Dr. Hank Liers, PhD biography about us HPDI integratedhealth formulator founder CEO scientist physicist wild bilberry and wild blueberry

Ultimate Protector contains resveratrol, as well as components from 29 different fruits, vegetables, and herbs. Each of these ingredients contain substances that may be considered to be polyphenols, antioxidants, and Nrf2 activators. In this article I will explore the ingredient resveratrol, which is added as a separate ingredient in addition to being a component in VitaBerry Plus® from Futureceuticals.

Resveratrol (3,5,4′-trihydroxy-trans-stilbene) is a stilbenoid, a type of natural phenol, and a phytoalexin produced naturally by several plants in response to injury or when the plant is under attack by pathogens such as bacteria and fungi. Natural sources of resveratrol include giant knotweed (Polygonum cuspidatum) and the skin of grapes, blueberries, raspberries, and mulberries. Resveratrol has two isomers: cis and trans, with the latter being the most abundant.  Piceid, also known as polydatin, is a glucoside form of resveratrol found in Japanese knotweed. HPDI includes the very pure 99% resveratrol form from giant knotweed in Ultimate Protector. This material contains greater than 96% of the trans form.

giant knotweed resveratrol

Knotweed (Polygonum cuspidatum) is a major source for resveratrol.



VitaBerry® (N1023) is the trade name for a line of high ORAC blends of fruit powders and fruit extracts, exclusively available through FutureCeuticals.

VitaBerry® is a proprietary formula that combines wild bilberry and wild blueberry, cranberry, raspberry, strawberry, prune, cherry, and grape whole powders and extracts into lines of custom blends. High in fruit polyphenols, anthocyanins, proanthocyanins, ellagic acid, chlorogenic acid, resveratrol, and quinic acid, VitaBerry offers 6,000 ORAC units in a single gram.

VitaBerry® Plus (N81.3) combines the standard blend of VitaBerry® with resveratrol and quercetin to deliver a minimum of 12,000 ORAC units per gram.


Resveratrol provides anti-oxidant protection, boosts cellular energy, and balances the immune system. It has been proven in studies to activate the SIRT1 longevity gene and enhance cellular productivity. Several research studies have shown that trans-resveratrol significantly modulates biomarkers of bone metabolism, inhibits pro-inflammatory enzymes such as COX-1 and COX-2, and exhibits chemopreventive properties, cardioprotective effects, neuroprotective properties, and caloric restrictive behavior. Trans-resveratrol has shown the ability to increase the number of mitochondria thereby increasing total daily energy. Studies have shown that trans-resveratrol promotes an increase in mitochondrial function, that translates into an increase in energy availability, improved aerobic capacity, and enhanced sensorimotor function. Resveratrol has been shown to be a powerful Nrf2 activator that can support the body’s endogenous production of protective enzymes.

Scientific Studies on the Antioxidant Effects of Resveratrol

Databases of scientific studies (like the National Institutes of Health (NIH) PubMed database) contain thousands of up-to-date studies and abstracts about resveratrol

Below, we provide a few relevant scientific studies on the antioxidant effects and potential health benefits of resveratrol.

Resveratrol confers endothelial protection via activation of the antioxidant transcription factor Nrf2.


Epidemiological studies suggest that Mediterranean diets rich in resveratrol are associated with reduced risk of coronary artery disease. Resveratrol was also shown to confer vasoprotection in animal models of type 2 diabetes and aging. However, the mechanisms by which resveratrol exerts its antioxidative vasculoprotective effects are not completely understood. Using a nuclear factor-E(2)-related factor-2 (Nrf2)/antioxidant response element-driven luciferase reporter gene assay, we found that in cultured coronary arterial endothelial cells, resveratrol, in a dose-dependent manner, significantly increases transcriptional activity of Nrf2. Accordingly, resveratrol significantly upregulates the expression of the Nrf2 target genes NAD(P)H:quinone oxidoreductase 1, gamma-glutamylcysteine synthetase, and heme oxygenase-1. Resveratrol treatment also significantly attenuated high glucose (30 mM)-induced mitochondrial and cellular oxidative stress (assessed by flow cytometry using MitoSox and dihydroethidine staining). The aforementioned effects of resveratrol were significantly attenuated by the small interfering RNA downregulation of Nrf2 or the overexpression of Kelch-like erythroid cell-derived protein 1, which inactivates Nrf2. To test the effects of resveratrol in vivo, we used mice fed a high-fat diet (HFD), which exhibit increased vascular oxidative stress associated with an impaired endothelial function. In HFD-fed Nrf2(+/+) mice, resveratrol treatment attenuates oxidative stress (assessed by the Amplex red assay), improves acetylcholine-induced vasodilation, and inhibits apoptosis (assessed by measuring caspase-3 activity and DNA fragmentation) in branches of the femoral artery. In contrast, the aforementioned endothelial protective effects of resveratrol were diminished in HFD-fed Nrf2(-/-) mice. Taken together, our results indicate that resveratrol both in vitro and in vivo confers endothelial protective effects which are mediated by the activation of Nrf2.


Mitochondrial Protection by Resveratrol

From: http://www.medscape.com/viewarticle/745451


Mitochondrial dysfunction and oxidative stress are thought to play important roles in mammalian aging. Resveratrol is a plant-derived polyphenol that exerts diverse antiaging activities, mimicking some of the molecular and functional effects of dietary restriction. This review focuses on the molecular mechanisms underlying the mitochondrial protective effects of resveratrol, which could be exploited for the prevention or amelioration of age-related diseases in the elderly.


Age-specific mortality rates from heart disease, stroke, complications of diabetes, Alzheimer disease, and cancer increase exponentially with age, which imposes a huge financial burden on the health care systems in the Western world. There is an urgent need for effective therapeutic strategies that have the potential to promote health in the elderly, simultaneously preventing or delaying the development of various diseases of aging. During the past decade, dietary supplementation with resveratrol (3,5,4′-trihydroxystilbene) has emerged as a promising approach to counteract age-related diseases. Resveratrol is a naturally occurring polyphenol found in more than 70 species of plants, including grapes (Vitis vinifera), cranberries (Vaccinium macrocarpon), and peanuts (Arachis hypogaea), which was shown to confer diverse physiological effects in laboratory animals including cancer protection, microvascular protection, neuroprotection, cardioprotection, and antidiabetic effects. In this review, we consider the evidence in support of the hypothesis that mitochondrial protective effects of resveratrol underlie its antiaging action that can prevent/delay the development of age-related diseases in the cardiovascular system and other organs. The use of resveratrol as a dietary supplement to promote mitochondrial health in the elderly and diabetic patients is discussed.


Resveratrol induces glutathione synthesis by activation of Nrf2 and protects against cigarette smoke-mediated oxidative stress in human lung epithelial cells

From: http://ajplung.physiology.org/content/294/3/L478 


Nuclear erythroid-related factor 2 (Nrf2), a redox-sensitive transcription factor, is involved in transcriptional regulation of many antioxidant genes, including glutamate-cysteine ligase (GCL). Cigarette smoke (CS) is known to cause oxidative stress and deplete glutathione (GSH) levels in alveolar epithelial cells. We hypothesized that resveratrol, a polyphenolic phytoalexin, has antioxidant signaling properties by inducing GSH biosynthesis via the activation of Nrf2 and protects lung epithelial cells against CS-mediated oxidative stress. Treatment of human primary small airway epithelial and human alveolar epithelial (A549) cells with CS extract (CSE) dose dependently decreased GSH levels and GCL activity, effects that were associated with enhanced production of reactive oxygen species. Resveratrol restored CSE-depleted GSH levels by upregulation of GCL via activation of Nrf2 and also quenched CSE-induced release of reactive oxygen species. Interestingly, CSE failed to induce nuclear translocation of Nrf2 in A549 and small airway epithelial cells. On the contrary, Nrf2 was localized in the cytosol of alveolar and airway epithelial cells due to CSE-mediated posttranslational modifications such as aldehyde/carbonyl adduct formation and nitration. On the other hand, resveratrol attenuated CSE-mediated Nrf2 modifications, thereby inducing its nuclear translocation associated with GCL gene transcription, as demonstrated by GCL-promoter reporter and Nrf2 small interfering RNA approaches. Thus resveratrol attenuates CSE-mediated GSH depletion by inducing GSH synthesis and protects epithelial cells by reversing CSE-induced posttranslational modifications of Nrf2. These data may have implications in dietary modulation of antioxidants in treatment of chronic obstructive pulmonary disease.


Effect of Nrf2 activators on release of glutathione, cysteinylglycine and homocysteine by human U373 astroglial cells

From: http://www.sciencedirect.com/science/article/pii/S2213231713000645


Neurons rely on the release and subsequent cleavage of GSH to cysteinylglycine (CysGly) by astrocytes in order to maintain optimal intracellular GSH levels. In neurodegenerative diseases characterised by oxidative stress, neurons need an optimal GSH supply to defend themselves against free radicals released from activated microglia and astroglia. The rate of GSH synthesis is controlled largely by the activity of γ-glutamyl cysteine ligase. Expression of γ-glutamyl cysteine ligase and of the Xc- system, which facilitates cystine uptake, is regulated by the redox-sensitive transcription factor, nuclear factor erythroid-2-related factor 2 (Nrf2). Compounds that can activate the Nrf2-ARE pathway, referred to as ‘Nrf2 activators’ are receiving growing attention due to their potential as GSH-boosting drugs.

This study compares four known Nrf2 activators, R-α-Lipoic acid (LA), tert-butylhydroquinone (TBHQ), sulforaphane (SFN) and Polygonum cuspidatum extract containing 50% resveratrol (PC-Res) for their effects on astroglial release of GSH and CysGly. GSH levels increased dose-dependently in response to all four drugs. Sulforaphane produced the most potent effect, increasing GSH by up to 2.4-fold. PC-Res increased GSH up to 1.6-fold, followed by TBHQ (1.5-fold) and LA (1.4-fold). GSH is processed by the ectoenzyme, γ-glutamyl transpeptidase, to form CysGly. Once again, SFN produced the most potent effect, increasing CysGly by up to 1.7-fold, compared to control cells. TBHQ and PC-Res both induced fold increases of 1.3, followed by LA with a fold increase of 1.2. The results from the present study showed that sulforaphane, followed by lipoic acid, resveratrol and Polygonum multiflorum were all identified as potent “GSH and Cys-Gly boosters”.

Resveratrol Upregulates Nrf2 Expression To Attenuate Methylglyoxal-Induced Insulin Resistance in Hep G2 Cells

From: http://pubs.acs.org/doi/abs/10.1021/jf302831d


Oxidative stress can result in insulin resistance, a primary cause of type-2 diabetes. Methylglyoxal (MG), a highly reactive dicarbonyl metabolite generated during glucose metabolism, has also been confirmed to cause pancreatic injury and induce inflammation, thereby resulting in insulin resistance. Recently, resveratrol has been reported to exert antioxidant properties, protecting cells from the generation of reactive oxygen species (ROS). The aim of this study was to evaluate resveratrol activation of nuclear factor erythroid 2-related factor 2 (Nrf2) to attenuate MG-induced insulin resistance in Hep G2 cells. Therefore, the molecular signaling events affecting resveratrol-mediated heme oxygenase-1 (HO-1) and glyoxalase expression levels were further investigated in this study. Our findings indicated that resveratrol activated the extracellular signal-regulated kinase (ERK) pathway but not the p38 or c-Jun N-terminal kinase (JNK) pathways, subsequently leading to Nrf2 nuclear translocation and elevation of HO-1 and glyoxalase expression levels. Moreover, resveratrol significantly elevated glucose uptake and protected against MG-induced insulin resistance in Hep G2 cells. In contrast, depletion of Nrf2 by small interfering RNA (si-RNA) resulted in the abrogation of HO-1 and glyoxalase expression in the MG-treated resveratrol group in Hep G2 cells. Administration of an appropriate chemopreventive agent, such as resveratrol, may be an alternative strategy for protecting against MG-induced diabetes.


Resveratrol restores sirtuin 1 (SIRT1) activity and pyruvate dehydrogenase kinase 1 (PDK1) expression after hemorrhagic injury in a rat model.

From: http://www.ncbi.nlm.nih.gov/pubmed/24395567


Severe hemorrhage leads to decreased blood flow to tissues resulting in decreased oxygen and nutrient availability affecting mitochondrial function. A mitoscriptome profiling study demonstrated alteration in several genes related to mitochondria, consistent with the mitochondrial functional decline observed after trauma hemorrhage (T-H). Our experiments led to the identification of sirtuin 1 (SIRT1) as a potential target in T-H. Administration of resveratrol (a naturally occurring polyphenol and activator of SIRT1) after T-H improved left ventricular function and tissue ATP levels. Our hypothesis was that mitochondrial function after T-H depends on SIRT1 activity. In this study, we evaluated the activity of SIRT1, a mitochondrial functional modulator, and the mitochondrial-glycolytic balance after T-H. We determined the changes in protein levels of pyruvate dehydrogenase kinase (PDK)-1 and nuclear c-Myc, peroxisome proliferator-activated receptor-γ coactivator (PGC)-1α and NF-E2-related factor (NRF)2 after T-H and after treatment with resveratrol or a combination of sirtinol (a SIRT1 inhibitor) and resveratrol. We have also tested the activity of mitochondrial complex 1. SIRT1 enzyme activity was significantly decreased after T-H, whereas resveratrol treatment restored the activity. We found elevated PDK1 and c-Myc levels and decreased PGC-1α, NRF2 and mitochondrial complex I activity after T-H. The reduced SIRT1 activity after T-H may be related to declining mitochondrial function, since resveratrol was able to reinstate SIRT1 activity and mitochondrial function. The elevated level of PDK1 (an inhibitor of pyruvate dehydrogenase complex) after T-H indicates a possible shift in cellular energetics from mitochondria to glycolysis. In conclusion, SIRT1 modulation alters left ventricular function after T-H through regulation of cellular energetics.


Resveratrol suppresses PAI-1 gene expression in a human in vitro model of inflamed adipose tissue.

From: http://www.ncbi.nlm.nih.gov/pubmed/23819014


Increased plasminogen activator inhibitor-1 (PAI-1) levels are associated with a number of pathophysiological complications; among them is obesity. Resveratrol was proposed to improve obesity-related health problems, but the effect of resveratrol on PAI-1 gene expression in obesity is not completely understood. In this study, we used SGBS adipocytes and a model of human adipose tissue inflammation to examine the effects of resveratrol on the production of PAI-1. Treatment of SGBS adipocytes with resveratrol reduced PAI-1 mRNA and protein in a time- and concentration-dependent manner. Further experiments showed that obesity-associated inflammatory conditions lead to the upregulation of PAI-1 gene expression which was antagonized by resveratrol. Although signaling via PI3K, Sirt1, AMPK, ROS, and Nrf2 appeared to play a significant role in the modulation of PAI-1 gene expression under noninflammatory conditions, those signaling components were not involved in mediating the resveratrol effects on PAI-1 production under inflammatory conditions. Instead, we demonstrate that the resveratrol effects on PAI-1 induction under inflammatory conditions were mediated via inhibition of the NF κ B pathway. Together, resveratrol can act as NF κ B inhibitor in adipocytes and thus the subsequently reduced PAI-1 expression in inflamed adipose tissue might provide a new insight towards novel treatment options of obesity.


Effects of resveratrol in experimental and clinical non-alcoholic fatty liver disease.

From: http://www.ncbi.nlm.nih.gov/pubmed/24799987


The prevalence of obesity and related conditions like non-alcoholic fatty liver disease (NAFLD) is increasing worldwide and therapeutic options are limited. Alternative treatment options are therefore intensively sought after. An interesting candidate is the natural polyphenol resveratrol (RSV) that activates adenosinmonophosphate-activated protein kinase (AMPK) and silent information regulation-2 homolog 1 (SIRT1). In addition, RSV has known anti-oxidant and anti-inflammatory effects. Here, we review the current evidence for RSV-mediated effects on NAFLD and address the different aspects of NAFLD and non-alcoholic steatohepatitis (NASH) pathogenesis with respect to free fatty acid (FFA) flux from adipose tissue, hepatic de novo lipogenesis, inadequate FFA β-oxidation and additional intra- and extrahepatic inflammatory and oxidant hits. We review the in vivo evidence from animal studies and clinical trials. The abundance of animal studies reports a decrease in hepatic triglyceride accumulation, liver weight and a general improvement in histological fatty liver changes, along with a reduction in circulating insulin, glucose and lipid levels. Some studies document AMPK or SIRT1 activation, and modulation of relevant markers of hepatic lipogenesis, inflammation and oxidation status. However, AMPK/SIRT1-independent actions are also likely. Clinical trials are scarce and have primarily been performed with a focus on overweight/obese participants without a focus on NAFLD/NASH and histological liver changes. Future clinical studies with appropriate design are needed to clarify the true impact of RSV treatment in NAFLD/NASH patients.


Modulatory role of resveratrol on cytotoxic activity of cisplatin, sensitization and modification of cisplatin resistance in colorectal cancer cells.

From: http://www.ncbi.nlm.nih.gov/pubmed/25815689


Colorectal cancer (CRC) is a leading cause of cancer-associated mortality worldwide. Cisplatin (CIS) is one of the most active cytotoxic agents in current use and it has proven efficacy against various human malignancies. However, its clinical usefulness has been restricted by detrimental side effects, including nephrotoxicity and myelosuppression. The aim of the present study was to attempt to decrease the required dose of CIS, in order to minimize its side effects, and increase its capability to arrest, delay or reverse carcinogenesis. In addition, the present study aimed to ameliorate CIS‑resistance in CRC cells, using the natural compound resveratrol (RSVL). RSVL (3,4′, 5‑trihydroxy‑trans‑stilbene) is a naturally occurring polyphenol present in the roots of white hellebore (Veratrum grandiflorum O. Loes) and extracted from >70 other plant species. RSVL can exert antioxidant and anti‑inflammatory activities, and it has been shown to be active in the regulation of numerous cellular events associated with carcinogenesis. The present study evaluated the effects of RSVL on sensitization of both parent and CIS‑resistant HCT‑116 CRC cells to the action of cisplatin. The CIS was administered at a dose of 5 and 20 µg/ml, and CIS cytotoxicity, apoptosis, cell cycle and cisplatin cellular uptake were examined in the presence and absence of RSVL (15 µg/ml). RSVL treatment showed anti‑proliferative effects and enhanced the cytotoxic effects of cis against the growth of both parent and CIS‑resistant HCT‑116 CRC cells, with a half maximal inhibitory concentration of 4.20 µg/ml and 4.72 µg/ml respectively. RSVL also induced a significant increase in the early apoptosis fraction and enhanced the subsequent apoptotic effects of CIS. The cellular uptake of CIS was significantly increased in the presence of RSVL, as compared with CIS treatment alone, and RSVL treatment sensitized the CIS‑resistant HCT‑116 cells. In conclusion, RSVL treatment increased the cytotoxic activity of CIS against the growth of both parent and CIS‑resistant HCT-116 CRC cells.


Resveratrol treatment rescues hyperleptinemia and improves hypothalamic leptin signaling programmed by maternal high-fat diet in rats.

From: http://www.ncbi.nlm.nih.gov/pubmed/25801629


PURPOSE: Perinatal high-fat diet is associated with obesity and metabolic diseases in adult offspring. Resveratrol has been shown to exert antioxidant and anti-obesity actions. However, the effects of resveratrol on leptinemia and leptin signaling are still unknown as well as whether resveratrol treatment can improve metabolic outcomes programmed by maternal high-fat diet. We hypothesize that resveratrol treatment in male rats programmed by high-fat diet would decrease body weight and food intake, and leptinemia with changes in central leptin signaling.

METHODS: Female Wistar rats were divided into two groups: control group (C), which received a standard diet containing 9 % of the calories as fat, and high-fat group (HF), which received a diet containing 28 % of the calories as fat. Dams were fed in C or HF diet during 8 weeks before mating and throughout gestation and lactation. C and HF male offspring received standard diet throughout life. From 150 until 180 days of age, offspring received resveratrol (30 mg/Kg body weight/day) or vehicle (carboxymethylcellulose).

RESULTS: HF offspring had increased body weight, hyperphagia and increased subcutaneous and visceral fat mass compared to controls, and resveratrol treatment decreased adiposity. HF offspring had increased leptinemia as well as increased SOCS3 in the arcuate nucleus of the hypothalamus, which suggest central leptin resistance. Resveratrol treatment rescued leptinemia and increased p-STAT3 content in the hypothalamus with no changes in SOCS3, suggesting improvement in leptin signaling.

CONCLUSIONS: Collectively, our data suggest that resveratrol could reverse hyperleptinemia and improve central leptin action in adult offspring from HF mothers attenuating obesity.



Resveratrol is an important polyphenol, antioxidant, and Nrf2 activator that helps to make Ultimate Protector such an outstanding nutritional supplement.




Consuming Organic Produce Reduces Dietary Exposure to Organophosphate Pesticides

Dr. Hank Liers, PhD dietary supplementFred Liers PhD dietary supplement dshea

We at HPDI have long advocated consuming organic produce. There are many reasons for choosing organic over conventional produce, including greater nutritional value and avoidance of genetically modified organisms (GMOs).

Another major reason for consuming organic produce is avoiding exposure to toxic pesticides, including organophosphate pesticides. Pesticide exposures can poison the body and weaken overall health. They especially can harm children, as well as disrupt normal development of unborn children.

Avoiding exposures to toxins (or preventing toxicity) is an important part of the HPDI Rejuvenation Program. It has become clear that consuming organic produce reduces pesticide exposures, and thereby helps reduce the body’s toxic load.

Consuming organic foods may not be sufficient to prevent toxicity or significant exposure to toxins given the fact that pesticides and other toxins are ubiquitous in the environment (air, water, and soil). Periodic juice cleansing for your liver or kidneys supports elimination of toxins from the body.

A recent study published in Environmental Health Perspectives (Environ Health Perspect; DOI:10.1289/ehp.1408197) highlights the important role played by consuming organic produce in reducing exposure to organophosphate pesticides.

spray pesticides farm equipment conventional gmo

Consuming organic foods is important because increasing amounts of pesticides are sprayed on crops.

The study is titled, “Estimating Pesticide Exposure from Dietary Intake and Organic Food Choices: The Multi-Ethnic Study of Atherosclerosis (MESA).” Here we present a summary of the study published in Environmental Health Perspectives.

Estimating Pesticide Exposure from Dietary Intake and Organic Food Choices: The Multi-Ethnic Study of Atherosclerosis (MESA)


Background: Organophosphate pesticide (OP) exposure to the US population is dominated by dietary intake. The magnitude of exposure from diet depends partly upon personal decisions such as which foods to eat and whether to choose organic food. Most studies of OP exposure rely on urinary biomarkers, which are limited by short half-lives and often lack specificity to parent compounds. A reliable means of estimating long-term dietary exposure to individual OPs is needed to assess the potential relationship with adverse health effects.

Objectives: We assessed long-term dietary exposure to 14 OPs among 4,466 participants in the Multi-Ethnic Study of Atherosclerosis, and examined the influence of organic produce consumption on this exposure.

Methods: Individual-level exposure was estimated by combining information on typical intake of specific food items with average OP residue levels on those items. In an analysis restricted to a subset of participants who reported rarely or never eating organic produce (“conventional consumers”), we assessed urinary dialkylphosphate (DAP) levels across tertiles of estimated exposure (n=480). In a second analysis, we compared DAP levels across subgroups with differing self-reported organic produce consumption habits (n=240).

Results: Among conventional consumers, increasing tertile of estimated dietary OP exposure was associated with higher DAP concentrations (p<0.05). DAP concentrations were also significantly lower in groups reporting more frequent consumption of organic produce (p<0.02).

Conclusions: Long-term dietary exposure to OPs were estimated from dietary intake data, and estimates were consistent with DAP measurements. More frequent consumption of organic produce was associated with lower DAPs.

Citation: Curl CL, Beresford SA, Fenske RA, Fitzpatrick AL, Lu C, Nettleton JA, Kaufman JD. Estimating Pesticide Exposure from Dietary Intake and Organic Food Choices: The Multi-Ethnic Study of Atherosclerosis (MESA). Environ Health Perspecthttp://dx.doi.org/10.1289/ehp.1408197.

Read this scientific article on Environmental Health Perspectives website: http://ehp.niehs.nih.gov/1408197/


Consuming organic foods not only means greater nutritional value and better taste, it also means you reduce exposure to toxins like organophosphate pesticides that can cause significantly harm.

More pesticides than ever are being applied, and more potent ones. This is due to a combination of factors, including the expansion of genetically modified (GMO) crops. In addition, the development of resistance to pesticides means more are used in order have the desired (i.e., toxic) effects.

Protect yourself from pesticide exposure by consuming more organic foods, and following other recommendations in the HPDI Rejuvenation Program.



Dr. Hank Liers, PhD dietary supplementFred Liers PhD dietary supplement dshea

In February 2015, the Orthomolecular Medicine News Service (OMNS) published an article reviewing the major scientific research studies on Vitamin D for the year 2014.

As noted by the author William B. Grant, PhD, “research into the health effects associated with vitamin D continued to be strong in 2014. The number of publications with vitamin D in the title or abstract listed at pubmed.gov increased from 3,119 in 2011 to 3,919 in 2014.”

Seven top vitamin D researchers selected the 20 papers they regard as making the greatest contribution to understanding the health effects of vitamin D for the year. Here we publish the article with permission. ~


by William B. Grant, PhD

(OMNS Feb 3, 2015) Higher vitamin D blood levels may reduce the risk of many types of disease including autoimmune diseases, cancers, cardiovascular disease, dementia, diabetes mellitus, and falls and fractures.

Research into the health effects associated with vitamin D continued to be strong in 2014. The number of publications with vitamin D in the title or abstract listed at pubmed.gov increased from 3,119 in 2011 to 3,919 in 2014. Seven vitamin D researchers (listed after this report) worked together to pick the 20 papers in 2014 that made the most contribution to understanding the health effects of vitamin D in 2014.

sunset at beach vitamin d research

Sunshine plays a major role in vitamin D production but foods/supplements can support optimal levels.

Papers are not in priority order, but instead grouped by type of study. For the purpose of this article “vitamin D” in the blood is a measurement of 25-hydroxyvitamin D or 25(OH)D.

Do randomized controlled trials work for vitamin D?

No one refutes the fact that vitamin D is beneficial to the skeletal system. There are many studies (randomized controlled trials [RCT] and also epidemiological) that support this hypothesis. What is at odds is whether or not vitamin D is beneficial to the non-skeletal system. There are many observational (epidemiological, or association) studies that show vitamin D is beneficial, and many RCTs that show it isn’t. Does that mean that vitamin D does not aid in disease prevention? Or does it mean that the RCT model does not work for nutrients?


Vitamin D3 supplementation in patients with chronic obstructive pulmonary disease [Martineau, 2014]

A vitamin D trial in the UK in which patients with chronic obstructive pulmonary disease (COPD) were given 120,000 IU vitamin D3 every two months for a year found that vitamin D3 supplementation was protective against moderate or severe exacerbation in those with baseline 25(OH)D concentrations < 50 nmol/L (20 ng/mL) but not for those with concentrations > 50 nmol/L. Vitamin D3 supplementation had no effect on upper respiratory infections. This is consistent with previous RCTs that used high doses at infrequent intervals, every 2 months in this case; however other trials that used an adequate dose given daily have shown reduction in upper respiratory tract infections.

Vitamin D promotes vascular regeneration [Wong, 2014]

This study demonstrated that vitamin D improved cardiovascular disease. The German team investigated this effect several ways. They showed that supplementation with 4000 IU/day of vitamin D3 increased the number of circulating angiogenic myeloid cells, which promote growth and vascular regeneration necessary for a healthy cardiovascular system. A similar result was found in a mouse model, which also demonstrated restoration of impaired angiogenesis (new vessel formation) function. They also examined the mechanisms by which vitamin D acted.

Vitamin D and depression: a systematic review and meta-analysis comparing studies with and without biological flaws. [Spedding, 2014]

This paper reported on a statistical average of many studies of vitamin D RCTs without methodological flaws and found that vitamin D supplementation resulted in a statistically significant improvement in clinical depression. However, the same analysis of vitamin D RCTs with methodological flaws found a statistically significant worsening of depression. The major flaws identified included not increasing 25(OH)D concentrations and not measuring baseline or final 25(OH)D concentrations. Vitamin D supplementation of > 800 IU/d was somewhat favorable in the management of depression.

Effect of vitamin D supplementation on antibiotic use: a randomized controlled trial. [Tran, 2014]

A post hoc (conducted after the study was completed) analysis of a vitamin D RCT involving 644 Australian residents aged 60-84 years found a significant reduction in prescribed antibiotics if they were over the age of 70 years and taking 60,000 IU of vitamin D3 monthly compared with the placebo groups. The effect was not significant for those < 70 years of age. This study suggests that taking an average of 2000 IU/day vitamin D3 reduces the risk of infections, most likely respiratory infections, in older adults.


Observational studies provide some of the strongest evidence to date for beneficial health outcomes related to vitamin D. Observational studies measure vitamin D status and health outcomes for every participant. Blood samples are taken at the time of enrollment and people are followed for several years. Vitamin D is said to be effective if positive health outcomes result.

Vitamin D and risk of cause specific death: systematic review and meta-analysis of observational cohort and randomised intervention studies [Chowdhury, 2014]

This paper was a review of observational and RCT studies that showed a correlation between vitamin D and specific mortality outcomes. One conclusion was that supplementation with vitamin D3 significantly reduces overall mortality among older adults. They used data from 73 cohort studies (849,412 participants) and 22 RCTs (30,716 participants). In the RCTs, all cause mortality rate was reduced by 11% for vitamin D3 supplementation but increased by 4% for vitamin D2 supplementation. In addition, their meta-analysis of cancer-specific incidence and mortality rates comparing those who started in the lowest third of vitamin D blood concentrations against those in the highest third suggests that vitamin D may have a much stronger impact on survival after developing cancer than on reducing the risk of developing cancer to start with.

Meta-analysis of all-cause mortality according to serum 25-hydroxyvitamin D [Garland, 2014]

An analysis of 32 observational studies found that as 25(OH)D concentrations increased from 13 nmol/L (5 ng/ml) to 90 nmol/L (36 ng/ml) there is a linear reduction in all-cause mortality. At concentrations greater than 90 nmol/L (36 ng/ml), no further improvement was observed. This finding is important in that it did not find any evidence for a U-shaped relationship showing higher risk for both low and high 25(OH)D concentrations as has been reported in some studies. Furthermore, the risk for all-cause mortality rate for those with 25(OH)D concentration < 25 nmol/L (10 ng/mL) was 1.9 compared to that for those with concentrations > 100 nmol/L (40 ng/mL).

Low vitamin D level is an independent predictor of poor outcomes in Clostridium difficile-associated diarrhea [Wang, 2014]

A study in New York found that 25(OH)D concentration and age were the only independent predictors of response to the highly fatal Clostridium difficile-associated diarrhea (CDAD). Subjects with 25(OH)D concentration < 53 nmol/L (21 ng/mL) were 4.75 times more likely to fail to resolve CDAD after 30 days than subjects with 25(OH)D concentrations > 75 nmol/L (30 ng/mL). This is an important finding since CDAD rates are increasing due to antibiotic resistant strains of CD.

Avoidance of sun exposure is a risk factor for all-cause mortality: results from the MISS cohort [Lindqvist, 2014]

An observational study in Sweden involving 29,518 women followed for up to 20 years with 2,545 reported deaths found that the mortality rate for those who avoided sun exposure was approximately twice as high as those who were most exposed to the sun. This difference explained 3% of all deaths and is important since UVB doses in Sweden are generally low and virtually absent for six months of the year. Production of vitamin D may explain most of the differences between sun exposure amounts, although other beneficial effects of solar UV exist, such as release of nitric oxide resulting in reduction of blood pressure, as well as vitamin D-independent effects on the immune system.

25-Hydroxyvitamin D in the range of 20 to 100 ng/ml and incidence of kidney stones [Nguyen, 2014]

GrassrootsHealth (510c3) initiated a voluntary reporting project called D*action. There are over 7,000 in the cohort, of which 2,012 have reported their data for a median of 19 months. In this cohort, there has been no evidence of an association of 25(OH)D and kidney stones. What was a risk factor for kidney stones in this study was high body mass index. This study counters the Women’s Health Initiative study that reported an elevated risk of kidney stones for women taking 400 IU/d vitamin D3 and 1500 mg/d calcium.

Prediagnostic circulating vitamin D levels and risk of hepatocellular carcinoma in European populations: a nested case-control study [Fedirko, 2014]

An observational study involving 520,000 participants in the European Prospective Investigation into Cancer and Nutrition (EPIC) cohort, of which 138 developed hepatocellular carcinoma (HCC) or liver cancer, found that higher levels of 25(OH)D reduced incidence of HCC. Each 10 nmol/L (4 ng/mL) increase in 25(OH)D concentration was associated with a 20% average decrease in risk of HCC. The large number of participants in the study with a very small number of cases indicates the difficulty of demonstrating the beneficial effect of vitamin D for the rare cancers. The authors noted that the result did “not change after adjustment for biomarkers of preexisting liver damage, nor chronic infection with hepatitis B or C viruses.”

Plasma vitamin D concentration influences survival outcome after a diagnosis of colorectal cancer [Zgaga, 2014]

A study in Ireland and Scotland involving 1,598 patients with stage I to III colorectal cancer, found that 25(OH)D concentrations (measured approximately 15 weeks after diagnosis of colorectal cancer) were associated with survival rates. Those in the highest third of 25(OH)D concentrations with a median concentration of 51 nmol/L (20 ng/mL) compared to the lowest third with a median concentration of 10 nmol/L (4 ng/mL) had a 32% lower risk of cancer-specific mortality rate and a 30% lower risk of all-cause mortality rate over a ten-year follow-up period. This study provides support for the idea that people diagnosed with cancer should raise their 25(OH)D concentration to above a minimum of 50 nmol/L (20 ng/mL),

Meta-analysis of vitamin D sufficiency for improving survival of patients with breast cancer [Mohr, 2014]

Two meta-analyses found significantly increased cancer survival rates with higher concentration of 25(OH)D at time of diagnosis. For breast cancer, results from five studies found that those with 25(OH)D concentration of 75 nmol/L (30 ng/mL) had half the 5-20 year mortality rate as those with a lower concentration of 30 nmol/L (12 ng/mL).

Could vitamin D sufficiency improve the survival of colorectal cancer patients? [Mohr, 2014]

In this meta-analysis for colorectal cancer, results from four studies found that those with 25(OH)D concentration of 80 nmol/L (32 ng/mL) had 60% of the 6-20 year mortality rate as those with 45 nmol/L (18 ng/mL).

Reduced 25-hydroxyvitamin D and risk of Alzheimer’s disease and vascular dementia [Afzal, 2014]

Two papers reported that those with low 25(OH)D concentrations had increased risk of developing vascular dementia and Alzheimer’s disease. This first one is from Denmark. A study involving 418 people followed for 30 years found a 25% increased risk of Alzheimer’s disease and a 22% increased risk of vascular dementia for those with baseline 25(OH)D concentration < 25 nmol/L (10 ng/ml) compared to > 50 nmol/L (20 ng/ml)

Vitamin D and the risk of dementia and Alzheimer disease [Littlejohns, 2014]

In this second paper on dementia and Alzheimer disease, a study in the United States involving 1,658 participants followed for 5.6 years found a 125% increased risk of Alzheimer’s disease for those with severely deficient 25(OH)D levels (< 25 nmol/L (10 ng/mL)), and a 53% increased risk for those with deficient levels ( ≥ 25 to < 50 nmol/L) compared to participants with sufficient concentrations ( ≥ 50 nmol/L (20 ng/mL)).


Post-hoc comparison of vitamin D status at three time points during pregnancy demonstrates lower risk of preterm birth with higher vitamin D closer to delivery [Wagner, 2014]

There is considerable interest in the role of vitamin D during pregnancy. In a reanalysis of results from two maternal vitamin D supplementation trials conducted in South Carolina, it was found that: “(1) maternal vitamin D status closest to delivery date was more significantly associated with preterm birth, suggesting that later intervention as a rescue treatment may positively impact the risk of preterm delivery, and (2) a serum concentration of 100 nmol/L (40ng/mL) in the 3rd trimester was associated with a 47% reduction in preterm births.”

Vitamin D in fetal development: Findings from a birth cohort study [Hart, 2014]

A study in Australia compared maternal 25(OH)D concentration at 18 weeks’ pregnancy with outcomes of the children years later. The authors found that “maternal vitamin D deficiency during pregnancy was associated with impaired lung development in 6-year-old offspring, neurocognitive difficulties at age 10, increased risk of eating disorders in adolescence, and lower peak bone mass at 20 years.”

Vitamin D and pre-eclampsia: original data, systematic review and meta-analysis [Hypponen, 2014]

A review of vitamin D supplementation and 25(OH)D concentrations during pregnancy found vitamin D reduces the risk of pre-eclampsia. For 25(OH)D concentration, the combined risk reduction was 48% with higher level circulating vitamin D. For vitamin D RCTs, the combined risk reduction was 34% for vitamin D supplementation vs. a placebo. This review provides further support for the importance of vitamin D supplementation and raising 25(OH)D concentrations during pregnancy.


An approach recently being applied to evaluating whether vitamin D can be considered causally linked to health outcomes is Mendelian randomization analysis. In this approach, genetic variants known to be affected by vitamin D are compared to health outcomes. The advantage of this approach is that the results should be independent of baseline 25(OH)D concentrations, which vary over time. The disadvantage is that only a few factors are considered and the most important ones affecting 25(OH)D concentrations may not be included.

Genetically low vitamin D concentrations and increased mortality: mendelian randomization analysis in three large cohorts [Azfal, 2014]

In a study involving 95,766 white participants of Danish descent, genetic variations of DHCR7 (related to vitamin D synthesis) and CYP2R1 (hepatic 25-hydroxylation), which slightly lower plasma 25(OH)D concentrations over the lifetime of the subjects, were examined. As 25(OH)D increased, significant reductions were found for all-cause, cancer and other mortality rates, but not for cardiovascular mortality. These results are interesting, but the method is not strong enough to rule out a protective role of vitamin D in reducing risk of cardiovascular disease. Some regard this approach as particularly weak, since the serum 25(OH)D concentration depends much more in the general population upon solar exposure than upon genes.

Guidelines for optimizing design and analysis of clinical studies of nutrient effects [Heaney, 2014]

Most vitamin D RCTs were based on guidelines designed for pharmaceutical drugs where the only source of the agent is the medication in the trial, and there is a linear dose-response relation between the agent and the outcome. Dr. Heaney asserts that neither assumption is valid for vitamin D trials.

Instead, vitamin D trials should:

  1. Start with an understanding of the 25(OH)D concentration-health outcome relationship. What are we expecting to find?
  2. Measure 25(OH)D concentrations of prospective trial participants and only enroll those with values near the low end of the relation.
  3. Supplement with enough vitamin D to raise 25(OH)D concentrations to near the upper end of the relation.
  4. Measure 25(OH)D concentrations throughout the trial.
  5. Optimize the status of other nutrients related to vitamin D so that vitamin D is the only limiting factor in the response.

Unfortunately, many of the ongoing vitamin D trials have not been designed with these or similar guidelines in mind. As a result, it may be some time before vitamin D RCTs will be able to provide adequate evidence to confirm or refute the findings of observational studies for non-skeletal diseases.


Research on the health benefits of solar UVB exposure and vitamin D continues at a rapid pace. We appear to be in the middle of the golden age of vitamin D research, a period with much progress in understanding the effects of UVB exposure and vitamin D for a large range of health outcomes. We are shifting from discovery to evaluation of previous findings and testing the role of vitamin D in prevention and treatment of various diseases.

While many of the findings from ecological and observational studies are strong, it appears that health systems and policy makers are awaiting results from large on-going RCTs before they accept UVB exposure and vitamin D as valid factors for health. Unfortunately, most of the RCTs currently underway and due to be completed before the end of the decade, including large-scale RCTs in several countries, have not been properly designed, so they may not shed light on vitamin D’s preventive powers. Thus, it may be another decade before the true health benefits of vitamin D and sunlight are accepted. Meanwhile, various types of research will continue and it will be up to individuals and their health care providers to evaluate the available evidence and act accordingly.

For additional information on solar UVB and vitamin D:



Other OMNS Press Releases on Vitamin D

This press release is the fifth in the series on vitamin D by the Orthomolecular Medicine News Service. Previous articles:

  1. Vitamin D Stops Cancer; Cuts Risk In Half. American Cancer Society Drags its Feet. Oct. 2, 2008. http://orthomolecular.org/resources/omns/v04n11.shtml
  2. Why You Need More Vitamin D. A Lot More. Sept. 16, 2011. http://orthomolecular.org/resources/omns/v07n07.shtml
  3. Top Vitamin D Papers of 2011, Dosage Recommendations and Clinical Applications. April 10, 2012; http://orthomolecular.org/resources/omns/v08n12.shtml
  4. Vitamin D is Now the Most Popular Vitamin. Jan. 17, 2013. http://orthomolecular.org/resources/omns/v09n01.shtml

Peer review by:

Barbara J Boucher, MD, FRCP, Centre for Diabetes, Blizard Institute, Bart’s & The London School of Medicine & Dentistry, Queen Mary University of London, London, UK.

John J. Cannell, MD, Director, Vitamin D Council, San Luis Obispo, CA, http://www.vitamindcouncil.org/

Cedric F. Garland, DrPH, Professor, Department of Family and Preventive Medicine, Division of Epidemiology, University of California San Diego, La Jolla, CA

William B. Grant, Ph.D., Director, Sunlight, Nutrition and Health Research Center, San Francisco, CA,  http://www.sunarc.org/

Michael F. Holick, M.D., Ph.D., Department of Medicine, Section of Endocrinology, Nutrition, and Diabetes, and the Vitamin D, Skin, and Bone Research Laboratory, Boston University Medical Center, Boston, MA,  http://drholick.com/, Interview at http://www.doctoryourself.com/holick.html

Henry Lahore, Director, http://www.vitaminDwiki.com, Port Townsend, WA

Pawel Pludowski, M.D., Department of Biochemistry, Radioimmunology and Experimental Medicine, The Children’s Memorial Health Institute, Warsaw, Poland



Afzal S, Bojesen SE, Nordestgaard BG. Reduced 25-hydroxyvitamin D and risk of Alzheimer’s disease and vascular dementia. Alzheimers Dement. 2014 May;10(3):296-302.

Afzal S, Brondum-Jacobsen P, Bojesen SE, Nordestgaard BG. Genetically low vitamin D concentrations and increased mortality: mendelian randomisation analysis in three large cohorts. BMJ. 2014 Nov 18;349:g6330. http://www.ncbi.nlm.nih.gov/pubmed/25406188

Chowdhury R, Kunutsor S, Vitezova A, Oliver-Williams C, Chowdhury S, Kiefte-de-Jong JC, Khan H, Baena CP, Prabhakaran D, Hoshen MB, Feldman BS, Pan A, Johnson L, Crowe F, Hu FB, Franco OH. Vitamin D and risk of cause specific death: systematic review and meta-analysis of observational cohort and randomised intervention studies. BMJ. 2014 Apr 1;348:g1903. http://www.bmj.com/content/348/bmj.g1903?view=long&pmid=24690623

Fedirko V, Duarte-Salles T, Bamia C, Trichopoulou A, Aleksandrova K, Trichopoulos D, Trepo E, Tjonneland A, Olsen A, Overvad K, Boutron-Ruault MC, Clavel-Chapelon F, Kvaskoff M, Kühn T, Lukanova A, Boeing H, Buijsse B, Klinaki E, Tsimakidi C, Naccarati A, Tagliabue G, Panico S, Tumino R, Palli D, Bueno-de-Mesquita HB, Siersema PD, Peters PH, Lund E, Brustad M, Olsen KS, Weiderpass E, Zamora-Ros R, S nchez MJ, Ardanaz E, Amiano P, Navarro C, Quir¢s JR, Werner M, Sund M, Lindkvist B, Malm J, Travis RC, Khaw KT, Stepien M, Scalbert A, Romieu I, Lagiou P, Riboli E, Jenab M. Prediagnostic circulating vitamin D levels and risk of hepatocellular carcinoma in European populations: a nested case-control study. Hepatology. 2014 Oct;60(4):1222-30.  http://www.ncbi.nlm.nih.gov/pubmed/24644045

Garland CF, Kim JJ, Mohr SB, Gorham ED, Grant WB, Giovannucci EL, Baggerly L, Hofflich H, Ramsdell J, Zeng K, Heaney RP.Meta-analysis of all-cause mortality according to serum 25-hydroxyvitamin D. Am J Pub Health. 2014 Aug;104(8):e43-50. http://www.ncbi.nlm.nih.gov/pubmed/24922127

Hart PH, Lucas RM, Walsh JP, Zosky GR, Whitehouse AJ, Zhu K, Allen KL, Kusel MM, Anderson D, Mountain JA. Vitamin D in fetal development: Findings from a birth cohort study. Pediatrics. 2015 Jan;135(1):e167-73. http://www.ncbi.nlm.nih.gov/pubmed/25511121

Heaney RP. Guidelines for optimizing design and analysis of clinical studies of nutrient effects. Nutr Rev. 2014 Jan;72(1):48-54. http://www.ncbi.nlm.nih.gov/pubmed/24330136

Hyppönen E, Cavadino A, Williams D, Fraser A, Vereczkey A, Fraser WD, B nhidy F, Lawlor D, Czeizel AE. Vitamin D and pre-eclampsia: original data, systematic review and meta-analysis. Ann NutrMetab. 2013;63(4):331-40. (published in 2014) http://www.ncbi.nlm.nih.gov/pubmed/24603503

Lindqvist PG, Epstein E, Landin-Olsson M, Ingvar C, Nielsen K, Stenbeck M, Olsson H. Avoidance of sun exposure is a risk factor for all-cause mortality: results from the MISS cohort. J Intern Med. 2014 Jul;276(1):77-86. http://www.ncbi.nlm.nih.gov/pubmed/24697969

Littlejohns TJ, Henley WE, Lang IA, Annweiler C, Beauchet O, Chaves PH, Fried L, Kestenbaum BR, Kuller LH, Lang KM, Lopez OL, Kos K, Soni M, Llewellyn DJ. Vitamin D and the risk of dementia and Alzheimer disease.Neurology. 2014 Sep 2;83(10):920-8.

Martineau AR, James WY, Hooper RL, Barnes NC, Jolliffe DA, Greiller CL, Islam K, McLaughlin D, Bhowmik A, Timms PM, Rajakulasingam RK, Rowe M, Venton TR, Choudhury AB, Simcock DE, Wilks M, Degun A, Sadique Z, Monteiro WR, Corrigan CJ, Hawrylowicz CM, Griffiths CJ. Vitamin D3 supplementation in patients with chronic obstructive pulmonary disease (ViDiCO): a multicentre, double-blind, randomised controlled trial. Lancet Respir Med. 2014 Dec 1. pii: S2213-2600(14)70255-3. doi: 10.1016/S2213-2600(14)70255-3. [Epub ahead of print] http://www.ncbi.nlm.nih.gov/pubmed/25476069

Mohr SB, Gorham ED, Kim J, Hofflich H, Cuomo RE, Garland CF. Could vitamin D sufficiency improve the survival of colorectal cancer patients? J Steroid Biochem Mol Biol. 2014 Dec 19. pii: S0960-0760(14)00316-1. doi: 10.1016/j.jsbmb.2014.12.010. [Epub ahead of print] http://www.ncbi.nlm.nih.gov/pubmed/25533386

Mohr SB, Gorham ED, Kim J, Hofflich H, Garland CF. Meta-analysis of vitamin D sufficiency for improving survival of patients with breast cancer. Anticancer Res. 2014 Mar;34(3):1163-6. http://www.ncbi.nlm.nih.gov/pubmed/24596354

Nguyen S, Baggerly L, French C, Heaney RP, Gorham ED, Garland CF. 25-Hydroxyvitamin D in the range of 20 to 100 ng/mL and incidence of kidney stones. Am J Public Health. 2014 Sep;104(9):1783-7.  http://www.ncbi.nlm.nih.gov/pubmed/24134366

Spedding S. Vitamin D and depression: a systematic review and meta-analysis comparing studies with and without biological flaws. Nutrients. 2014 Apr 11;6(4):1501-18. http://www.ncbi.nlm.nih.gov/pubmed/24732019

Tran B, Armstrong BK, Ebeling PR, English DR, Kimlin MG, van der Pols JC, Venn A, Gebski V, Whiteman DC, Webb PM, Neale RE. Effect of vitamin D supplementation on antibiotic use: a randomized controlled trial. Am J Clin Nutr. 2014 Jan;99(1):156-61. http://www.ncbi.nlm.nih.gov/pubmed/24108783

Wagner CL, Baggerly C, McDonnell SL, Baggerly L, Hamilton SA, Winkler J, Warner G, Rodriguez C, Shary JR, Smith PG, Hollis BW. Post-hoc comparison of vitamin D status at three time points during pregnancy demonstrates lower risk of preterm birth with higher vitamin D closer to delivery. J Steroid Biochem Mol Biol. 2014 Nov 13. pii: S0960-0760(14)00268-4. doi: 10.1016/j.jsbmb.2014.11.013. [Epub ahead of print] http://www.ncbi.nlm.nih.gov/pubmed/25448734

Wang WJ, Gray S, Sison C, Arramraju S, John BK, Hussain SA, Kim SH, Mehta P, Rubin M. Low vitamin D level is an independent predictor of poor outcomes in Clostridium difficile-associated diarrhea. Therap Adv Gastroenterol. 2014 Jan;7(1):14-9. http://www.ncbi.nlm.nih.gov/pubmed/24381644

Wong MS, Leisegang MS, Kruse C, Vogel J, Schürmann C, Dehne N, Weigert A, Herrmann E, Brüne B, Shah AM, Steinhilber D, Offermanns S, Carmeliet G, Badenhoop K, Schröder K, Brandes RP. Vitamin D promotes vascular regeneration. Circulation. 2014 Sep 16;130(12):976-86. http://www.ncbi.nlm.nih.gov/pubmed/25015343

Zgaga L, Theodoratou E, Farrington SM, Din FV, Ooi LY, Glodzik D, Johnston S, Tenesa A, Campbell H, Dunlop MG. Plasma vitamin D concentration influences survival outcome after a diagnosis of colorectal cancer. J Clin Oncol. 2014 Aug 10;32(23):2430-9. http://www.ncbi.nlm.nih.gov/pubmed/25002714

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Ian Brighthope, M.D. (Australia)
Ralph K. Campbell, M.D. (USA)
Carolyn Dean, M.D., N.D. (USA)
Damien Downing, M.D. (United Kingdom)
Michael Ellis, M.D. (Australia)
Martin P. Gallagher, M.D., D.C. (USA)
Michael Gonzalez, D.Sc., Ph.D. (Puerto Rico)
William B. Grant, Ph.D. (USA)
Michael Janson, M.D. (USA)
Robert E. Jenkins, D.C. (USA)
Bo H. Jonsson, M.D., Ph.D. (Sweden)
Peter H. Lauda, M.D. (Austria)
Thomas Levy, M.D., J.D. (USA)
Stuart Lindsey, Pharm.D. (USA)
Jorge R. Miranda-Massari, Pharm.D. (Puerto Rico)
Karin Munsterhjelm-Ahumada, M.D. (Finland)
Erik Paterson, M.D. (Canada)
W. Todd Penberthy, Ph.D. (USA)
Gert E. Schuitemaker, Ph.D. (Netherlands)
Robert G. Smith, Ph.D. (USA)
Jagan Nathan Vamanan, M.D. (India)
Atsuo Yanagisawa, M.D., Ph.D. (Japan)

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