Natural Liver Protection

October 20, 2009 Written by JP       [Font too small?]

The word “detoxification” is frequently mentioned in holistic circles. Perhaps the most important organ involved in this process is the liver. Without it, the body could not handle exposure to alcohol, environmental contaminants, junk food and even medications. The liver is responsible for promoting healthy blood (via the production of albumin and clotting factors) and combats fatigue by storing fat as an source of energy. Furthermore, it also aids in the absorption of life promoting nutrients such as CoQ10, Vitamins A, D, E and K. Simply put, without a properly functioning liver, one cannot live a vigorous life.

An herb known as milk thistle (Silybum marianum) is probably the best known natural remedy that supports healthy liver function. It has garnered this reputation with good reason. But there are some other lesser known ways to protect the liver as well. (1,2,3)

Liver Protector #1 – Coffee

A new study appearing in the journal Hepatology examined a proposed link between coffee consumption and hepatitis C outcomes. 766 Hep C patients were medically evaluated every 3 months for almost 4 years. During that time, they reported their average coffee and tea intake. Researchers found a dose dependent protective effect afforded by regular coffee use. The relative risk of disease progression was 30% lower in those drinking 1-3 cups of coffee per day and 53% lower in participants drinking 3 or more cups daily. An interesting side note is that black and green tea did not appear to confer the same benefit. Prior population studies appear to support the superiority of coffee vs. tea in this particular circumstance. The exact mechanism by which coffee imparts this protective effect isn’t clear at this time. However, some scientists suspect that certain phytochemicals in coffee (cafestol, diterpenes and kahweol) may block the damaging effects of toxins on this vital organ. (4,5,6)

Liver Protector #2 – Coenzyme Q10

Coenzyme Q10 is a vitamin-like substance produced by the body that plays an integral role in maintaining a healthy cardiovascular system and supporting cellular energy. The liver is one of the richest sources of CoQ10. Perhaps this is why a recent study presented in the journal Biochemical Pharmacology points to its application in protecting against liver damage caused by a poor diet.

  • A group of mice was fed a junk food diet or a “balanced diet” for 8 weeks.
  • The unhealthy diet was higher in fat and included 21% added fructose in the water supply.
  • Some of the mice receiving the unhealthy drink and food were also supplemented with CoQ10.

The researchers reported that the junk food mice ate more, gained weight and demonstrated elevated blood sugar and “impaired glucose tolerance”. There was also a significant increase in inflammation and oxidative stress – particularly with regard to liver metabolism. On the other hand, CoQ10 supplementation countered some of these ill effects by decreasing liver inflammation and stress markers via altered gene expression in the liver. This is not the first mention of a hepatoprotective effect of CoQ10 in the medical literature. Other trials have concluded that this coenzyme may combat symptoms of cirrhosis and even mitigate the harmful effects of certain medications on the liver. (7,8,9)

Liver Protector #3 – Krill Oil

Krill oil is a valuable source of omega-3 fatty acids, phospholipids and a potent antioxidant known as astaxanthin, a carotenoid that gives wild salmon its distinctive pink color. The October 2009 edition of the Journal of Agricultural Food Chemistry points to a relatively new method for shielding the heart and liver against dietary insults. Much like the previous study using CoQ10, the mice in this experiment were fed two different types of diet: 1) a “standard feed” that was used for comparison purposes; and 2) a heavily processed feed that was intended to tax the cardiovascular system and liver. The researchers then added krill oil to the chow of some of the lab animals that were fed the unhealthy diet.

  • The mice who received krill oil while eating the unhealthy diet showed a reduction in liver fat content and liver weight.
  • Lower levels of blood sugar, cholesterol and triglycerides were also detected in the krill supplemented group.

It’s also interesting to note that krill oil provoked an increase in adiponectin levels. This is a substance released by fat cells that helps to regulate lipids (cholesterol and triglycerides) and promotes insulin sensitivity. Higher levels of this hormone are connected to improved cardiovascular health and a reduced risk of diabetes. In general, marine-based omega-3 fats have been shown to support hepatic health. But krill oil appears to be more effective than fish oil in this regard. However, this conclusion needs to be interpreted with caution because it’s based on a very limited number of studies. (10,11,12)

Source: Can Fam Physician 2007;53:857-863 (link)

The single best way to support the liver is to avoid harming it in the first place. We all understand that abusing alcohol and drugs can ruin virtually any organ or system in the body. But not everyone is aware of the damage caused by consuming excessive carbohydrates on a regular basis. Even moderate amounts of carbs in the form of added sweeteners can lead to harmful shifts in lipid profiles and liver health markers. This is according to a new study conducted at the VA Puget Sound Health Care System in Seattle, Washington. The worst sweeteners appear to be the fructose based variety – agave nectar, crystalline fructose and high fructose corn syrup. A recent review in the Journal of Nutritional Biochemistry again points to fructose as a primary culprit in the development of nonalcoholic fatty liver disease. On the flip side of the coin, the October 2009 issue of the American Journal of Clinical Nutrition explains that higher protein intake may actually lower fatty deposits in the liver – via increased bile acid production. (13,14,15)

There may never be a drug, food or supplement that allows us to eat and live recklessly without suffering the consequences. However, I am a realist and do understand that most people don’t always eat and exercise as they should. Coffee, CoQ10 and krill oil may help overcome genetic weaknesses or the occasional dietary indulgence. But ultimately it’s important to remember that “supplements are meant to supplement an otherwise healthy lifestyle”. When used in that fashion, they can often be the body’s best friend.

Note: Please check out the “Comments & Updates” section of this blog – at the bottom of the page. You can find the latest research about this topic there!

Be well!


Bookmark and Share

Related Posts:

Tags: , ,
Posted in Detoxification, Food and Drink, Nutritional Supplements

17 Comments & Updates to “Natural Liver Protection”

  1. Nina K. Says:

    Thanks JP,

    good to know that my morning coffee is good for my liver :-) . The krill oil issue is interessting, looking for krill oil know….

    thanks and greetings,
    Nina K.

  2. liverock Says:

    Milk thisle is also very good protection against heavy metals passing through the liver because it boosts the liver’s glutathione levels.

  3. JP Says:


    I’m always happy to find good news about a favorite drink or food. Coffee is also my morning beverage of choice. :)

    re: krill oil

    It’s not inexpensive but the recommended dosage is quite low (usually 1,000 mg daily is adequate). Please let me know if you have any questions while looking into krill oil.

    Be well!


  4. JP Says:


    Indeed. I really need to write a full column about milk thistle. It’s an incredible herb. As you probably know, it’s not just for the liver either. Lately, there’s been a lot of interest in it’s cancer fighting potential. Pretty amazing.

    Be well!


  5. Angie Says:

    Wow… and I always thought daily coffee was bad for my liver.

  6. JP Says:


    I think many people (and even physicians) think that. In general, coffee is still regarded as an unhealthy brew that should be enjoyed by few and only on occasion. I agree that it’s not appropriate for everyone. But modern science is making a pretty strong case showing that benefits of coffee typically far outweigh the downside of it. Good to know, right? :)

    Be well!


  7. JP Says:

    A reason to consider Chlorella:

    Health Promot Perspect. 2014 Jul 12;4(1):107-15. doi: 10.5681/hpp.2014.014. eCollection 2014.

    The Effect of Chlorella vulgaris Supplementation on Liver En-zymes, Serum Glucose and Lipid Profile in Patients with Non-Alcoholic Fatty Liver Disease.

    Ebrahimi-Mameghani M1, Aliashrafi S2, Javadzadeh Y3, AsghariJafarabadi M4.


    Non-alcoholic fatty liver disease (NAFLD) is becoming a public health problem worldwide and using microalgae is a new approach on its treatment. The aim of this study was to investigate the effect of Chlorella vulgaris supplementation on liver enzymes, serum glucose and lipid profile in patients with NAFLD.


    This double-blind randomized placebo-controlled clinical trial was conducted on 60 NAFLD patients from specialized clinics of Tabriz University of Medical Sciences from December 2011 to July 2012. The subjects were randomly allocated into 2 groups: 1) “intervention” (n=30) received 400 mg/day vitamin E plus four 300 mg tablets of Chlorella vulgaris and, 2) “placebo” (n=30) received 400 mg/day vitamin E and four placebo tablets per day for 8 weeks. Weight, liver enzymes and metabolic factors were assessed in fasting serum and dietary data was collected at baseline and end of the study.


    Weight, liver enzymes, fasting blood sugar (FBS) and lipid profile decreased significantly in both groups (P<0.05). The differences in weight, ALP and FBS between the two groups were statistically significant (P=0.01, P=0.04 and P=0.02, respectively).


    C. vulgaris seems to improve FBS and lipid profile and therefore could be considered as an effective complementary treatment in NAFLD.

    Be well!


  8. JP Says:

    Update: More support for the role that coffee in fatty liver protection …

    Eur J Clin Nutr. 2015 Mar 25.

    Coffee but not green tea consumption is associated with prevalence and severity of hepatic steatosis: the impact on leptin level.

    BACKGROUND/OBJECTIVES: Most of the studies that have investigated the association between coffee consumption and hepatic steatosis have been experimental and small-scale clinical studies. As a result, epidemiological studies are scarce. To clear the association, we conducted a cross-sectional study and investigated the effects of coffee consumption with those of green tea consumption.

    SUBJECTS/METHODS: We analyzed 1024 Japanese male workers. The diagnosis of hepatic steatosis was based on ultrasonography. We divided coffee and green tea consumption into the following three categories: non-drinker; 1-2 cups/day and ⩾3 cups/day. To investigate the association between hepatic steatosis and coffee or green tea consumption, we calculated the odds ratio (OR) and adjusted the means of leptin levels on each severity of hepatic steatosis.

    RESULTS: A total of 265 of our subjects (25.9%) were diagnosed with hepatic steatosis. The ORs of the group of subjects who drank >3 cups of coffee/day was significantly lower compared with that of the noncoffee drinker group (OR 0.59, 95% confidence intervals 0.38-0.90, P=0.03). Although there was a significant difference between coffee consumption and leptin level only in the asymptomatic group, we found a decreasing trend in the asymptomatic and moderate-severe hepatic steatosis group. We did not find the same relationships in green tea consumption.

    CONCLUSIONS: Although we did not find an association between hepatic steatosis and green tea consumption, coffee may have beneficial effects on hepatic steatosis. In addition, we produced one possible hypothesis that coffee consumption negatively associates with leptin levels in hepatic steatosis.

    Be well!


  9. JP Says:

    Update 06/01/15:

    Nutr Metab Cardiovasc Dis. 2015 Apr 25.

    A double-blind, placebo-controlled randomized trial to evaluate the efficacy of docosahexaenoic acid supplementation on hepatic fat and associated cardiovascular risk factors in overweight children with nonalcoholic fatty liver disease.

    BACKGROUND AND AIMS: Very little information is available on whether docosahexaenoic acid (DHA) supplementation has a beneficial effect on liver fat and cardiovascular disease (CVD) risk factors in children with nonalcoholic fatty liver disease (NAFLD). In a double-blind, placebo-controlled randomized trial we investigated whether 6-month treatment with DHA improves hepatic fat and other fat depots, and their associated CVD risk factors in children with biopsy-proven NAFLD.

    METHODS AND RESULTS: Of 58 randomized children, 51 (25 DHA, 26 placebo) completed the study. The main outcome was the change in hepatic fat fraction as estimated by magnetic resonance imaging. Secondary outcomes were changes in visceral adipose tissue (VAT), epicardial adipose tissue (EAT), and left ventricular (LV) function, as well as alanine aminotransferase (ALT), triglycerides, body mass index-standard deviation score (BMI-SDS), and insulin sensitivity. At 6 months, the liver fat was reduced by 53.4% (95% CI, 33.4-73.4) in the DHA group, as compared with 22.6% (6.2-39.0) in the placebo group (P = 0.040 for the comparison between the two groups). Likewise, in the DHA group VAT and EAT were reduced by 7.8% (0-18.3) and 14.2% (0-28.2%), as compared with 2.2% (0-8.1) and 1.7% (0-6.8%) in the placebo group, respectively (P = 0.01 for both comparisons). There were no significant between-group changes for LV function as well as BMI-SDS and ALT, while fasting insulin and triglycerides significantly decreased in the DHA-treated children (P = 0.028 and P = 0.041, respectively).

    CONCLUSIONS: DHA supplementation decreases liver and visceral fat, and ameliorates metabolic abnormalities in children with NAFLD.

    Be well!


  10. JP Says:

    Update 07/10/15:

    J Am Coll Nutr. 2015 Jul 9:1-8.

    Functions of Coenzyme Q10 Supplementation on Liver Enzymes, Markers of Systemic Inflammation, and Adipokines in Patients Affected by Nonalcoholic Fatty Liver Disease: A Double-Blind, Placebo-Controlled, Randomized Clinical Trial.

    BACKGROUND: Nonalcoholic fatty liver disease (NAFLD) is a chronic liver disorder related to inflammation. Coenzyme Q10 (CoQ10) is a natural compound that has recently been considered as an anti-inflammatory factor. In the current study we aimed to evaluate the effects of CoQ10 supplementation on liver enzymes, inflammation status, and adipokines in patients with NAFLD.

    METHODS: Forty-one subjects with NAFLD participated in the current randomized, double-blind, placebo-controlled trial. The participants were randomly divided into 2 groups: one group received CoQ10 capsules (100 mg once a day) and the other received placebo for 12 weeks. Blood samples of each patient were taken before and after the 12-week intervention period for measurement of liver aminotransferases, inflammatory biomarkers, and adipokines (adiponectin and leptin).

    RESULTS: Taking 100 mg CoQ10 supplement daily resulted in a significant decrease in liver aminotransferases (aspartate aminotransferase [AST] and gamma-glutamyl transpeptidase [GGT]), high-sensitivity C-reactive protein (hs-CRP), tumor necrosis factor α, and the grades of NAFLD in the CoQ10 group in comparison to the control group (p < 0.05). In addition, patients who received CoQ10 supplement had higher serum levels of adiponectin (p = 0.016) and considerable changes in serum leptin (p = 0.053). However, no significant changes occurred in serum levels of interleukin-6 in both groups.

    CONCLUSION: The present study suggested that CoQ10 supplement at a dosage of 100 mg could be effective for improving the systemic inflammation and biochemical variables in NAFLD.

    Be well!


  11. JP Says:

    Update 07/14/15:

    MMW Fortschr Med. 2014 Dec 15;156 Suppl 4:120-6.

    [Effect of silymarin on liver health and quality of life. Results of a non-interventional study].

    BACKGROUND: Many drugs are known to have hepatotoxic side effects. The effect of silymarin on liver function and liver-injury-impaired quality of life under daily practice conditions in patients with elevated values of liver enzymes was evaluated in the present non-interventional study.

    METHOD: Patients with drug-induced elevated aminotransferase levels and indication for silymarin (Legalon forte) treatment for 2 to 3 months were documented prospectively over 4 months. At baseline, after 2 and 4 months, respectively, the following parameters were documented: alanine transaminase (ALT), aspartate transaminase (AST), γ-glutamyltransferase (GGT), alkaline phosphatase, total bilirubin, presence of liver-related skin symptoms and discoloured urine, severity of liver-related symptoms and quality of life.

    RESULTS: In total, 190 patients (53.2% male, median age 60.0 years [range 19-81]) from 48 centres participated in the non-interventional study. Among potentially hepatotoxic drugs, analgesics/anti-inflammatory drugs were used most frequently (45.8%). These drugs have been administered for a median period of 2.8 years (range 0.0-26.1). At baseline, all patients had elevated levels of ALT, AST or GGT. Fatigue, flatulence, upper abdominal discomfort, lethargy, and joint complaints were the most severe liver-related symptoms and prevalent in over 62% of patients. Quality of life was affected in 88.7% of patients. Significant reductions were achieved in all documented laboratory parameters (p < 0.001), leading to marked improvement in liver-related symptoms and increased quality of life already after 2 months. The percentage of patients with liver enzymes in the normal range increased considerably within 4 months. No adverse drug reactions were observed.

    CONCLUSIONS: Silymarin is a safe and efficacious treatment option for patients with elevated liver enzymes. A benefit in terms of liver-related symptoms as well as quality of life and performance was demonstrated already after 2 months of treatment.

    Be well!


  12. JP Says:

    Updated 07/20/15: (full text)

    Hepatobiliary Surg Nutr. 2015 Jun;4(3):161-71.

    Carotenoids and non-alcoholic fatty liver disease.

    Non-alcoholic fatty liver disease (NAFLD) is a growing health problem around the world, especially in developed countries. NAFLD includes all cases of fatty liver disease from simple steatosis to cirrhosis, without excessive alcohol intake, use of steatogenic medication or hereditary disorders. Pathogenesis is associated with dietary high fat intake, decreased free fatty acid (FFA) oxidation, increased hepatic lipogenesis and lipolysis from the adipose tissue. These metabolic alterations contribute to the hepatic fat accumulation. Consequently, stimulated oxidative stress and inflammation play a major role in hepatocellular damage. Therefore, antioxidant and anti-inflammatory agents may have a role in the prevention of this disease. Carotenoids are potent antioxidant and anti-inflammatory micronutrients, which have been investigated in the prevention and treatment of NAFLD. The main sources of the carotenoids are fruits and vegetables. In this article we review the potential role and possible molecular mechanism of carotenoids in NAFLD.

    Be well!


  13. JP Says:

    Updated 07/30/15:

    J Hum Nutr Diet. 2015 Jul 27.

    n-3 polyunsaturated fatty acid supplementation reduces insulin resistance in hepatitis C virus infected patients: a randomised controlled trial.

    BACKGROUND: Insulin resistance promotes liver disease progression and may be associated with a lower response rate in treated hepatitis C virus (HCV) infected patients. n-3 polyunsaturated fatty acid (PUFA) supplementation may reduce insulin resistance. The present study aimed to evaluate the effect of n-3 PUFA supplementation on insulin resistance in these patients.

    METHODS: In a randomised, double-blind clinical trial, 154 patients were screened. After applying inclusion criteria, 52 patients [homeostasis model assessment index of insulin resistance (HOMA-IR ≥2.5)] were randomly divided into two groups: n-3 PUFA (n = 25/6000 mg day-1 of fish oil) or control (n = 27/6000 mg day-1 of soybean oil). Both groups were supplemented for 12 weeks and underwent monthly nutritional consultation. Biochemical tests were performed at baseline and after intervention. Statistical analysis was performed using the Wilcoxon Mann-Whitney test for comparisons and the Wilcoxon test for paired data. Statistical package r, version 3.02 (The R Project for Statistical Computing) was used and P < 0.05 (two-tailed) was considered statistically significant.

    RESULTS: Comparisons between groups showed that n-3 PUFA supplementation was more effective than the control for reducing HOMA-IR (P = 0.015) and serum insulin (P = 0.016). The n-3 PUFA group not only showed a significant reduction in HOMA-IR 3.8 (3.2-5.0) versus 2.4 (1.8-3.3) (P = 0.002); serum insulin 17.1 (13.8-20.6) μIU mL-1 versus 10.9 (8.6-14.6) μIU mL-1 (P = 0.001); and glycated haemoglobin 5.4% (5.0-5.7%) versus 5.1% (4.8-5.6%) (P = 0.011), but also presented an increase in interleukin-1 97.5 (0.0-199.8) pg mL-1 versus 192.4 (102.2-266.8) pg mL-1 (P = 0.003) and tumour necrosis factor 121.2 (0.0-171.3) pg mL-1 versus 185.7 (98.0-246.9) pg mL-1 (P = 0.003).

    CONCLUSIONS: n-3 PUFA supplementation reduces insulin resistance in genotype 1 HCV infected patients.

    Be well!


  14. JP Says:

    Updated 09/16/15:

    Eur Rev Med Pharmacol Sci. 2015 Aug;19(16):3118-3124.

    Effect of silymarin plus vitamin E in patients with non-alcoholic fatty liver disease. A randomized clinical pilot study.


    Non-alcoholic fatty liver disease (NAFLD) is an increasingly recognized health problem. Various treatment strategies such as thiazolidinediones, metformin, lipid-lowering agents and antioxidants have been evaluated. So far, no single intervention has convincingly improved liver histology. Experience of using silymarin alone or in combination with other agents in patients with NAFLD is limited in the medical literature. The present study was conducted to evaluate the efficacy of silymarin plus vitamin E in the treatment of NAFLD.


    A sample of 36 patients was enrolled. The diagnosis of NAFLD was confirmed by percutaneous liver biopsy. All patients were randomized to one of the following intervention groups: group I: treated with 2 tablets per day of silymarin plus vitamin E (Eurosil 85®, MEDAS SL) and a lifestyle modification program consisting of hypocaloric diet (1520 kcal, 52% of carbohydrates, 25% of lipids and 23% of proteins) and exercise for 3 months and group II (only with the hypocaloric diet). Anthropometric variables as waist circumference, weight, body mass index (BMI) were measured. Biochemical parameters: Glucose, triglycerides, AST, ALT, GGt levels and insulin resistance (HOMA-IR) were determined under fasting conditions. Non-invasive NAFLD-index were applied before and after the treatments: Fatty liver index (FLI), liver accumulation product (LAP) and NAFLD-Fibrosis score (FS).


    The mean age was 47.4 ± 11.2 years old (range 18-67); 22 men and 14 women. In group I, 11 patients (61%) have a NAS-score > 5 and 10 (55.5%) in the group II (NS). Anthropometric parameters decreased after treatment in both groups. Patients in both groups showed a decrease in GGt levels after treatment (group I: 68 IU/L vs. 46.2 ± 27 IU/L; p < 0.05 and group II 80.5 ± 46 IU/L vs. 50.3 ± 27 IU/L; p < 0.05). Only in group II we observed a significant decrease in AST and ALT levels. In both groups, we observed a decrease in: FLI index (group I: 86.2 ± 19 vs. 76.9 + 20; p < 0.05 and in group II: 85.2 ± 18 vs. 77.5 ± 23; p < 0.05), and NAFLD-FS index (group I: -1.6 ± 1.8 vs. -2.1 ± 1.5; p < 0.05 and in group II -1 ± 1.9 vs. -1.5 ± 2.1; p < 0.05). Patients in group I who did not get a 5% loss of weight also displayed decreased GGt levels, and in the FLI and NAFLD-FS indexes; whereas patients in group II without decrease of 5% by weight showed no improvement in any of the analyzed parameters.


    Treatment with silymarin plus vitamin E and a hypocaloric diet ameliorate function hepatic test, and non-invasive NAFLD index. Silymarin can be an alternative valid therapeutic option particularly when other drugs are not indicated or have failed or as a complementary treatment associated with other therapeutic programs.

    Be well!


  15. JP Says:

    Updated 1/28/16:

    Int J Obes (Lond). 2016 Jan 20.

    Strong and persistent effect on liver fat with a Paleolithic diet during a two-year intervention.

    BACKGROUND/OBJECTIVES: Our objective was to investigate changes in liver fat and insulin sensitivity during a 2-year diet intervention. An ad libitum Paleolithic diet was compared to a conventional, low-fat diet.

    SUBJECTS/METHODS: Seventy healthy, obese, postmenopausal women were randomized to either a Paleolithic diet or a conventional, low-fat diet. Diet intakes were ad libitum. Liver fat was measured with proton magnetic resonance spectroscopy. Insulin sensitivity was evaluated with oral glucose tolerance tests and calculated as HOMA-IR/Liver IR index for hepatic insulin sensitivity and OGIS/Matsuda for peripheral insulin sensitivity. All measurements were performed at 0, 6, and 24 months. 41 women completed the examinations for liver fat and were included.

    RESULTS: Liver fat decreased after 6 months by 64% (95% CI: 54-74%) in the Paleolithic diet group and by 43% (27-59%) in the low-fat diet group (P<0.01 for difference between groups). After 24 months liver fat decreased 50% (25-75%) in the Paleolithic diet group and 49% (27-71%) in the low-fat diet group. Weight reduction between baseline and 6 months was correlated to liver fat improvement in the low-fat diet group (rs=0.66, P<0.01) but not in the Paleolithic diet group (rs=0.07, P=0.75). Hepatic insulin sensitivity improved during the first 6 months in the Paleolithic diet group (P<0.001 for Liver IR index and HOMA-IR), but deteriorated between 6 and 24 months without association to liver fat changes.

    CONCLUSIONS: A Paleolithic diet with ad libitum intake had a significant and persistent effect on liver fat and differed significantly from a conventional low-fat diet at six months. This difference may be due to food quality, e.g. a higher content of mono- and polyunsaturated fatty acids in the Paleolithic diet. Changes in liver fat did not associate to alterations in insulin sensitivity.

    Be well!


  16. JP Says:

    Updated 02/27/16:

    Br J Nutr. 2016 Feb 26:1-8.

    High serum carotenoids are associated with lower risk for developing elevated serum alanine aminotransferase among Japanese subjects: the Mikkabi cohort study.

    Many recent studies have shown that antioxidant vitamins and/or carotenoids may reduce liver disease, but this association has not been well established with thorough longitudinal cohort studies. The objective of this study was to longitudinally investigate whether serum carotenoids at baseline are associated with the risk of developing elevated serum alanine aminotransferase (ALT) among Japanese subjects. We conducted a follow-up study of 1073 males and females aged between 30 and 79 years at baseline from the Mikkabi prospective cohort study. Those who participated in the baseline study and completed follow-up surveys were examined longitudinally. Exclusions included excessive alcohol consumption (≥60 g alcohol/d), hepatitis B and C and having a history of medication use for liver disease. A cohort of 213 males and 574 females free of elevated serum ALT (>30 IU/ml) at baseline was studied. Over a mean follow-up period of 7·4 (sd 3·1) years, thirty-one males and forty-nine females developed new elevated serum ALT. After adjustments for confounders, the hazard ratios for elevated serum ALT in the highest tertiles of basal serum β-carotene, β-cryptoxanthin and total provitamin A carotenoids against the lowest tertiles were 0·43 (95 % CI 0·22, 0·81), 0·51 (CI 0·27, 0·94) and 0·52 (CI 0·28, 0·97), respectively. For α-carotene and lycopene, borderline reduced risks were also observed; however, these were not significant. Our results further support the hypothesis that antioxidant carotenoids, especially provitamin A carotenoids, might help prevent earlier pathogenesis of non-alcoholic liver disease in Japanese subjects.

    Be well!


  17. JP Says:

    Updated 03/18/16:

    Int J Food Sci Nutr. 2016 Mar 17:1-9.

    Flaxseed supplementation in non-alcoholic fatty liver disease: a pilot randomized, open labeled, controlled study.

    A two-arm randomized open labeled controlled clinical trial was conducted on 50 patients with non-alcoholic fatty liver disease (NAFLD). Participants were assigned to take either a lifestyle modification (LM), or LM +30 g/day brown milled flaxseed for 12 weeks. At the end of the study, body weight, liver enzymes, insulin resistance and hepatic fibrosis and steatosis decreased significantly in both groups (p< 0.05); however, this reduction was significantly greater in those who took flaxseed supplementation (p < 0.05). The significant mean differences were reached in hepatic markers between flaxseed and control group, respectively: ALT [-11.12 compared with -3.7 U/L; P< 0.001], AST [-8.29 compared with -4 U/L; p < 0.001], GGT [-15.7 compared with -2.62 U/L; p < 0.001], fibrosis score [-1.26 compared with -0.77 kPa; p = 0.013] and steatosis score [-47 compared with -15.45 dB/m; p = 0.022]. In conclusion, flaxseed supplementation plus lifestyle modification is more effective than lifestyle modification alone for NAFLD management.

    Be well!


Leave a Comment

To prove you're a person (not a spam script), type the security word shown in the picture. Click on the picture to hear an audio file of the word.
Click to hear an audio file of the anti-spam word