What's in our food packaging?

By NICHOLAS D. KRISTOF
Published: November 7, 2009 New York Times

Your body is probably home to a chemical called bisphenol A, or BPA. It’s a synthetic estrogen that United States factories now use in everything from plastics to epoxies — to the tune of six pounds per American per year. That’s a lot of estrogen. More than 92 percent of Americans have BPA in their urine, and scientists have linked it — though not conclusively — to everything from breast cancer to obesity, from attention deficit disorder to genital abnormalities in boys and girls alike.

Now it turns out it’s in our food.

Consumer Reports magazine tested an array of brand-name canned foods for a report in its December issue and found BPA in almost all of them. The magazine says that relatively high levels turned up, for example, in Progresso vegetable soup, Campbell’s condensed chicken noodle soup, and Del Monte Blue Lake cut green beans.


The magazine also says it found BPA in the canned liquid version of Similac Advance infant formula (but not in the powdered version) and in canned Nestlé Juicy Juice (but not in the juice boxes). The BPA in the food probably came from an interior coating used in many cans.

Should we be alarmed?

The chemical industry doesn’t think so. Steven Hentges of the American Chemistry Council dismissed the testing, noting that Americans absorb quantities of BPA at levels that government regulators have found to be safe. Mr. Hentges also pointed to a new study indicating that BPA exposure did not cause abnormalities in the reproductive health of rats.

But more than 200 other studies have shown links between low doses of BPA and adverse health effects, according to the Breast Cancer Fund, which is trying to ban the chemical from food and beverage containers.

“The vast majority of independent scientists — those not working for industry — are concerned about early-life low-dose exposures to BPA,” said Janet Gray, a Vassar College professor who is science adviser to the Breast Cancer Fund.

Published journal articles have found that BPA given to pregnant rats or mice can cause malformed genitals in their offspring, as well as reduced sperm count among males. For example, a European journal found that male mice exposed to BPA were less likely to make females pregnant, and the Journal of Occupational Health found that male rats administered BPA had less sperm production and lower testicular weight.

This year, the journal Environmental Health Perspectives found that pregnant mice exposed to BPA had babies with abnormalities in the cervix, uterus and vagina. Reproductive Toxicology found that even low-level exposure to BPA led to the mouse equivalent of early puberty for females. And an array of animal studies link prenatal BPA exposure to breast cancer and prostate cancer.

While most of the studies are on animals, the Journal of the American Medical Association reported last year that humans with higher levels of BPA in their blood have “an increased prevalence of cardiovascular disease, diabetes and liver-enzyme abnormalities.” Another published study found that women with higher levels of BPA in their blood had more miscarriages.

Scholars have noted some increasing reports of boys born with malformed genitals, girls who begin puberty at age 6 or 8 or even earlier, breast cancer in women and men alike, and declining sperm counts among men. The Endocrine Society, an association of endocrinologists, warned this year that these kinds of abnormalities may be a consequence of the rise of endocrine-disrupting chemicals, and it specifically called on regulators to re-evaluate BPA.

Last year, Canada became the first country to conclude that BPA can be hazardous to humans, and Massachusetts issued a public health advisory in August warning against any exposure to BPA by pregnant or breast-feeding women or by children under the age of 2.

The Food and Drug Administration, which in the past has relied largely on industry studies — and has generally been asleep at the wheel — is studying the issue again. Bills are also pending in Congress to ban BPA from food and beverage containers.

“When you have 92 percent of the American population exposed to a chemical, this is not one where you want to be wrong,” said Dr. Ted Schettler of the Science and Environmental Health Network. “Are we going to quibble over individual rodent studies, or are we going to act?”

While the evidence isn’t conclusive, it justifies precautions. In my family, we’re cutting down on the use of those plastic containers that contain BPA to store or microwave food, and I’m drinking water out of a metal bottle now. In my reporting around the world, I’ve come to terms with the threats from warlords, bandits and tarantulas. But endocrine disrupting chemicals — they give me the willies.

XMRV video helps explain the research....

XMRV VIDEO!

CFS /CFIDS/ ME link to XMRV - Retrovirus Similar to HIV, HTLV and Leukaemia Viruses

OVERTAKING CHRONIC FATIGUE: An electron micrograph 

shows the XMRV retrovrius in the blood of a patient with chronic fatigue syndrome.

WHITTENMORE PETERSON INSTITUTE.

From the website of M.E. Research UK, October 2009:

XMRV and ME/CFS — A stunning find

The discovery of a potential retroviral link to ME/CFS, which is estimated to affect some 17 million people worldwide, has certainly caught the world’s attention — no bad thing for an under-researched and often-overlooked illness! The scientific report, entitled “Detection of infectious retrovirus, XMRV, in the blood cells of CFS patients”, appeared online in Science, one of the most prestigious scientific journals in the world, on 8th October 2009 and described the findings of a consortium of researchers from the Whittemore Peterson Institute (WPI, located at the University of Nevada, Reno), the National Cancer Institute (part of the National Institutes of Health) and the Cleveland Clinic, Ohio.

ME Research UK welcomes good-quality outline applications from Research Units anywhere in the world for funding to replicate and/or extend the work on the possible links between XMRV and ME/CFS. Applications will be processed rapidly, and the peer-review process expedited, for such applications.

The findings

The headline finding of the research paper was that DNA from a human gammaretrovirus, xenotropic murine leukemia virus-related virus (XMRV), could be detected in the peripheral blood mononuclear cells of 68 out of 101 ME/CFS patients (67%) compared with only 8 out of 218 healthy controls (3.7%). The extent of this difference in proportions is unusual, as it is the norm for scientific researchers to find relatively small yet significant differences between patients and closely matched control groups; in the modern world, novel associations of such magnitude are rarely found between long-standing chronic illnesses and infectious agents. In addition to the headline finding, the researchers determined that XMRV proteins were being expressed in blood cells from ME/CFS patients at very high levels compared with controls, and through cell culture experiments they showed that patient-derived XMRV was infectious and transmissible. So, as well as being the first to show infection with this novel virus in ME/CFSpatients, the researchers appear to have been the first to be able to isolate XMRV particles from the blood, and to show direct transmission of this virus between blood cells — dramatic observations indeed.

What has caught the attention of the scientific world is that these observations seem to fit neatly, at least at a first glance, with what is already known about ME/CFS as a chronic illness. For example, viruses related to XMRV have been reported to be involved in damage to blood vessels and nerves, and natural killer cells (historically low in ME/CFS) are said to be susceptible to infection by XMRV. Also, the fact that retroviruses like XMRV are known to be able to activate some other (latent) viruses might explain why ME/CFS has been associated with a range of different viral triggers, such as herpesviruses like Epstein-Barr, over the years. Again, as Dr Judy Mikovits and colleagues point out in their paper, some of the most commonly reported features of ME/CFS include neurological symptoms and immune dysfunction with inflammatory cytokine and chemokine upregulation, and some of these observations could be accounted for by infectious XMRV in lymphocytes. The fact that such pieces seem to fit so well together is suggestive only at this stage, however, and a virologist at Tufts University was surely wise to say in New Scientist that while it’s not impossible that infection with this agent might cause a disease with neurological and immunological consequences, we don’t know for sure as yet.

The background

The scientific journey towards this discovery is an extremely interesting one, and includes several strands: prostate cancer, the RNAse L immune pathway, the discovery of the novel virus XMRV, and ME/CFS. XMRV is a human retrovirus similar to HIV, HTLV-1 and a group of endogenous murine leukaemia viruses found in the genomes of wild mice (see  the informative presentation on retroviruses by Dr Jones of SAIC-Frederick/NCI-Frederick), and was first identified only in 2006 by Prof. Robert H. Silverman of the Cleveland Clinic, a co-author on the 2009 ME/CFS study. Prof. Silverman initially showed the presence of XMRV in prostate cancer tissue samples (PLoS Pathog, 2006), and subsequent work has confirmed XMRV protein expression in 23% of 334 prostate cancer biopsies (Proc Natl Acad Sci USA, 2009). Importantly, the men with prostate cancer initially studied by Prof. Silverman all had a specific genetic defect in their antiviral defences, the RNase L antiviral pathway which Prof. Silverman had been studying for 30 years, a lifetime’s work of scientific progression described in his fascinating essay, “Journey through the 2-5A/RNase L System”.

RNase L is the terminal enzyme in the 2,5A synthetase/RNase L antiviral pathway, and plays an essential role in the elimination of viral mRNAs. The enzyme has been the focus of research interest in ME/CFS patients for nearly 20 years, and deregulation of this pathway in subsets of ME/CFS patients has been reported extensively in the scientific literature (reviewed by Nijs and Fremont, 2008). In ME/CFS, a wide spectrum of “cleavage” of RNase L can be observed (a phenomenon also seen in multiple sclerosis patients), and such altered RNase L activity profoundly affects cellular physiology, including apoptosis. Overall, an upregulated RNase L pathway in ME/CFS is consistent with an activated immune state and a role for persistent viral infection in the pathogenesis of the disorder — and it is because of these and other findings that many researchers have come to view ME/CFS as primarily a disorder of the innate immune system (see Klimas and Kineru, 2008). It was thanks to the insight of Dr Judy Mikovits and her team at WPI that the potential connection between RNase L dysfunction inXMRV-infected prostrate cancer and in ME/CFS was recognised, and an exploration undertaken to test for the presence of the virus in the banked blood samples in the WPI tissue repository, the largest ME/CFS sample repository in the world.

What we don’t know

A plethora of unanswered questions arise from this discovery. Chief among these concerns cause and effect: the researchers’ work has shown a suggestive, significant association between the presence of XMRV and a diagnosis of ME/CFS, but this is far from proof that the virus has a direct or even indirect role in the development or maintenance of the illness. This and other points have been well-put in a fine “perspective” in Science by National Academy of Sciences member and expert retrovirologist, Prof. John Coffin, and colleague Jonathan Stoye, who say, “There is still much that we do not understand. Whether the virus plays a causative role in either chronic fatigue syndrome or prostate cancer is unknown.” They go on to point out thatXMRV infection might be higher, by co-incidence, in the same locations as clusters of patients; that patients with ME/CFS or prostate cancer might be more readily infected due to immune activation; that XMRV might prefer to proliferate in cells that are dividing rapidly, and that the presence of these cells in these illnesses might simply make it easier to detect infection; and that the mechanism of viral transmission remains unknown, as does the prevalence or distribution XMRV in human or animal populations. In the aftermath of all initial scientific reports of a potentially major find, the unknown wildly exceeds the known — an exciting place for ME/CFS research to find itself.

The next steps

The researchers say that since publication they have continued to refine their test for XMRV, finding that 95% of 330 ME/CFS samples have tested positive for XMRV antibodies in the plasma (showing that these patients have at least been in contact with the virus at some time). They plan to continue their in-depth studies of XMRV to clarify its effects on the human immune system, and are clinically validating a blood test for the detection of XMRV in ME/CFS and other human diseases. And they will shortly begin the work of determining if any currently approved drugs, such as AZT, might be useful for suppressing XMRV. If these efforts are successful, human clinical trials to determine the most effective patient treatments in a clinical setting would surely be close behind.

At the same time, other independent laboratories across the world will be attempting to replicate the findings in their own local populations of ME/CFS patients. Since the WPI researchers used samples selected from several regions in the US where “outbreaks of CFS” had been documented (using patients diagnosed on CDC-1994 and 2003 Canadian Clinical criteria ), blood samples from patients in other countries (possibly diagnosed with less stringent criteria) might throw up very different results. Furthermore, it will be particularly important for independent laboratories to conduct double-blind studies to search for XMRV in ME/CFS patients and healthy matched controls, to strengthen the evidence base as a whole.

The long-term

This is a stunning find — like a comet from a cloudless sky to patients across the world. Yet it is too early to know whether the discovery will change the ME/CFS landscape or not. At worst, the discovery will be just one of a number of false dawns that have arrived over the years — albeit one that has brought, suddenly, the world’s attention to a neglected field largely ignored by mainstream biomedical medicine. In this scenario, XMRV might prove to be simply a passenger virus carried by an immune-depressed ME/CFS patient population, with little or no influence on the illness. At best, however, XMRV might be found to be the casual factor in the development and maintenance of ME/CFS, and a combination of anti-viral drugs will be found to eradicate the viral load from patients. One consequence of this “jackpot” scenario would be a demolition of the existing diagnostic criteria for the “syndrome” CFS (currently a ragbag of common non-specific symptoms, with many causes, shared with other illnesses), as well as the older criteria for myalgic encephalomyelitis. These would be replaced by objective diagnostic criteria based on state-of-the-art methodology — surely a welcome liberation for both CFS and ME patients currently parked in a Diagnostic Terminal. Indeed, the WPI group has already suggested that a new disease entity — X associated neuro-immune disease, or XAND — might arise from the rubble, implying (one assumes) that the one-third of ME/CFS patients found to be “negative” forXMRV in the WPI report would also acquire new, more appropriate diagnoses.

Like Dr Dan Peterson, medical director of the WPI, we are hopeful. As he says, “Patients with ME/CFS (XAND) deal with a myriad of health issues as their quality of life declines. I’m excited about the possibility of providing patients who are positive for XMRV a definitive diagnosis, and hopefully very soon, a range of effective treatment options.”

Starting to understand CFIDS / ME / CFS

From Weighed Down by Sophie Meredith

She tells me to just get started. I protest that I want to write something interesting and engaging but honestly, when I feel well enough to consider that, I forget what it actually feels like to be down under the grimy covers of ME / CFIDS / CFS. Now, I am peering through one eye, my head is pounding. My throat is tight and lumpy like a clogged sink. My facial muscles want to be touched and soothed. My bones feel like they hurt from the inside-out. My whole body wants to be touched and warmed and soothed. I am tired but hyper and frustrated inside. I cannot sleep and I have an innate sense that it is not fair that I should have to in broad day-light. A vein in my right hand throbs irritatingly as I type. I feel alone. I desperately want someone to understand. I sweat between moments of stillness and rest and those of fighting to appear well and racing to do something, anything, with my day. I feel alone, but at least I am alone. In company, I feel confused, anxious, stupid and slow, unengaging.

We all can forget how ill we felt when we are all at once well again. When I am more able-bodied or able-minded, I forget how it feels to have a real ‘CFS-day’ (as I describe it to my girlfriend, Al). I feel angry, though, that anyone could have taken me too seriously, including myself. I think, ‘I am a brilliant and well person who should be trusted to do things. Give me responsibility! I can do anything the same as you. Give me a drink or a social group, and I will be as fun as I have ever been. Give me a yoga mat and I will show you the fit person that I am.' Inevitably, very soon after the outburst, I am forced to remember with a crash just what CFS is and I lie here with the consequences of having been reckless enough to have behaved like…a normal person.

When something’s bad, we may have a socially understood ‘event’ to remind us. People refer to times like ‘when I was in hospital’ and know that it MUST have been bad. We sometimes consciously leave ourselves a reminder. When Al fell off her bike, we took photos of the imposingly gargantuan bruises and though she may sometimes forget what a pain it was not be able to get around for so long, one glance at the photo, brings it all back.

With ME/CFS, I forget again and again only to remember all over. As with severe food poisoning, you think ‘please don’t let me ever feel like this anymore. Let this be over.’ ‘Normal’ has never been such a tantalising concept. You are apparently calling out to a higher being --whom you are not accustomed to chatting with -- out of sheer desperation. Next day you almost forget all about it.. until the next time.

I feel like this sometimes every other day, or week or morning or afternoon. I do not know how to predict it. I may be chatting away confidently when a thick fog sweeps from my nose up my forehead and into my skull and my left eye feels like it is shrinking. I begin to wonder why you are talking to me, or even, at the worst times, who you are in relation to me. I may become dizzy and want to lie down. I will either become completely vacant, or, if I try to fight it, frowning and irritable. I now know that I crave quiet and clear air, though I did not recognise that before I was diagnosed.

If I do not relieve my symptoms with rest or withdrawal, I deteriorate. I become anxious and irritable. I do not want to be alone, but there is nowhere else quiet enough. .. and yet, I must prove I am okay. I may look okay. What will this person think if I tell them I am tired or have a headache? How lame will that sound? I am not the kind of person who shies away from a chat or a job or a shopping expedition on account of a headache.

My reluctance to calmly and confidently allay these symptoms for fear of what other people might think, is, as far as I can work out at the moment, one of the few things in my control. I can work on this to make my life, and other’s around me, easier. I remind myself that I cannot make people understand but I can do what I need to do for myself and do what I can, to let people know.

I intend for this ME/CFS condition to teach me things for life about how energy is best spent, and what I take for granted. I do not have the energy to stress. It is a luxury I can no longer wish to waste my daily dosage on! That is currently an idea that I have yet to work out fully how to implement. I begin Cognitive Behavioural Therapy on Monday to help me work on managing this. Acceptance is my starting stone.

My conscious challenge in curing self is to work with CFS/ME/CFIDS not against it, and to accept help, not isolate myself. Just as an able-bodied person might remind themselves how lucky they are, I have to remind myself how fortunate I am with a miraculously supportive, proactive and loving girlfriend and a beautiful and kind family who are doing everything they can to understand and to have such persistent and loyal friends, despite my apparent withdrawal.