Overview Liver and vitamin D

Created November 2011

  • Fact: A properly functioning liver is needed for the efficient activation of vitamin D in the body

  • Fact: Liver diseases often result in lower levels of vitamin D

  • Fact: Various pain relievers damage the liver function

  • Fact: Lower levels of vitamin D result in osteoporosis and many other diseases

  • Options with a poorly functioning liver appear to be:

  1. Increased vitamin D (example: 2X more vitamin D if Liver is 1/2 as efficient)

  2. Increase the response you get from vitamin D

  3. Increase sunshine / UVB,

  4. Get the response you get from the sun/UVB

  5. Consider supplementing with Iron - a patented Iron supplement appears to work very well

  6. Get prescription for active form of vitamin D ( Calcitriol ) which does not need the liver or kidney to get the benefits of vitamin D in the body

  7. Get Calcidiol which does not need the liver

  8. Use Topical Vitamin D - activation by the skin etc does not require the liver

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Click on image for ways of getting vitamin D even if Liver is not functioning well

Renamed NAFLD => MASLD; NASH => MASH July 2023

  • NAFLD renamed July 2023 ==> metabolic dysfunction–associated steatotic liver disease = MASLD

  • Also renamed NASH ==> Metabolic dysfunction–associated steatohepatitis, or MASH

  • Both renamings the result of 3-year effort involving some 236 panelists from 56 countries

See VitaminDWiki

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Inflammatory diseases: review of vitamin D, with many tables – May 2014 which has a summary table

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Most of the people with the diseases have less than 20 ng of vitamin D

See also Web

Should monitor Liver Cirrhosis for Vitamin D, A and Zinc - 2018

An Argument for Vitamin D, A, and Zinc Monitoring in Cirrhosis.

Ann Hepatol. 2018 Oct 16;17(6):920-932. doi: 10.5604/01.3001.0012.7192.

📄 Download the PDF from VitaminDWiki

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Malnutrition is prevalent in cirrhosis. Vitamin and mineral deficiencies, including vitamin D, vitamin A, and zinc, are common and have been shown to correlate with survival. Our aim was to review the mechanisms of vitamin D, vitamin A, and zinc deficiencies in cirrhosis and the clinical assessment of affected patients, their outcomes based on the current literature, and management. This is a narrative review including the relevant literature for cirrhosis and vitamin D, vitamin A, and zinc deficiencies. Vitamin D deficiency has important effects in cirrhosis, regardless of the cause of chronic liver disease.These effects include associations with fibrosis and outcomes such as infections, hepatocellular carcinoma, and mortality. Vitamin A deficiency is associated with liver disease progression to cirrhosis and clinical decompensation, including occurrence of ascites or hepatic encephalopathy. Zinc deficiency can lead to hepatic encephalopathy and impaired immune function. Such deficiencies correlate with patient survival and disease severity. Caution should be applied when replacing vitamin D, vitamin A, and zinc to avoid toxicity. Identification and appropriate treatment of vitamin and mineral deficiencies in cirrhosis may reduce specific nutritional and cirrhosis-related adverse events. Routine monitoring of vitamin A, vitamin D and zinc levels in cirrhosis should be considered.

Chronic Liver Diseases might be treated by Vitamin D - Dec 2014

New insight of vitamin D in chronic liver diseases

Hepatobiliary Pancreat Dis Int. 2014 Dec;13(6):580-5. PMID: 25475859

Chen EQ1, Shi Y, Tang H.

CONCLUSIONS:

Although the exact role and mechanisms of vitamin D have not been fully elucidated in chronic liver diseases,

it is potentially beneficial in the treatment of chronic liver diseases.

Further mechanistic studies are needed to validate its clinical application.

📄 Download the PDF from VitaminDWiki.

Low vitamin D = 2X worse liver cancer prognosis

Severe 25-hydroxyvitamin D deficiency identifies a poor prognosis in patients with hepatocellular carcinoma - a prospective cohort study.

Aliment Pharmacol Ther. 2014 May;39(10):1204-12. doi: 10.1111/apt.12731. Epub 2014 Mar 29.

Finkelmeier F1, Kronenberger B, Köberle V, Bojunga J, Zeuzem S, Trojan J, Piiper A, Waidmann O.

BACKGROUND: Vitamin D is involved in many biological processes. The role of vitamin D in patients with hepatocellular carcinoma (HCC) remains inconclusive, although there is evolving evidence that vitamin D may modulate cancer development and progression.

AIM: To evaluate serum vitamin D as prognostic parameter in HCC, we performed a prospective cohort study.

METHODS: HCC patients were prospectively recruited and 25-hydroxyvitamin D3 (25(OH)D3 ) levels were determined. 25(OH)D3 levels were compared to stages of cirrhosis and HCC stages with nonparametric Kruskal-Wallis tests and Spearman correlations in 200 HCC patients. The association of the 25(OH)D3 levels and overall survival (OS) was assessed in uni- and multivariate Cox regression models.

RESULTS: Two-hundred patients with HCC were included. The mean follow-up time was 322 ± 342 days with a range of 1-1508 days. Nineteen patients underwent liver transplantation and 60 patients died within the observation time. The mean serum 25(OH)D3 concentration was 17 ± 13 ng/mL with a range of 1-72 ng/mL. 25(OH)D3 serum levels negatively correlated with the stage of cirrhosis as well as with stages of HCC. Patients with severe 25(OH)D3 deficiency had the highest mortality risk ( hazard ratio 2.225 , 95% confidence interval 1.331-3.719, P = 0.002). Furthermore, very low 25(OH)D3 levels were associated with mortality independently from the MELD score and high alpha-Fetoprotein levels (>400 ng/mL) in a multivariate Cox regression model.

CONCLUSIONS: We conclude that 25(OH)D3 deficiency is associated with advanced stages of hepatocellular carcinoma and it is a prognostic indicator for a poor outcome.

Progression of Liver damage

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NAFLD inversely related to Vitamin D only in whites - Sept 2019

Serum 25-hydroxyvitamin-D and nonalcoholic fatty liver disease: Does race/ethnicity matter? Findings from the MESA cohort

Nutr Metab Cardiovasc Dis. 2019 Sep 10. pii: S0939-4753(19)30342-4. doi: 10.1016/j.numecd.2019.09.004

El Khoudary SR1, Samargandy S2, Zeb I3, Foster T4, de Boer IH5, Li D6, Budoff MJ7.

BACKGROUND AND AIMS:

Low serum 25-hydroxyvitamin D (25(OH)D) is associated with higher nonalcoholic fatty liver disease (NAFLD) risk in studies of mainly white participants. Significant racial/ethnic differences exist in serum 25(OH)D and NAFLD prevalence questioning extending this association to other racial/ethnic groups. We tested whether the association between serum 25(OH)D and NAFLD vary by race/ethnicity.

METHODS AND RESULTS:

This was a cross-sectional analysis from the Multi-Ethnic Study of Atherosclerosis (MESA) that included 3484 participants (44% male; 38.4% Whites, 27.8% African-Americans, 23.5% Hispanics, and 10.3% Chinese-Americans) who had serum 25(OH)D and upper abdominal CT images available at baseline. Serum 25(OH)D was measured by high-performance liquid chromatography-tandem mass spectrometry. NAFLD was identified if liver-to-spleen Hounsfield-Unit ratio was <1. Whites had the highest 25(OH)D level and African-Americans had the lowest level (mean ± SD: 29.5 ± 10.4 vs.19.9 ± 9.1, respectively). Six hundred and eleven (17.5%) participants had NAFLD;

  • Hispanics had the highest prevalence (26.2%) followed by

  • Chinese-Americans (19.8%),

  • Whites (15.8%) and

  • African-Americans (11.7%), P < 0.0001.

In adjusted model, the association of 25(OH)D with NAFLD differed by race/ethnicity (P < 0.0001). Negative association was only evident in Causations (OR (95% CI):1.23 (1.03, 1.47) per 1 SD lower serum 25(OH)D). For other racial/ethnic groups, BMI, triglycerides, diabetic status and/or smoking, but not serum 25(OH)D, were common independent risk factors for NAFLD.

CONCLUSIONS:

The negative association between serum 25(OH)D and NAFLD in Whites may not be broadly generalizable to other racial/ethnic groups. Modifiable risk factors including BMI, triglycerides, diabetic status and/or smoking associated with NAFLD risk in non-white racial/ethnic groups beyond 25(OH)D.

Liver factoids from The Body, by Bill Bryson, 2019

  • The liver takes part in some five hundred metabolic processes.

  • 2/3 of the liver can be removed and it regenerates

  • third of us are thought to have early stages of NAFLD, but luckily for most of us it never progresses beyond that.

    * NAFLD is starting to be found in young children—somewhere it had never been seen before until recently. An estimated 10.7 percent of US children

  • Hepatitis C can live within victims for forty years or more, stealthily demolishing their livers, without their being aware of it. The CDC estimates that if all those people could be identified and treated, 120,000 lives would be saved in America alone.

Alcohol-Related Liver Disease might be associated with Low Mg, Vitamin D, Zinc, Selenium - Sept 2021

The Role of Micronutrients in the Pathogenesis of Alcohol-Related Liver Disease

Alcohol Alcohol. 2021 Sep 7;agab060. doi: 10.1093/alcalc/agab060

Ruairidh Nicoll 1, Konstantinos Gerasimidis 2, Ewan Forrest 1

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Aims: Chronic alcohol consumption may result in liver injury and chronic liver disease, but other factors are likely to influence disease progression. Malnutrition, specifically micronutrient deficiency, is frequently associated with both alcohol use disorder and chronic liver disease. We hypothesize that micronutrient deficiencies may affect the progression of liver disease in this population.

Methods: Systematic integrative review of the medical literature; electronic search of MEDLINE 1950-2021; studies investigating role of any micronutrient in the acceleration of alcohol-related liver injury in humans or animals. Studies which specifically related to alcoholic hepatitis were excluded. Outcomes were extracted and recorded in tabulated form and discussed narratively.

Results: We identified 46 studies investigating the role of micronutrient deficiencies in the pathogenesis of alcohol-related liver disease. Specific micronutrients which were identified included folic acid or related B vitamins (n = 9 studies), Vitamin D (n = 9 studies), magnesium (n = 8 studies), zinc (n = 8 studies) and selenium (n = 12 including one systematic review). Observational evidence suggests a potential role of magnesium deficiency in accelerating alcohol-related liver injury with weak or negative evidence for other micronutrients.

Conclusions: Magnesium deficiency may increase the risk of alcohol-related liver injury and adverse liver outcomes. However, currently, there is insufficient evidence to support magnesium supplementation except for clinically relevant magnesium deficiency. Long-term prospective cohort studies assessing the impact of micronutrients on liver disease progression in patients with alcohol use disorder are lacking and may help determine whether there is a causal role for micronutrient deficiencies in alcohol-related liver injury.

Tags: Liver Overview