney found that if you regularly take
2,200 IU per day, you have about 12 days supply of vitamin D in your body.
He explained, “What this indicates is that fat reserves of the vitamin are
essentially running on empty and that . . . additional vitamin D inputs are
[converted to 25(OH)D] almost immediately.” . . “The currently recommended
intake of vitamin D needs to be revised upward by at least an order of

What is not known, at least by me, is what happens when cholecalciferol
intake far exceeds the body’s requirement. We know it is stored in the body,
mainly in fat and muscle, but what does the body do to control excess
cholecalciferol from building up in the body? Professor Reinhold Vieth has
written that much of it will simply be excreted unchanged in the bile, but
how does that system work exactly, to get rid of excess cholecalciferol? We
know it works because the few patients with vitamin D toxicity reported in
the literature – almost always due to industrial errors – reduce their
vitamin D levels rather quickly by simply stopping the vitamin D and staying
out of the sun.

*Zocor has no effect on vitamin D levels.*

I know several studies have found statins raise vitamin D levels but
different scientists report different findings. This paper found Zocor had
no effect of vitamin D levels while a previous paper found Crestor almost
tripled vitamin D levels. What’s the truth? I don’t know. The above study
did find that higher vitamin D levels were strongly associated with better
triglycerides and weakly associated with higher HDL (the good cholesterol)

Rejnmark L, Vestergaard P, Heickendorff L, Mosekilde L. Simvastatin does not
affect vitamin d status, but low vitamin d levels are associated with
dyslipidemia: results from a randomised, controlled trial. Int J Endocrinol.

*Vitamin D lowers statin blood levels*

This study makes the point that things are often more complex than they
first appear. Almost nothing is known of vitamin D’s drug-drug interactions.
That is, how does vitamin D affect the blood level of other drugs? The below
study measured the effects of vitamin D on Lipitor levels and cholesterol
levels hours after Lipitor was given to patients taking vitamin D. The
authors were looking for drug-drug interactions and found them.

Schwartz JB. Effects of vitamin D supplementation in atorvastatin-treated
patients: a new drug interaction with an unexpected consequence. Clin
Pharmacol Ther. 2009

The above study found vitamin D not only lowered Lipitor levels, but vitamin
D lowered bad cholesterol levels as well. That is, the lowest bad
cholesterol levels were found in patients on vitamin D with the lowest
Lipitor levels, just the opposite of what one would think. I mean, wouldn’t
higher Lipitor levels result in lower cholesterol levels? Not when vitamin D
was taken into account. If you think my explanation of this study is
confusing, you should read the study.

*Intensive treatment with vitamin D, statins, and omega-3 fish oil reverses
coronary calcium scores.*

The below open study by Dr. William Davis and colleagues studied 45 adults
with evidence of calcified coronary arteries, treating them with high dose
statins, niacin, fish oil (not cod liver oil) capsules, and enough vitamin D
(average of about 4,000 IU/day) to obtain 25(OH)D levels of 50 ng/ml. They
found that regimen reduced coronary calcium scores in 20 patients and slowed
progression in 22 additional patients. That is, it reversed the coronary
calcification process in about half of patients and slowed its progression
in most of the rest.

Davis W, Rockway S, Kwasny M. Effect of a combined therapeutic approach of
intensive lipid management, omega-3 fatty acid supplementation, and
increased serum 25 (OH) vitamin D on coronary calcium scores in asymptomatic
adults. Am J Ther. 2009

Most studies have shown high dose statins on their own do not reverse
coronary arthrosclerosis, so we know it was not the statins alone. What
would vitamin D levels of 70 ng/ml do? So, if you have coronary artery
disease: ask your cardiologist about statins and niacin, take 5-10 fish oil
capsules per day, and at least 5,000 IU of vitamin D3 per day.

A word about fish oil is in order. Fish oil means fish body oil, not fish
liver oil. And, four or five capsules of omega-3 fish oil a day will do very
little if you do not limit your intake of omega-6 oils. Your ratio of
omega-6 to omega-3 is the crucial number, your want that ratio at 2 or
below, which means no chips, no French fries and no processed foods, a
difficult diet. Omega-6 oils are vegetable oils such as corn oil, safflower
oil, soybean oil, sunflower oil and cottonseed oil. Read the packages to see
what is in them and if they contain the above oils do not eat them. In
additions to taking fish oil capsules, try to eat wild-caught salmon three
times a week.

*Our group’s second paper on influenza is now the most accessed paper in the
history of Virology Journal.*

I was asked to write the paper by the editor of another journal, who then
refused it! I almost decided to scrap the paper but, in the end, submitted
it to Virology Journal. I’m glad I did.

Virology Journal: Top 20 most accessed articles for all

I was glad to see that six other experts recently recommended that the
diagnosis and treatment of vitamin D deficiency be part of our national
preparedness for the H1N1 pandemic.

Edlich RF, Mason SS, Dahlstrom JJ, Swainston E, Long WB 3rd, Gubler
K. Pandemic preparedness for swine flu influenza in the United States. J
Environ Pathol Toxicol Oncol.

In addition, I hear through the grapevine that the CDC has discovered that,
of the 329 American children who have died so far from H1N1, vitamin D
levels in the dead children were lower than in children who survived the
swine flu. Maybe something can be done to save our children by next winter?
Not to mention the 16,000 adult Americans the CDC thinks died from H1N1.

Reuters. Up to 80-million Americans have been infected with H1N1.

*Low vitamin D levels mean higher death rates in patients with kidney

The below study is the first of its kind; Dr. Rajnish Mehrota and his eight
colleagues studied 3,000 of the 28 million U.S. adults who have chronic
kidney disease, finding those with vitamin D levels below 15 ng/ml had a 50%
increased risk of death compared to those with levels above 30 ng/ml over
the nine years of the study. These researchers from UCLA, Harvard, the Los
Angeles Biomedical Research Institute, and other institutions concluded:
“The broad public health implications of our findings cannot be
overemphasized given the high prevalence of vitamin D deficiency among
individuals with chronic kidney disease, and the ease, safety, and low cost
of maintaining replete vitamin D levels.”

Mehrotra R Mehrotra R, Kermah DA, Salusky IB, Wolf MS, Thadhani RI, Chiu YW,
Martins D, Adler SG, Norris KC.. Chronic kidney disease, hypovitaminosis D,
and mortality in the United States. Kidney Int. 2009

These words are music to my ears; these words are strong words, urgent
words, and, better yet, they are not my words. This is the first large study
looking at a representative group of Americans with kidney disease, before
dialysis, finding about 1/3 of them died over the 9 years of the study.
Those with low vitamin D levels were more likely to die; in fact, they were
more likely to have about every chronic disease you can think of before they
died. The average age of those with kidney disease was only 55. This is a
very important study, well written and well-conducted.

However, there is a scandal in medicine, a scandal not openly discussed in
scientific papers, one not yet reported by the mainstream press. The scandal
is this: if you are on dialysis, the chances are very high that your kidney
doctor thinks he is giving you vitamin D when he is doing no such thing and
some drug companies encourage such ignorance.

Drug companies market very lucrative activated vitamin D drugs to
nephrologists as “vitamin D.” The kidney doctors, in turn, think they are
giving vitamin D to their dialysis patients when they are doing no such
thing. If anything, the activated vitamin D analogs nephrologists use in
kidney disease will lower 25(OH)D levels by turning on the enzyme that gets
rid of vitamin D.

The ugly secret is that plain old dirt-cheap vitamin D would lower the
amount of activated vitamin D analogs needed to treat kidney disease. We
used to think it was all or none, the kidneys would either make activated
vitamin D to maintain blood calcium or the kidneys would not, as in renal
failure. However, it is not all or none; the more vitamin D building blocks
available to the diseased kidneys, the more activated vitamin D diseased
kidneys can make. And, tissues other than the kidney, such as the skin,
pancreas, adrenal medulla, and certain white blood cells, can contribute to
serum activated vitamin D levels, and probably would if they had enough of
the building block (plain old, dirt-cheap old, regular old, vitamin D).

*Just out: Vitamin D administration (plain old vitamin D) to renal dialysis
patients reduces the need for expensive vitamin D analogues, reduces
inflammation, reduces the need for medication that increases red blood
count, and improves cardiac function.*

As I was about to finish this tirade about vitamin D and kidney failure, the
below open study was published on March 4, 2010 and I ordered it. (By the
way, the Council has to pay $11.00 for every paper I get and only one paper
in ten is worth reporting on). The study below confirms what the above
authors predicted; plain old cheap vitamin D helps patients with kidney

Matias PJ, Jorge C, Ferreira C, Borges M, Aires I, Amaral T, Gil C, Cortez
J, Ferreira A. Cholecalciferol Supplementation in Hemodialysis Patients:
Effects on Mineral Metabolism, Inflammation, and Cardiac Dimension
Parameters. Clin J Am Soc Nephrol. 2010 Mar

Dr. Patricia Matias and colleagues in Portugal gave vitamin D3 to 158
patients on renal dialysis, using a sliding scale of vitamin D3
administration dependent on baseline 25(OH)D levels. Some patients got
50,000 IU per week, some got 10,000 IU per week, etc. Their dosing regimen
increased 25(OH)D levels from a mean of 22 ng/ml at the beginning of the
study to a mean of 42 ng/ml during treatment, indicating half of patients
still had levels lower than 42 ng/ml after treatment. Interestingly, most of
the patients who did not increase their 25(OH)D very much had diabetes,
suggesting the metabolic clearance (how quickly it is used up) of vitamin D
is increased in diabetes. By the way, we know the patients took the vitamin
D; the doctors gave it to them when they came in for dialysis.

The results of this study were amazing. After vitamin D administration,
parathyroid hormone, albumin, CRP (a measure of inflammation), brain
natriuretic peptide (a measure of heart failure), and left ventricular mass
index (a measure of heart function) all improved significantly. The dose of
activated vitamin D (Zemplar in this case) was reduced, and some patients
were able to stop it all together. Also, the dose of two other drugs used in
kidney failure, one to bind phosphorus and the other to raise hemoglobin,
was reduced.

It is a tragedy that drug companies sell more expensive vitamin D analogs by
having their drug salesman assure kidney doctors that the expensive vitamin
D analogues are vitamin D, even if it kills their clients. But, with the
brand new knowledge that kidney failure patients live much longer on vitamin
D, the drug companies might want to do some simple math. They might make
even more money if they kept their patients alive longer. True, they will
need less vitamin D analogues and other expensive kidney drugs every day,
but the patients may live many more days.

John Cannell, MD

This newsletter is now copyrighted but may be reproduced for non-economic
reasons as long as proper attribution to its source is clearly stated in the
reproduction. Please reproduce it, post it on Internet sites, and forward it
to your friends.

Remember, we are a non-profit and rely on your donations to publish our
newsletter, maintain our website, and pursue our objectives. Send your
tax-deductible contributions to:

The Vitamin D Council<>
1241 Johnson Ave., #134
San Luis Obispo, CA 93401

Obesity linked to kidney cancer

On January 22, 2010, in Uncategorized, by Andrea

Not a good day.

From Medscape:

Obesity Linked to Clear-Cell Renal Cell Carcinoma

Laurie Barclay, MD

January 22, 2010 — Obesity is associated with an increased risk for clear-cell renal cell carcinoma (RCC), according to the results of a case series reported in the January issue of BJU International.

“Recent scientific breakthroughs about what causes clear-cell RCC have led to the development of new targeted therapies,” lead author William T. Lowrance, from Memorial Sloan-Kettering Cancer Center (MSKCC), New York, NY, said in a news release. “This makes it more important than ever to identify those people who face an increased risk of developing this variant, which is on the rise in the USA.”

The goal of the study was to evaluate the association between body mass index (BMI) and histologic features of RCC in a contemporary cohort of 1640 patients with renal cortical tumors being surgically removed at MSKCC from January 2000 to December 2007. Of these tumors, 12% were benign and 88% were malignant; of these, 61% were clear-cell RCCs.

The association of BMI with RCC histologic features was examined with multivariable logistic regression.

“The widespread use of abdominal imaging has definitely contributed to increased detection of RCC, but fails to account for it entirely,” Dr. Lowrance said. “A number of studies have suggested that obesity could be a risk factor for RCC, but the exact reason is unknown. Researchers suggest it might be secondary to hormonal changes, decreased immune function, hypertension or diabetes in obese patients.”

Obesity, defined as a BMI of more than 30 kg/m2, was present in 38% of patients. Median BMI was 28 kg/m2 (interquartile range, 25 – 32 kg/m2). BMI was significantly associated with clear-cell histologic features, after adjustment for tumor size, age, sex, American Society of Anesthesiologists score, estimated glomerular filtration rate, hypertension, diabetes mellitus, and smoking.

For each unit of BMI, the odds ratio (OR) was 1.04 (95% confidence interval [CI], 1.02 – 1.06; P < .001), and OR was 1.48 for obese vs nonobese patients (95% CI, 1.19 – 1.84; P < .001). BMI was still an independent predictor of clear-cell histology in the subgroup of patients with RCC (excluding benign renal cortical tumors; OR, 1.04; 95% CI, 1.02 – 1.06; P = .001).

“We also looked at other health and lifestyle factors, like diabetes, hypertension and smoking,” Dr. Lowrance said. “This showed that the only other factors that were independent predictors of clear-cell RCC were male gender and tumour size.”

Limitations of this study include retrospective case series, lack of a control group, referral/selection bias, and BMI calculation at a single point in time.

“Although we still need to find out more about the pathology of clear-cell RCC, this study is useful as it provides individual predictors of the chance of developing this form of cancer,” Dr. Lowrance concluded. “Of these, obesity provides the strongest association.”

The Stephen Hanson Family Fellowship, National Institutes of Health, and the Sidney Kimmel Center for Prostate and Urologic Cancers supported this study. The study authors have disclosed no relevant financial relationships.

BJU Int. 2010;105:16-20.

Obesity increases cancer risk

On January 22, 2010, in Uncategorized, by Andrea

Yet another mark against obesity.

From Medical News Today:

How Does Obesity Increase Cancer Risk?

Obesity comes with plenty of health risks, but there’s one that’s perhaps not so well known: an increased risk of developing cancer, and especially certain types of cancer like liver cancer. Now, a group of researchers reporting in the January 22nd issue of the journal Cell, a Cell Press publication, have confirmed in mice that obesity does indeed act as a “bona fide tumor promoter.” They also have good evidence to explain how that happens.

“Doctors always worry about our weight, but the focus is often on cardiovascular disease and type 2 diabetes, both of which can be managed pretty well with existing drugs,” said Michael Karin of the University of California, San Diego. “However, we should also worry about elevated cancer risk. If we can reduce cancer deaths by as many as 90,000 per year, that’s a lot of people – a lot of lives.”

Karin’s team shows that liver cancer is fostered by the chronic inflammatory state that goes with obesity, and two well known inflammatory factors in particular. The findings suggest that anti-inflammatory drugs that have already been taken by millions of people for diseases including rheumatoid arthritis and Crohn’s disease may also reduce the risk of cancer in those at high risk due to obesity and perhaps other factors as well, Karin said.

The epidemiological studies reported earlier showed that obese people have about a 1.5-fold increase in their risk of cancer overall. That may not necessarily sound like a lot, Karin said, but it equates to about 90,000 extra cancer deaths per year in the United States alone. When it comes to liver cancer, the study showed obese people have a 4.5-fold greater risk.

Given the apparent connection between obesity and liver cancer in particular, Karin’s team decided to investigate in mice prone to develop hepatocellular carcinoma (HCC). The mice are typically given HCC either by exposure to a chemical carcinogen, known as DEN, when they are two weeks old, or by exposure to that same carcinogen at three months of age followed by the tumor-promoting chemical phenobarbitol.

In the new study, the researchers gave two-week-old mice DEN and then divided them into two groups – one fed a normal, relatively low-fat food and the other fed on high-fat chow. “It was clear that the mice on the high fat diet developed more liver cancer,” Karin said.

To further confirm the link, they gave DEN to two-week-old mice that were fed a normal diet but carried a gene that made them obesity-prone. Those mice, too, developed more liver cancers, evidence that it wasn’t the high-fat diet that led to cancer, but rather something about the animals obese state.

But Karin said perhaps the biggest surprise came in studies of mice on a high-fat diet who were given DEN a little later in life, when they were three-months-old. Normally, mice on the standard diet given the chemical at that age really don’t develop liver cancer unless DEN exposure is followed up with phenobarbitol, Karin explained. But the obese mice developed the disease without that extra push.

“We expected to see more cancer in our first experiments, but I was stunned to see here that only the mice who were obese developed the cancer,” Karin said. “Obesity appears to be as strong as phenobarbitol; we can conclude, at least in mice, that obesity is a real tumor promoter.”

His team was able to trace the source of obesity’s tumor-promoting effect to a rise in two inflammatory factors known as IL-6 and TNF. Obese mice lacking either the TNF receptor or IL-6 don’t show the same rise in liver cancer.

Those treatments also led the mice to accumulate less fat in their livers, he said. “They still get fat, but the distribution of the fat is different,” he said. “The fat goes to other places, but not to the liver.”

Karin suggests that clinical studies of people who are already taking anti-TNF drugs should be done, to find out if their livers are less fatty and cancer-free.

The researchers include Eek Joong Park, Jun Hee Lee, Guann-Yi Yu, Guobin He, Syed Raza Ali, Ryan G. Holzer, Christoph H.Osterreicher, Hiroyuki Takahashi, and Michael Karin, of University of California, San Diego, La Jolla, CA.

Source: Cathleen Genova
Cell Press

Please note!  From sun exposure.  This study did not, did not, did not! study high levels of vitamin D from supplemental use.  There is much evidence that shows that a high D level actually helps in heart disease, stroke, and several cancer risks.

With that in mind, high levels of serum D have been linked to basal cell carcinoma.  That’s skin cancer.

I post this only because many times, docs tell us to go outside to get our D rather than take our supplements.  I’m thinking I’d rather take a 10,000 IU pill…

From Medscape:

Higher Vitamin D Levels Linked to Risk for Basal Cell Carcinoma

NEW YORK (Reuters Health) Jan 18 – Even years after measurement, high serum levels of vitamin D (25(OH)D) are associated with an elevated risk of basal cell carcinoma, findings from a nested case-control study suggest.

According to the report in the December 31 advanced online issue of the Journal of Investigative Dermatology, “The same spectrum of UV radiation causes both DNA damage to keratinocytes and vitamin D synthesis by these cells.”

This could mean that “vitamin D formation in keratinocytes may be an innate protective mechanism against UV damage,” according to the authors. On the other hand, they add, in vitro and in vivo evidence suggests that vitamin D and its receptor are involved in cutaneous carcinogenesis.

But until now, no one has directly examined the relationship between serum vitamin D levels and basal cell carcinoma in humans.

Lead author Dr. Maryam M. Asgari and colleagues did just that, using a Kaiser Permanente electronic database of pathology specimens of basal cell carcinomas. The pathology reports were matched with data on each patient’s serum level of 25(OH)D before the skin cancer developed.

In the 220 Caucasian patients and 220 controls, 25(OH)D had been measured between 1968 and 1970. Cancer cases were diagnosed between 1974 and 1979. The mean time between measurement and diagnosis was 8.74 years.

Dr. Asgari, from Kaiser Permanente Northern California, Oakland, and her team found that for every 1 ng/mL rise in serum 25(OH)D levels, the risk of basal cell carcinoma rose by 3%. For subjects with levels in the highest quintile, the unadjusted odds ratio was 2.32 compared with the lowest quintile (p = 0.03 for trend).

Moreover, individuals who had clinically sufficient 25(OH)D levels (at least 30 ng/mL) were at significantly increased risk compared with those who were deficient (< 10 ng/mL), with an unadjusted odds ratio of 3.98 (p < 0.01).

In multivariate analysis adjusted for body mass index, smoking status, education, estimates of sun exposure, X-ray exposure, and personal history of cancer, the risk of basal cell carcinoma rose by 2% with each ng/mL increase in 25(OH)D. Comparing sufficient with deficient levels still yielded an adjusted odds ratio of 3.61 (p = 0.03).

This analysis was limited by the use of surrogates for sun exposure (e.g., leisure time activities, occupation), none of which was associated with levels of serum 25(OH)D or a significant risk factor for basal cell carcinoma, the authors note. Moreover, the model did not take into account variables such as supplemental vitamin D use or healthcare screening bias.

“Future studies that can accurately measure acute and intermittent sun exposure, supplemental vitamin D use, and other potential confounding factors may be warranted,” the research team concludes.

J Invest Dermatol 2009.


On December 25, 2009, in Uncategorized, by Andrea

Really?  Must be a European thing, cause I’ve not seen a whole lotta PSA’s saying “gain weight or you’re gonna die from malnourishment!”

From Medical News Today:

Adverse Consequences Of Obesity May Be Greater Than Previously Thought, UK

Article Date: 25 Dec 2009 – 0:00 PST

The link between obesity and cardiovascular mortality may be substantially underestimated, while some of the adverse consequences of being underweight may be overstated, concludes a study published on .

This means that the adverse influence of higher BMI and obesity in a population is of greater magnitude than previously thought, say the authors.

Numerous studies have already investigated the link between body mass index (BMI) and mortality. They show that high BMI is associated with higher rates of death from cardiovascular causes, diabetes, and some cancers, while low BMI is associated with increased mortality from other causes, such as respiratory disease and lung cancer.

But there are inconsistencies in the evidence that low body mass index actually increases the risk of causes of death such as respiratory disease and lung cancer.

Some researchers argue that this association may be biased by a process called reverse causality, where a severe illness, such as lung cancer, leads to both weight loss and higher mortality. Other factors such as smoking and poor socioeconomic circumstances may also lead to biasing estimates. This is known as confounding.

So a team from the University of Bristol and the Karolinska Institute in Sweden set out to obtain a valid estimate of the association between body mass index (BMI) and mortality by comparing, for over one million Swedish parent-son pairs, the BMI of the sons as young adults with mortality among their parents.

Using offspring BMI as an indicator of parental BMI avoids problems of reverse causality and is less influenced by confounding, explain the authors.

Their analysis shows strong associations between high offspring BMI (used as a so-called instrumental variable) and parental mortality from cardiovascular disease, diabetes, and some cancers, as reported in other studies of own BMI with mortality. However, unlike previous studies, there was no evidence of an association between low BMI and an increased risk of respiratory disease and lung cancer mortality.

These findings suggest that the apparent adverse consequences of low BMI on respiratory disease and lung cancer mortality may be overstated, whereas the adverse consequences of higher BMI on cardiovascular disease mortality may be substantially underestimated, say the authors.

These conclusions have important implications for public health practice because they suggest that reducing population levels of overweight and obesity (or preventing their rise) will have a considerable benefit to population health, they add. Suggestions to the contrary, which have received considerable media attention over recent years, are probably misguided.

Link to paper

British Medical Journal