Neonics in the news.
Beekeepers in Washington State Leading an Effort to Control Neonics
I take another look at Imidacloprid, below. Links to the papers in the bibliography will bring you the pdfs.
Honeybee colony losses continue to be unacceptably high. In the US this spring, colonies brought in to California to pollinate almonds from throughout the country, about half of the colonies were lost (New York Times, March 29, 2013). It is generally accepted that multiple pathogens ultimately bring down stressed colonies (Cornman 2012). However the role of pesticide stress on colonies remains controversial. Chronic exposure studies are often poorly constructed and frequently do not follow the exposed insects long enough for effects of the toxin to become evident. The best studies look at mortality, or behavioral effects, over a substantial fraction of the insect’s lifespan while varying the toxin concentration or dose. Time-to-effect studies lend themselves to a simple time dependent “power law” empirical model which can guide expectations for field toxicity effects (Tennekes 2011, Sánchez-Bayo 2009). Other reviews of the toxicity of imidacloprid (Cresswell 2011) attempt to establish specific “acute” or “chronic” levels, but this seems useless if the time of exposure is not explicitly included.
Hence, I’ve made an effort to identify relevant time-to-effect studies in the literature most specifically for imidacloprid with insects of order hymenoptera, which includes bees and ants. As it turns out, there is an interest in concocting ant baits that proffer sub-lethal doses of toxin to forager ants. A study done by Rust, et.al. 2004, has time-dependent toxicity measurements for imidacloprid on Argentine ants.
For the honeybee data, we have the paper by Suchail et.al. 2001 that I discussed previously. However, there is general concern in the research community that there is something wrong with the Suchail results. Many other studies do not show such a high sensitivity to the toxin. So I looked for other experiments that also include time-to-effect measurements. There is a study by DEFRA (2007) that has time-to-effect figures, and also a compilation to many researchers’ LD50 numbers for 24, 48, 72, and 96 hr. periods (FERA 2013). To be able to plot both chronic and acute data on the same graph, I take the acute LD50 numbers and divide by the time interval for the measurement to obtain daily dose rates. At higher concentrations there is an anti-feedant effect that reduces the consumption rate, so I’ve plotted the reported consumption of toxin (ng/day) versus the time of exposure until half the bees have died (LT50).
Many studies only follow the bees for 10 days or less. At lower concentrations, the LT50 time is never reached in the experiments. However, there is a paper by Dechaume-Moncharmont, et al. 2003, which contains a couple of data points with time-to-effect numbers for relatively low sub-lethal concentrations. The data show that 4-8 ppb samples eventually kills bees in about 30 days. All of these data are plotted in the chart below. I had to estimate the consumption rate for the ants in order to plot it with the other data, but an incorrect estimate would shift the curve left or right, but not change its slope. I show the power law best-fit line for each data set, where the Dechaume-Moncharmont points (blue squares) are included with LD50 averages from the FERA 2013 paper.
First notice that the LT50 times for the Argentine ants do a remarkably good job of following a simple power law with roughly t1.7 dependence. This adds confidence to the utility of the empirical power law model for imidacloprid. Recall that simple accumulation to a toxic threshold would appear as directly proportional to time ( t1.0 ). An exponent larger than one can be interpreted as coming from damaging secondary physiological effects that take time to develop.
The DEFRA data stands out as not falling with the averages of other researchers. In general, there appears to be a wide variation between experiments, and hence individual colonies or strains of bees, to the sensitivity of this insecticide. The DEFRA study has time-to-effect numbers and consumption data, so it provides a good data set for looking at time scaling, even if the DEFRA bees are not particularly representative of most other bees tested. Again we see the data taken can be very well explained by the power law formulation, this time with about t1.6 dependence. We might expect that healthy individuals of similar species would exhibit similar temporal effects to the same toxin, and this seems to be the case. Finally, the average LD50 numbers from many researchers also fits the power law model. I also included the Dechaume-Moncharmont data in the power law fit, here about t2 . The Dechaume-Moncharmont data extends the model into the high field-realistic exposure range when approaching the lifespan of summer bees. If we extrapolate the curve to the lifespan of winter bees, we are well into the range of field-realistic exposure (0.01 ng/day). Hence, even with healthy bees, exposure to modest field-realistic levels of imidacloprid will compromise the longevity of winter bees, and could easily cause problems getting the bees through the winter.
It is known that imidacloprid is relatively quickly metabolized in the honeybee. The metabolic half-life is about 5 hours (Suchail 2004). Yet the effects of the poison are cumulative and long-lasting. This seeming paradox is explained by the fact that when the imidacloprid molecule binds to the nAChR receptor sites in the nervous system of the insect, it binds strongly and essentially irreversibly. So while free circulating imidacloprid may decay away, the damaging bound molecules remain, continuously compromising the nervous system.
The imidacloprid toxicity graph tells us that we need to be careful not to expose bees to more than a very few parts per billion (ppb) of toxin if we wish there to be no effect over the lifespan of the bees. Reports of levels of neonicotinoids from treated agricultural crops are frequently in the 1 to 5 ppb range. Typical honeybee consumption is about 20 µl/d, so at 5 ppb, the ingested toxin would be 0.1 ng/day which is the upper end of the yellow zone in the figure.
The Suchail (2001) results show a much higher sensitivity to imidacloprid than would fit the trends we see with the other data sets. Rather than the t2 dependence, lethal effect seems to scale as toxic concentration times t5. It is tempting to disregard the Suchail results, however one test site in trials by Shmuck (2004) also showed very high sensitivity to imidacloprid as well. Hence it is worth considering a secondary stressors that could result in a higher sensitivity to the toxin. The logical culprits would be pathogens, bacterial, viral or the microsporidian nosema.
Pathogen interactions with a host could lead to several time-dependent processes. First, damage to the host immune system has to occur for a pathogen to get a foothold. Then, before the host succumbs to the pathogen, the infectious organism must grow and multiply to lethal levels. Damage from the pathogen itself may take time to manifest in the host organism. Several of these time-dependent processes happening simultaneously would lead to a higher order time dependence.
The interaction between nosema and imidacloprid was studied by Alaux, et. al. (2010). The study fed bees 200,000 nosema spores to initiate infection and subject the bees to various doses of imidacloprid. There was some interaction between the pesticide and the pathogen, but the study only followed the bees for ten days so it is hard to draw conclusions at field-realistic doses, and the nosema infection dominated the experiment. Two data points from the study are plotted on our graph (blue diamonds).
A very good study, Aufauvre (2012), looks at the interaction of the systemic insecticide fipronil and nosema infection, and finds a strong synergy between the pesticide and the pathogen. The figure from that paper, below, shows what happens when sub lethal infection levels are combined with sub lethal insecticide exposure.
The curves (purple) show what happens with both the pathogen and the toxin combined. Neither nosema alone (red) nor fipronil alone (green) are very different from the control (blue), since low doses were used. However, the combination, given enough time, is especially lethal. The study examines the effects of the relative timing of the exposure and infection, but finds synergistic interaction between the pathogen and the toxin in all cases. The study followed the bees for twenty-two days, significantly longer than the typical ten-day chronic studies. The added time is crucial for the delayed toxic and synergistic effects to show up. The same is true with the Dechaume-Moncharmont experiment, where there were no deaths in either the control or exposed bees at the ten-day point, yet the toxic effect was clearly evident by day 30.
The choice of nosema as the pathogen for this study is convenient because the infection is easily accomplished with a spore solution, and the progress of the infection can be followed with microscopic examination of the bees. Curiously, the level of the nosema infection as measured by spore counts, was not much different with or without the pesticide exposure. Viruses are much more difficult to use as the infectious agent because of the difficulty of diagnosing their presence and quantifying the infectious dose and infection progress. However, viruses are more ubiquitous in honeybee colonies than nosema, and could easily have a similar synergistic interaction with pesticides on the bee’s health.
Cornman et al. (2012) found that CCD (colony collapse disorder) colonies were more likely to have higher levels of a wide variety of pathogens than weak, but non-CCD, colonies. Not only were the levels of pathogens higher, but multiple agents were frequently found in combinations not typical of non-CCD colonies. The figure below from that paper does a great job of graphically illustrating the situation.
It looks like the immune system has gone awry. Could it be a few parts per billion of insecticide that makes the difference? More research is still needed here, perhaps looking at pesticide interaction with KBV or AMPV virus, since these viruses show up in CCD colonies.
Extrapolating LD50 numbers or 10-day chronic LC50 values to the lifetime of bees wintering in the honeybee colony requires some understanding of the time-dependent nature of the toxin. We have shown that the published LD50 and LC50 data can be empirically modeled using a simple power law. For imidacloprid with healthy honeybees, the time dependence is approximately t2 , indicating that not only is the exposure cumulative, but also that there are delayed toxic effects.
Queen bees can live for several years. Queen bees also need to consume large amounts of food in order to churn out the thousands of eggs they lay every day. This make queen bees especially susceptible to such a toxin. Queen failure was one of the precursors to colony mortality found by vanEngelsdorp et al. (2013). Queen failure, even if the bees succeed in raising a new one, will leave the colony without a fresh supply of young bees. A colony with pesticide stress may be relying on young bees to make up for those that disappear before their time.
I only looked at studies that addressed bee mortality. Bees affected by pesticide may not immediately die, but they may be practically useless to the colony, or may be unable to forage or navigate, and hence become lost and perish outside the hive. Quantifying behavioral effects is more difficult than counting dead bees, but one might expect that the time-to-effect scaling would be similar to the mortality data.
Alaux, C., Brunet, J.-L., Dussaubat, C., Mondet, F., Tchamitchan, S., Cousin, M., Brillard, J., Baldy, A., Belzunces, L. P. and Le Conte, Y. (2010), Interactions between Nosema microspores and a neonicotinoid weaken honeybees (Apis mellifera). Environmental Microbiology, 12: 774–782. doi: 10.1111/j.1462-2920.2009.02123.x
vanEngelsdorp D, Tarpy DR, Lengerich EJ, Pettis JS, Idiopathic brood disease syndrome and queen events as precursors of colony mortality in migratory beekeeping operations in the eastern United States. Preventive Veterinary Medicine, 108, 2–3, February 2013, Pages 225–233.
Suchail, S., Debrauwer, L. and Belzunces, L. P. (2004), Metabolism of imidacloprid in Apis mellifera. Pest. Manag. Sci., 60: 291–296. doi: 10.1002/ps.772
Tennekes HA, Sánchez-Bayo F (2011) Time-Dependent Toxicity of Neonicotinoids and Other Toxicants: Implications for a New Approach to Risk Assessment. J Environment Analytic Toxicol S4:001. doi:10.4172/2161-0525.S4-001
The DateTrike made its debut last summer. Since them there have been a few refinements, and finishing details that have given the craft a more finished look and some added features.
I finished the rear deck which includes a storage area under a sliding door for a place to carry travel essentials. Lighting was also added. A front hub generator provides ready power for both a nice bright headlight and the pair of LED tail lights. Good lighting makes for a pleasurable ride home from the theatre late a t night.
Sammy the dog is always ready to go for a run with the trike, and so is Ellen!
Even though the trike is now officially complete, there is one more accessory that is still to come, and that is the canopy. If all goes well, the DateTrike will be coming to Black Rock City later this year and we will need the shade.
There are quite a number of studies that show imidacloprid and other neonicotinoid insecticides don’t do much damage to honeybees at levels expected in field conditions. Yet there is plenty of evidence that “country” bees do better than “farm” bees.
The big migratory beekeepers are the one’s suffering the most, often with losses over 100% a year, only staying in business by continually making splits from stronger colonies and adding new queens. Then, come fall, they combine the weaker colonies so they can get through the winter. These practices essentially allow more than one queen to help make young bees for the eventually recombined colonies that winter over. These beekeepers are moving bees from field to field in agricultural areas and the bees are frequently in range of crops treated with neonicotinoids.
But the bees don’t always die. Sometimes they are sitting next to treated fields and they do just fine. So what is going on?
A little history is in order. The first study that really hinted at big problems with imidacloprid was done by Suchail, et.al. in 2001. This is the data I presented in The Case Against Imidacloprid. The researchers found lethal effects on the bees at very small doses ~1-10 ppb when fed chronically over ten days. As a response to this study, Bayer commissioned a study reported by Shmuck in 2004 to confirm or discredit the Suchail study. That study purports to show the imidacloprid is quite safe, but it deserves a closer look.
The Bayer study used four test sites, three in Germany and one in the UK and did pretty much the same experiments at each site. Three of the sites did not see much in the way of increase bee mortality at the sub lethal levels tested over several days. But one site did see a substantial effect. A good fraction of the Shmuck paper is an attempt to explain away the results of the Germany II site. The author suggests it was because of poor randomization procedures when they loaded the bees into the cages as the reason. But that doesn’t ring true because the absolute mortality levels are higher than any other site, as well as evidence for a strong effect of the toxin. If you are selling insecticide, you do not want to look very hard at why one of your tests shows such acute toxicity for chronic exposures. But it begs the question – what was different about this test site, and also the Suchail 2001 experiments, that showed such high chronic toxicity compared to the other tests sites and other published studies?
We can either throw out the work of the researchers involved, or look more closely for the missing factor(s). We really now have two independent studies where very low chronic doses of imidacloprid caused a very high percentage of the bees to die. We also have several studies where the bees seem not to be effected at the same low chronic doses. The statistics for all of the studies are fairly conclusive; we are not talking about doubt because of a small effect. We really have two very different sets of results, so why?
One thing that Shmuck noted was that in the Suchail study the bees only consumed ~12 µl/bee/day of sugar solution, whereas in his studies, most of the bees were eating 45-75 µl/bee/day. However, Shmuck’s Germany II site, the bees were only consuming about 38-40 µl/bee/day. Perhaps Suchail’s bees and Shmuck’s bees at the Germany II site were not as healthy as they could have been. The Shmuck paper should be seen as confirmation that there are times when very small chronic levels of imidacloprid can kill bees in some circumstances – probably when they are already somewhat sick.
Usually researchers try their best to only change a single variable at a time. When studying toxins, one wants to start with healthy bees. Undoubtedly, none of the hives sampled were outwardly sick. If as seems likely, a low dose of neoncotinoids can cause damage that is commonly not lethal, then we are fortunate that the two studies did find lethal effects.
Other studies have shown learning disabilities for bees give low doses of imidacloprid (Decourtye, 2004). The presence of insecticide may reduce individual bee’s performance in their hive duties, but such non-lethal impairment is not recorded by lethality studies. Bees which lose the ability to find their way home are effectively lost to the colony even if they have not died. Nervous system deterioration due to low levels of neonicotinoid insecticides may not kill bees directly, and so is invisible to studies that only count dead bees. However any number of added stressors could give rise to the death of already damaged bees.
What the two experiments are telling us is that the presence of very small levels of imidacloprid can be fatal to an otherwise tolerable colony. This observation goes a long way to help us understand the dynamics of CCD. Without the pesticide, the bees natural immune response is able to keep infection under control. Disease surveys usually find many pathogens present in healthy bee hives at non-threatening levels. External stresses can precipitate an outbreak of disease. Healthy, non-poisoned colonies may get sick, but with the natural immune response of the bees, the colony can usually recover from such outbreaks. Not so for bees with damaged nervous systems. Once a pathogen gets a foothold, it is likely to multiply and infect neighboring colonies, and a CCD outbreak is born.
I’m often asked which products are OK and which should be avoided. Hence the mnemonic in the title to help you remember I’m getting rid of Imidacloprid. Say it three times out loud, and when you read the labels at the garden store you will remember: I’m getting rid of Imidacloprid.
When it comes to insecticides, first ask yourself , do you really need them? Rather than automatically reaching for a spray bottle, first take a close look at your foe. Do you know what it is, its life cycle? What will happen if you do nothing? Are there any natural predators around? Open your eyes to the fascinating world of insects and their daily dramas before killing them all.
Attentive gardeners are always on the lookout for the pests they have come to know. I expect cabbage caterpillars to appear as soon as I see the pretty white butterflies flitting about. So I watch the plants for any sign of the worms and many times I notice predatory wasps patrolling with me. I don’t get all of the worms by hand picking; there are always some left for the wasps. Between us, we don’t need anything else to keep the worms off the broccoli. Hand picking works for many garden pests.
Healthy plants are more resistant to insect pest. Good growing conditions, water and organic fertilizer are your first choices to solve problems. A good resource when you have problem is NCAP’s solution tool box. Occasionally you may be driven to need something more. So lets look at the good, the bad, and the ugly, when it comes to garden chemicals.
The Good: Soaps and Oils
The least toxic chemicals are often soap or fat/oil based emulsions that disrupt the pest with little environmental impact. Safer Brand and EcoSmart products are generally a good choice for chemical products that have low toxicity and are usually derived from organic ingredients. The major pesticide brands like Ortho and Bayer also have lines of less toxic chemicals but I would suggest patronizing brands that generally avoid the worst chemicals in all of their products. Read the labels!
The Bad: Neonicotinoid Pesticides
There are plenty of bad chemicals. I’m mostly concerned about the insidious, highly toxic neonicotinoid insecticides because they are long-lasting in the environment and sub-lethal amounts of toxin will accumulate and cause harm in bees and other beneficial insects. The list of products that contain neonicotinoid insecticides is a long one. Common on this list are foliar sprays for direct control of insect pests.
Ortho brand sprays usually contain acetamiprid, a neonicotinoid that is less toxic and more quickly degrades than imidacloprid. Bayer foliar sprays contain imidacloprid. The extended length of time the chemicals continue to kill insects can clue you in on how much active ingredient is being spread about and their relative environmental impact. The Bayer Complete Insect Killer has a lot of active ingredient and really belongs with the ugly product below.
The Ugly: Mindless-Use, Soil-Contaminating, Neonicotinoid Pesticides
These are the real problems. Insecticides that are applied in the soil need to have more active ingredient in order that enough is taken up by the plant to be effective. This means that much more is still left in the soil where it can contaminate non-target plants for many years and eventually move into the ground water.
Tree and shrub product use large amounts of chemical. Many flowering shrubs are prime bee forage, make an attractive and deadly combination. The soil around treated trees will grow toxic flowers for years. The “all-in-one” and “protect & feed” products contain fertilizer as well as imidacloprid. This leads to mindless needless insecticide use and soil contamination. The Bayer All-in-One Rose and Flower Care also contains clothianidin, another deadly neonicotinoid, in addition to imidacloprid. Please do not use these chemicals, for the sake of the bees and the entire invertebrate eco-system.
Remember, I’m getting rid of imidacloprid!
Ever since French beekeepers saw their bees dying as they collected pollen from treated sunflowers back in 1996, beekeepers have been concerned that their bees are being harmed the highly toxic neonicotinoid insecticides, with imidacloprid most widely used. The use of this class of insecticide has grown steadily ever since. Bee losses have become chronic as well. However, unlike the first case in France where bees were literally falling dead while gathering pollen, the widespread colony losses today are less explainable, often associated with outbreaks of a variety of diseases, and with very high winter colony mortality. So why blame the insecticides?
To see why the bees are dying, and why these pesticides are still being sold, we must examine the toxicology of the neonicotinoid chemicals as well as the history and science of pesticide regulation. The toxic nature of a chemical is characterized by its “LD50″ level. This is the amount of chemical that will kill half of the test organisms in short order. For many traditional pesticides (organophosphates), the LD50 level provides an adequate overall characterization of toxic effect. These pesticides tend to be short-lived and generally do not bio-accumulate in the target organism. If the dose doesn’t kill the organism, the toxic compound will be metabolized and excreted. Since the organophospate pesticides — which for many years made up the majority of pesticides sold — could be characterized easily with the single LD50 number, the culture of pesticide regulation largely accepts the acute LD50 as determinative for all toxic effects.
The acute LD50 characterization works poorly for substances that bio-accumulate and/or have a relatively long time-to-effect characteristic. Substances that fall into this category are heavy metals that are known to accumulate in certain tissues, and some carcinogens where an initial single exposure can give rise to cancers much later in the life of the organism. Neonicotinoid insecticides also fit into this category. These insecticide molecules bond strongly and irreversibly at nicotine receptor sites in the central nervous system. There is also evidence of delayed time-to-effect of several days for exposures below the acute LD50 [Suchail et. al.(2001)].
Toxicologists attempt to model the time-dependent effects of chemicals at various dose levels [Tennekes, (2010)]. One of the simplest empirical models assumes the dose/effect relationship can be characterized by a simple “power law” where the effect is proportional to the dose multiplied by the time-of-exposure raised to a power, b.
Effect = Dose x Timeb
Instead of a single number, now we have two numbers to characterize toxicity, the dose and the time exponent. When a power law is plotted with logarithmic scales, one gets a straight line with slope equal to the exponent, b, and intercept equal to the Dose. The time-independent, acute LD50 model is the special case when b=0. For a simple bio-accumulation model, one would expect linearity in time with b=1. Time-to-effect mechanisms require b>0. Combinations of effects for a given organism and chemical will result in a Dose vs Effect curve with characteristic slope that includes all of the time-dependent mechanisms embedded in the value of the exponent.
The plot above shows some published data on imidacloprid toxicity on a log-log graph. Data for two species of small aquatic crustaceans, Daphnia magna (red squares) and Cypridopsis vidua (blue diamonds) illustrates the large range of toxicity difference between organisms, and also the large range of applicability of the model, spanning more than three orders of magnitude in concentration. [Sánchez-Bayo et. al. 2009] Honeybees (green triangles) also have high toxicity over a wide range of concentrations [Suchail et al.(2001)].
The best-fit power law curves are shown in the plot. In all cases, the fit parameter, R2, is greater than 0.85. The time exponent for Daphnia, 1.3, is barely more than linear, where as for Cypridopsis and honeybees the exponent is close to 5. This means that there are strong time-dependent delayed effects from the chemical for the Cypriopsis and honeybees. The time5 dependence of the toxicity of imidacloprid for honeybees is the big problem. Very low levels of exposure, with sufficient time, will be lethal. The power law model suggests that we should extend the time of exposure to the lifetime of the organism in order to determine the minimum dose that will have no effect. Honeybees, including the larval stage, live ~50 days in the summer and ~100 days for wintering bees. Extrapolating the green dashed line trying to reach 50 to 100 days would require reducing continuous exposure to less than 0.0001 parts per billion (ppb). This minuscule exposure level is far below the detectable limits of present technology (~1 ppb). What we can detect are residual levels in nectar and pollen on treated plants commonly in the 1 – 10 ppb range; even these small levels are more than 10000 times the level that the power law model suggests would cause no harm to adult bees. Looked at another way, if one bee in 10,000 returns to the colony with pollen gather from a treated plant, that would be enough toxin to begin to cause damage to the colony.
Collecting toxicity data about bees is a complex process, involving multiple trials, caged bees to limit their activity to the test sample, etc. Aquatic crustaceans provide an easier test subject where dosage can be controlled by dilution of the water they live in. The fact that the crustaceans conform to the power law model confirms that imidacloprid is bio-accumulative. The same finding by Suchail et.al. for bees should not be surprising, given that both organisms have central nervous systems with nicotine receptors.
What about mammals and humans? Very little time-dependent information is available. There are a couple of data points on the plot above for mice. One point was the LD50 for short time exposure and the other the threshold for immune system compromise exposed for 28 days. The data for mammals is just not available yet, but even much more modest sensitivity to the chemical could present problems for long-lived species such as humans. There is also fear that these biologically persistent chemicals could be fueling world-wide wild life declines in many species [Mason, R. et. al. 2012].
Our regulators, (EPA) are not adequately considering the time-dependent nature of the lethal effects of the neonicotinoid class of pesticides. The most toxic and long-lived chemicals, imidacloprid, clothanidin, and thiamethoxam should be removed from the market before more harm is done, as is happening in Europe. Other insecticides in this class should be subject to further scrutiny as well.
The social nature of bees naturally draws one to a human analogy. Imagine that a toxic chemical is slowly poisoning our brains. (Think lead pipes and the Romans.) Instead of healthy people living into their 70′s, the toxic effects are bringing on Alzheimer’s-like symptoms to folks in their 40′s and 50′s. The younger healthier part of the population has its hands full, providing for themselves and those that no longer support their own livelihood. Everyone is hungry. Now introduce a bad case of the flu, or the plague, and the already weakened population is devastated. That is what our bees are facing today. The levels of poison are rising as more and more of these pesticides are being used, building up in our soil and in treated plants. The bees are dying younger, and we are gradually eliminating a host of insects and creatures we don’t even know we are poisoning.
Tennekes, H, A. The significance of the Druckrey-Kupfmuller equation for the risk assessment — the toxciity of neonicotinoid insecticides to arthropods is reinforced by exposure time. Toxicology. 2010 Sep 30;276(1):1-4
Last week three major home store chains in the UK took insecticides with troublesome neonicotinoid systemics off their shelves. The chains, Wicks, B&Q, and HomeBase no longer have insecticides containing clothianidin, imidacloprid and thiamethoxam, the three neonicotinoids deemed most toxic and problematic to honeybees in a recent announcement from the European Food Safety Authority (EFSA). The EFSA recommends, among other things, that for the three most toxic neonics, “only uses on crops not attractive to honey bees were considered acceptable.” The voluntary ban by the major store chains is the latest development in the deliberative effort going on in Europe concerning bee losses and systemic insecticides. The body of evidence for the problems with neonicotinoid insecticides is growing larger. In December 2012, the European Parliament issued a report, Existing Scientific Evidence of the Effects of Neonicotinoid Pesticides on Bees, as they struggle to decide what to do about increasing bee losses in Europe. The authors recommend banning or severely restricting use of the worst offenders. This is on the heels of a very complete, 265 page report issued by the EFSA in May 2012, Scientific Opinion on the science behind the development of a risk assessment of Plant Protection Products on bees (Apis mellifera, Bombus spp. and solitary bees) which goes into detail about hazards of the neonics. The process in Europe is deliberative. The consensus-building necessary for new Europe-wide regulations began with the compilation of all the scientific evidence, pro and con, concerning the safety of these chemicals. The scientific reports document the known problems and also raise the issue that there are no adequate studies of long-term sub-lethal effects of these very toxic chemicals that focus on whole-colony dynamics with honey bees or consider other native species. The next step in the process would be for the EU to write language to actually institute a Europe-wide ban the use of the insecticides where they are harmful to bees. This is likely to happen in the coming months. In the meantime, reaction to the recent announcement has been mixed. Bayer and other manufacturers of the chemicals have denounced the recommendation, predicting dire consequences to the corn crop if the chemicals are banned. However, in the UK, the home center stores have voluntarily removed products containing the troubling insecticides from their shelves. In the US, the Environmental Protection Agency (EPA) has been slower to act. Despite the concerns of beekeepers and environmentalists that resulted in EPA consideration of a petition in 2012, the agency refused to make any changes in the regulatory status of clothianidin. The threat in the US is not only with chemicals marketed to industrial agriculture. Increasingly, Bayer is including neonics in their home garden insecticides aimed at individual home owners and gardeners. This is especially troubling in our communities where urban beekeeping must coexist with urban gardeners. Colony losses continue to mount. Early reports for colony health coming through this winter are discouraging. It is likely that for the first time there will not be sufficient bees available in the US for the California almond pollination event. Beekeepers my have difficulty finding package bees this spring, as demand to replace dead colonies exceeds the capabilities of the southern producers. In our community, the Oregon Sustainable Beekeepers have begun circulating a letter requesting local garden centers to stop selling neonicotinoid insecticides. Although our EPA may not be protecting us from these chemicals, we think that especially with the evidence and recommendations coming from Europe, there is very good reason to get these chemicals out of our communities. Local activism is our only choice.
It is always exciting to encounter a fresh topic that has escaped attention, yet with a little investigation, demands it. So it is with the story of A1 / A2 milk. I first became aware of the existence of this issue at a potluck dinner with health-conscious fellow diners. As it turns out, this is old news to residents of New Zealand, where a few researchers and entrepreneurs have been promoting the virtues of A2 milk for about a decade. The story is about the role of a milk protein, beta-casein, that can take on two very similar forms, called A1 and A2, depending upon a single simple mutation of one gene. The A1 form of the beta-casein, upon digestion, breaks down into beta-casomorphin-7 (BCM7), a fairly stable and strong opiate which appears to cause health problems in some people some of the time. Meanwhile, the A2 beta casein proteins are digested completely and don’t generate the problematic BCM7.
The evidence suggests that BCM7 can trigger the auto-immune response responsible for Type 1 diabetes, and it is implicated in arterial damage and consequently could be a factor in heart disease. In addition, there is evidence for connections between BCM7 and autism, schizophrenia, sudden infant death syndrome (SIDS) and milk intolerance.
The story is well-told by Keith Woodford in his book, Devil in the Milk: Illness, Health and the Politics of A1 and A2 Milk. The author has a nice synopsis of the major scientific findings on his website. I find the evidence and the arguments he presents for the case against A1 milk quite compelling. But what makes this story particularly interesting, and the book fascinating reading, are the personalities that have shaped policy surrounding the science and the agriculture, and the all-too-predictable response of large organizations against making any kind of change.
The solution to the A1 milk problem is easy. Just stop breeding dairy cows using bulls with A1 genes, and in a few cow generations the milk will have a lot less A1 beta casein in it. The cost for such an adjustment is minimal. Many of the dairy bulls used for artificial insemination have already been genetically tested and their A1/A2 status is known. The cost of genetic A1/A2 testing is only a few dollars per head; nothing compared to the cost of raising breeding stock.
But we live in a world where brand is everything. Any hint that milk might not be the most wholesome of foods just cannot be allowed to reach the public. In New Zealand, where this issue first became known, the large milk marketing company Fonterra was always ready to downplay and counter any scientific findings that hit the public media. The milk companies and government regulators have been content to let reasonable scientific skepticism serve as an excuse for doing nothing, and presently this is the state of affairs.
Let’s look at just a bit of the evidence for the A2 milk hypothesis, just to give readers a glimpse of the argument and potential health consequences. We will look at the results from a study by Murray Laugesen and Robert Elliott, published in Journal of the New Zealand Medical Association in 2003. The graph below shows the death rate from ischemic heart disease as a function of A1 beta-casein consumption for several countries that all have established health care systems. The trend is obvious and is highly unlikely to be due to chance.
The authors look at other correlations, such as total milk protein, butter fat, or other dietary differences, but nothing has as strong a correlation as A1 beta-casein consumption. The study also looked at the correlation of A1 beta-casein consumption with the incidence of Type 1 diabetes, and here the correlation was even stronger.
If you take the study numbers at face value, and assume that, in the US, the milk supply could become free of A1 beta-casein, then you might expect a reduction of about 40 deaths per 100,000 annually due to heart disease, just extrapolating from the linear correlation coefficient in the chart above. This would amount to about 60,000 fewer deaths from heart disease every year. (For perspective, auto accidents kill about half that number.)
Scientific “proof” that there is a problem with A1 beta casein is a standard that will not be reached until long-term double-blind studies are done on humans – which could be decades in the future, if ever. The cost of such studies could easily be more than the cost of just solving the problem! That the solution is so simple with such low costs, the down-side risks virtually nonexistent, and the potential public health benefits so large, make this issue a fascinating case study in the politics of indecision.
The best solution would be for some industry group or public entity to promote or require farmers in a defined geographic area to begin the switch to only A2 milk-producing cows. In the matter of a few years, with good record-keeping and now with a significant sample size, the change in A1 beta-casein content in the milk supply should show up in a change in the incidence of Type 1 diabetes and heart disease statistics.
Individually, the risks from milk are not high, just as riding in a car is not particularly dangerous. However, if the driver is drunk, or the body is prone to other compromises, even individual risks can become significant. In the US, the only source of milk that does not contain A1 beta-casein is goat milk, or milk from cows that are known to be genetically A2A2 homozygous individuals — difficult if not impossible to find. In other parts of the world, A2 milk is becoming more available.
I suspect that someday there will be no more A1 beta casein allowed in milk, but that time is a long time away. In the mean time, don’t expect our health watch-dogs to protect you any better than they did from cigarette smoking.