What are the Health Benefits of Wasabi?

A lesser-known member of the Brassica family that includes broccoli, cabbage, and horseradish is the Japanese vegetable wasabi (Wasabia japonica Matsumura).

Wasabi is best known for its presence alongside sushi in Japanese restaurants. But be careful, this
lovely green condiment is pungent!

Antimicrobial Benefits of Wasabi

Interestingly, wasabi and allyl isothiocyanate, the compound responsible for wasabi’s taste, have been found to inhibit the bacterium V. parahaemolyticus in tuna meat, indicating that its use as an accompaniment to sushi and sashimi adds more than flavor.1

Wasabi roots, stems, and leaves have also shown activity against the ulcer-causing bacterium H. pylori.2 While the bacterial activity of the leaves was higher than that of the roots, its leaves have a lower amount of allyl isothiocyanate, leading researchers to conclude that other components in wasabi have an antibacterial action. Subsequent research in animals infected with H. pylori and exposed to physical stress found a reduction in resultant oxidative DNA damage in the stomach and peripheral red blood cells in association with the administration of wasabi leaf extract.3

Of ten foods tested, including banana, coriander, mustard, and mugwort, wasabi had the strongest antibacterial activity against the intestinal bacterium Escherichia coli.4 The researchers identified 6-(methylsulfinyl)hexyl isothiocyanate (6-MITC) as wasabi’s active compound, and found that related compounds in other cruciferous plants were active against E. coli and Staphylococcus aureus (staph infection).

Anticancer Effects of Wasabi

One of the first studies to investigate wasabi was a rat study in which male animals received drinking water that contained MNNG, which induces gastric cancer.5 Some of the animals also received diets that contained 10% wasabi powder for 40 weeks. Among the 30 animals that received the carcinogen alone, nine animals developed stomach or duodenal cancers, in comparison with two rats among the group that also received wasabi. “These results indicated that glandular stomach carcinogenesis induced by MNNG was suppressed by the administration of wasabi,” the authors concluded.

6-MITC significantly inhibited mutation in the skin cells of mice that received a topical application of the carcinogen DMBA.6 6-MITC was also shown to suppress the growth of two mouse tumor cell lines.

In rats given 1,2-dimethylhydrazine (DMH) to induce the formation of premalignant lesions known as aberrant crypt foci and beta-catenin-accumulated crypts in the colon, the addition of 6-MITC to the diet during the initiation phase was associated with a reduction in the number of aberrant crypt foci as well as a decrease in those of larger size compared to treatment with DMH alone.7 6-MITC was also associated with a decrease in beta-catenin-accumulated crypts. A study involving colon cancer cells treated with wasabi extract resulted in the induction of autophagy and apoptosis (programmed cell death), which was verified in animals that received transplanted cancerous tumors.8

Apoptosis was also the inhibitory mechanism in a study involving human monoblastic leukemia cells, which the researchers attributed to its 6-MITC content.9 6-MITC also induced apoptosis in a stomach cancer cell line. Other research found an inhibitory effect for 6-MITC against the growth and survival of breast cancer and melanoma cell lines.10

In mice inoculated with either of two types of triple negative breast cancer cells, orally administered 6-MITC decreased tumor weight in mice that received one cell line and reduced tumor volume in both cell lines.11 In vitro, 6-MITC induced apoptosis in both lines (as well as an estrogen receptor positive line), while downregulating nuclear factor-kappa beta (NF-kB). 6-MITC and a derivative compound have also shown inhibitory effects against the growth of human pancreatic cancer cells.12

Identification of wasabi as the most potent inducer of glutathione S-transferase (GST, a phase II detoxification enzyme involved in protection against carcinogenesis) following an extensive screening of vegetable extracts led to the identification of 6-MITC as wasabi’s major GST inducer.13 Researchers Yasujiro Morimitsu and colleagues concluded that 6-MITC “may be a chemoprotector against tumors evoked by a number of chemical carcinogens and can be regarded as a readily available promising new cancer chemopreventive agent.”

Other Protective Properties of Wasabi

In addition to wasabi’s anticarcinogenic properties, Dr. Morimitsu reports an ability to inhibit platelet aggregation, indicating a potential role in the prevention of cardiovascular disease.14 He was also a contributor to research that screened a number of Brassica vegetables for their ability to promote the formation of neurites in rat cells, which found that wasabi had the strongest activity and that 6-MITC was one of wasabi’s major enhancers of neuritogenesis.15 In a mouse model of Parkinson’s disease, 6-MITC showed neuroprotective effects, attributable to a reduction in apoptotic cell death and activation of glutathione-dependent antioxidant systems.16

Wasabi has shown antioxidant and superoxide scavenging properties.17 In mouse cells, 6-MITC inhibited cyclooxygenase-2 (COX-2) expression induced by lipopolysaccharide and interferon-gamma, indicating an anti-inflammatory effect.18,19 In human umbilical vein endothelial cells, 6-MITC suppressed cell adhesion and lowered inflammation.20

Additionally, in a mouse model of atopic dermatitis, wasabi rhizome extract added to the diet reduced scratching behavior as well as levels of histamine, IgE and other plasma factors.21

It has been suggested that some of the wasabi served in Japanese restaurants is not true wasabi, but is actually horseradish. While horseradish has its own health benefits, make sure you obtain true wasabi if you seek to avail yourself of its protective effects. The rhizome (stem of a plant that is usually found underground) of wasabi is also available as a dietary supplement.


  1. Hasegawa N et al. Int J Food Microbiol. 1999 Aug 1;49(1-2):27-34.
  2. Shin IS et al. Int J Food Microbiol. 2004 Aug 1;94(3):255-61.
  3. Sekiguchi H et al. Biosci Biotechnol Biochem. 2010;74(6):1194-9.
  4. Ono H et al. Biosci Biotechnol Biochem. 1998 Feb;62(2):363-5
  5. Tanida N et al. Nutr Cancer. 1991;16(1):53-8.
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  7. Kuno T et al. Oncol Lett. 2010 Mar;1(2):273-278.
  8. Hsuan SW et al. Eur J Nutr. 2016 Mar;55(2):491-503.
  9. Watanabe M et al. Phytochemistry. 2003 Mar;62(5):733-9.
  10. Nomura T et al. Cancer Detect Prev. 2005;29(2):155-60.
  11. Fuke Y et al. Nutr Cancer. 2014;66(5):879-87.
  12. Chen YJ et al. Evid Based Complement Alternat Med. 2014;2014:494739.
  13. Morimitsu Y et al. J Biol Chem. 2002 Feb 1;277(5):3456-63.
  14. Morimitsu Y et al. Biofactors. 2000;13(1-4):271-6.
  15. Shibata T et al. J Neurochem. 2008 Dec;107(5):1248-60.
  16. Morroni F et al. Brain Res. 2014 Nov 17;1589:93-104.
  17. Kinae N et al. Biofactors. 2000;13(1-4):265-9.
  18. Uto T et al. Biochem Pharmacol. 2005 Dec 5;70(12):1772-84.
  19. Uto T et al. Oncol Rep. 2007 Jan;17(1):233-8.
  20. Okamoto T et al. J Nat Med. 2014 Jan;68(1):144-53.
  21. Nagai M et al. J Nutr Sci Vitaminol (Tokyo). 2009 Apr;55(2):195-200.


How To Get Relief from Menopause with Black Cohosh

Cimicifuga racemosa or, as it is more commonly known, black cohosh, is a native American herb used primarily by women seeking relief from menopausal or menstrual disorders. The so-called "woman's herb," which is a member of the buttercup family, is prized in herbalism for the benefits of its rhizomes and roots.

How Does Black Cohosh Work?

Its effects in women were initially thought to be due to the presence of estrogenic compounds; however, they may be due in greater part to the herb's serotonin receptor activators. A double-blind, randomized trial reported in 2002 found a lack of change in vaginal cytology measures or female hormone levels in women given black cohosh for 24 weeks, which suggests an absence of an overall estrogenic effect despite significant relief from menopausal symptoms in the majority of women who received either of two doses.2

What is Black Cohosh Used for?

Two early reviews concluded effectiveness and safety for black cohosh for the alleviation of menopausal symptoms, including hot flashes, profuse perspiration, sleep disturbances and depression.3,4 It has been suggested as an alternative for estrogen replacement therapy among women for whom hormone therapy is not recommended or for those who otherwise choose to forego it. Interestingly, a survey of 100 eligible women found that perceived quality of life was highest among women who used dietary supplements for menopause, including black cohosh, in comparison with those who used hormone replacement therapy, a combination of supplements and hormones, or no treatment.5

The Clinical Efficacy of Black Cohosh

A study of 20 women with menopausal complaints treated with 40 milligrams black cohosh daily for six months had a decrease in Kupperman's Index values (which scores 11 menopausal symptoms) from an average of 30.2 points to 8.5 points after three months, which further decreased to 2.6 points after six months.6 No changes in hormone profiles or other biochemical values were observed. In a comparison of fluoxetine (PROZAC®) and black cohosh in 120 women with menopausal symptoms, Kupperman's Index values were significantly lower after three months of treatment among the black cohosh group.7

Monthly hot flash and night sweat scores were also lower in comparison to those who received fluoxetine. At the end of six months, women who received black cohosh reported an 85% reduction in hot flash scores, compared to 62% in association with fluoxetine, leading the researchers to conclude that the herb was more effective for hot flashes and night sweats, while fluoxetine was better for depression.

In a randomized, double-blind trial that evaluated the effect of black cohosh in 48 postmenopausal women with sleep disturbance, the herb increased sleep efficiency and decreased wakefulness after sleep onset duration compared to a placebo.8

A meta-analysis of nine randomized trials of black cohosh for the treatment of menopausal complaints found significant improvements in comparison with a placebo in six trials and an overall 26% improvement in vasomotor symptoms.9

Does Black Cohosh Cause Cancer?

While the majority of research involving phytoestrogens has indicated an inhibitory effect against the growth of estrogen-responsive malignancies, a concern exists in regard to whether phytoestrogens could, in some cases, stimulate breast or other female cancers. An evaluation of four herbs used during menopause, one of which was black cohosh, failed to find estrogenic activity or stimulatory effects in cultured breast cancer cells.10

In fact, other research has shown that black cohosh antagonized estradiol-induced activities, indicating a possible protective effect against estradiol-fueled conditions.11 A study in estrogen receptor-positive and estrogen receptor-negative breast cancer cells found antiestrogenic activity in the former and growth inhibition in both cell lines.12 And in another study of estrogen receptor-positive and receptor-negative cells, black cohosh decreased growth and dose-dependently inhibited the conversion of estrone sulfate to estradiol, which is considered by some researchers to be the preferred pathway of estradiol synthesis in the breast.13

Black cohosh has also been demonstrated to suppress the invasiveness of estrogen-receptor negative human breast cancer cells.14

In a case-control study involving 949 women with breast cancer and 1,524 controls, women who used black cohosh had a 61% lower risk of breast cancer than those who did not report using the herb.15 In another study, none of the 65 women who completed a trial of daily black cohosh experienced an increase in mammographic breast density or experienced breast cell proliferation as ascertained by fine needle aspiration biopsies.16 And in a retrospective study of 18,861 breast cancer patients among whom 1,102 had used black cohosh extract, recurrence of the disease developed in 14% of nonusers after 2 years compared to 6.5 years among users.17

In a review of plant-based menopause treatments, a study in rats was cited which found that black cohosh extract was associated with many of the benefits of 17beta-estradiol, including effects in the brain, bone and urinary bladder, without causing uterine growth.18 The authors conclude that the extract "would appear as an ideal SERM (selective estrogen receptor modulator) and may therefore be an alternative to hormone replacement therapy."

A study that involved 400 postmenopausal women with estrogen deficiency symptoms who were treated for a year with 40 milligrams black cohosh daily found a reduction in intensity and number of hot flashes and no incidence of increased endometrial thickness (which can occur when women consume unopposed estrogen).19

A one year randomized, double-blind, placebo-controlled trial that involved 351 women (the Herbal Alternatives for Menopause Study) concluded that black cohosh, used alone or as part of a multibotanical supplement with or without the addition of dietary soy, had no effects on the endometrium, vaginal epithelium or reproductive hormones.20

Nevertheless, if you have or have had breast, ovarian or endometrial cancer, it is suggested that you discuss the use of black cohosh with your physician.

The Bottom Line

Black cohosh is not just for perimenopausal and postmenopausal women. It can be used by younger women who have undergone surgical removal of their ovaries, and by those experiencing menstrual disorders.21 Its general ability to help relieve pain makes it useful for men as well.


  1. Ross SM. Holist Nurs Pract. 2007 May-Jun;21(3):162-3.
  2. Liske E et al. J Womens Health Gend Based Med. 2002 Mar;11(2):163-74.
  3. Liske E. Adv Ther. 1998 Jan-Feb;15(1):45-53.
  4. Lieberman S. J Womens Health. 1998 Jun;7(5):525-9.
  5. Kam IW et al. Menopause. 2002 Jan-Feb;9(1):72-8.
  6. Radowicki S et al. Ginekol Pol. 2006 Sep;77(9):678-83.
  7. Oktem M et al. Adv Ther. 2007 Mar-Apr;24(2):448-61.
  8. Jiang K et al. Climacteric. 2015;18(4):559-67.
  9. Shams T et al. Altern Ther Health Med. 2010 Jan-Feb;16(1):36-44.
  10. Amato P et al. Menopause. 2002 Mar-Apr;9(2):145-50.
  11. Zierau O et al. J Steroid Biochem Mol Biol. 2002 Jan;80(1):125-30.
  12. Garita-Hernandez M et al. Planta Med. 2006 Mar;72(4):317-23.
  13. Rice S et al. Maturitas. 2007 Apr 20;56(4):359-67.
  14. Hostanska K et al. In Vivo. 2007 Mar-Apr;21(2):349-55.
  15. Rebbeck TR et al. Int J Cancer. 2007 Apr 1;120(7):1523-8.
  16.  Hirschberg AL et al. Menopause. 2007 Jan-Feb;14(1):89-96.
  17. Henneicke-von Zepelin HH et al. Int J Clin Pharmacol Ther. 2007 Mar;45(3):143-54.
  18. Wuttke W et al. Maturitas. 2003 Mar 14;44 Suppl 1:S9-20.
  19. Raus K et al. Menopause. 2006 Jul-Aug;13(4):678-91.
  20. Reed SD et al. Menopause. 2008 Jan-Feb;15(1):51-8.
  21. McKenna DJ et al. Altern Ther Health Med. 2001 May-Jun;7(3):93-100.


How Colostrinin Helps the Aging Brain - Life Extension Blog

Colostrinin is a polypeptide derived from colostrum, which lactating mothers produce prior to the
production of breast milk. Colostrum ensures the delivery of disease-protecting antibodies to newborn mammals. Polypeptides are chains of approximately 50 or fewer bonded amino acids.

Colostrinin is rich in the amino acid proline, which is one of the amino acids recommended by Linus Pauling to lower the risk of cardiovascular disease.

Some of the earliest published research concerning colostrinin suggests an immune system benefit. It has been reported that colostrinin induces the maturation and differentiation of thymus cells in mice.1

Experimental research suggests that colostrinin could benefit those with allergies. In a mouse model of allergic airway inflammation, IgE/IgG1 production, airway eosinophilia, mucin production and hypersensitivity were reduced in response to exposure to extracts from ragweed pollen grains and house dust mites.2

While colostrinin has many published studies focusing on immune support, it has also shown the ability to modulate production of tau and amyloid beta proteins, which are associated with cognitive decline.

Alzheimer’s Disease and Cognitive Decline

Recently, colostrinin has shown promise against cognitive dysfunction and Alzheimer’s disease. In experiments with rats, intraperitoneal (abdominal cavity) injection of colostrinin improved spatial learning in 13-month-old rats, but not in young, 3-month old-animals.3 Incidental learning was also enhanced in association with colostrinin. “Given the fact that colostrum is the first nutritive agent of neonates, it might be speculated that its peptides may facilitate the early postnatal development of the cerebral neurons and their plasticity,” write authors P. Popik and colleagues at the Polish Academy of Sciences.

Acting on these and other positive animal findings, colostrinin was evaluated in a clinical trial.4 Forty-six patients with Alzheimer’s disease were assigned to receive 100 micrograms of colostrinin every other day, 100 micrograms of selenium every other day, or a placebo for 3 weeks, followed by a 2-week period during which no treatment was received. After ten cycles, 15 patients who received colostrinin experienced improvement and seven of them had stabilized. While selenium was associated with disease stabilization in 13 out of 15 who received it, just half of the placebo patients had stabilized by the end of the trial evaluation.

In a similar trial, 105 participants with Alzheimer’s disease received 100 micrograms of colostrinin or a placebo on alternate days for three weeks followed by two treatment-free weeks for three cycles.5 This was followed by a 15 week phase during which all subjects received colostrinin. Tests that evaluated cognitive function, instrumental activities of daily living, and other areas were administered at the beginning of the study and at weeks 15 and 30. At 15 weeks, colostrinin was associated with stabilization of cognitive and daily living functions. Overall patient response also favored colostrinin. A better cognitive response to colostrinin was observed among those with less advanced disease.

In chicks trained in a task involving memory, injection of colostrinin into the mesopallium intermediomediale (a region of bird brains that is important for memory formation) prior to training improved long term memory retention, while control animals injected with saline failed to show improvement.6 Injection of colostrinin into the peritoneum was also effective. “These data extend the known efficacy of colostrinin from mammals demonstrating its widespread efficacy as a cognitive enhancer,” authors M. G. Stewart and D. Banks observe.

While some of the research has evaluated the use of colostrinin as an injection, it can also be taken orally as a supplement.

How Colostrinin Works

Research has revealed that colostrinin decreases lipid peroxidation and reduces intracellular levels of reactive oxygen species.7 In an in vitro study, colostrinin inhibited the aggregation of amyloid beta that results in the brain plaques characteristic of Alzheimer’s disease.8 It was observed that amyloid beta formed fibrils after 24 to 48 hours, however, colostrinin completely abolished fibril formation. As late as the 17th day, preformed fibers were dissolved upon the addition of colostrinin. When the effects of amyloid beta were evaluated in human neuroblastoma cells, preincubation of colostrinin with amyloid nearly completely prevented cell toxicity that would have otherwise occurred. Lower doses of colostrinin appeared to be as effective as high doses. The researchers concluded that colostrinin’s neuroprotective effects are related to the reduction of amyloid beta fibrils. Similar anti-amyloid effects have been demonstrated for colostrinin in other experiments.


In mouse diploid fibroblast cells, which are used as a model of cellular aging, the administration of colostrinin slowed senescence and increased population doubling levels.9 This was associated with a decrease in intracellular reactive oxygen species levels. “These data suggest that colostrinin may delay the development of cellular aging at the level of the organism,” A. Bacsi and colleagues conclude. “Thus, colostrinin may be used in the prevention and/or therapy of diseases associated with aging processes.”

In a review of colostrinin’s effects, I. Boldogh and M. L. Kruzel of the University of Texas Medical Branch at Galveston note that “Studies on cultured cells showed that colostrinin modulates intracellular levels of reactive oxygen species (ROS), via regulation of glutathione metabolism, activity of antioxidant enzymes and mitochondria function. Due to an improvement in senescence-associated mitochondrial dysfunction and a decrease in ROS generation, colostrinin decelerates the aging processes of both cultured cells and experimental animals. When given orally to mice, colostrinin increased the lifespan and improved various motor and sensory activities.”10

They conclude that “Although the molecular basis by which colostrinin exerts its diverse effects are still under investigation, the regulatory effect on the cellular redox state via maintenance of mitochondrial function and modification of ROS-induced cell signaling seem to be of great importance.”10


  1. Sokal I et al. Arch Immunol Ther Exp (Warsz). 1998;46(3):193-8.
  2. Boldogh I et al. Int Arch Allergy Immunol. 2008;146(4):298-306.
  3. Popkik P et al. Pharmacol Biochem Behav. 1999 Sep;64(1):183-9.
  4. Leszek J et al. Arch Immunol Ther Exp (Warsz). 1999;47(6):377-85.
  5. Bilikiewicz A et al. J Alzheimers Dis. 2004 Feb;6(1):17-26.
  6. Stewart MG et al. Neurobiol Learn Mem. 2006 Jul;86(1):66-71.
  7. Boldogh I et al. J Mol Neurosci. 2003 Apr;20(2):125-34.
  8. Schuster D et al. Neuropeptides. 2005 Aug;39(4):419-26.
  9. Bacsi A et al. Neuropeptides. 2007 Apr;41(2):93-101.
  10. Boldogh I et al. J Alzheimers Dis. 2008 Apr;13(3):303-21.


4 Triggers of Panic Attacks and How to Defeat Them - Life Extension Blog

Jackie Edwards

Panic attacks are described by the Mayo Clinic as feeling a sense of intense fear or impending doom, triggering a strong physical response when there is no real danger or a cause that is apparent to an observer. For those who regularly experience panic attacks, they can be exhausting, frightening, and may make you feel like you're losing control.

Even though they are distinct, and with different modes of action, panic attacks typically stem from anxiety. They are a vicious response to intense stress. If these panic attacks are consistently unexpected and are characterized by long periods of crippling fear, then you may be experiencing a chronic disorder.

Understanding the Symptoms of a Panic Attack

Panic attacks occur suddenly, striking at almost any time. Even though most people have preset triggers, it requires careful introspection or the help of a therapist to identify them. Physical manifestations also occur, like heart palpitations or feeling like you are experiencing a heart attack. Sweaty palms, hot flashes, waves of nausea, and dizzying headaches also tend to be baseline symptoms.

4 Common Triggers to a Panic Attack

  • Undiagnosed heart problems. Heart palpitations and a feeling of an actual heart attack aren't just your imagination. About a third of people who have experienced a heart attack or heart surgery encounter symptoms similar to someone going through a panic attack. Women are particularly at risk.
  • Alcohol and drug consumption can trigger a panic attack. Research has shown that sufferers try to self-medicate with the help of alcohol or drugs, sometimes being used together in a dangerous bid to control anxiety. Unfortunately, narcotic use can contribute to the frequency of panic attacks and lead to further complications.
  • Stimulants. Being over-caffeinated can have an adverse impact for those who are at risk for anxiety disorders. The jittery effect from being over-caffeinated shares similarities with a panic attack — a shortness of breath, a vicious cycle of the fight or flight response, and anxiety can bring about a panic attack. Switch to decaffeinated coffee, which typically has less than 15 milligrams of caffeine, compared to an eight ounce cup of coffee that can have almost 100 milligrams.
  • Prescription drugs. Inform your doctor that you may be experiencing anxiety or panic attacks. Certain medications can inadvertently contribute to feelings of despair. Be cognizant of drugs that utilize a thyroid medicine, or medication used to manage asthmatic problems.
Being informed of the signs associated with a panic attack will allow you to control your anxiety. Active mindfulness and breathing exercises can help with panic attacks. Therapy, medication, and proper nutrition can help you manage your response to potential triggers.

About Jackie Edwards: After taking a career sabbatical to become a mother, Jackie now writes full time on topics ranging from health and wellness, right through to news and current affairs. She has in the past battled problems with anxiety and panic, and in her spare time she volunteers for a number of local charities that support people with mental health issues.


Should We Worry about Mercury in Fish Oil? - Life Extension Blog

Fish and fish oils, which are high in the omega-3 polyunsaturated fatty acids eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA), are among the super foods whose known benefits continue to expand over decades of research.

Studies have documented protection against chronic inflammation, cardiovascular disease, depression, age-related macular degeneration, attention deficit disorder, cognitive decline, arthritis, and much more in association with fish and/or fish oil intake.

The extent of the research documenting the benefits of fish is so impressive as to have led one gerontologist to quip that “We ought to put fish in the water.” The predicament is consumers are concerned about consuming [enough] fish because of the potential for mercury contamination.

Mercury is a naturally occurring element that has no known benefit in the human body.

The element, which is present in the air due to natural and manmade causes, becomes methylmercury in water.

Larger fish that are higher on the food chain concentrate more methylmercury in their bodies than small fish.

Some of these fish, including swordfish, tilefish, shark, king mackerel and, to a lesser extent, white albacore tuna, have high methylmercury levels and pregnant women are advised to avoid consuming them due to an associated risk of brain damage, vision and hearing problems in their infants.

At one time, pregnant women were advised to limit the intake of other fish as well, but this is no longer the case.

Risk vs. Benefit Analysis

In 2002, the American Heart Association issued a Scientific Statement recommending the intake of omega-3 from fish and plants to help protect the heart.1 While plants such as soy and flax contain the omega-3 fatty acid alpha linoleic acid (ALA), this fatty acid has not been associated with as many benefits as EPA and DHA, which are found in fish or the algae they consume.

A review published in 2006 in the Journal of the American Medical Association evaluated the effects of fish or fish oil on cardiovascular risk, methylmercury and fish oil's effect on early neurodevelopment, mercury's risks in adults, and the health impact of dioxins and polychlorinated biphenyls (PCBs) contained in fish. Authors Dariush Mozaffarian, MD, DrPH, and E. B. Rimm, ScD, concluded that “For major health outcomes among adults, based on both the strength of the evidence and the potential magnitudes of effect, the benefits of fish intake exceed the potential risks. For women of childbearing age, benefits of modest fish intake, excepting a few selected species, also outweigh risks.”2

In 2008, research reported in the American Journal of Clinical Nutrition, scientists at Harvard and the Statens Serum Institut in Cophenhagen concluded that mothers who consumed more fish during pregnancy and breastfeeding actually had children who experienced improved development in comparison with children whose mothers consumed less.3

Seven years later, the journal published a study of Seychelles Islanders, where the larger fish intakes result in methylmercury exposures that are ten times higher as compared to people in the U.S.4 "These findings show no overall association between prenatal exposure to mercury through fish consumption and neurodevelopmental outcomes," reported study coauthor Edwin van Wijngaarden, PhD, of the University of Rochester Department of Public Health Sciences. "It is also becoming increasingly clear that the benefits of fish consumption may outweigh, or even mask, any potentially adverse effects of mercury."

Interestingly, a study of rats exposed to methylmercury found that supplementation with fish oil  protected DNA from damage that normally results from mercury exposure.

The authors of the study suggest this benefit is due to fish oil’s ability to reduce inflammation.5

An investigation of five brands of fish oil conducted by researchers at Massachusetts General Hospital and Harvard Medical School found levels of mercury that ranged from negligible to nondetectable.6 Authors S. E. Foran and colleagues noted that the mercury content of fish oils was similar to that which normally occurs in human blood. They suggest that consuming fish oils may be safer than eating fish.

Recent advancements in fish oil production have made the likeliness of any significant presence of mercury even lower than indicated by studies such as these. An effort is made by fish oil suppliers to obtain fish from areas of the ocean that have low contaminant levels. High quality fish oil is distilled, extracted and redistilled which ensures removal of any potential contaminants and a higher concentration of EPA and DHA.

The Bottom Line

While it’s still a good idea to avoid eating swordfish, tilefish, shark and king mackerel, there’s no reason to be concerned about mercury in fish oil if purchased from a reliable supplier. Look for a fish oil that has a Five-Star International Fish Oil Standards (IFOS™) rating to ensure top quality and safety.


  1. Kris-Etherton PM et al. Circulation. 2002 Nov 19;106(21):2747-57.
  2. Mozaffarian D et al. JAMA. 2006 Oct 18;296(15):1885-99.
  3. Oken E et al. Am J Clin Nutr. 2008 Sep;88(3):789-96.
  4. Strain JJ et al. Am J Clin Nutr. 2015 Mar;101(3):530-7.
  5. Grotto D et al. Ecotoxicol Environ Saf. 2011 Mar;74(3):487-93.
  6. Foran SE et al. Arch Pathol Lab Med. 2003 Dec;127(12):1603-5.

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