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VItamin Benefits- read four studies below

Diagnosis and treatment of vitamin D deficiency.

Expert Opin Pharmacother. 2008 Jan;9(1):107-118.

Cannell J, Hollis B, Zasloff M, Heaney R.
1Atascadero State Hospital, 10333 El Camino Real, Atascadero, California 93422, USA +1 805 468 2061 ; , 2Medical University of South Carolina, Departments of Biochemistry and
Molecular Biology, Charleston, South Carolina, USA, 3Georgetown University, Departments of Surgery and
Pediatrics, Washington, District of Columbia, USA, 4Creighton University Medical Center, Department of
Medicine, Omaha, Nebraska, USA.

The recent discovery - in a randomised, controlled trial - that
daily ingestion of 1100 IU of colecalciferol
(vitamin D) over a 4-year period
dramatically reduced the incidence of non-skin cancers makes it
difficult to overstate the potential medical, social and economic implications of treating vitamin D deficiency.
Not only are such deficiencies common, probably the rule, vitamin D deficiency stands implicated in a host
of diseases other than cancer. The metabolic product of vitamin D is a potent, pleiotropic, repair and
maintenance, secosteroid hormone that targets > 200 human genes in a wide variety of tissues, meaning it
has as many mechanisms of action as genes it targets. A common misconception is that government
agencies designed present intake recommendations to prevent or treat vitamin D deficiency. They did not.
Instead, they are guidelines to prevent particular metabolic bone diseases. Official recommendations were
never designed and are not effective in preventing or treating vitamin D deficiency and in no way limit the
freedom of the physician - or responsibility - to do so. At this time, assessing serum 25-hydroxy-vitamin D is
the only way to make the diagnosis and to assure that treatment is adequate and safe. The authors believe
that treatment should be sufficient to maintain levels found in humans living naturally in a sun-rich
environment, that is, > 40 ng/ml, year around. Three treatment modalities exist: sunlight, artificial ultraviolet
B radiation or supplementation. All treatment modalities have their potential risks and benefits. Benefits of
all treatment modalities outweigh potential risks and greatly outweigh the risk of no treatment. As a
prolonged 'vitamin D winter', centred on the winter solstice, occurs at many temperate latitudes, </= 5000 IU
(125 mug) of vitamin D/day may be required in obese, aged and/or dark-skinned patients to maintain
adequate levels during the winter, a dose that makes many physicians uncomfortable.
PMID: 18076342 [PubMed - as supplied by publisher]

Cytotoxicity of ascorbate [Vit. C], lipoic acid, and other antioxidants in hollow
fibre in vitro tumours

Br J Cancer 2001 (Vol. 84, Issue 11) 1544-50.

Casciari, J. J., Riordan, N. H., Schmidt, T. L., Meng, X. L., Jackson, J. A., Riordan, H. D.

Vitamin C (ascorbate) is toxic to tumour cells, and has been suggested as an adjuvant cancer treatment.
Our goal was to determine if ascorbate, in combination with other antioxidants, could kill cells in the SW620
hollow fibre in vitro solid tumour model at clinically achievable concentrations. Ascorbate anti-cancer
efficacy, alone or in combination with lipoic acid, vitamin K3, phenyl ascorbate, or doxorubicin, was
assessed using annexin V staining and standard survival assays. 2-day treatments with 10 mM ascorbate
increased the percentage of apoptotic cells in SW620 hollow fibre tumours.
Lipoic acid synergistically
enhanced ascorbate cytotoxicity
, reducing the 2- day LC(50)in hollow fibre tumours from 34 mM to 4
mM. Lipoic acid, unlike ascorbate, was equally effective against proliferating and non- proliferating cells.
Ascorbate levels in human blood plasma were measured during and after intravenous ascorbate infusions.
Infusions of 60 g produced peak plasma concentrations exceeding 20 mM with an area under the curve (24
h) of 76 mM h. Thus, tumoricidal concentrations may be achievable in vivo. Ascorbate efficacy was
enhanced in an additive fashion by phenyl ascorbate or vitamin K3. The
effect of ascorbate on
doxorubicin efficacy was concentration dependent; low doses were protective while high doses
increased cell killing

In vivo effect of lipoic acid on lipid peroxidation in patients with diabetic

In Vivo 2000 (Vol. 14, Issue 2) 327-30.

Androne, L., Gavan, N. A., Veresiu, I. A., Orasan, R.

BACKGROUND: The diabetic state, in both humans and experimental animals, is associated with oxidative
stress. Lipid peroxidation of nerve membranes has been suggested as a mechanism by which peripheral
nerve ischemia and hypoxia could cause neuropathy. Lipoic acid (LA) is a powerful inhibitor of
iron-dependent lipid peroxidation and reactive oxygen species. The treatment of diabetic peripheral and
cardiac autonomic neuropathy with LA is based on good clinical and experimental evidence. MATERIALS
AND METHODS: To investigate the magnitude of the oxidative stress, serum ceruloplasmin (Cp) and lipid
peroxide (Lp) levels were measured in 10 patients with diabetic neuropathy, before and 70 days after
treatment with single dose of 600 mg LA/day. For other 12 healthy age- and sex-matched control subjects
the serum Cp and Lp levels were evaluated. RESULTS: Our results show that hyperglycemia is a factor for
an increase in serum ceruloplasmin in patients with diabetic neuropathy compared to healthy subjects (p <
0.0001). High serum ceruloplasmin (Cp) level in patients with diabetes may be related to antioxidant
defense. The treatment of diabetic neuropathy with LA does not affect significantly the serum Cp activity.
The serum Lp levels after LA administration were significantly lower (p < 0.005) than those before
treatment. CONCLUSIONS: The antioxidant
therapy with LA improves and may prevent diabetic
. This improvement is associated with a reduction in the indexes of lipid peroxidation. Oxidative
stress appears to be primarily due to the processes of nerve ischemia and hyperglycemia autooxidation.

L-Carnitine treatment reduces severity of physical and mental fatigue and
increases cognitive functions in centenarians: a randomized and controlled
clinical trial.

Am J Clin Nutr. 2007 Dec;86(6):1738-44.

Malaguarnera M, Cammalleri L, Gargante MP, Vacante M, Colonna V, Motta M.

Department of Senescence, Urological, and Neurological Sciences, University of Catania, Catania, Italy.

BACKGROUND: Centenarians are characterized by weakness, decreasing mental health, impaired mobility,
and poor endurance. l-Carnitine is an important contributor to cellular energy metabolism. OBJECTIVE: This
study evaluated the efficacy of l-carnitine on physical and mental fatigue and on cognitive functions of
centenarians. DESIGN: This was a placebo-controlled, randomized, double-blind, 2-phase study. Sixty-six
centenarians with onset of fatigue after even slight physical activity were recruited to the study. The 2
groups received either 2 g levocarnitine once daily (n = 32) or placebo (n = 34). Efficacy measures included
changes in total fat mass, total muscle mass, serum triacylglycerol, total cholesterol, HDL cholesterol, LDL
cholesterol, Mini-Mental State Examination (MMSE), Activities of Daily Living, and a 6-min walking corridor
test. RESULTS: At the end of the study period, the levocarnitine-treated centenarians, compared with the
placebo group, showed significant improvements in the following markers: total fat mass (-1.80 compared
with 0.6 kg; P < 0.01), total muscle mass (3.80 compared with 0.8 kg; P < 0.01), plasma concentrations of
total carnitine (12.60 compared with -1.70 mumol; P < 0.05), plasma long-chain acylcarnitine (1.50
compared with -0.1 mumol; P < 0.001), and plasma short-chain acylcarnitine (6.0 compared with -1.50
mumol; P < 0.001). Significant differences were also found in physical fatigue (-4.10 compared with -1.10; P
< 0.01), mental fatigue (-2.70 compared with 0.30; P < 0.001), fatigue severity (-23.60 compared with 1.90;
P < 0.001), and MMSE (4.1 compared with 0.6; P < 0.001). CONCLUSIONS: Our study indicates that
administration of l-carnitine produces a reduction of total fat mass, increases total muscular
mass, and facilitates an increased capacity for physical and cognitive activity by reducing fatigue
and improving cognitive functions.

PMID: 18065594 [PubMed - in process]