BHT In My Cereal?

cereal-bagCan there be too much of a good thing? Drinking too much water can dilute the electrolytes in the body and short circuit the wiring.  It’s called water intoxication, and can lead to death.  Though eating too much candy might not cause a person to die, the resultant stomach distress might bring on the wish to expire early.  If there can be too much of a good thing, can there also be too little of a bad thing, meaning how much of a toxin can I consume before the symptoms show up or I keel over? Such is the case with some food additives. If enough people pronounce a falsehood as fact, does that make it true merely by the sheer number of proponents? Let’s talk about BHT and you decide whether it’s good or bad.

Butylated Hydroxytoluene is a horrendous sounding name.  Its presence lets us to keep a box of cereal in the cabinet for weeks at a time, and allows the product to withstand its protracted journey from maker to kitchen.  Its absence, on the other hand, yields a noxious aroma akin to a week-old dishrag that really needs a bath.  The culprit?  Rancid fats.  But what does BHT do to people?

BHT and its relative, BHA, have been used extensively as antioxidants for decades.  BHT was patented in 1947.  Since then it has become the most prevalent and approved antioxidant in the world.  The FDA, disbelieved by many consumers, approved BHT as an additive to foods and food packaging in 1954.  BHT is a phenol derivative that slows the rate of oxidation.  Oxygen prefers BHT to the fats in our foods.  The public gets upset when it learns that a material used to make non-foods appears in their victuals.  Yes, it is true that BHT is used in the manufacture of tires, some plastics and diesel fuel.   But it does what it is supposed to do without adverse effects.  It’s even been certified Kosher by the Union of Orthodox Jewish Congregations of America, and also certified Halal by the Islamic Food Nutrition Council of America.

Toxicology studies that added BHT to animal feed found that adverse effects were dose-dependent.  Amounts of BHT in excess of 526 mg/kg/day resulted in pleural and peritoneal hemorrhage in laboratory rats. (Takahashi.  1978) A human consumes in the neighborhood of 0.1 mg/kg/day of BHT.  Research shows that 500 times this amount yields no injurious effects.  (Branen.  1975)  This study added that 7 ounces of BHT per pound of body weight would result in pathological, enzyme, and lipid alterations that may be causative of certain cancers.  (Ibid.)

Some scientific research deals with topics and events that are way out there, seeming to have no bearing on real health issues.  (Gee, if I swallow a handful of number eight woodscrews and drink a cup of WD-40, will the screws still rust?)  There’s a similarly inane study in which lab animals were given more than four ounces of BHT per pound of body weight a day for three days, combined with a healthy dose of E.coli bacteria to learn of adverse effects on the liver.  What do you think happened?  The conclusion was that there is risk of liver damage with high-dose BHT in the presence of pathogenic bacteria.  (Engin. 2011)  This makes you wonder whose dime is in the phone booth.

The World Health Organization (WHO) asked its expert committee on food additives to evaluate the intake of BHT in ten participating countries in 1999.  After identifying certain foods as major contributors to overall intake, the committee agreed that 0.3 mg/kg of body weight a day is tolerable. (WHO, Geneva. 1999)  It is interesting to note that more BHT is allowable in the United States than in the other countries.  This might be explained by the fact that packaging materials are also treated with BHT, and that these plastics and waxed papers may carry as much as 7.8 mg/kg.  (Xiong. 2011)

That BHT has antioxidant properties was acknowledged by Korean researchers when they determined that, according to the National Health and Nutrition Survey, first conducted in 1971 and regularly afterward, one hundred thirty-three foods in twelve categories actually held significantly less BHT than the maximum limits. (Suh. 2005)  For most of these foods, less than 0.008 mg/kg was consumed.  Not to be outdone, Dutch scientists sought a connection between BHT intake and gastric cancers, studying a group of more than 120 thousand individuals, starting in 1986.  This longitudinal study examined BHT foods that included mayonnaise, cooking fats and oils, creamy salad dressings, and dried soups.  Via food frequency questionnaire, it was ascertained that the average intake of BHT was 351 micrograms a day total, not per pound or kilogram.  No association with gastric cancer was observed.  Oddly, an inverse association was found.  (Botterweck. 2000)

Around the time Christopher Columbus was floating in the Atlantic and Caribbean, a Swiss physician named Paracelsus, the first guy to call zinc, zinc, who is also known as the father of toxicology, was attributed with the dictum, “The dose makes the poison.”  His intended meaning was that a substance considered toxic may be harmless in small doses and that, conversely, an ordinarily harmless substance may be toxic in large doses—like water.  Such may be the case with BHT.

BHT was lauded as being protective against atherosclerosis in work performed in Sweden in the early 1990’s, where BHT was added to a 1% cholesterol diet in rabbits, whose digestive prowess parallels humans’.  Although lipid profiles were elevated, atherosclerotic involvement was considerably lower in the BHT rabbits than in those not receiving the substance in the same diet.  These investigators concluded that the antioxidant character of BHT prevented unwelcomed cardiac influences, although modulation of monocyte adhesion may be a factor.  (Björkhem. 1991)  Further study along this line, using a similar dietary protocol, discovered that LDL from other BHT-fed rabbits was less sensitive to oxidation than LDL from rabbits whose diets lacked BHT.
(Freyschuss. 2001)  It is accepted that oxidized LDL is the cause of ischemic heart disease.

What about cancer?  Pathologists at New York Medical College assessed BHT as a food additive in meta-analyses that inferred no cancer hazard at levels commonly used in food processing and manufacturing.  (Williams. 1999)  Laboratory animals that were purposely exposed to carcinogenic substances, notably aflatoxins that cause liver cancer, were spared from disease when administered BHT at doses of 1.5 mg/kg total over a period of twenty weeks (about 25 micrograms/kg, 3 x a week).  (Williams. 1986)  Other substances used to model liver carcinogenesis were almost completely neutralized in the presence of BHT, as reported in a study performed more than three decades ago.  (Ulland. 1973)

The dermatological use of BHT, as in cosmetics and other topically administered products, tells a somewhat different story in laboratory animals, since BHT is absorbed through the skin.  Stomach acid and digestive fluids appear to attenuate any pathogenic activity of the chemical.  Although the mechanism has not been completely explained, acute doses of BHT, as much as 1.0 g/kg, have caused some renal and hepatic damage in lab rats.  That is not to say that the same thing will happen to a human, since people are not likely to have exposure to such concentrated amounts.  (Lanigan. 2002)

For the time being, it looks like your cereal is off the hook.  There is one lingering question, though.  If natural vitamin E, as d-alpha-tocopherol, can do the same thing as BHT, why isn’t it being used?  It must be the money.

References

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    O. Takahashi, K. Hiraga
    Dose-response study of hemorrhagic death by dietary butylated hydroxytoluene (BHT) in male rats
    Toxicology and Applied Pharmacology.  Volume 43, Issue 2, February 1978, Pages 399-406

    A.L. Branen
    Toxicology and biochemistry of Butylated Hydroxyanisole and  Butylated Hydroxytoluene
    J Am Oil Chem Soc. 1975, Feb.; 52(2): 59-63

    Engin AB, Bukan N, Kurukahvecioglu O, Memis L, Engin A.
    Effect of butylated hydroxytoluene (E321) pretreatment versus l-arginine on liver injury after sub-lethal dose of endotoxin administration.
    Environ Toxicol Pharmacol. 2011 Nov;32(3):457-64. Epub 2011 Sep 10.

    WORLD HEALTH ORGANIZATION
    INTERNATIONAL PROGRAMME ON CHEMICAL SAFETY

    World Health Organization, Geneva, 1999
    IPCS - International Programme on Chemical Safety
    EVALUATION OF NATIONAL INTAKE ASSESSMENTS OF
     BUTYLATED HYDROXYTOLUENE (BHT)
    http://www.inchem.org/documents/jecfa/jecmono/v042je24.htm 
      Xiong Z, Wang L, Li N, Yu Y, Jia X
    Determination of antioxidant residues in polymer food package using gas chromatography.
    Se Pu. 2011 Mar;29(3):273-6.

    Suh HJ, Chung MS, Cho YH, Kim JW, Kim DH, Han KW, Kim CJ.
    Estimated daily intakes of butylated hydroxyanisole (BHA), butylated hydroxytoluene (BHT) and tert-butyl hydroquinone (TBHQ) antioxidants in Korea.
    Food Addit Contam. 2005 Dec;22(12):1176-88

    Botterweck AA, Verhagen H, Goldbohm RA, Kleinjans J, van den Brandt PA.
    Intake of butylated hydroxyanisole and butylated hydroxytoluene and stomach cancer risk: results from analyses in the Netherlands Cohort Study.
    Food Chem Toxicol. 2000 Jul;38(7):599-605.

    Björkhem I, Henriksson-Freyschuss A, Breuer O, Diczfalusy U, Berglund L, Henriksson P.
    The antioxidant butylated hydroxytoluene protects against atherosclerosis.
    Arterioscler Thromb. 1991 Jan-Feb;11(1):15-22.

    Freyschuss A, Al-Schurbaji A, Björkhem I, Babiker A, Diczfalusy U, Berglund L, Henriksson P.
    On the anti-atherogenic effect of the antioxidant BHT in cholesterol-fed rabbits: inverse relation between serum triglycerides and atheromatous lesions.
    Biochim Biophys Acta. 2001 Dec 30;1534(2-3):129-38.

    G.M Williams, M.J Iatropoulos, J Whysner
    Safety Assessment of Butylated Hydroxyanisole and Butylated Hydroxytoluene as Antioxidant Food Additives
    Food and Chemical Toxicology.  Vol 37, Iss 9-10, Sep-Oct 1999, Pages 1027-1038

    Williams GM, Tanaka T, Maeura Y.
    Dose-related inhibition of aflatoxin B1 induced hepatocarcinogenesis by the phenolic antioxidants, butylated hydroxyanisole and butylated hydroxytoluene.
    Carcinogenesis. 1986 Jul;7(7):1043-50.

    B.M. Ulland, J.H. Weisburger†, R.S. Yamamoto, Elizabeth K. Weisburger
    Antioxidants and carcinogenesis: butylated hydroxytoluene, but not diphenyl-p-phenylenediamine, inhibits cancer induction by N-2-fluorenylacetamide and by N-hydroxy-N-2-fluorenylacetamide in rats*
    Food and Cosmetics Toxicology.  Volume 11, Issue 2, 1973, Pages 199-207

    Lanigan RS, Yamarik TA.
    Int J Toxicol. 2002;21 Suppl 2:19-94.
    Final report on the safety assessment of BHT(1).

*These statements have not been evaluated by the FDA.
These products are not intended to treat, diagnose, cure, or prevent any disease.

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