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Vitamin D, aging, and cancer. Pentti Tuohimaa. 2008; Nutrition Reviews - Wiley InterScience
Vitamin D, aging, and cancer.
Tuohimaa P.
Nutr Rev. 2008 Oct;66(10 Suppl 2):S147-52. Review.
PMID: 18844842
DOI: 10.1111/j.1753-4887.2008.00095.x
Deficiency of the prohormone calcidiol (25OH vitamin D3) seems to be associated with several aging-related chronic diseases including cancer. Our results suggest that calcidiol is mainly responsible for differentiation homeostasis, whereas calcitriol might be more involved in calcium homeostasis. Therefore, an imbalance of calcidiol rather than calcitriol is a risk factor for cancer and chronic diseases. Calcidiol insufficiency, as well as insufficient solar exposure, is associated with increased risk of several solid cancers. Both a vitamin D3 deficiency and a high concentration of calcidiol may increase cancer risk. Similarly, aging phenomena show a U-shaped association with vitamin D bioactivity. Therefore, the chronic diseases and cancers related to aging might be prevented by an optimal concentration of serum calcidiol, which remains to be determined.
Vitamin D and aging. [J Steroid Biochem Mol Biol. 2009] - PubMed result
Vitamin D and aging.
Tuohimaa P.
J Steroid Biochem Mol Biol. 2009 Mar;114(1-2):78-84. Review.
PMID: 19444937
The role of Vitamin D3 metabolism in prostate cancer - ScienceDirect - The Journal of Steroid Biochemistry and Molecular Biology
The role of Vitamin D3 metabolism in prostate cancer.
Lou YR, Qiao S, Talonpoika R, Syvälä H, Tuohimaa P.
J Steroid Biochem Mol Biol. 2004 Nov;92(4):317-25. Epub 2004 Dec 19. Review.
PMID: 15663995
doi:10.1016/j.jsbmb.2004.10.007
In summary, the local metabolism of hormonal Vitamin D seems to play an important role in the development and progression of prostate cancer.
Calcidiol and prostate cancer - ScienceDirect - The Journal of Steroid Biochemistry and Molecular Biology
Calcidiol and prostate cancer.
Tuohimaa P, Golovko O, Kalueff A, Nazarova N, Qiao S, Syvälä H, Talonpoika R, Lou YR.
J Steroid Biochem Mol Biol. 2005 Feb;93(2-5):183-90. Epub 2005 Jan 22. Review.
PMID: 15860261
n-3 fatty acid dietary recommendations and food sources to achieve essentiality and cardiovascular benefits.
n-3 fatty acid dietary recommendations and food sources to achieve essentiality and cardiovascular benefits.
Gebauer SK, Psota TL, Harris WS, Kris-Etherton PM.
Am J Clin Nutr. 2006 Jun;83(6 Suppl):1526S-1535S. Review.
PMID: 16841863
Dietary recommendations have been made for n–3 fatty acids, including {alpha}-linolenic acid (ALA), eicosapentaenoic acid (EPA), and docosahexaenoic acid (DHA) to achieve nutrient adequacy and to prevent and treat cardiovascular disease. These recommendations are based on a large body of evidence from epidemiologic and controlled clinical studies. The n–3 fatty acid recommendation to achieve nutritional adequacy, defined as the amount necessary to prevent deficiency symptoms, is 0.6–1.2% of energy for ALA; up to 10% of this can be provided by EPA or DHA. To achieve recommended ALA intakes, food sources including flaxseed and flaxseed oil, walnuts and walnut oil, and canola oil are recommended. The evidence base supports a dietary recommendation of {approx}500 mg/d of EPA and DHA for cardiovascular disease risk reduction. For treatment of existing cardiovascular disease, 1 g/d is recommended. These recommendations have been embraced by many health agencies worldwide. A dietary strategy for achieving the 500-mg/d recommendation is to consume 2 fish meals per week (preferably fatty fish). Foods enriched with EPA and DHA or fish oil supplements are a suitable alternate to achieve recommended intakes and may be necessary to achieve intakes of 1 g/d.
Clinical Prevention of Sudden Cardiac Death by n-3 Polyunsaturated Fatty Acids and Mechanism of Prevention of Arrhythmias by n-3 Fish Oils -- Leaf et al. 107 (21): 2646 -- Circulation
Clinical prevention of sudden cardiac death by n-3 polyunsaturated fatty acids and mechanism of prevention of arrhythmias by n-3 fish oils.
Leaf A, Kang JX, Xiao YF, Billman GE.
Circulation. 2003 Jun 3;107(21):2646-52. Review.
PMID: 12782616
doi: 10.1161/01.CIR.0000069566.78305.33
This review will be limited specifically to the beneficial prevention by the n-3 polyunsaturated fatty acids (PUFAs) of arrhythmic deaths, including sudden cardiac death, which annually causes some 300 000 deaths in the United States and millions more worldwide. We will also show that the growing body of positive clinical studies is supported by what has been learned in animal and laboratory studies regarding the mechanism by which n-3 PUFAs prevent cardiac arrhythmias.
n-3 Fatty acids and cardiovascular disease -- Breslow 83 (6): S1477 -- American Journal of Clinical Nutrition
n-3 fatty acids and cardiovascular disease.
Breslow JL.
Am J Clin Nutr. 2006 Jun;83(6 Suppl):1477S-1482S. Review.
PMID: 16841857
The results of prospective cohort studies indicate that consuming fish or fish oil containing the n–3 fatty acids eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) is associated with decreased cardiovascular death, whereas consumption of the vegetable oil–derived n–3 fatty acid {alpha}-linolenic acid is not as effective. Randomized control trials (RCTs) in the context of secondary prevention also indicate that the consumption of EPA plus DHA is protective at doses <1 g/d. The therapeutic effect appears to be due to suppression of fatal arrhythmias rather than stabilization of atherosclerotic plaques. At doses >3 g/d, EPA plus DHA can improve cardiovascular disease risk factors, including decreasing plasma triacylglycerols, blood pressure, platelet aggregation, and inflammation, while improving vascular reactivity. Mainly on the basis of the results of RCTs, the American Heart Association recommends that everyone eat oily fish twice per week and that those with coronary heart disease eat 1 g/d of EPA plus DHA from oily fish or supplements. Directions for future research include 1) RCTs to confirm the initial trials showing that EPA plus DHA decreases cardiovascular death and additional studies to determine whether this effect is due to EPA, DHA, or the combination; the dosage of the effective components; and whether the mechanism of action in humans is prevention of fatal arrhythmias. 2) Clinical studies to determine whether the reduction in cardiovascular disease risk factors is due to EPA, DHA, or the combination and the dosage of the effective components. 3) Clinical studies to determine whether vegetable oil–derived {alpha}-linolenic acid added to a diet enriched in n–6 fatty acids can effectively substitute for fish oil–derived EPA plus DHA.
Effect of Fish Oil on Heart Rate in Humans: A Meta-Analysis of Randomized Controlled Trials -- Mozaffarian et al. 112 (13): 1945 -- Circulation
Effect of fish oil on heart rate in humans: a meta-analysis of randomized controlled trials.
Mozaffarian D, Geelen A, Brouwer IA, Geleijnse JM, Zock PL, Katan MB.
Circulation. 2005 Sep 27;112(13):1945-52. Epub 2005 Sep 19.
PMID: 16172267
doi: 10.1161/CIRCULATIONAHA.105.556886
Conclusions— In randomized controlled trials in humans, fish oil reduces HR, particularly in those with higher baseline HR or longer treatment duration. These findings provide firm evidence that fish oil consumption directly or indirectly affects cardiac electrophysiology in humans. Po
n-3 Fatty acids and cardiovascular disease: mechanisms underlying beneficial effects -- Jung et al. 87 (6): 2003S -- American Journal of Clinical Nutrition
n-3 Fatty acids and cardiovascular disease: mechanisms underlying beneficial effects.
Jung UJ, Torrejon C, Tighe AP, Deckelbaum RJ.
Am J Clin Nutr. 2008 Jun;87(6):2003S-9S.
PMID: 18541602
Dietary n–3 fatty acids, particularly eicosapentaenoic acid and docosahexaenoic acid, are important nutrients through the life cycle. Evidence from observational, clinical, animal, and in vitro studies indicates a beneficial role of n–3 fatty acids in the prevention and management of cardiovascular disease. Although the precise mechanisms are still unclear, clinical and preclinical studies indicate that the cardioprotective effects of n–3 fatty acids may be attributed to a number of distinct biological effects on lipid and lipoprotein metabolism, blood pressure, platelet function, arterial cholesterol delivery, vascular function, and inflammatory responses.
Substantial evidence supports n–3 fatty acids as a practical, therapeutic adjuvant for promoting cardiovascular health and preventing and treating disease. n–3 Fatty acids modulate a number of important physiologic responses that can contribute to their cardioprotective effects. The multiple and complex mechanisms through which DHA and EPA exert their action appear to be distinct but also complementary. However, more studies are needed to quantify their protective effects and to define exact mechanisms of action.
n-3 Fatty acids and gene expression -- Deckelbaum et al. 83 (6): S1520 -- American Journal of Clinical Nutrition
n-3 fatty acids and gene expression.
Deckelbaum RJ, Worgall TS, Seo T.
Am J Clin Nutr. 2006 Jun;83(6 Suppl):1520S-1525S. Review. Erratum in: Am J Clin Nutr. 2006 Oct;84(4):949.
PMID: 16841862
Accumulating evidence in both humans and animal models clearly indicates that a group of very-long-chain polyunsaturated fatty acids, the n–3 fatty acids (or omega-3), have distinct and important bioactive properties compared with other groups of fatty acids. n–3 Fatty acids are known to reduce many risk factors associated with several diseases, such as cardiovascular diseases, diabetes, and cancer. The mechanisms whereby n–3 fatty acids affect gene expression are complex and involve multiple processes. As examples, n–3 fatty acids regulate 2 groups of transcription factors, such as sterol-regulatory-element binding proteins and peroxisome proliferator-activated receptors, that are critical for modulating the expression of genes controlling both systemic and tissue-specific lipid homeostasis. Modulation of specific genes by n–3 fatty acids and cross-talk between these genes are responsible for many effects of n–3 fatty acids.
Quantitative Analysis of the Benefits and Risks of Consuming Farmed and Wild Salmon -- Foran et al. 135 (11): 2639 -- Journal of Nutrition
Quantitative analysis of the benefits and risks of consuming farmed and wild salmon.
Foran JA, Good DH, Carpenter DO, Hamilton MC, Knuth BA, Schwager SJ.
J Nutr. 2005 Nov;135(11):2639-43.
PMID: 16251623
Contaminants in farmed Atlantic and wild Pacific salmon raise important questions about the competing health benefits and risks of fish consumption. A benefit-risk analysis was conducted to compare quantitatively the cancer and noncancer risks of exposure to organic contaminants in salmon with the (n-3) fatty acid-associated health benefits of salmon consumption. Recommended levels of (n-3) fatty acid intake, as eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA), may be achieved by consuming farmed or wild salmon while maintaining an acceptable level of noncarcinogenic risk. However, the recommended level of EPA+DHA intake cannot be achieved solely from farmed or wild salmon while maintaining an acceptable level of carcinogenic risk. Although the benefit-risk ratio for carcinogens and noncarcinogens is significantly greater for wild Pacific salmon than for farmed Atlantic salmon as a group, the ratio for some subgroups of farmed salmon is on par with the ratio for wild salmon. This analysis suggests that risk of exposure to contaminants in farmed and wild salmon is partially offset by the fatty acid-associated health benefits. However, young children, women of child-bearing age, pregnant women, and nursing mothers not at significant risk for sudden cardiac death associated with CHD but concerned with health impairments such as reduction in IQ and other cognitive and behavioral effects, can minimize contaminant exposure by choosing the least contaminated wild salmon or by selecting other sources of (n-3) fatty acids.
The Effect of Select Nutrients on Serum High-Density Lipoprotein Cholesterol and Apolipoprotein A-I Levels -- Mooradian et al. 27 (1): 2 -- Endocrine Reviews
The effect of select nutrients on serum high-density lipoprotein cholesterol and apolipoprotein A-I levels.
Mooradian AD, Haas MJ, Wong NC.
Endocr Rev. 2006 Feb;27(1):2-16. Epub 2005 Oct 21. Review.
PMID: 16243964
One of the factors contributing to the increased risk of developing premature atherosclerosis is low plasma concentrations of high-density lipoprotein (HDL) cholesterol (HDLc). Multiple potential mechanisms account for the cardioprotective effects of HDL and its main protein apolipoprotein A-I (apo A-I). The low plasma concentrations of HDL could be the result of increased fractional clearance and reduced expression of apo A-I. To this end, nutrients play an important role in modulating the fractional clearance rate, as well as the rate of apo A-I gene expression. Because medical nutrition therapy constitutes the cornerstone of management of dyslipidemias, it is essential to understand the mechanisms underlying the changes in HDL level in response to alterations in dietary intake. In this review, we will discuss the effect of select nutrients on serum HDLc and apo A-I levels. Specifically, we will review the literature on the effect of carbohydrates, fatty acids, and ketones, as well as some of the nutrient-related metabolites, such as glucosamine and the prostanoids, on apo A-I gene expression. Because there are multiple mechanisms involved in the regulation of serum HDLc levels, changes in gene transcription do not necessarily correlate with clinical observations on serum levels of HDLc.
Are statins analogues of vitamin D? : The Lancet
Are statins analogues of vitamin D?
Grimes DS.
Lancet. 2006 Jul 1;368(9529):83-6. Review.
PMID: 16815382
doi:10.1016/S0140-6736(06)68971-X
There are many reasons why the dietary-heart-cholesterol hypothesis should be questioned, and why statins might be acting in some other way to reduce the risk of coronary heart disease. Here, I propose that rather than being cholesterol-lowering drugs per se, statins act as vitamin D analogues, and explain why. This proposition is based on published observations that the unexpected and unexplained clinical benefits produced by statins have also been shown to be properties of vitamin D. It seems likely that statins activate vitamin D receptors.
Traditional Chinese Medicine in Treatment of Metabolic Syndrome
Traditional chinese medicine in treatment of metabolic syndrome.
Yin J, Zhang H, Ye J.
Endocr Metab Immune Disord Drug Targets. 2008 Jun;8(2):99-111. Review.
PMID: 18537696
Berberine from rhizoma coptidis is an oral hypoglycemic agent. It also has anti-obesity and anti-dyslipidemia activities. The action mechanism is related to inhibition of mitochondrial function, stimulation of glycolysis, activation of AMPK pathway, suppression of adipogenesis and induction of low-density lipoprotein (LDL) receptor expression.
Berberine - Altern Med Rev. 2000 Apr;5(2):175-7.
Berberine.
[No authors listed]
Altern Med Rev. 2000 Apr;5(2):175-7.
PMID: 10767672
Berberine is a plant alkaloid with a long history of medicinal use in both Ayurvedic and Chinese medicine. It is present in Hydrastis canadensis (goldenseal), Coptis chinensis (Coptis or goldenthread), Berberis aquifolium (Oregon grape), Berberis vulgaris (barberry), and Berberis aristata (tree turmeric). The berberine alkaloid can be found in the roots, rhizomes, and stem bark of the plants. Berberine extracts and decoctions have demonstrated significant antimicrobial activity against a variety of organisms including bacteria, viruses, fungi, protozoans, helminths, and chlamydia. Currently, the predominant clinical uses of berberine include bacterial diarrhea, intestinal parasite infections, and ocular trachoma infection
The Vitamin D-Antimicrobial Peptide Pathway and Its Role in Protection Against Infection (printer-friendly) - Future Microbiol. 2009 Nov;4:1151-65. - Medscape
The vitamin D-antimicrobial peptide pathway and its role in protection against infection.
Gombart AF.
Future Microbiol. 2009 Nov;4:1151-65.
PMID: 19895218
Vitamin D deficiency has been correlated with increased rates of infection. Since the early 19th century, both environmental (i.e., sunlight) and dietary sources (cod liver) of vitamin D have been identified as treatments for TB. The recent discovery that vitamin D induces antimicrobial peptide gene expression explains, in part, the 'antibiotic' effect of vitamin D and has greatly renewed interest in the ability of vitamin D to improve immune function. Subsequent work indicates that this regulation is biologically important for the response of the innate immune system to wounds and infection and that deficiency may lead to suboptimal responses toward bacterial and viral infections. The regulation of the cathelicidin antimicrobial peptide gene is a human/primate-specific adaptation and is not conserved in other mammals. The capacity of the vitamin D receptor to act as a high-affinity receptor for vitamin D and a low-affinity receptor for secondary bile acids and potentially other novel nutritional compounds suggests that the evolutionary selection to place the cathelicidin gene under control of the vitamin D receptor allows for its regulation under both endocrine and xenobiotic response systems. Future studies in both humans and humanized mouse models will elucidate the importance of this regulation and lead to the development of potential therapeutic applications
Vitamin D and cancer: current dilemmas and future research needs -- Davis 88 (2): 565S -- American Journal of Clinical Nutrition
Vitamin D and cancer: current dilemmas and future research needs.
Davis CD.
Am J Clin Nutr. 2008 Aug;88(2):565S-569S. Review.
PMID: 18689403
A diversity of scientific literature supports a role for vitamin D in decreasing colorectal cancer incidence, but the available evidence provides only limited support for an inverse association between vitamin D status and the risk of other types of cancer. We need additional studies analyzing the dose-response relation between vitamin D status and cancer risk, the optimal level of 25-hydroxyvitamin D, the length of time required to observe an effect, and the time period of life when exposure is most relevant. Studies of vitamin D receptor polymorphisms have found that not all polymorphisms have the same association with cancer, and the cancer site could further dictate which polymorphisms might be most important; this indicates a need for more research on gene-environment interactions. Several dietary components and the balance between energy intake and expenditure influence vitamin D metabolism. These studies show that scientists need to identify confounders and modifiers of the biological response to vitamin D, including dietary factors, lifestyle factors such as exercise, and race or ethnicity. Transgenic and knockout animals are powerful tools for identifying the molecular targets of bioactive food components. Scientists should therefore make increased use of these models to identify molecular targets for vitamin D. Many research gaps relate to the need to develop predictive, validated, and sensitive biomarkers, including biomarkers that researchers can use to reliably evaluate intake or exposure to vitamin D, assess one or more specific biological effects that are linked to cancer, and effectively predict individual susceptibility as a function of nutrient-nutrient interactions and genetics.
Mortality in vegetarians and nonvegetarians: detailed findings from a collaborative analysis of 5 prospective studies -- Key et al. 70 (3): 516 -- American Journal of Clinical Nutrition
Mortality in vegetarians and nonvegetarians: detailed findings from a collaborative analysis of 5 prospective studies.
Key TJ, Fraser GE, Thorogood M, Appleby PN, Beral V, Reeves G, Burr ML, Chang-Claude J, Frentzel-Beyme R, Kuzma JW, Mann J, McPherson K.
Am J Clin Nutr. 1999 Sep;70(3 Suppl):516S-524S.
PMID: 10479225
Further categorization of diets showed that, in comparison with regular meat eaters, mortality from ischemic heart disease was 20% lower in occasional meat eaters, 34% lower in people who ate fish but not meat, 34% lower in lactoovovegetarians, and 26% lower in vegans. There were no significant differences between vegetarians and nonvegetarians in mortality from cerebrovascular disease, stomach cancer, colorectal cancer, lung cancer, breast cancer, prostate cancer, or all other causes combined.
See especially
TABLE 7. All-studies death rate ratios and 95% CIs and the number of deaths by diet category
http://www.ajcn.org/cgi/content/full/70/3/516S/T7
Vitamin D and breast cancer. - Ann Epidemiol. 2009 Jul (full text PDF)
Vitamin D and breast cancer.
Bertone-Johnson ER.
Ann Epidemiol. 2009 Jul;19(7):462-7. Epub 2009 Feb 20. Review.
PMID: 19230714
Though the relationship between vitamin D and breast cancer remains unclear, a growing body of evidence suggests that vitamin D may modestly reduce risk. A large number of in vitro studies indicate that vitamin D can inhibit cell proliferation and promote apoptosis and cell differentiation in breast tumor tissue. Results from analytic studies of sunlight exposure and dietary intake have been inconsistent but together generally support a modestly protective role of vitamin D, at least in some population subgroups. Studies using blood vitamin D metabolites to assess vitamin D status may be less prone to misclassification than those of diet and sunlight exposure. Overall, the two prospective and four case-control studies of 25-hydroxyvitamin D and 1,25-dihydroxyvitamin D tend to support a protective effect in older women. The relationship between common vitamin D receptor polymorphisms and risk remains unclear. Many questions about this relationship clearly remain, including the utility of assessing vitamin D through diet and sunlight exposure, the relationship between plasma metabolites, and the potential modifying effects of age, menopausal status and tumor characteristics. Given that vitamin D status is modifiable, additional prospective studies are necessary to determine if vitamin D may have important potential for breast cancer prevention.
Ecological studies of ultraviolet B, vitamin D and cancer since 2000. - Ann Epidemiol. 2009 Jul (full text PDF)
Ecological studies of ultraviolet B, vitamin D and cancer since 2000.
Grant WB, Mohr SB.
Ann Epidemiol. 2009 Jul;19(7):446-54. Epub 2009 Mar 9. Review.
PMID: 19269856
CONCLUSION: These findings provide strong evidence that vitamin D status plays an important role in controlling the outcome of cancer. Support for the UVB-vitamin D-cancer theory is now scientifically strong enough to warrant use of vitamin D in cancer prevention, and as a component of treatment. More research studies would help to explore whether there are benefits beyond the substantial effects that have been observed.
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