Carrageenan Concerns go Mainstream,0,2164837.story

Doubts surface about safety of common food additive, carrageenan

March 18, 2013 - Chicago Tribune

March 18–Sara Baker says the light went on in her head after a cup of hot cocoa set off a storm in her stomach.

“I went back and looked at the package, and there it was: carrageenan,” said Baker, a career services coordinator from Bloomington, in central Illinois.

Baker had been taking medication for ulcerative colitis for years but still suffered debilitating digestive flare-ups without warning. She had read warnings about carrageenan in a natural health newsletter but didn’t take them seriously. After all, researchers haven’t conclusively linked the common food additive to gastrointestinal problems in humans.

This time, though, “it really clicked,” she said. “It took awhile to learn just how many things it’s in, but now that know, I can avoid it, and I no longer have the problems.”

Experiences like Baker’s have led some people with gastrointestinal problems to sidestep mainstream medical advice and avoid carrageenan, a seaweed-derived texturizer found in meat, dairy and other processed foods — including some organic products.

For scientists, however, these are just anecdotes. Though studies on lab animals and human cells have suggested that carrageenan can cause gastrointestinal inflammation, many researchers and physicians say it’s unclear whether the additive has the same impact on people who consume it.

Scientists at the University of Illinois at Chicago and University of Chicago are seeking to address that question with a controlled clinical trial that Baker is participating in.

“I believe it’s worth investigating and doing the science to find out,” said Dr. Stephen Hanauer, a medical professor and chief of gastroenterology and nutrition at University of Chicago Medicine.

His co-researcher, UIC physician and professor Joanne Tobacman, has been looking at the health effects of carrageenan for more than a decade and is concerned enough to have petitioned the U.S. Food and Drug Administration in 2008 to prohibit the use of carrageenan in food.

Her petition cited decades of publicly funded, peer-reviewed science — including her own — on carrageenan-induced inflammation in animals and cells. In June, the FDA responded with a letter of denial.

Tobacman said “it was disappointing that, with such clear evidence about the effects of carrageenan on inflammation, the FDA did not restrict the use of carrageenan, particularly in infant formula.” Europe doesn’t allow the ingredient in formula.

The additive, which lends a uniform, creamy texture to food, can be found in soy milk, yogurt, ice cream, cheeses, some meats, diet soft drinks and even toothpaste.

Michael Adams, deputy director of the FDA’s Office of Food Additive Safety, said the petition didn’t make a compelling case to re-examine the safety of carrageenan. “It has been reviewed repeatedly by FDA scientists and other international organizations, and in the judgment of those experts there hasn’t been a problem,” he said.

Adams called a rat study from 2006 “the gold standard for us because it exactly mimics the exposure consumers are going to get when they eat these carrageenan-containing foods.”

That study was funded and performed by a manufacturer of carrageenan. Adams said he didn’t know that but added: “If you look at the science and you believe it’s well done, it doesn’t matter where the money comes from.”

The Cornucopia Institute, a Wisconsin-based organic industry watchdog group, was expected to release a report Sunday night on carrageenan called “How a Natural Food Additive Is Making Us Sick.”

Charlotte Vallaeys, Cornucopia’s director of food policy, said the group felt “an ethical obligation” to raise awareness. “If government agencies weren’t going to protect consumers, then it seemed we needed to let consumers know about this so they could protect themselves.”

The institute also is challenging the FDA’s denial of Tobacman’s petition. Among other objections, Cornucopia’s letter to the agency asks why officials didn’t consider any studies on carrageenan published in the last four years.

Adams said the FDA’s scientific evaluation in response to the petition was finished in May 2009, after which it spent more than three years in what he calls the “administrative chain.”

Regarding infant formula, Adams said, Europe takes a different approach to food additives than the U.S., sometimes banning a substance when toxicity studies raise concerns but aren’t conclusive. “The Europeans do their business that way, but we don’t,” he said. “We would base it more on the science we have rather than waiting for science to be developed.”

While the Chicago researchers proceed with their work and advocates seek federal action, some consumers and activists have made an impact on their own by lobbying manufacturers directly to phase out the ingredient.

Last month Stonyfield joined a number of manufacturers who have removed or have pledged to remove carrageenan from their organic products. Organic Valley says it has removed the ingredient from most food items but is still working on reformulations for soy milk, chocolate milk and one version of its whipping cream.

A representative of the organic dairy company Horizon Organic and soy milk maker Silk (each majority-owned by Dean Foods) said both view carrageenan as safe and wouldn’t comment on any plans to remove it.

The U.S. National Organic Standards Board reapproved the use of carrageenan in most organic foods last year but decided to prohibit its use in organic infant formula.

Carrageenan manufacturers, the FDA, the United Nations food additives committee and some scientists say it is safe, as evidenced by centuries of use.

Marinalg International, a Brussels-based trade association representing producers of carrageenan, notes in an online statement that the U.N. additives committee has approved the use of carrageenan without a specific limit — with the exception of infant formula.

Among the studies the panel looked at, Marinalg said, was “a valuable, scientifically critical literature review” of carrageenan by Drs. Samuel Cohen and Nobuyuki Ito. The fact that Marinalg funded the 2002 report didn’t influence the “thorough and sound” review, according to Cohen, a physician and professor of medicine at the University of Nebraska.

James McKim, chief scientific officer at the toxicological research firm CeeTox Inc., said industry-funded science is not unusual and should be taken seriously. Marinalg recently hired McKim to review the last 30 years of carrageenan safety studies. His paper hasn’t been published yet, but he says it will affirm carrageenan’s safety.

The Tribune asked Marinalg and McKim if they were aware of any peer-reviewed scientific research that supported the safety of carrageenan but wasn’t performed by industry-funded scientists. They agreed to look but provided no examples after three weeks. The Tribune made a similar request to the FDA, which also provided no immediate examples.

In 2001, Tobacman published a scientific review in a National Institute of Health journal suggesting that consumption of carrageenan in lab animals was associated with “intestinal ulcerations” and tumors. She concluded that the “widespread use of carrageenan in the Western diet should be reconsidered.”

Beyond the acute reaction it triggers in some, Tobacman said in a recent email, carrageenan may also promote low levels of chronic internal inflammation, a factor linked to common chronic disorders such as diabetes, atherosclerosis and arthritis.

Still, many gastroenterologists are not convinced carrageenan is dangerous.

“There are some studies in rats and mice showing that carrageenan exposure can lead to GI inflammation that mimics things like Crohn’s” disease, said Dr. Sunanda Kane, a Mayo Clinic physician and medical adviser to the Crohn’s and Colitis Foundation of America. “But it’s never been shown on human tissue in humans walking around.”

Over the last 50 years, incidence of inflammatory bowel disease has risen as people eat more processed food, Kane said. “But is it carrageenan or that we don’t exercise or have lots of other additives and preservatives or fructose in our food supply?”

In Hanauer and Tobacman’s study, people whose ulcerative colitis is in remission are being put on a carrageenan-free diet, then given either a controlled dose of carrageenan or a placebo.

So far, the research has been hampered by low volunteer rates — currently, fewer than 20 subjects. Hanauer notes that the prospect of re-inflaming one’s inactive ulcerative colitis isn’t particularly attractive.

But Baker, who was one of more than 120 people who responded when Cornucopia asked to hear from those with carrageenan-related digestive problems, said she was willing to go through it to help establish human science on the topic.

“I believe there are people who are as sick as I was, or even worse, who need this information,” she said.



Hey, thanks for the article.Really thank you! Conway


I’m so glad you’re out there reading. And I hope it’s with an open mind, too. If so, I think I’ll risk telling you that there are many actual FOODS (as opposed to food additives) which aren’t optimal for human digestion and, yet, still have the potential to cause ill health effects similar to the ones incurred by the consumption of carrageenan. But you would likely have to have some knowledge of nutrition, biochemistry, and maybe even human evolution in order to really understand that beyond what you might read or happen to be told by your favorite government agency or authority dujour.

That the FDA considers carrageenan safe—all I can say is WOW! Then it must be. After all, their track record is exemplary! Aspartame, artificial colors, Olestra…No harm there. And it’s gotta be tough to get their approval. I explore this subject here: and here: Yet I wonder—do they ever “approve” of products before issuing a recall?

Fen-Phen—24 yrs on the market despite heart disease and other pulmonary problems.

DES—37 yrs on the market when in 1971 it was connected to a rare tumor that kept appearing in the daughters of women who had taken it. The FDA only banned DES prescriptions to women because no such problems have been found in men.

Baycol—4 yrs on the market is reportedly responsible for more than 100,000 deaths

Vioxx—5 yrs on the market and then found to be responsible for increased risk of heart attack and stroke.

Read more: The Ten Worst Drug Recalls In The History Of The FDA – 24/7 Wall St.

But back to Carrageenan—maybe some of the below reading from the FDA’s own website would interest you:

There it clearly states that “significant abnormalities appear to be induced in the anaphase figures of human embryoic lung cells in tissue culture at dosages that are slightly above average daily human intake. It is of further concern that parenterally administered carrageenan is reported to inhibit the activity of complement, excert cytotoxic effects on macrophases, suppress delayed hypersensitivity reactions in some tuberculin sensitive animals, activate factors causing procoagulant activity in human blood platelets, increase vascular permeabiltiy, and liberate kinin in vitro, all of which point to the possibility of the generation of toxic effects that could cause adverse responses followint the oral consumption of carrageenan if, during pregnancy or in the presence of infectious challenge or metabolic disorder, appropriate amounts of carrageenan should be absorbed from the gastrointestinal tract.”

And so my readers may read Dr. Tobacman’s position, you can find a 2012 letter along with attached studies here:

Or the following studies by others:

Pathol Biol (Paris). 1979 Dec;27(10):615-26.
[Biological and pharmacological effects of carrageenan (author’s transl)].
[Article in French]
Roch-Arveiller M, Giroud JP.
Carrageenan is sulfated polysaccharide which has been extensively used as emulsifier and thickening agent in the food industry, for its ability to induce acute inflammation in pharmacology and for its selectively toxic effect for macrophages in immunology. Carrageenan is a complex substance which displays various biological properties. The authors have shown the extent of these actions and reviewed the latest investigations on this subject.

J Allergy Clin Immunol. 1995 May;95(5 Pt 1):933-6.
Anaphylaxis to carrageenan: a pseudo-latex allergy.
Tarlo SM, Dolovich J, Listgarten C.
Toronto Hospital, Western Division, Ontario, Canada.
Anaphylactic reactions during a barium enema have been attributed to allergy to latex on the barium enema device. The observation of anaphylaxis during barium enema without latex exposure or latex allergy led to the performance of an allergy skin test to the barium enema solution.
Individual components of the barium enema solution were obtained for double-blind skin testing. A RAST to identify specific IgE antibodies to the skin test active agent was established.
Carrageenan, a component of the barium enema solution, produced positive reactions to allergy skin test and RAST. Gastrointestinal symptoms for which the patient was being investigated by the barium enema subsequently disappeared with a diet free of carrageenan.
Carrageenan is a previously unreported cause of anaphylaxis during barium enema. It is an allergen widely distributed in common foods and potentially could account for some symptoms related to milk products or baby formula.

Food Addit Contam. 1989 Oct-Dec;6(4):425-36.
Intestinal uptake and immunological effects of carrageenan–current concepts.
Nicklin S, Miller K.
Carrageenans are a group of high molecular weight sulphated polygalactans which find extensive use in the food industry as thickening, gelling and protein-suspending agents. Although there is no evidence to suggest that the persorption of small amounts of carrageenans across the intestinal barrier poses an acute toxic hazard, they are known to be biologically active in a number of physiological systems and extended oral administration in laboratory animals has been shown to modify both in vivo and in vitro immune competence. Whereas this effect could be attributed to carrageenan having a selective toxic effect on antigen-processing macrophages, additional studies suggest that macrophages can also influence immune responses by the timed release of immunoregulatory mediators. Evidence in support of this comes from in vitro studies which demonstrate that carrageenan-treated macrophages can, depending on conditions and time of administration, release either stimulatory or inhibitory factors. The former is known to be the immunostimulatory agent interleukin 1 (IL-1). The inhibitory factor, which is produced at an early stage following exposure to non-toxic doses of carrageenans, has yet to be formally identified but it is believed to be a prostaglandin because of its specific mode of action and short biological half-life. At present it is impossible to relate these studies to the human situation. Although it is established that carrageenans can cross the intestinal barrier of experimental animals, there is no evidence to suggest that the limited uptake that may occur in man in any way interferes with normal immune competence. Nevertheless, increased exposure may occur in the neonate during weaning, and adults and children following allergic reactions and episodes of gastrointestinal disease. Further studies under such conditions now seem warranted in order to elucidate the possible immunological consequences which may be associated with enhanced uptake of carrageenans in vulnerable groups.

Environ Health Perspect. 2001 October; 109(10): 983–994.
Review of harmful gastrointestinal effects of carrageenan in animal experiments.
J K Tobacman
In this article I review the association between exposure to carrageenan and the occurrence of colonic ulcerations and gastrointestinal neoplasms in animal models. Although the International Agency for Research on Cancer in 1982 identified sufficient evidence for the carcinogenicity of degraded carrageenan in animals to regard it as posing a carcinogenic risk to humans, carrageenan is still used widely as a thickener, stabilizer, and texturizer in a variety of processed foods prevalent in the Western diet. I reviewed experimental data pertaining to carrageenan’s effects with particular attention to the occurrence of ulcerations and neoplasms in association with exposure to carrageenan. In addition, I reviewed from established sources mechanisms for production of degraded carrageenan from undegraded or native carrageenan and data with regard to carrageenan intake. Review of these data demonstrated that exposure to undegraded as well as to degraded carrageenan was associated with the occurrence of intestinal ulcerations and neoplasms. This association may be attributed to contamination of undegraded carrageenan by components of low molecular weight, spontaneous metabolism of undegraded carrageenan by acid hydrolysis under conditions of normal digestion, or the interactions with intestinal bacteria. Although in 1972, the U.S. Food and Drug Administration considered restricting dietary carrageenan to an average molecular weight > 100,000, this resolution did not prevail, and no subsequent regulation has restricted use. Because of the acknowledged carcinogenic properties of degraded carrageenan in animal models and the cancer-promoting effects of undegraded carrageenan in experimental models, the widespread use of carrageenan in the Western diet should be reconsidered.

Food Chem Toxicol. 1990 Dec;28(12):807-11.
The effects of carrageenan on drug-metabolizing enzyme system activities in the guinea-pig.
Pintauro SJ, Gilbert SW.
Carrageenans are seaweed extracts comprising high molecular weight sulphated polygalactosides. They are used in foods at concentrations of up to 2.5% as thickening and gelling agents. When degraded to lower molecular weight forms, they have been shown to induce ulcerative colitis and colon cancer in laboratory animals. Furthermore, undegraded carrageenan (CG) has been shown to promote azoxymethane and methylnitrosourea initiated carcinogenesis, but the promotion mechanism is unclear. To determine if this mechanism involves alterations of tissue drug-metabolizing enzyme system (DMES) activities, six groups of five guinea-pigs each were administered 0.2% kappa undegraded, 0.2% i undegraded, 1% kappa degraded or 1% i degraded CG, or control solutions in the drinking-water for 8 wk. Microsomal and cytosolic DMES activities of the liver, small intestine and colon were determined. The kappa undegraded CG group exhibited significant (P less than 0.05) increases in small intestine cytochrome P-450 levels and benzo[a]pyrene hydroxylase activities. These data suggest that undegraded CG may selectively induce DMES activities in the small intestine mucosa.

J Pharm Pharmacol. 1989 Jun;41(6):423-6.
Rapid production of ulcerative disease of the colon in newly-weaned guinea-pigs by degraded carrageenan.
Marcus AJ, Marcus SN, Marcus R, Watt J.
In a dose-response study, degraded carrageenan (Eucheuma spinosum) was supplied in the drinking fluid at 1.2 and 3% concentrations over two weeks to young adult guinea-pigs. Ulceration of the large bowel was produced in 100% of animals, the severity and extent of damage probably being dose-related. In a time-course study, 3% degraded carrageenan solution supplied to newly-weaned guinea-pigs produced in 100% of animals ulceration in the caecum by four days and in the ascending colon by seven days. The onset of ulceration occurred as early as the second day. This model is convenient and economic for the screening of drugs of potential therapeutic value in human ulcerative colitis.

Gut. 1971 Feb;12(2):164-71.
Carrageenan-induced ulceration of the large intestine in the guinea pig.
Watt J, Marcus R.
A 5% aqueous solution of degraded carrageenan derived from the red seaweed Eucheuma spinosum was fed to guinea pigs in their drinking water over a period of 20-45 days. Occult blood in the faeces and multiple ulcers in the caecum, colon and rectum occurred in 100% of animals by the 30th day. The clinical and pathological features bear a close resemblance to human ulcerative colitis. The method provides a simple experimental model for the study of various aspects of the pathology of ulcerative lesions in the large intestine as well as the effects of therapeutic agents.

Int J Exp Pathol. 1992 Aug;73(4):515-26.
The pre-ulcerative phase of carrageenan-induced colonic ulceration in the guinea-pig.
Marcus SN, Marcus AJ, Marcus R, Ewen SW, Watt J.
The pre-ulcerative phase of carrageenan-induced colonic ulceration was investigated in guinea-pigs supplied 3% degraded carrageenan as an aqueous solution as drinking fluid for 2 or 3 days during which no ulceration of the bowel was observed with the naked eye or dissecting microscope. Mucosal microscopic changes, from caecum to rectum, were multifocal and included cellular infiltrates, dilatation of glands, crypt abscesses, micro-ulcers and sulphated polysaccharide in the lamina propria. Sulphated polysaccharide was also demonstrated histologically for the first time within the surface epithelium and showed ultrastructural features similar to carrageenan. The results indicate that colonic epithelium in the guinea-pig is capable of macromolecular absorption. Carrageenan, a highly active polyanionic electrolyte, within the surface epithelial cells is most likely a primary factor in the breakdown of mucosal integrity. Macromolecular absorption causing enteropathy of the large bowel is a new pathophysiological concept which may have implications in man, particularly in the pathology of large bowel disease.

Methods Achiev Exp Pathol. 1975;7:56-71.
Experimental ulcerative disease of the colon.
Watt J, Marcus R.
The oral administration to guinea-pigs of an aqueous solution of carrageenan derived from the red seaweed, Eucheuma spinosum, provides a useful, readily available experimental model for the study of ulcerative disease of the colon. Two types of ulcerative disease can be produced within a 4-6 week period, viz., ulceration localised mainly to the caecum by using 1% undegraded carrageenan in the drinking fluid, and extensive ulceration involving caecum, colon, and rectum by using 5% degraded carrageenan. Ulceration is probably due to the local action of carrageenan in the bowel.

J Natl Cancer Inst. 1977 Apr;58(4):1171-2.
Promotion of incidence of adenovirus type 12 transplantable tumors by carrageenan, a specific antimacrophage agent.
Lotzová E, Richie ER.
Carrageenan, a sulfated polygalactose with known macrophage-toxic properties, was used to ascertain the role of macrophages in resistance to adenovirus type 12 transplantable tumors. A single ip injection of 5 or 10 mg carrageenan led to increased incidence and more rapid growth of tumors in C3H mice. Carrageenan was most effective if given 1 day before tumor inoculation; the effectiveness decreased with increasing intervals before or after tumor cell injection. The macrophage stabilizer poly-2-vinylpyridine N-oxide injected sc (150 mg/kg) 1 day before carrageenan was given reduced the incidence of tumors. These data lend further support to the importance of macrophages in tumor immunity.

Biomedicine. 1975 Sep;22(5):387-92.
Involvement of macrophages in genetic resistance to bone marrow grafts. Studies with two specific antimacrophage agents, carrageenan and silica.
Lotzova E, Gallagher MT, Trentin JJ.
Carrageenans and silica, agents toxic for macrophages, were used in this study to examine the role of macrophages in resistance of irradiated mice to inbred parental and rat bone marrow grafts. Administration of 2.5 mg of carrageenans or 2.5-5 mg of silica particles intravenously to prospective graft recipients resulted in a prompt abrogation of hybrid and xenogeneic resistance. The macrophage stabilizer poly-2-vinylpyridine N-oxide (PVNO) injected subcutaneously in the dose of 150 mg/kg, 24 hr before silica prevented or reduced the suppression of resistance. PVNO, however, did not antagonize the suppression of resistance by carrageenen, horse anti-mouse thymocyte serum and cyclophosphamide. These results suggest that a) a subpopulation is involved in marrow graft rejection by irradiated mice; b) carrageenan and silica apparently act on macrophages by different mechanisms c) horse anti-mouse thymocyte serum and cyclophosphamide may act on cells other than macrophages or they act on macrophages by a different mechanism than silica, to resistance to bone marrow transplantation.

Agents Actions. 1981 May;11(3):265-73.
Carrageenan: a review of its effects on the immune system.
Thomson AW, Fowler EF.
Carrageenans (kappa, lambda and iota) are sulphated polysaccharides isolated from marine algae that can markedly suppress immune responses both in vivo and in vitro. Impairment of complement activity and humoral responses to T-dependent antigens, depression of cell-mediated immunity, prolongation of graft survival and potentiation of tumour growth by carrageenans have been reported. The mechanism responsible for carrageenan-induced immune suppression is believed to be its selective cytopathic effect on macrophages. This property of carrageenan has led to its adoption as a tool for analysing the role of these cells in the induction and expression of immune reactivity. Systemic administration of carrageenan may, however, induce disseminated intravascular coagulation and inflict damage on both the liver and kidney. This is an important consideration in the interpretation of the effects of carrageenan in vivo and precludes its use as a clinical immune suppressant.

Biomedicine. 1978 May-Jun;28(3):148-52.
Carrageenan and the immune response.
Thomson AW.
Since the biological effects of carrageenan were reviewed in 1972 by Di Rosa it has become clear from a large number of reports that this algal polysaccharide markedly influences immune responses. Profound suppression of immunity evidenced by impaired antibody production, graft rejection, delayed hypersensitivity and anti-tumour immunity, has been observed in carrageenan-treated animals and the immunodepressive ability of carrageenan confirmed by in vitro studies. Efforts at analysis of carrageenan-induced immune suppression have focussed on the selective cytotoxic effect of this agent on mononuclear phagocytes. Faith in the ability of carrageenan to eliminate those cells has led to its use in examination of the role played by mononuclear phagocytes in various aspects of immune reactivity. This review documents and discusses the effects of carrageenan on immune responses and assesses the value of carrageenan as a useful tool in both current and future work aimed at broadening our knowledge of mechanisms underlying immune reactions.

Biomedicine. 1976 May;24(2):102-6.
Evaluation of carrageenan as an immunosuppressive agent and mediator of intravascular coagulation.
Thomson AW, Wilson AR, Cruickshank WJ, Horne CH.
Carrageenan suppressed antibody responses to SRBC in mice and rats, measured in terms of splenic IgM PFC production. The effect, in mice, was dependent on dose and on the temporal relationship between treatment and antigen administration. Carrageenan was found to alter the time course of the PFC response and also to produce disseminated intravascular coagulation. Some correlation between the observed effects and the use of chemically distinct carrageenans was found. The possible mode of actio2n of carrageenan is discussed in the light of these, and other findings.

J Pathol. 1980 Sep;132(1):63-79.
Histological and ultrastructural changes following carrageenan injection in the mouse.
Fowler EF, Simpson JG, Thomson AW.
Mice were injected intravenously with either uncharacterised potassium carrageenan or purified iota carrageenan and tissue was examined by light and electron microscopy 1 hr and 24 hr later. The survival of animals injected with these carrageenans was monitored over a 6-month period. Histological examination of liver and kidney was carried out on animals which died during this time and in the surviving mice at 28 weeks. Histological and ultrastructural evidence of disseminated intravascular coagulation was observed within 24 hr of carrageenan injection. The changes were more severe in animals given potassium carrageenan. Electro-microscopic examination of liver revealed carrageenan within membrane-bound vacuoles in Küpffer cells. These cells were largely unaffected by phagocytosis of iota carrageenan but uptake of potassium carrageenan resulted in marked ultrastructural changes and occasional damage to adjacent hepatocytes. Mice given potassium carrageenan had the poorer long-term survival and many animals in this group showed chronic renal damage with features which suggested obstructive nephropathy. A smaller proportion of mice injected with iota carrageenan displayed similar changes. There was no evidence of long-term hepatotoxicity in either group although both types of carrageenan persisted within liver macrophages for at least 6 months after injection.

Am J Pathol. 1971 Aug;64(2):387-404.
Spectrum and possible mechanism of carrageenan cytotoxicity.
Catanzaro PJ, Schwartz HJ, Graham RC Jr.
Carrageenan, a sulfated polygalactose which suppresses established delayed hypersensitivity in vivo, is shown to be cytotoxic to macrophages but not to lymphocytes in vitro. This cytotoxicity depends on the carrageenan concentration and degree of lysosomal differentiation but is independent of serum. Survival of macrophages in the presence of carrageenan can be enhanced temporarily by corticosteroids. Ultrastructural studies reveal that carrageenan is readily taken up by macrophages and stored in lysosomes, which subsequently swell and rupture, apparently resulting in cell death. The presence of corticosteroids temporarily retards lysosome swelling. It is suggested that carrageenan may exert its cytotoxic effect by causing osmotic rupture of lysosomes. The possible immunologic significance of these findings is discussed.

Cancer Lett. 1978 Mar;4(3):171-6.
Induction by degraded carrageenan of colorectal tumors in rats.
Ashi KW, Inagaki T, Fujimoto Y, Fukuda Y.
Degraded carrageenan derived from the red seaweed Eucheuma spinosum was given to Sprague—Dawley rats through the diet, in drinking water or by stomach tube for up to 24 months. Carrageenan-induced squamous cell carcinomas, adenocarcinomas and adenomas in the colorectum were observed. Some rats had metastases to the regional lymph nodes of squamous cell carcinomas. These results show that degraded carrageenan is carcinogenic to the colorectum of the rat.

Toxicol Lett. 1981 Jun-Jul;8(4-5):207-12.
Effect of degraded carrageenan on the intestine in germfree rats.
Hirono I, Sumi Y, Kuhara K, Miyakawa M.
The role of intestinal bacterial flora in display of the effect of degraded carrageenan was investigated by feeding 9 germfree and 12 conventional female Wistar rats on diet containing 10% carrageenan for 63 days. Animals were sacrificed 7, 20, 35, and 63 days after the start of feeding and histological changes induced by carrageenan were studied. The germfree rats showed mucosal lesions, such as macrophage aggregates, erosion, and squamous metaplasia of the large intestine, and these lesions were more extensive than those in the conventional rats. Therefore, it was concluded that bacterial flora are not essential for display of the biological effects of degraded carrageenan.

Food Chem Toxicol. 1987 Feb;25(2):113-8.
Intestinal permeability changes in rodents: a possible mechanism for degraded carrageenan-induced colitis.
Delahunty T, Recher L, Hollander D.
Rats and guinea-pigs were treated with degraded carrageenan (50 g/litre in the drinking-water) and their intestinal permeability was studied at weekly intervals over the last 4 wk of the test period by determining the recovery of orally administered tracer doses of [3H]polyethylene glycol (PEG-900) or D-[3H]mannitol in 16-hr urine collections. A freely diffusible dye, Azure A, was administered simultaneously to compensate for non-intestinal factors that could modify renal excretion. Animals were killed after a total treatment period of 5 months for rats and 6 wk for guinea-pigs. After 3 wk of carrageenan treatment, excretion of PEG-900 (expressed as a ratio of the Azure A excretion) in guinea-pigs showed a statistically significant increase over that in the control group. At autopsy, the caeca showed numerous macroscopically visible erosions of the entire mucosal surface and histological examination showed ulcerations largely in the mucosa with abscesses in the crypts. Although no such histological changes were seen in the intestines of the treated rats, even after 5 months, a statistically significant increase in PEG-900 excretion was again found compared with the control group. This increase did not occur when deoxycholate was administered with the carrageenan solution. No effect of carrageenan treatment on mucosal permeability to D-[3H]mannitol was demonstrated in either species. The results suggest that degraded carrageenan-induced colitis could be a result of increased intestinal permeability, since ingestion of this polysaccharide by rats increased PEG-900 absorption without causing mucosal damage.

Cancer Detect Prev. 1981;4(1-4):129-34.
Harmful effects of carrageenan fed to animals.
Watt J, Marcus R.
An increased number of reports have appeared in the literature describing the harmful effects of degraded and undegraded carrageenan supplied to several animal species in their diet or drinking fluid. The harmful effects include foetal toxicity, teratogenicity, birth defects, pulmonary lesions, hepatomegaly, prolonged storage in Kupffer cells, ulcerative disease of the large bowel with hyperplastic, metaplastic, and polypoidal mucosal changes, enhancement of neoplasia by carcinogens, and, more ominously, colorectal carcinoma. Degraded carrageenan as a drug or food additive has been restricted in the United States by the FDA, but undegraded carrageenan is still widely used throughout the world as a food additive. Its harmful effects in animals are almost certainly associated with its degradation during passage through the gastrointestinal tract. There is a need for extreme caution in the use of carrageenan or carrageenan-like products as food additives in our diet, and particularly in slimming recipes.

Food and Cosmetics Toxicology
Volume 14, Issue 2, 1976, Pages 85-93
Carrageenan: The effect of molecular weight and polymer type on its uptake, excretion and degradation in animals
K.A. Pittmana, L. Golberga, F. Coulstona
A variety of τ-, κ- and λ-carrageenans was given to guinea-pigs, monkeys and rats, either in the drinking-water, by gavage or in the diet. Faecal and liver samples were examined qualitatively by gel electrophoresis, to determine any changes in the apparent molecular weight of carrageenans after administration. Quantitative measurements of carrageenans were carried out on samples of liver and urine. That there was little or no absorption of carrageenans of high molecular weight was evidenced by the absence of carrageenan from the livers of guinea-pigs or rats or from the urine of guinea-pigs or monkeys. By contrast, substantial amounts of carrageenan were found in the livers of guinea-pigs and rats given low-molecular-weight carrageenans (Mn ⩽ 40,000). Intermediate amounts of carrageenan were found in livers of animals given carrageenans ranging in Mn between 40,000 and 150,000. Urinary excretion of carrageenan was limited to low-molecular-weight material (Mn ⩽ 20.000). Qualitative and quantitative evidence indicated that there was an upper limit to the size of carrageenan molecules absorbed, but estimates of this upper limit ranged from 10,000 to 85.000 depending upon the analytical approach. Absorption of carrageenan from the drinking-water may differ qualitatively from absorption from the diet. Analysis of faecal samples by gel electrophoresis showed that degradation of high-molecular-weight carrageenan had occurred, either in the gut or in the faeces.

Cancer Letters
Volume 14, Issue 3, December 1981, Pages 267-272
A study on carcinogenesis induced by degraded carrageenan arising from squamous metaplasia of the rat colorectum
Yasuyuki Oohashi, Tomonori Ishioka, Kazuo Wakabayashi, Noriyuki Kuwabara
We have undertaken studies on carcinogenesis arising from precancerous lesions, such as squamous metaplasia and ulcerative lesions of the rat colorectum, after termination of degraded carrageenan administration. Rates of tumor incidence in groups that were given a 10% diet of degraded carrageenan for 2, 6 and 9 months were 5 rats out of 39 (12.8%), 8 out of 42 (19.0%) and 17 out of 42 (40.5%), respectively. The colorectal squamous metaplasia persisted in all rats and progressed irreversibly. Degraded carrageenan was deposited not only in the colorectal propria mucosa, but also in the other reticuloendothelial organs. These results show that, even with short-term degraded carrageenan administration, degraded carrageenan is carcinogenic to the colorectum of the rat after a prolonged period.

Cancer Res. 1997 Jul 15;57(14):2823-6.
Filament disassembly and loss of mammary myoepithelial cells after exposure to lambda-carrageenan.
Tobacman JK.
Carrageenans are naturally occurring sulfated polysaccharides, widely used in commercial food preparation to improve the texture of processed foods. Because of their ubiquity in the diet and their observed preneoplastic effects in intestinal cells, their impact on human mammary myoepithelial cells in tissue culture was studied. At concentrations as low as 0.00014%, lambda-carrageenan was associated with disassembly of filaments with reduced immunostaining for vimentin, alpha-smooth muscle-specific actin, and gelsolin; increased staining for cytokeratin 14; and cell death. The absence of mammary myoepithelial cells is associated with invasive mammary malignancy; hence, the destruction of these cells in tissue culture by a low concentration of a widely used food additive suggests a dietary mechanism for mammary carcinogenesis not considered previously.

Acta Pathol Microbiol Scand A. 1980 May;88(3):135-41.
Stereomicroscopic and histologic changes in the colon of guinea pigs fed degraded carrageenan.
Olsen PS, Poulsen SS.
A colitis-like state induced in Guinea Pigs fed degraded carrageenan orally. By means of a combined semimacroscopic and histologic technique the course of the disease was followed during 28 days. The changes were primarily seen and became most prominent in the caecum. The first lesions were observed following 24 hours of treatment as small rounded foci initially with degenerative changes and inflammation in the surface epithelium, later forming superficial focal ulcerations. Ulcerative changes gradually progressed during the experiment, forming linear and later large, geographical ulcerations. Topographically the ulcerative process was strongly related to the larger submucosal vessels. Nonulcerated parts of the mucosa were not changed until following 7-14 days of treatment. The mucosa became bulging, granulated and finally villus-like. Accumulation of macrophages was found under the surface epithelium after 7-17 days. Possible pathogenetic mechanisms are discussed, especially the development of the early lesions and the significance of the macrotphages.

Teratology. 1981 Apr;23(2):273-8.
Teratogenic effect of lambda-carrageenan on the chick embryo.
Monis B, Rovasio RA.
Carrageenans are widely used as food additives. Thus, it seemed of interest to test their possible teratogenic action. For this purpose, 530 chick eggs were injected in the yolk sac with 0.1 ml of a solution of 0.1% lambda-carrageenan in 0.9% sodium chloride. As controls, 286 eggs were injected with 0.1 ml of 9.0% sodium chloride. In addition, 284 eggs received no treatment. After incubation for 48–50 hours at 39 degrees C, embryos were fixed, cleared, and observed with a stereoscopic microscope. The frequency of abnormal embryos in the group receiving lambda-carrageenan was higher than in the controls (p less than 0.04). Partial duplication of the body, abnormal flexures of the trunk, anencephaly, a severely malformed brain, thickening of the neural tube wall, an irregular neural tube lumen with segmentary occlusion and a reduction in crown-rump length and number of somites were distinctly seen in the lambda-carrageenan-injected group. Moreover, the average number of anomalies per embryo in the lambda-carrageenan-injected group was nearly twice that in the controls. Present data indicate that lambda-carrageenan has teratogenic effects on early stages of the development of the chick embryo.

Let me know if I can provide more reading material for you, Debbie. In the meantime, I would strongly urge you to stop listening to your government while ignoring what your body is trying to tell you. Paying attention here just may save your health.



Q. What is Carrageenan??

A. Carrageenan is a naturally-occurring seaweed extract. It is widely used in foods and non-foods to improve texture and stability. Common uses include meat and poultry, dairy products, canned pet food, cosmetics and toothpaste.
Q. Why the controversy?
A. Self-appointed consumer watchdogs have produced numerous web pages filled with words condemning carrageenan as an unsafe food additive for human consumption. However, in 70+ years of carrageenan being used in processed foods, not a single substantiated claim of an acute or chronic disease has been reported as arising from carrageenan consumption. On a more science-based footing, food regulatory agencies in the US, the EU, and in the UN’s Food and Agriculture Organization/World Health Organization (FAO/WHO) repeatedly review and continue to approve carrageenan as a safe food additive.
Q. What has led up to this misrepresentation of the safety of an important food stabilizer, gelling agent and thickener?
A. It clearly has to be attributed to the research of Dr. Joanne Tobacman, an Associate Prof at the University of Illinois in Chicago. She and a group of molecular biologists have accused carrageenan of being a potential inflammatory agent as a conclusion from laboratory experiments with cells of the digestive tract. It requires a lot of unproven assumptions to even suggest that consumption of carrageenan in the human diet causes inflammatory diseases of the digestive tract. The objectivity of the Chicago research is also flawed by the fact that Dr Tobacman has tried to have carrageenan declared an unsafe food additive on weak technical arguments that she broadcast widely a decade before the University of Chicago research began.

Q. What brings poligeenan into a discussion of carrageenan?
A. Poligeenan (“degraded carrageenan” in pre-1988 scientific and regulatory publications) is a possible carcinogen to humans; carrageenan is not. The only relationship between carrageenan and poligeenan is that the former is the starting material to make the latter. Poligeenan is not a component of carrageenan and cannot be produced in the digestive tract from carrageenan-containing foods.
Q. What are the differences between poligeenan and carrageenan?
A. The production process for poligeenan requires treating carrageenan with strong acid at high temp (about that of boiling water) for 6 hours or more. These severe processing conditions convert the long chains of carrageenan to much shorter ones: ten to one hundred times shorter. In scientific terms the molecular weight of poligeenan is 10,000 to 20,000; whereas that of carrageenan is 200,000 to 800,000. Concern has been raised about the amount of material in carrageenan with molecular weight less than 50,000. The actual amount (well under 1%) cannot even be detected accurately with current technology. Certainly it presents no threat to human health.
Q. What is the importance of these molecular weight differences?
A. Poligeenan contains a fraction of material low enough in molecular weight that it can penetrate the walls of the digestive tract and enter the blood stream. The molecular weight of carrageenan is high enough that this penetration is impossible. Animal feeding studies starting in the 1960s have demonstrated that once the low molecular weight fraction of poligeenan enters the blood stream in large enough amounts, pre-cancerous lesions begin to form. These lesions are not observed in animals fed with a food containing carrageenan.

Q. Does carrageenan get absorbed in the digestive track?
A. Carrageenan passes through the digestive system intact, much like food fiber. In fact, carrageenan is a combination of soluble and insoluble nutritional fiber, though its use level in foods is so low as not to be a significant source of fiber in the diet.
Carrageenan has been proven completely safe for consumption. Poligeenan is not a component of carrageenan.
Closing Remarks
The consumer watchdogs with their blogs and websites would do far more service to consumers by researching their sources and present only what can be substantiated by good science. Unfortunately we are in an era of media frenzy that rewards controversy.
Additional information available:
On June 11th, 2008, Dr. Joanne Tobacman petitioned the FDA to revoke the current regulations permitting use of carrageenan as a food additive.
On June 11th, 2012 the FDA denied her petition, categorically addressing and ultimately dismissing all of her claims; their rebuttal supported by the results of several in-depth, scientific studies.
If you would like to read the full petition and FDA response, they can be accessed at!searchResults;rpp=25;po=0;s=FDA-2008-P-0347

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