Re: Vitamin D status predicts physical performance and its decline in older persons

On Tue, 13 Mar 2007 00:42:14 +0200, Matti Narkia <mna@xxxxxxxx> wrote:

On Mon, 12 Mar 2007 19:58:21 GMT, Jim Chinnis <jchinnis@xxxxxxxxxxxx>
wrote:

CliffMacgillivray <nospam@xxxxxxxxxxxxxx> wrote in part:

Matti Narkia wrote:
just published online, found that low vitamin D status is common in
older persons and associated with poorer physical performance and a
greater decline in physical performance. Below the abstract of this
study:

*gasp* So old people that are too frail to go outside into the sunlight
have low vitamin D levels!?!? I think that being too frail to go outside
leads to the vitamin D deficiency and not the other way around.

Right. I also think the "discovery" of lower vit D in those with diabetes
type 2 is similar: they got diabetes (many of them) because they didn't go
out and bike/walk/run/swim enough and they got low vit D because they didn't
go out and bike/walk/run/swim enough.

That's logical, but I don't think that the observation of relatively
high prevalence of low vitamin D status among type 2 diabetes patients
was a main point of this study. IMHO it was the association of low
vitamin D status within this population with increased
atherosclerosis. An excerpt from the abstract:

"In multivariate regression analysis, low 25(OH)D
concentrations independently predicted carotid IMT (P <
0.001) in people with type 2 diabetes after adjustment for
classical risk factors, diabetes duration, HbA1c, calcium,
renal function tests, inflammatory markers, use of
medications, and presence of the metabolic syndrome"

As for the relation between low vitamin D status and type 2 diabetes,
I take a couple of IMHO interesting quotes from

Zittermann A.
Vitamin D in preventive medicine: are we ignoring the evidence?
Br J Nutr. 2003 May;89(5):552-72. Review.
PMID: 12720576 [PubMed - indexed for MEDLINE]
<http://www.ingentaconnect.com/content/cabi/bjn/2003/00000089/00000005/art00002?token=00531a0783f6da2dd5264f65263a3d4f58762f467c405847447b23442f7b317b763b6b674c7a2d1245d>
(full text available from that page)

"Experimental studies have demonstrated that a reduction in
vitamin D activity can result in both increased insulin
resistance and reduced insulin secretion (Boucher, 1998).
Epidemiological data have shown a four- to five-fold higher
prevalence of non-insulin-dependent diabetes in dark-skinned
Asian immigrants in comparison with British Caucasians
indicating that low vitamin D status may contribute to the
pathogenesis of diabetes (McKeigue et al. 1992). Moreover, in
elderly subjects the subgroup with the lowest tertile of
25(OH)D levels had a significantly higher blood glucose
increase and higher blood insulin increase after an oral
glucose-tolerance test in comparison with the subgroup with
the highest tertile of 25(OH)D levels (Baynes et al. 1997).
Data indicate that vitamin D insufficiency may result in
insulin resistance. Results are in line with the suggestion
that enhanced levels of TNF-alpha, a cytokine with is
inversely related to 25(OH)D and calcitriol (see p. 560),
promote insulin resistance (Hotamisligil & Spiegelman, 1994).

[...]

It should be mentioned that hypertension, cardiovascular
diseases, and diabetes mellitus are often associated with
obesity. Obese subjects have an increased risk for low
circulating 25(OH)D levels (Bell et al. 1985; Wortsman et al.
2000) due to the storage of vitamin D and 25(OH)D in adipose
tissue (Wortsman et al. 2000). The alterations in vitamin D
metabolism of obese subjects in comparison with lean subjects
are also associated with functional alterations such as
elevated PTH levels (Bell et al. 1985; Wortsman et al. 2000).
Obesity might thus contribute to insufficient circulating
25(OH)D levels."

Here a few more references about the relation between low vitamin D
status and insulin resistance or type 2 diabetes

Pittas AG, Harris SS, Stark PC, Dawson-Hughes B.
The Effects of Calcium and Vitamin D Supplementation on Blood Glucose
and Markers of Inflammation in Non-diabetic Adults.
Diabetes Care. 2007 Feb 2; [Epub ahead of print]
PMID: 17277040 [PubMed - as supplied by publisher]
<http://care.diabetesjournals.org/cgi/content/abstract/dc06-1994v1>

"Conclusions. In healthy older adults with impaired fasting
glucose, supplementation with calcium and vitamin D may
attenuate increases in glycemia and insulin resistance that
occur over time. However, our findings should be considered
hypothesis generating and need to be confirmed in randomized
trials specifically designed for the outcomes of interest."

Mathieu C, Gysemans C, Giulietti A, Bouillon R.
Vitamin D and diabetes.
Diabetologia. 2005 Jul;48(7):1247-57. Epub 2005 Jun 22. Review.
PMID: 15971062 [PubMed - indexed for MEDLINE]
DOI: 10.1007/s00125-005-1802-7
<http://www.springerlink.com/content/q21433360tv03407/>

"Vitamin D deficiency predisposes individuals to type 1 and
type 2 diabetes, and receptors for its activated
form - 1alpha,25-dihydroxyvitamin D3 - have been identified in
both beta cells and immune cells. Vitamin D deficiency has
been shown to impair insulin synthesis and secretion in
humans and in animal models of diabetes, suggesting a role in
the development of type 2 diabetes. Furthermore,
epidemiological studies suggest a link between vitamin D
deficiency in early life and the later onset of type 1
diabetes. In some populations, type 1 diabetes is associated
with certain polymorphisms within the vitamin D receptor
gene. In studies in nonobese diabetic mice, pharmacological
doses of 1alpha,25-dihydroxyvitamin D3, or its structural
analogues, have been shown to delay the onset of diabetes,
mainly through immune modulation. Vitamin D deficiency may,
therefore, be involved in the pathogenesis of both forms of
diabetes, and a better understanding of the mechanisms
involved could lead to the development of preventive
strategies."

Chiu KC, Chu A, Go VL, Saad MF (2004)
Hypovitaminosis D is associated with insulin resistance and beta cell
dysfunction.
Am J Clin Nutr 79:820-825
<http://www.ajcn.org/cgi/content/full/79/5/820>

"CONCLUSIONS: The data show a positive correlation of 25(OH)D
concentration with insulin sensitivity and a negative effect
of hypovitaminosis D on beta cell function. Subjects with
hypovitaminosis D are at higher risk of insulin resistance
and the metabolic syndrome. Further studies are required to
explore the underlying mechanisms.

[...]

Our data show that, in glucose-tolerant subjects, 25(OH)D
concentration has a positive relation to insulin sensitivity
and a negative effect on beta cell function. These relations are
independent of confounding factors. Therefore,
hypovitaminosis D is a risk factor for type 2 diabetes and
the metabolic syndrome. Although there is to date no report
on both of these associations in a single study such as the
current study, separate reports have shown the association of
hypovitaminosis D with insulin resistance (16) and beta cell
dysfunction (8).

[...]

To our knowledge, the current study is the first to show the
relation of 25(OH)D concentration to insulin sensitivity and
secretion by using a hyperglycemic clamp technique in a group
of healthy, glucose-tolerant subjects. We also observed that
hypovitaminosis D is a risk factor for the metabolic
syndrome. Extrapolation from the observations in the current
study suggests that increasing 25(OH)D from 10 to 30 ng/mL
can improve insulin sensitivity by 60%, from 3.8128 to 6.1176
(micromol/L) * m^(-2) * min^(-1) * (pmol/L)^(-1). This improvement
in insulin resistance could potentially eliminate the burden on
beta cells and reverse abnormal glucose tolerance. Furthermore,
the 60% improvement in insulin sensitivity that results from
vitamin D treatment indicates that that treatment is more
potent than either troglitazone or metformin treatment (54%
and 13% improvement in insulin sensitivity, respectively;
36). The modest effect of vitamin D on insulin sensitivity in
individual persons may translate into a dramatic effect in
the population as a whole because of the high prevalence of
hypovitaminosis D, which, in a large population, carries an
attributable risk for type 2 diabetes and the metabolic
syndrome. Although a review of the literature suggests non-
calcium-mediated effects, the underlying molecular mechanism
remains to be elucidated."


--
Matti Narkia
.

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