The West’s Changed Climate: Burning It Up!

Here’s a report that should be of interest to those who stumble across it… Thanks to the NRDC. Here’s to a burning wild west. **** Hotter and Drier The West’s Changed Climate Human activities are already changing the climate of the American West. This report by the Rocky Mountain Climate Organization (RMCO) and the Natural Resources Defense Council (NRDC), drawn from 50 scientific studies, 125 other government and scientific sources, and our own new analyses, documents that the West is being affected more by a changed climate than any other part of the United States outside of Alaska. When compared to the 20th century average, the West has experienced an increase in average temperature during the last five years that is 70 percent greater than the world as a whole. Responding quickly at all levels of government by embracing the solutions that are available is critical to minimizing further disruption of this region’s climate and economy. http://www.nrdc.org/globalWarming/west/contents.asp Fact Sheet http://www.nrdc.org/globalWarming/west/fwest.pdf Full Report http://www.nrdc.org/globalWarming/west/west.pdf

The sting of poverty: psychologically pricey

The more poor you get the less you want to deal with it.  I liken it to the same as digging yourself in a really deep hole.  On the flip side of this concept it the more you get, the less you appreciate what you’ve gotten.  Giving people more money to deal with a mountain of troubles isn’t going to work in the face of this thinking.  One has to lower the mountain so that the person sees there’s actually a chance of dealing with it.  

This kind of reminds of chemistry though the analogy isn’t perfect.  There are 2 ways to get a chemical reaction going – you either pump more energy into it or let it release it or you lower the “activation energy” so it’s easier for the reaction to go up the hill.  What Karelis in the article below is talking about is lowering the energy “hill” so it’s easier to climb – psychologically.  

Thanks to Doug Brugge for this article.

****

What bees and dented cars can teach about what it means to be poor – and the flaws of economics

By Drake Bennett 

March 30, 2008

IMAGINE GETTING A bee sting; then imagine getting six more. You are now in a position to think about what it means to be poor, according to Charles Karelis, a philosopher and former president of Colgate University.

In the community of people dedicated to analyzing poverty, one of the sharpest debates is over why some poor people act in ways that ensure their continued indigence. Compared with the middle class or the wealthy, the poor are disproportionately likely to drop out of school, to have children while in their teens, to abuse drugs, to commit crimes, to not save when extra money comes their way, to not work.

To an economist, this is irrational behavior. It might make sense for a wealthy person to quit his job, or to eschew education or develop a costly drug habit. But a poor person, having little money, would seem to have the strongest incentive to subscribe to the Puritan work ethic, since each dollar earned would be worth more to him than to someone higher on the income scale. Social conservatives have tended to argue that poor people lack the smarts or willpower to make the right choices. Social liberals have countered by blaming racial prejudice and the crippling conditions of the ghetto for denying the poor any choice in their fate. Neoconservatives have argued that antipoverty programs themselves are to blame for essentially bribing people to stay poor.

Karelis, a professor at George Washington University, has a simpler but far more radical argument to make: traditional economics just doesn’t apply to the poor. When we’re poor, Karelis argues, our economic worldview is shaped by deprivation, and we see the world around us not in terms of goods to be consumed but as problems to be alleviated. This is where the bee stings come in: A person with one bee sting is highly motivated to get it treated. But a person with multiple bee stings does not have much incentive to get one sting treated, because the others will still throb. The more of a painful or undesirable thing one has (i.e. the poorer one is) the less likely one is to do anything about any one problem. Poverty is less a matter of having few goods than having lots of problems.

Poverty and wealth, by this logic, don’t just fall along a continuum the way hot and cold or short and tall do. They are instead fundamentally different experiences, each working on the human psyche in its own way. At some point between the two, people stop thinking in terms of goods and start thinking in terms of problems, and that shift has enormous consequences. Perhaps because economists, by and large, are well-off, he suggests, they’ve failed to see the shift at all.

If Karelis is right, antipoverty initiatives championed all along the ideological spectrum are unlikely to work – from work requirements, time-limited benefits, and marriage and drug counseling to overhauling inner-city education and replacing ghettos with commercially vibrant mixed-income neighborhoods. It also means, Karelis argues, that at one level economists and poverty experts will have to reconsider scarcity, one of the most basic ideas in economics.

“It’s Econ 101 that’s to blame,” Karelis says. “It’s created this tired, phony debate about what causes poverty.”

In challenging decades of poverty research, Karelis draws on some economic data and some sociological research. But, more than that, he makes his case as a philosopher, arguing by analogy and induction. This approach means that he remains relatively unknown, even among poverty researchers. The book in which he laid out his argument, “The Persistence of Poverty: Why the Economics of the Well-Off Can’t Help the Poor,” wasn’t widely read when it was published last year.

A few, though, have taken notice, and are arguing that Karelis does have something important to say.

“There’s not much evidence in the book, and there are a lot of bold claims, but it’s great that he’s making them,” says Tyler Cowen, an economics professor at George Mason University. It “was a really great book, and it was totally neglected.”

The economist’s term for the idea Karelis takes issue with is the law of diminishing marginal utility. In brief, it means the more we have of something, the less any additional unit of that thing means to us. It undergirds, among other things, how the US government taxes people. We assume that taking $40,000 in taxes from Warren Buffett will be a lot less onerous to him than to an elementary school teacher, because he has so much more to begin with.

In many cases, Karelis says, diminishing marginal utility certainly does apply: Our seventh ice cream cone will no doubt be less pleasurable than our first. But the logic flips when we are dealing with privation rather than plenty. To understand why, he argues, we need only think about how we all deal with certain familiar situations.

If, for example, our car has several dents on it, and then we get one more, we’re far less likely to get that one fixed than if the car was pristine before. If we have a sink full of dishes, the prospect of washing a few of them is much more daunting than if there are only a few in the sink to begin with. Karelis’s name for goods that reduce or salve these sort of burdens is “relievers.”

Karelis argues that being poor is defined by having to deal with a multitude of problems: One doesn’t have enough money to pay rent or car insurance or credit card bills or day care or sometimes even food. Even if one works hard enough to pay off half of those costs, some fairly imposing ones still remain, which creates a large disincentive to bestir oneself to work at all.

“The core of the problem has not been self-discipline or a lack of opportunity,” Karelis says. “My argument is that the cause of poverty has been poverty.”

The upshot of this for policy makers, Karelis believes, is that they don’t need to fret so much about the fragility of the work ethic among the poor. In recent decades, experts and policy makers all along the ideological spectrum have worried that the more aid the government gives the poor, the less likely they are to work to provide for themselves. David Ellwood, an economist and the dean of Harvard’s John F. Kennedy School of Government, has called this “the helping conundrum.” It was this concern that drove the Clinton administration’s welfare reform efforts.

But, according to Karelis, that argument is exactly backward. Reducing the number of economic hardships that the poor have to deal with actually make them more, not less, likely to work, just as repairing most of the dents on a car makes the owner more likely to fix the last couple on his own. Simply giving the poor money with no strings attached, rather than using it, as federal and state governments do now, to try to encourage specific behaviors – food stamps to make sure money doesn’t get spent on drugs or non-necessities, education grants to encourage schooling, time limits on benefits to encourage recipients to look for work – would be just as effective, and with far less bureaucracy. (One federal measure Karelis particularly likes is the Earned Income Tax Credit, which, by subsidizing work, helps strengthen the “reliever” effect he identifies.)

Few economists are familiar with Karelis’s work, and when it’s presented to them, they tend to be skeptical of its explanatory power. If Karelis is right, we should see even more defeatist behavior than we do from the poor, says Kevin Lang, chairman of the Boston University economics department and author of “Poverty and Discrimination.” Plus, he argues, there’s little evidence that simply making poor people less poor increases their work ethic – and some evidence that it does the opposite. In the early 1970s, a large-scale study gave poor people in four cities a so-called “negative income tax,” a no-strings-attached payment based on how little money they made. The conclusion: the aid tended to discourage work.

Karelis responds that the data from that experiment is in fact quite ambiguous, and there has been debate among economists over how to interpret the results. But ultimately, he believes, the strength of his arguments is less in how they fit with the economic work that’s been done to date on poverty – much of which he is suspicious of anyway – but in how familiar they feel to all of us, rich or poor.

“The bee sting argument, or the car dent one,” he says, “I’ve never had anybody say that that isn’t true.”

Drake Bennett is the staff writer for Ideas. E-mail drbennett@globe.com.

© Copyright 2008 Globe Newspaper Company.

The Big Fat Fix: Missing the Point?

You’ll find this article interesting if you read it all.  It talks about the social factors, the genetics, the polluted environmental factors, the evolutionary factors and more that are linked to the obesity/diabetes epidemic.  Essentially alluding to the many problems in society that most are unwilling to face.  It’s the wholesome view where the sum of the individual parts is greater than each part alone.  Alas, it’s in terms of a less positive issue…

 

It’s not entirely the fault of the “individual” as opposed to the collective problem of today’s “modern society”.  

 

Some of the facts about the real causes of obesity include:

1.  Social status:  low income people, people of colour, new immigrants are at greater risk.  That’s because they have access to more junk food, high calorie food, food lacking A LOT of important nutrients.

2.  Location:  you find that diabetes and obesity is highest where people with low income are found.  

3.  Genetics:  having an obese parent or older parent means your kid is more likely to be obese (in cell biology a process called methylation can turn on/off certain genes which are passed on to your children).  

4.  Hormones:  Our highly polluted environments (I tend to think of places like malls too where the chemicals from clothing, etc tends to leach into the air) with thousands of chemicals that mess with your hormones has an effect too.  Think about how this influences your weight and then think back to point #3.  A vicious cycle eh?

5.  Physiology:  The fat cells in your body are as important as any other part of your body.  It helps to control the amount of toxic chemicals in your bloodstream.  Ever wonder why people who diet can’t keep the weight off?  Well the chemicals pretty much shut down your fat burning system.  Your body has to produce more fat cells to suck up the toxins in your bloodstream (so they don’t destroy your brain, heart or liver – as quickly).  This is one fact that skipped my mind until now.  The fascinating wonders of the human body…

6.  Evolution:  Well if people who have more fat survive better in today’s toxic environments (#5) it may translate into having more children (as such studies have indicated).  Low and behold, more obese children may be born which only serves to reinforce point #3.  Unfortunately, being overweight and obese is going to the extreme on its own and you have to deal with heart disease, diabetes.  Of course that won’t kill you before you have kids in some cases so this point still works (that was a bit of evolutionary biology for you).  

 

****

 

The Big Fat Fix

Obesity is a problem that is chronic, stigmatised, costly to treat and rarely curable. Why? Because we are looking in the wrong places for a solution. Pat Thomas reports

 

Date:01/11/2006 Author:Pat Thomas

 

 

Open a newspaper and on any given day you can usually find a story about the growing  number of overweight and obese people throughout the UK, and indeed the world.  Obesity is now officially an ‘epidemic’. GPs are ‘alarmed’. The Department of Health is ‘concerned’. And dozens of local authorities are gearing up to ‘do something about it’. 

 

The figures are shocking. Globally the prevalence of overweight and obesity has increased steadily since 1970. In August of this year, it was reported that the number of overweight people in the world has topped one billion, considerably outnumbering the 800 million who are undernourished.

 

It’s not just an aesthetic problem. Obesity is a health risk associated with higher rates of diabetes, heart disease and cancer. In the UK, 43 per cent of men and 34 per cent of women are overweight and one in four adults, and one in 10 children under 15, are obese. The direct cost to the NHS is £480 million. The indirect costs are estimated to be in

the region of £2.5 billion per year, including costs to the NHS and costs to industry through sickness and absence. In the US, medical expenses for overweight and obesity accounted for 9.1 percent of total US medical expenditures in 1998, costing around $78.5 billion (equivalent to $92 billion today).

 

Most reports in the media trot out the same causes – the gluttony and sloth of modern society – and the same old solutions – eat less and exercise more. And yet if weight loss was simply a matter of cutting calories and being more active then our population should be in pretty good shape. At any given time as much as 50 per cent of the population in the UK is on a diet and/or exercise regime.

 

But one recent report contained a signpost to a truth about obesity that was nonetheless missed by almost everyone who read it. In September of this year a ‘fat map’ of Britain was published by Dr Foster Intelligence, an independent health research organisation that works closely with the NHS, and Experian, a market research company. 

 

The analysis was a complex synthesis of data from two surveys – the Health Survey for England and the British Market Research Bureau’s quarterly survey of 25,000 Britons – that provided details of lifestyle, body mass index (BMI, an indication of how overweight a person is) and geographical location. Its conclusion was that people living in northern industrial towns were fatter than those living in London and more rural areas of the UK. 

 

Across the board the reportage was unremarkable. The results, after all, echoed those of a survey produced by Experian two years ago. Having heard it all before, the newspapers avoided original analysis and focused instead on the marvels of modern technology that allow us to pinpoint, down to a street, the places where the fattest people live.

 

A rent-a-quote from Dr Foster Intelligence about the threat of obesity, and the benefits of surveys like this one, made all the papers: “We need to reduce levels of obesity, and detailed health maps like these show where the risks of obesity are highest,” commented the organisation’s marketing development manager, Dr Marc Farr. “This will enable

health authorities to target weight-loss drives in areas where this is a problem. Until now they have not had access to this accurate database; this should make a difference.”

 

At first it may be difficult to see how knowing where people are fattest will make a dramatic difference to the problem of obesity. Surely the real question that needs answering is why are we so fat? On this point, Farr fell back on mainstream thinking to conclude: “The reasons for obesity [in these northern towns] are not uncommon and shared by many areas: availability of cheap, high sugar food products, unemployment, age-related failure to engage in physical activity, understanding the nature and dangers of obesity and changes to more sedentary forms of employment.”

 

This oft-repeated explanation, of course, has some merit but misses the vital point; that the where and the why of being overweight are intricately linked.

 

Urban Fatties

 

The reductionist explanation for the increase in overweight and obese individuals is a simple equation: calories in/calories out. A more global view, however, would acknowledge the multifaceted effect of urbanisation and industrialisation, which have had a devastating impact on what we eat, when we eat, how much we eat, how often we eat

and the quality of the food we eat, as well as on our levels of daily physical exertion.

 

In the West these simple ‘whys’ of obesity are rarely questioned anymore and have become largely obscured by the solution-oriented focus of quick weight-loss schemes. But in developing nations the startling parallel between the rise in obesity and the rapid acceptance of urban/industrial lifestyles and diets is all too apparent.

 

Speaking in September at the International Congress on Obesity in Sydney Dr. Philip James, the British chairman of the International Obesity Task Force (IOTF), noted that in China the rate of obesity has risen from almost zero in the 1980s to about 10 percent of the population in 2006, and that the rise can be pinned down to the growing problems of urbanisation and the infiltration of a generally nutritionally poor Western diet, which favours high-fat, high-energy products over basic fruits and vegetables. Similar increases have been noted among more affluent urban dwellers in India.

 

Diet failures

 

And so we diet to fight the flab. Yet over and over again surveys show that the majority of people who lose weight on a given diet will subsequently regain that lost weight, and more besides. There is even evidence to suggest that dietary regimes that severely restrict calories as well as types of foods (fats, carbohydrates etc) in the short-term, actually encourage rebound weight gain over the long-term. 

 

This rebound effect, which is well known to dieters and well documented in the medical literature, may have deep roots in human evolution. In our hunter-gatherer stage, when the next meal was not predictable, we became programmed to overeat when food was

available. In times of food deprivation (including when we diet), our hard-wiring changes. Our bodies develop mechanisms, largely driven by hormones, to store calories by over-riding signals of satiety and increasing hunger signals, even when food becomes plentiful again. In essence, the body is storing up calories in anticipation of the next period of food deprivation, even if it never comes. 

 

According to the data, this effect is more dramatic when food and drink is freely available, when the foods available are calorie dense – such as crisps, sodas, Big Macs etc – and energy expenditure is low due to reduced physical activity. 

 

Medical science has determined a biological basis for this storage effect. When we lose weight, our basal metabolic rate (BMR) – the minimum amount of energy the body requires at rest, to keep itself alive and to maintain weight at a constant ’set point’ – decreases. BMR is related to the actual amount of body tissue so it naturally decreases when the amount of body tissue is reduced through dieting. Constant yo-yoing of weight through dieting and bingeing plays havoc with the body’s BMR and set point, in some cases wiping it out altogether, leaving the body with no blueprint for maintaining a healthy weight.

 

A more complex equation

 

In spite of the failure of conventional diets, the comforting equation of calories in/calories out still informs most weightloss initiatives, possibly because it makes the job of ‘doing something about it’ so effortless. Weight management programmes centred on this simple equation are easy to devise – anyone with a calculator, a calorie reference guide and an exercise manual can do it – and they shift the responsibility for the success or failure of the regime squarely onto the individual.

 

It’s an all too familiar scenario when faced with difficult cultural problems, where challenging the status quo could raise uncomfortable questions. Consider the way that individuals are encouraged to switch off standby electronics and change to energy efficient lightbulbs in order to ‘do something about’ climate change, or to recycle to end waste. Focusing on individual efforts – and failures – in this way deflects attention that away from bigger, and arguably more powerful influences, such as the government subsidies that keep polluting airlines and industries in business.

 

Nevertheless, the ongoing failure of ‘gold standard’ solutions like calorie counting has motivated some scientists to suggest that we must be missing something, and to look beyond the usual explanations. This year, a paper in the International Journal Of Obesity, for instance, attempted to explore the ‘roads less travelled’ in obesity research and suggested at least 10 additional causes of obesity that have nothing to do with gluttony and sloth. 

 

The authors, made up of a panel of doctors from across the US, concluded that medical science had a tendency to “focus overwhelmingly on food-marketing practices and technology and on institution-driven reductions in physical activity (the ‘Big Two’), eschewing the importance of other influences.”

 

The panel went on to say that the influence of the Big Two on the global obesity epidemic is “largely circumstantial”, relying as it does on broad surveys – not unlike the recent Dr Foster report – rather than epidemiological data focused on individuals, or large randomised studies.

 

They further noted that the acceptance of the idea that too much food and too little exercise is the sole cause of obesity “.has created a hegemony whereby the importance of the Big Two is accepted as established and other putative factors are not seriously explored. The results may be well-intentioned, but ill-founded proposals for reducing obesity.”

 

In an effort to broaden the debate the authors recommended that other influential aspects of modern life (see box opposite) are influential. Among these and of particular relevance to the results of the Dr Foster survey, was exposure to hormone-disrupting pollutants – the kind you might find in excess in any industrial town in the North of the UK, where once there were mines, refineries, factories and tall chimneys belching out smoke and where now there are chemical factories, incinerators and waste transfer facilities regularly releasing toxins into the air, water and soil.

 

Hormone havoc

 

Hormones play a major role in determining and maintaining metabolism and the body’s set point. When levels of these hormones (produced by the thyroid, sympathetic nervous system and reproductive organs) deviate from the norm, problems with weight can ensue.

 

Thus in January 2004, at a conference titled Obesity: Developmental Origins and Environmental Influences, the US National Institutes of Health made an urgent call for more research on the link between hormone-disrupting chemicals and obesity, noting that exposure during adulthood and, crucially, in the womb, can permanently disrupt the body’s weight control mechanisms. 

 

But, according to at least one scientist, if you look hard enough, the research is already out there. In 2002 Dr Paula Baillie-Hamilton, a visiting Fellow at the Occupational and Environmental Health Research Group, Stirling University, published a paper in which she proposed that chemical toxins were to blame for the global obesity epidemic.

 

Baillie-Hamilton’s hypothesis, the culmination of many years of forensic investigation  into the way that pollution is changing us from the inside out, had its roots in an article she stumbled upon that explained how toxic chemicals in the environment were affecting the fertility of wildlife.

 

“I couldn’t understand how someone like myself, an academic with a load of scientific qualifications and papers behind me, had never heard of all these different chemicals that were out there. Yet if these chemicals were affecting the fertility of wildlife they must be affecting hormones significantly. And of course, hormones control a number of other functions in the body, including weight control.

 

“I spent a couple of years intensively identifying each major category of chemical and then working out how each individual substance affected the body’s weight control system. I looked at all the mechanisms involved, from the nerves and hormones to metabolism, and the levels of nutrients in the body, and found that the same chemicals that at high doses can cause weight loss, seemed to cause a fattening effect at very low levels – the same low levels that we are exposed to in everyday life.”

 

It was an arduous task made more difficult by the fact that weight gain is not always documented in trials of toxic chemicals. “For many years this data has been ignored or suppressed in the conclusions of scientific papers because there was no way to explain why it happened. And of course it wasn’t accepted at the time that weight gain in animals exposed to substances like DDT could be anything other than positive,” continues Baillie-Hamilton. “If weight gain was mentioned, it would be buried in the text of the paper, rather than the conclusion. Essentially what this meant was starting from scratch and reading through every single paper to find some mention of these effects.”

 

What else makes you fat?

 

Being overweight or obese is a modern problem and, as the results of a recent investigation in the International Journal Of Obesity show, many of the putative contributors to the problem have their roots in modern life. The authors suggest that even if some of these causes have only a small effect, they may interact with each other and with other factors in ways that greatly magnify their individual effects.

 

Sleep debt: Too many of us are getting too little sleep and the resulting ’sleep debt’ can alter hormone levels and trigger an increase in body weight. Sleep debt is also associated with insulin resistance and diabetes, and with increased hunger and appetite.

 

Pollution: Hormones control body weight and many of today’s pollutants drastically alter levels of key hormones. 

 

Air conditioning: We burn more calories when the environment is too hot or too cold for comfort. But more people than ever live and work in temperature-controlled homes and offices.

 

Decreased smoking: Smoking, because of its effects on circulation and the nervous system, reduces weight. In many developed countries people are smoking much less than they used to.

 

Prescription medications: Many different drugs – including contraceptives, steroid hormones, diabetes drugs, some antidepressants, and blood pressure drugs – can cause weight gain. Use of these drugs has risen exponentially in recent decades.

 

Population age and ethnicity: Middle-aged people and those of African and Hispanic origin have a tendency to be more obese than younger people of European descent. Throughout the world the population is getting older and more ethnically diverse.

 

Older mothers: There’s some evidence that the older a woman is when she gives birth, the higher her child’s risk of obesity. The average age at which a women has her first child is rising.

 

Ancestry and environment: Some health problems are passed down through the generations. A tendency towards gestational diabetes will produce a child prone to obesity (who are in turn more likely to produce obese children). Very high-fat diets during pregnancy have been shown, in animals, to skew the metabolism of offspring two generations down the line.

 

Obesity linked to fertility: Some evidence suggests that overweight and obese people are more fertile than lean ones. If obesity has a genetic component that makes it a dominant characteristic, the percentage of obese people in the population is likely to increase.

 

Unions of obese spouses: Obese women tend to marry obese men. If there are fewer thin people around – and if obesity is a dominant genetic characteristic – then these couples will produce obese children, who will then go on to produce more obese children.

 

A Chemical Cosh

 

Industrial chemicals – and specifically those that act like hormone disrupters – profoundly alter several aspects of human metabolism and appetite control. Research at the University of Laval in Quebec has added greatly to the understanding of just how wide-ranging the effects of an overpolluted body can be.

 

In the late 1990s Professor Angelo Tremblay and his team began to study, first in animals and then in people, the metabolic effects of organochlorines. Their interest was sparked by earlier Italian research which showed that overweight people who underwent gastric bypasses, to encourage weight loss, experienced dramatic increases in levels of the pesticide DDT and one of its breakdown products, DDE, in their blood as their bodyweight declined. The Laval studies of humans undergoing an average weight-loss programme also showed that concentrations of these chemicals rose as the pounds were shed.

 

Once in the body organochlorines and other industrial pollutants are generally stored in human fat cells. During weight loss the fat cells shrink and release these chemicals back into the bloodstream. The scientists at Laval found that as levels of these now freely circulating pollutants rose in dieters, levels of essential thyroid hormones – necessary for maintaining an efficient metabolism – fell dramatically.

 

A drop in basal metabolic rate (BMR) – the rate at which the body burns calories – is not uncommon in dieters. Studies into dieting show that as metabolism slows down during weight loss, levels of thyroid hormones also drop naturally. This slowdown is referred to as ‘adaptive thermogenesis’.

 

The worrying discovery of the Laval scientists was that higher levels of organochlorine compounds were associated with much lower levels of thyroid hormones than would be produced by weight loss alone. In dieters with these newly liberated toxins circulating throughout the body, BMR also slowed more dramatically, as did energy expenditure and levels of skeletal muscle oxidative enzymes (which determine how efficiently the muscles use energy – when levels are not optimum, energy gets stored as fat).

 

“If I were to put this in journalistic terms,” says Tremblay “I might say that the organochlorines essentially shut down the metabolic furnace that helps the body burn fat.”

 

Professor Tremblay’s research has focused on organochlorine compounds, for instance the pesticides DDT (and its breakdown product DDE), chlordane, aldrin, dieldrin and heptachlor, as well as PCBs, dioxins and chlorophenols. But the list of chemicals that can cause weight gain and promote obesity extends well beyond these to include a wide variety of everyday chemicals associated with manufacturing and a polluted environment (see Chemical calories, page 42).

 

A key effect, says Dr Baillie-Hamilton, is the way industrial pollutants interact with the sympathetic nervous system. This system releases hormones like adrenaline and noradrenaline that suppress our appetite, particularly for fat. These hormones also increase the ability and desire to exercise, as well as increasing body temperature, so that while you are exercising you are also burning calories more efficiently.

 

“Chemicals like organochlorines act directly on the sympathetic nervous system attacking  each and every part of the way it works,” she explains. “It’s like a chemical cosh. They reduce levels of important hormones necessary for weight balance and also block and even destroy the hormone receptors in fat cells. This means the hormones can’t  communicate with the fat cell and the cell becomes less sensitive to those metabolism-regulating hormones that are in circulation.”

 

Adapt and survive

 

Research at Laval continues to confirm that high circulating levels of organochlorines alter metabolism and may be one of the most important contributors to adaptive  thermogenesis and the rebound weight gain so depressingly familiar to dieters.

 

But once liberated by weight loss these chemicals are also free to attack vital organs such as the brain, liver and kidneys, and this threat triggers an even more intriguing response. As chemicals build up beyond a level with which the body’s detoxification pathways can cope, the body begins to ‘dilute’ the amount of circulating toxins – the majority of which are fat soluble – by making new fat cells to store them in. 

 

Recent evidence even suggests that the presence of some industrial pollutants such as  bisphenol-A and organotins can signal dormant ‘baby’ fat cells, known as preadipocytes, to grow into fully mature fat cells, or adipocytes. As the number of fat cells increases it can become harder to keep weight down. In addition, with increasing weight the body detoxification system, which would normally facilitate the excretion of toxins, appears to shut down in preference to simply storing any toxins in available fat.

 

Professor Tremblay admits there is still much that is unknown about the way these chemicals interfere with metabolism. But, apart from triggering hormonal changes, the presence of organochlorines and other toxins can also act as inflammatory triggers.

 

Intelligent fat

 

Some physicians such as Dr. Leo Galland, author and internationally recognised expert in nutrition, believe industrial pollutants can also trigger allergies and allergic responses that can cause, or worsen, the problem of chronic systemic inflammation.

 

For Dr. Galland, it is the problem of chronic inflammation that is most relevant to rising levels of obesity. Inflammation, he argues, causes the body to release a range of  chemicals that make the system resistant to the relatively recently discovered hormone, leptin. Professor Tremblay agrees that this is “entirely possible”.

 

The discovery of leptin 12 years ago in New York at the Rockefeller Institute changed the whole map of our understanding of obesity. 

 

“Prior to that,” says Galland, “the way that everyone thought about fat was that it was just a bag of unused calories that was totally inert. The key thing about leptin is not just that it is a hormone that affects appetite, metabolism and fat stores. It’s that leptin is produced

by fat cells exclusively. So all of a sudden fat became an active player in the body. Really, fat is an organ and its function is just as intricate as any other organ in the body in that it interacts with the immune system, with the nervous system and with other systems

and can produce changes that can be very complex.”

 

Galland admits that the science is difficult, and yet some understanding of it is crucial if we are to get to grips with the problems of hard to shift overweight and obesity.

 

“Whenever there is inflammation, the cells respond by producing anti-inflammatory chemicals known as SOCS – suppressors of cytokine signalling. Two of these, SOCS1 and SOCS3, interfere with leptin by blocking the signal in the cells. The mechanism is very similar to the development of insulin resistance, which is also due to inflammation In fact, inflammation also causes production of the fight or flight hormone cortisol from the adrenal glands. Cortisol blocks leptin and it also raises blood sugar, which in turn decreases the response to any given amount of insulin.”

 

The bigger picture of what these scientists are saying is staggering. Inflammation is fundamentally a protective process necessary, for instance, for wound healing as well as for curing infection. If inflammation arises in a polluted body it’s highly likely that it is a protective response to the presence of toxins.

 

Body fat also has a protective effect. For example, studies show that animals that are exposed to environmental toxins while at the same time encouraged to gain weight through a high calorie diet will survive better than exposed animals that are not allowed to gain weight. In other words, body fat, because it is a repository of these toxins, also becomes a survival mechanism. Thus it is possible that the obesity epidemic, as Tremblay postulated as far back as 2000, is in reality an adaptive response by the body to a chemically toxic environment.

 

The bigger picture 

 

Viewed in this way, obesity could be seen as the response of an intelligent body trying to cope and maintain balance in an overwhelmingly polluted world. Sadly, in an  environment where we are overwhelmed with pollutants, this intelligent adaptation is proving lethal and continued advice to simply decrease calorie intake dramatically in order to speed weight loss may even be making the problem worse. 

 

Clinical practice has been frustratingly slow to catch up with the conceptual changes prompted by the link between environmental pollutants and obesity. 

 

Says Dr Baillie-Hamilton, “There is still no academic textbook that brings it all together and it takes time to get through to people’s consciousness. If you are talking to an obesity specialist, whose professional life has been spent telling people that if they eat too much

and don’t exercise they are going to gain weight, he may not have a clue about the link between industrial pollutants and weight gain. And until the professionals do get a clue their conclusions, and the solutions they propose, will continue to be very limited.”

 

Dr Galland agrees. “There is a worldwide epidemic and it is definitely associated with industrialisation and pollution. And yes, of course, there may be confounding factors because industrialisation and pollution are also associated with dietary changes and changes in activity patterns. But the reality is that the results of most weight loss treatments are lousy and creative new approaches are urgently needed.”

 

To an intelligent health service the ‘fat map’ of Britain would be seen as a wakeup call, an opportunity to get to grips with a difficult and challenging problem. Instead, NHS and government advice remains stubbornly allied to the calories in/calories out equation. For example, the latest Department of Health (DoH) patient leaflet ‘Your Weight, Your Health’ makes clear that excess weight is due to ‘energy imbalance’, explains the number of calories needed per day, suggests ways to reduce the calories you take in each day and lists the benefits of being active.

 

Another booklet from the DoH, The Obesity Care Pathway, for health professionals advises much the same thing and suggests that a sensitive, empathetic, non-judgemental approach should underpin all obesity-related interventions – advice that is intended to complement the National Institute of Clinical Excellence (NICE) guidelines on the prevention, identification, assessment, treatment and weight management of overweight and obesity in adults and children due to be published this month (November).

 

Certainly, not blaming the victims when conventional diets fail would be a good first step. Given the available data on the environmental complexity of obesity this is rather like blaming the poverty striken of the world for being lazy and feckless, the victims of starvation for not having had the foresight to stock up on food, and the people murdered in the twin towers for going to work that day.

 

There also needs to be a much more comprehensive and honest focus on the double bind in which some of the nation’s poorest people find themselves in relation to good health. People in lower income brackets may already be subsisting on poor quality food that is high in sugar and fat and low in nutrition. Their general level of health will already be

compromised. Add the chemical cosh of industrial pollution to the mix and the metabolic and detoxification pathways that should be protecting the body may break down entirely.

 

Uncomfortable questions

 

There is also a need to address the obvious question of why the people in polluted cities like London and New York remain slimmer than those in industrial towns and cities. Given what is already known about polluted bodies, it is a fair bet that such research might show that being thin is not the only, or even the best indicator, of a healthy population. That the particulate pollution from traffic and lighter forms of industry in and around major capitals like these behaves in a distinct way in the body and causes its own kind of chemical chaos. New Yorkers and Londoners may be thinner, but are they also, for example, more infertile or more prone to allergies and asthma and generally more immune compromised?

 

What stands in the way of recognising the need for such solutions, says Professor  Tremblay, is simply that the concept of industrial pollutants altering body chemistry invites far too many uncomfortable questions about the world in which we live. Most of these pertain to the economic consequences of acknowledging this issue.

 

“There is a global context here,” says Tremblay. “You see it with George W Bush’s position regarding the Kyoto agreement. He says it is out of the question to move towards any solution that might lead to what he sees as economic vulnerability. It’s the same with

obesity. The response is always framed by the politics and economics of addressing the reality, not by the potential health problems of exposure to substances like organochlorines.”

 

But just as the US President should be worried about global warming, he should also be worried about the fact that the ‘fat map’ of Britain was not unique to the UK. A just-published survey by the Trust for America’s Health found that the 10 fattest states in the US – Mississippi, Alabama, West Virginia, Louisiana, Kentucky, Tennessee, Arkansas, Indiana, South Carolina and Texas – were in located in the industrial South of the nation. The report failed to mention any aspect of environment, yet the Mississippi River, which runs through several of these states, is officially the most polluted river in the US. Likewise, West Virginia, Texas, Indiana, Alabama, Louisiana and Georgia are home to some of the top 20 mercury polluting power plants in the US. Fish and wildlife in some southern states like Alabama, Arkansas and Tennessee are regularly found contaminated by organochlorines like DDT and PCBs – due to the former production of these chemicals in these areas. 

 

Instead of falling over ourselves to promote a lot of PC nonsense about not being judgemental about overweight and obesity, perhaps it would be more productive to acknowledge that the most pressing human problems, the biggest human disasters, don’t just apparate out of thin air. They evolve in the industrial, environmental and politcial milieu of modern life – and modern life can be a much dirtier business in certain parts of the country. 

 

The health problems associated with polluted bodies are usually unseen. Some, like cancer or Alzheimer’s disease, can take decades to develop. The problems of overweight and of obesity offer us a rare and very visible cue that tells us that pollution is killing us, inch by everexpanding inch.

 

The recognition that chemical pollutants could have such a direct effect on our bodies is possibly one of the most important new ideas in public health; one which demands a difficult but necessary shift in our conceptual understanding of the dynamics of weight control. Allied to this there is an urgent need to acknowledge the way that our actions shape our environment and our environment, in turn, shapes our lives.

 

In July of this year members of the Women’s Institute in the UK took the initiative and dumped carloads of unnecessary food packaging back on the doorstep of supermarkets countrywide, with the message ‘you created this problem, now you clean it up’. The time has come to dump the problem of overweight and obesity back on the doorstep of industry and government with the same unflinching message. 

 

Chemical Calories

 

In addition to organochlorines, a range of other industrial and everyday chemicals are known to encourage weight gain. These include:

 

ORGANOPHOSPHATES

Organophosphate pesticides, such as malathion, dursban, diazanon and carbonates,  constitute 40 per cent of all pesticides used. These chemicals are mainly used inside buildings as opposed to in agriculture. They are neurotoxins and hormone disrupters.

 

CARBAMATES 

Including aldicarb, bendiocarb, carbaryl, propoxur and thiophanate methyl, are used extensively in agriculture, forestry and gardening, and are suspected hormone disrupters.

 

ORGANOTINS 

These chemicals, which include tributyltin (TBT) and the mono and dibutyltins (MBT, DBT), have many applications, including stabilisers in PVC and catalysts in chemical reactions. They are also found in glass coatings, agricultural pesticides, biocides in marine antifoulant paints and wood treatments and preservatives They are damaging

to the thyroid and immune system and potential hormone disrupters.

 

BISPHENOL

A Estrogen mimic used to make clear, hard, reusable plastic products; also used in the manufacture of polymers, fungicides, antioxidants, dyes, polyester resins, flame retardants and rubber chemicals and some dental resins.

 

PHTHALATES

Hormone disrupting chemicals, produced in large volumes, and commonly detected in groundwater, rivers and drinking water as well as in meat and dairy products. Around 95 per cent of phthalate production over the last few decades is tied to the PVC industry. Can be found in many plastics and consumer products – everything from hair spray and nail varnish to plastic water bottles and tshirts.

 

POLYBROMINATED FLAMERETARDANTS

Added to many products, including computers, TVs and household textiles to reduce fire risk. Also found in baby mattresses, foam mattresses, car seats and PVC products. Office workers who use computers, hospital cleaners and workers in electronics-dismantling plants are at particular risk from these chemicals. Polybrominated flame-retardants are oestrogen mimics and can also affect the thyroid.

 

BENZO[A]PYRENE 

A common food pollutant that belongs to a family of chemicals known as polycyclic  aromatic hydrocarbons (PAHs). It is derived from coal tar and enters the atmosphere as a result of incomplete combustion of fossil fuels. In animals it has been shown to cause weight gain in the absence of any detectable change in food intake. It is possible that other PAHs may have a similar effect.

 

SOLVENTS

Neurotoxic chemicals that include xylene, dichlorobenzene, ethylphenol, styrene, toluene, acetone and trichloroethane are commonly found in human blood samples.  Necessary for a wide range of industrial processes and found widely in adhesives, glues, cleaning fluids, paint and felt-tip pens, perfumes, paints, varnishes, pesticides, petrol, and household cleaners and waxes.

 

CADMIUM

Principally used as a protective plating for steel, in electrode material in nickel-cadmium batteries and as a component of various alloys. It is also present in phosphate fertilisers, fungicides and pesticides. Cadmium in the soil is taken up through the roots of plants and distributed to edible leaves, fruits and seeds, and eventually passed on to humans and other animals, where it can build up in milk and fatty tissues. Neurotoxic and a potential hormone disrupter.

 

LEAD

Professions that put their employees at risk of exposure to this neurotoxin include lead-smelting, -refining and -manufacturing industries, brass/bronze foundries, the rubber and plastics industries, steel-welding and -cutting operations, and battery manufacturing plants. Construction workers and people who work in municipal waste incinerators, in the pottery and ceramics industries, radiator-repair shops and other industries that use lead solder may also be among the high-exposure groups.

 

http://www.theecologist.org/archive_detail.asp?content_id=646

Sky High Wheat $ = Expensive Bread + Butter

As powerful businesses rush to cash in on the biofuel gold rush, food prices are going up worldwide not just in Canada.  Here’s another article about that issue as we turn land for food into land for fuel for cars and trucks (to transport food and other consumer goods far and away).  

****

(Feb 18, 2008) (The Canadian Press) REGINA — It’s fixing to get a lot more expensive to bring home the bread as skyrocketing wheat prices squeeze bakers, pasta makers and anyone else who relies on flour to produce their wares.

gllg.php

Bake shops across the country report that the cost of a bag of flour has doubled or more in a matter of months, making it impossible to hold the line on the prices they charge their customers. The increased cost of eggs, butter, shortenings, fruit and other farmed ingredients is compounding the situation. 

“It’s not an industry that is doing well at this time, and that’s an understatement,” said Paul Hetherington, president of the Baking Association of Canada, based in Mississauga, Ont.. “To say the situation is dire — I tend not to want to use words like that, but I think it is fair in this case.” 

Shrinking global grain stocks are behind the wheat price hikes. 

Australia has gone through two years of drought, and nagging weather problems in other parts of the world have put a dent in yields. 

The biofuels movement has been blamed for leading grain farmers to switch to other crops. But the effects on wheat prices are unclear because wheat is not grown in the same parts of the world as corn, which is the main crop used for ethanol. 

World wheat stocks at the end of this marketing year are expected to be the lowest they’ve been since the late 1970s, and in the United States stocks are the tightest they’ve been since just after the end of the Second World War, says Bruce Burnett with the Canadian Wheat Board. 

“It’s a very, very tight situation,” he says. “World production has been under consumption in the last couple of years, so we have been drawing stocks down … and we’ve finally hit levels that have made the market very, very concerned about supplies and rightly so.” 

Generally, the situation has meant prices have doubled in most of the main wheat classes and are likely to remain high for at least the next 18 months, Burnett says. 

“It will take a couple of production cycles, even with the most optimistic yields, to help build the stock levels up in the world to a comfortable level.”

• spacer

• Ethanol may increase greenhouse gas emissions, not reduce them

• The all-natural pint

• Biofuels, barley and beer

At the Bee-Bell Health Bakery in Edmonton’s trendy Old Strathcona district, it has meant the cost of a 20-kilogram bag of bread flour has risen to $18 from $9.50 last September. 

General manager Pete Plaizier can remember a time, not that long ago, when a 25- or 30-cent increase in the price would send the industry into a tizzy. The last two price increases — both within the last month — were more than $2. 

“It’s unbelievable, it’s just going crazy,” Plaizier says. 

The shop has boosted its prices twice in the last two months. A $2 loaf of bread, for example, now costs about $2.60. 

“That’s unheard of in baking.” 

In Toronto, Sal Cofone says he is worried about the future of his business. Cofone’s Queen’s Pasta has been distributing fresh-made and frozen product to some of the city’s finest restaurants for the last 25 years. 

A year ago Cofone was paying $24 for 40 kilograms of flour. Now he is paying $54. Eggs, which come from chickens fed with grain, have also gone up. 

“We cannot go like this, it’s just terrible,” Cofone says. “We can only absorb so much, but people, the users, the restaurants, they don’t understand that.” 

Cofone recently raised his prices by 10 per cent, but that angered his customers. 

“Everybody put their hands in the air and say, `Why, why?’ I say, `What do you want me to do, serve you or close the doors?”‘ 

The higher wheat costs will take longer to hurt larger food producers who lock into long-term supply contracts, but that protection will only last so long, Hetherington says. 

“It’s an industry problem,” he says. “The reality is, if you have escaped the worst of it to date, you are going to be experiencing those same types of cost pressures when your contract expires.” 

Plaizier figures his shop will be paying $25 for a 20-kilogram bag of bread flour before prices stabilize. 

“We can’t wait to react. You have to be quick — you can’t say, `Well, let’s look at this in four or five months,’ because by that time you could have lost $20,000,” he says. 

“You have to keep up. It’s almost a full-time job.”

Tags: barley, biofuels, ethanol.

Climate Chaos is Killing Our Food Crops

Nothing enjoys shocking changes – that goes for plants as well as for people.  Climate change or “chaos” is evident in the extreme changes in our weather.  One day it’s -10 C and before you know it it’s 5 C.  Plants depend on the the right, consistent signals.  Well it seems our changing world know longer knows what signals to send. 

If you stick an object that’s been super heated into something very cold, the extreme changes in temperature cause it to become brittle and vulnerable to breaking easily (like a freshly boiled egg hit with cold water).  Try it with a glass bowl and see what happens (grins).  Now that’s stress.  

****

From: American Institute of Biological Sciences 

Published March 3, 2008 09:12 AM

Will global warming increase plant frost damage?

Widespread damage to plants from a sudden freeze that occurred across the Eastern United States from 5 April to 9 April 2007 was made worse because it had been preceded by two weeks of unusual warmth, according to an analysis published in the March 2008 issue of BioScience. The authors of the report, Lianhong Gu and his colleagues at the Oak Ridge National Laboratory and collaborators at NASA, the University of Missouri, and the National Oceanic and Atmospheric Administration, found that the freeze killed new leaves, shoots, flowers, and fruit of natural vegetation, caused crown dieback of trees, and led to severe damage to crops in an area encompassing Nebraska, Maryland, South Carolina, and Texas. Subsequent drought limited regrowth.

Rising levels of atmospheric carbon dioxide are believed to reduce the ability of some plants to withstand freezing, and the authors of the BioScience study suggest that global warming could lead to more freeze and thaw fluctuations in future winters. This pattern is potentially dangerous for plants because many species must acclimate to cold over a sustained period. Acclimation enables them to better withstand freezes, but unusual warmth early in the year prevents the process. A cold spring in 1996, in contrast to the 2007 event, caused little enduring damage because it was not preceded by unusual warmth.

The 2007 freeze is likely to have lasting effects on carbon balance in the region. Plants cannot resorb nutrients from dead tissue that would normally be remobilized within the plants during autumnal senescence, so many nutrients became less available for plants in 2008. Wildlife is expected to have suffered harm from lack of food, and changes to plant architecture could have long-term implications.

Gu and his colleagues propose that the 2007 spring freeze should not be viewed as an isolated event, but as a realistic climate-change scenario. Further study of its long-term consequences could help refine scenarios for ecosystem changes as carbon dioxide levels increase and the climate warms.

My Forbidden Fruits (and Vegetables)

The farmer who wrote this article found that the rules give him a catch-22:  if he grows fruits and vegetables for local consumption on even a part of his land he loses all the US subsidy money that would support him.  If he grows only cash crops like corn or soy then he can’t thrive and earn a better living on local markets.  The trade and subsidy rules have been designed to primarily support big food export business.  

I always find it funny that nearly 70% of these big grain crops (i.e.  corn, wheat, soy – StatsCan data mind you) often go to feeding animals to produce meat at a time when people are eating way more than the recommended 2-4 servings/day…

****

March 1, 2008

OP-ED CONTRIBUTOR

My Forbidden Fruits (and Vegetables)

By JACK HEDIN

Rushford, Minn.

IF you’ve stood in line at a farmers’ market recently, you know that the local food movement is thriving, to the point that small farmers are having a tough time keeping up with the demand.

But consumers who would like to be able to buy local fruits and vegetables not just at farmers’ markets, but also in the produce aisle of their supermarket, will be dismayed to learn that the federal government works deliberately and forcefully to prevent the local food movement from expanding. And the barriers that the United States Department of Agriculture has put in place will be extended when the farm bill that House and Senate negotiators are working on now goes into effect.

As a small organic vegetable producer in southern Minnesota, I know this because my efforts to expand production to meet regional demand have been severely hampered by the Agriculture Department’s commodity farm program. As I’ve looked into the politics behind those restrictions, I’ve come to understand that this is precisely the outcome that the program’s backers in California and Florida have in mind: they want to snuff out the local competition before it even gets started.

Last year, knowing that my own 100 acres wouldn’t be enough to meet demand, I rented 25 acres on two nearby corn farms. I plowed under the alfalfa hay that was established there, and planted watermelons, tomatoes and vegetables for natural-food stores and a community-supported agriculture program.

All went well until early July. That’s when the two landowners discovered that there was a problem with the local office of the Farm Service Administration, the Agriculture Department branch that runs the commodity farm program, and it was going to be expensive to fix.

The commodity farm program effectively forbids farmers who usually grow corn or the other four federally subsidized commodity crops (soybeans, rice, wheat and cotton) from trying fruit and vegetables. Because my watermelons and tomatoes had been planted on “corn base” acres, the Farm Service said, my landlords were out of compliance with the commodity program.

I’ve discovered that typically, a farmer who grows the forbidden fruits and vegetables on corn acreage not only has to give up his subsidy for the year on that acreage, he is also penalized the market value of the illicit crop, and runs the risk that those acres will be permanently ineligible for any subsidies in the future. (The penalties apply only to fruits and vegetables — if the farmer decides to grow another commodity crop, or even nothing at all, there’s no problem.)

In my case, that meant I paid my landlords $8,771 — for one season alone! And this was in a year when the high price of grain meant that only one of the government’s three crop-support programs was in effect; the total bill might be much worse in the future.

In addition, the bureaucratic entanglements that these two farmers faced at the Farm Service office were substantial. The federal farm program is making it next to impossible for farmers to rent land to me to grow fresh organic vegetables.

Why? Because national fruit and vegetable growers based in California, Florida and Texas fear competition from regional producers like myself. Through their control of Congressional delegations from those states, they have been able to virtually monopolize the country’s fresh produce markets.

That’s unfortunate, because small producers will have to expand on a significant scale across the nation if local foods are to continue to enter the mainstream as the public demands. My problems are just the tip of the iceberg.

Last year, Midwestern lawmakers proposed an amendment to the farm bill that would provide some farmers, though only those who supply processors, with some relief from the penalties that I’ve faced — for example, a soybean farmer who wanted to grow tomatoes would give up his usual subsidy on those acres but suffer none of the other penalties. However, the Congressional delegations from the big produce states made the death of what is known as Farm Flex their highest farm bill priority, and so it appears to be going nowhere, except perhaps as a tiny pilot program.

Who pays the price for this senselessness? Certainly I do, as a Midwestern vegetable farmer. But anyone trying to do what I do on, say, wheat acreage in the Dakotas, or rice acreage in Arkansas would face the same penalties. Local and regional fruit and vegetable production will languish anywhere that the commodity program has influence.

Ultimately of course, it is the consumer who will pay the greatest price for this — whether it is in the form of higher prices I will have to charge to absorb the government’s fines, or in the form of less access to the kind of fresh, local produce that the country is crying out for.

Farmers need the choice of what to plant on their farms, and consumers need more farms like mine producing high-quality fresh fruits and vegetables to meet increasing demand from local markets — without the federal government actively discouraging them.

Jack Hedin is a farmer.

http://www.nytimes.com/2008/03/01/opinion/01hedin.html?ei=5070&en=9e667ebba91a7259&ex=1205125200&emc=eta1&pagewanted=print

Buzzing On City Honey: Toronto Style

Sasha Chapman

Feb. 23/08

Globe and Mail 

http://www.theglobeandmail.com/servlet/story/LAC.20080223.INSATIABLE23/TPStory/?query=bees

 

Toronto Bees: Raised on the Roof

Much ink has been spilled over the worldwide disappearance of honeybees over the past couple of years. There are many threats to this sensitive species, from parasitic varroa mites to industrial agriculture to the mysterious colony collapse disorder that seems to be plaguing hives south of the border. But the biggest threat to our city’s bees may be the Ontario Beekeeping Act, which makes it illegal to put a hive within 30 metres of an urban dwelling. Which is a shame, because Toronto honey tastes so good.

 

Most cities around the world keep bees, whether it’s legal or not. In Paris, there are hives on the roof of the opera house. In New York, high-rise bees produce honey for the Union Square Market. And in Vancouver, city councillors recently introduced a loophole to allow apiculturists to keep bees in the city.

 

So far, there’s been no relaxing of the rules at our own City Hall. Instead, dedicated beekeepers are quietly finding ways to work around the act. A couple of years ago, Brian Hamlin, a beekeeper with hives’ all over Ontario, found a secret corner on the Toronto Islands where he could install a few hives. He now produces a couple hundred pounds of raw honey each year, which Murray Graziano sells at the Golden Orchards stall in the St. Lawrence Market. “We only have two jars left,” Mr. Graziano says. “People wait for it.”

 

FoodShare is a non-profit organization that works to bring healthy, affordable, local food to Torontonians. About five years ago, it tucked a dozen hives underneath the Gardiner Expressway near its offices on Eastern Avenue, where the bees were kept out of the public eye and had easy access to the Don Valley. They thrived, producing about 700 kilograms of honey each year for FoodShare and the volunteer Toronto Beekeepers Cooperative that tends them. (FoodShare sells 500-millilitre jars for $5 at its offices.) Complex and full of character, FoodShare’s semi-solid honey is more interesting than a lot of country honeys and certainly better than the Chinese and South American honey that is sometimes added to the mass-produced “Canadian” brands.

 

“I suspect it’s because the forage in the city is so diverse,” says Cathy Kozma, a real-estate agent and one of the volunteers who tends FoodShare’s hives. “In the country, it’s all monocultures.”

 

But when FoodShare moved its offices to a larger location at Bloor and Dufferin a year ago, their new landlord, the Toronto District School Board, wasn’t keen on having bees as tenants, and the hives were temporarily banished to Guelph, while a cadre of volunteers tried to find a new Toronto home for them. Honey production plummeted.

 

“You could tell that the bees weren’t happy,” Ms. Kozma says. The volunteers weren’t very happy, either – they had to drive to Guelph to tend the hives.

 

The bees are finally returning to the city next month, though not to FoodShare’s offices. Some will be housed, improbably, on top of the Fairmont Royal York, across from Union Station, and the rest will be installed at the Brick Works in the Don  Valley. Although the Fairmont is situated in the middle of downtown, the bees will be kept on a 14th-floor roof garden – more than 30 metres above street level, or any other “urban dwellings” nearby.

 

David Garcelon, the executive chef at Fairmont, got the buzz when he was harvesting herbs in the hotel’s rooftop garden and noticed somebody else’s honeybees foraging there. “Wild honeybees are virtually non-existent in the city, so we figured somebody had to be keeping hives close by maybe on the island,” Mr. Garcelon says. The chef began to wonder if he could put his own hives on the roof.

 

He contacted the Toronto Beekeepers Cooperative – the same volunteer organization that tends FoodShare’s hives. Soon, they were talking logistics, trying to figure out how many hives they could build in the rooftop garden. “When we first started talking about it, people thought we were crazy,” says Mr. Garcelon, who spent months convincing hotel management that the project was worthwhile.

 

Last fall, the chef and his apprentices built a couple of hives. Now, they are just waiting for some warmer weather to move the bees from Guelph. This year, Mr. Garcelon hopes to harvest 200 to 300 kilograms of honey, which he will use in the kitchen and package as gift items for guests.

 

The rest of the hives will go to the Brick Works, where Evergreen plans to use the hives as a program piece, for public education.

 

Honeybees are far less likely to sting people than the carnivorous yellow jackets that plague our picnics, and there are good reasons to keep them in the city. They pollinate our gardens, helping our flowers bloom and our vegetables grow. And they are also a good indicator of the health of our environment.

 

In the meantime, FoodShare has not given up hope on housing its own hives – it continues to negotiate with the TDSB and make nice with its neighbours, in the hopes that one day it might be able to install a few hives on its roof.

 

Sasha Chapman’s column ” INSATIABLE”  appears every other Saturday  Special to The Globe and Mail

Eggs from the Backyard Anyone?

Urban chicken farming is environmentally sustainable, but illegal

 

Kim Covert, Canwest News Service; With files from Global News

Published: Tuesday, February 26

Montreal Gazette – Montreal,Quebec,Canada

http://www.canada.com/montrealgazette/news/story.html?id=5e8ddb61-3657-455b-84c2-6f8253380c46

Three chickens were forced to fly their city coop in Halifax yesterday, depriving their owner of fresh eggs – but also reigniting the discussion about where our food should come from.

Some say that in the era of the zero-mile diet, urban agriculture is something that will have to be dealt with more constructively than by setting the government foxes on the henhouses.

The woman who owned the chickens, Louise Hanavan, says she believes people in cities should be able to grow some of their own food, and she wants the city of Halifax to change a bylaw prohibiting that.

“I’d really like to see the city take a more active position in promoting urban agriculture, and encouraging people to do creative things like this to promote sustainability in urban areas,” she said.

Mike Levenston agrees. He’s executive director of City Farmer, a small non-profit group of urban gardeners, defined as anyone who lives in an urban area who grows things to eat on a non-commercial basis, from the window sill herb garden to the big backyard – or rooftop – garden.

“In 1978, we put out a small newspaper called City Farmer, and our first cover story was ‘Chickens in Soup’ about a Vancouver woman in trouble with the municipality for raising chickens at home.”

He recently wrote a blog post called “Chickens Still in Soup” because of the number of stories that have come across his desk recently, including Hanavan’s.

Levenston says sympathy is growing, “around North America, certainly, around changing the bylaws. I think earlier on it was: ‘Hey, we’re urbanites, we’re not farmers, we’re not rural, there’s a difference.’

“But now, with the whole local food (movement) … people are thinking: ‘Hey, we want to get involved in our food.’ So I think it’s becoming ultra-urban chic now to have this take place in the city,” he said from his office in Vancouver.

Some urbanites worry about smell when it comes to livestock, others worry about noise, or about mice and rats being attracted to the feed. Levenston says the smart thing to do would be to work with experts – say at a university agricultural program – to set standards for housing livestock and storing feed, and then issue permits to keep livestock based on those standards.

People are now lobbying the Halifax Regional Municipality to allow limited poultry farming there, echoing similar movements across Canada, said Jayme Melrose, Community Garden Co-ordinator for the Nova Scotia Public Interest Research Group.

“Food (in)security is a massive impending issue that should be of serious concern to federal, provincial and municipal governments across the country!” Melrose said in an e-mail to Canwest News Service.

Marla MacLeod, Food Miles Co-ordinator for the Ecology Action Centre in Nova Scotia, says her group was surprised at the continuing public outcry over Hanavan’s chickens, which were moved yesterday to a farm outside Halifax.

There are at least two Facebook groups dedicated to Hanavan with over 600 members, and two petitions were presented to city council in February with more than 1,000 names demanding she be allowed to keep her poultry and that bylaws be amended.

Asked what she thought prompted the interest, MacLeod pointed to recent food scares.

“People are really worried about where their food is coming from,” MacLeod said. “Local food was the news item for 2007, ‘locavore’ was the word of the year in the Oxford English dictionary. … People are wanting to reconnect with their food. And I think that was part of why this story really took off.”

Is plastic making us fat?

Might as well be aware of what’s going on.  I’m also doing research on this subject in terms of PFOA or perfluorooctanoic acid – a substance that is so indestructible that every molecule produced will stay with us forever even if we stopped.  The likely impacts (even at low yet constant doses) on pregnant women and of course the children needs to be remembered.  The article below brings home a more vivid impact on our waistlines from a related indestructible chemical – bisphenol A.  

 

If we walk, let us walk in knowledge and not in fear or despair.  

Then at least we have the choice to do something about it.  

-SL

 

****

 

Researchers are exploring whether exposure to common chemicals during early development could set us up for a lifetime battle with the bulge

By Beth Daley 

Globe Staff / January 14, 2008

Boston Globe

 

Being fat has long been seen as a personal problem, fixed only by struggling against the proliferation of fast food restaurants, unlucky genes, and a sedentary life.

 

But could something in the environment also be making Americans fat in epidemic numbers?

 

Animal studies in recent years raise the possibility that prenatal exposure to minuscule amounts of common chemicals – found in everything from baby bottles to toys – could predispose a body to a life of weight gain. The chemicals, known as endocrine disrupters, mimic natural hormones that help regulate, for example, how many fat cells a body makes and how much fat to store in them.

 

These findings have led some scientists to put forth a provocative argument: They say diet and too little exercise clearly are key reasons for the worldwide rise in obesity in the past 20 years, but they may not be the only ones. Food intake and exercise just haven’t changed that much in that period, they argue. And while genetics obviously play a role – just think of someone you know who can eat three Big Macs a day and never gain an ounce – these researchers say it would be impossible to see such widespread genetic change in just two decades, giving them more reason to suspect the environment.

 

“This is a really new area . . . but from multiple labs on multiple levels we are getting preliminary data that all say the same thing: Chemicals can play a role,” said Jerry Heindel, a program administrator for the National Institute of Environmental Health Sciences. “We know that nutrition and exercise are very, very important, but underlying that could be environmental exposures during development that alter your physiology, including how you respond to food and exercise.”

 

Thousands of chemicals have come on the market in the past 30 years, and some of them are showing up in people’s bodies in low levels. Scientists studying obesity are focusing on endocrine disrupters – which have already been linked to reproductive problems in animals and humans – because they have become so common in the environment and are known to affect fat cells.

 

One key researcher in the field, Bruce Blumberg of the University of California, Irvine, has even coined a new word for chemicals that can make you fat: Obesogens.

 

A recent US Centers for Disease Control and Prevention study found that about 93 percent of the US population had bisphenol A, a chemical that can be found in canned goods and in hard, clear plastic items such as baby bottles and hiking containers, in their body. A study at the University of Missouri-Columbia showed that mice fed bisphenol A during early development – at lower amounts than what would have resulted in the levels found in most people in the CDC study – become markedly more obese as adults than those that weren’t fed the chemical. Tufts University scientists observed similar phenomenon in rats.

 

The chemical industry, however, disputes those studies and says dozens of others that examined bisphenol A showed no weight gain.

 

more stories like this

 

“The scientific evidence shows that bisphenol A . . . does not have any effect on body weight,” said Steven Hentges, executive director of the polycarbonate/BPA global group of the American Chemistry Council, which represents chemical manufacturers.

 

Bisphenol A is only one of the chemicals scientists are studying. Blumberg’s lab has also studied tributyltin, an endocrine disrupter that is used as an antifungal agent in agriculture and in marine paints to keep ship hulls free of barnacles. Female mollusks exposed to the chemical were seen to grow male sex organs. Lab mice exposed to tiny levels of tributyltin during prenatal development became fatter adults than those not given the chemical.

 

“It predisposed them for life,” said Blumberg.

 

These scientists are focusing on early development because it is a critical time for determining a baby’s long-term health and weight. For example, studies show that babies born underweight are likely to be fatter later in life, possibly because undernourished fetuses learn to use fat cells more efficiently – and it gets embedded in their physiology. Researchers suspect the same thing may be taking place with chemical exposures.

 

Exposure “can be critical on the front end of one’s life where the rest of your life’s physiology is being programmed,” said Frederick vom Saal, a biological scientist at the University of Missouri-Columbia who studies bisphenol A.

 

His lab is studying genes in the fat cells of mice to better understand why the animals became fatter when exposed to the chemical.

 

Growing up with more fat cells isn’t necessarily a problem if you are running around a lot, says Pete Myers, chief scientist for Environmental Health Sciences, which publishes the online journal Environmental Health News. But in a world where exercise is down and poor diets abound, it could exacerbate a weight problem.

 

Vom Saal says as people become adults, they may be able to shake off the weight with extreme diet and exercise, but it won’t be easy. “It is a very intractable thing to change,” he said.

 

Scientists who study obesity’s link to chemicals say the research is still in its infancy. Among the many unanswered questions that remain: How do the changes happen? What about the combined impact of exposure to many chemicals? Are humans affected by the chemicals the same way as animals?

 

For those who don’t want to wait until all the evidence is in, there is another question: How to avoid these chemicals now?

 

“It can be difficult,” said Felix Grun, assistant researcher in the department of developmental and cell biology at the University of California who works with Blumberg. To minimize exposure to bisphenol A, Grun said people can avoid buying plastics with the recycling number 7 marked on the bottom, but similar types of chemicals abound in other products, too. “These compounds are everywhere, the carpet fibers, the PVC piping, etc,” he said.

 

Scientists say years of research into a once-popular synthetic hormone – diethylstilbestrol (DES) – also bolsters their belief that chemical exposure during early development can affect weight later in life. DES was once given to women to prevent miscarriages until it was linked to cancer in female offspring. Now, research by Retha R. Newbold at the National Institute of Environmental Health Sciences shows that mice exposed to DES in utero are fatter than those not given the chemical.

 

Ana Soto, a Tufts University professor who studies endocrine disrupters and development, says scientists already know that the most serious health problems of DES impact mice and humans similarly. Now that mice exposed to low levels of bisphenol A are behaving much the same way they do when exposed to DES, it makes sense to conclude that humans may be at risk too. She wants the chemicals like bisphenol A to be regulated by the federal government.

 

“What else are we waiting for?” Soto asked. “There is evidence these chemicals have a multitude of deleterious effects in animals. . . We should be worried.”

 

Beth Daley can be reached at bdaley@globe.com

© Copyright 2008 Globe Newspaper Company.

The Cholesterol Con – Misinformation for $

 

It was funny that I should have run into this article (see below).  What a coincidence.  I’d just watched an episode on Daily Planet where Jay Ingram was talking about how reducing inflammation in the past was what really allowed us to live longer and grow taller.  It wasn’t necessarily the diseases in the past at all.  An examination of the the past records by scientists indicate that chronic inflammation may have played the biggest role in shortening lives and killing people.  It’s like being constantly stressed – your body spends energy fighting that instead of growing taller or living longer.  

 

Anyways, how does it relate to this article on statins and cholesterol?  Well it turns out that statins are probably no better than eating things like omega 3 fatty acids and vitamin E.  Considering its high price and additional side effects, one might as well just go for the o-3 and vitamins.  According to the growing research it’s really about preventing inflammation (i.e.  vitamin E is one of many anti-inflammatory compounds – inflammation also causes allergy suffering).  If Jay’s research and what I’ve learnt over the last few years is making some sense then drug companies just want to make a profit off of people by having government agencies sell their product to the masses when more natural, effective and simple methods exist.  

 

****

 

The Cholesterol Con – Where Were the Doctors? Part I   [and reporters] 

 

By Maggie Mahar 

Health Beat 

 

 Wednesday 20 February 2008 

 

http://www.truthout.org/issues_06/022908HA.shtml 

 

 

After the stock market bubble burst, the New York Times asked: “Where were the analysts? Why didn’t they warn us?” 

 

    To be perfectly honest, this was a somewhat disingenuous question. As experienced financial journalists understood all too well, the analysts plugging the high-flying issues of the 1990s were employed by Wall Street firms raking in billions as investors bet their nest eggs on one hot stock after another. It really wasn’t in their employers’ interest for analysts to tell us that their products were wildly over-priced. When a small investor wades into the financial world, there are two words he needs to keep in mind: “caveat emptor.” 

 

    But physicians, I firmly believe, are different from the folks employed by Merrill Lynch. (I don’t mean to knock people who work at ML. I am simply saying that they have a very different job description.) When consulting with your doctor, you should not have to be wary. You are not a customer; you are a patient. And your physician is a professional who has pledged to put your interests ahead of his or her own. 

 

    This brings me to the question I ask in my headline: during the many years of the Cholesterol Con – where were the doctors? When everyone from the makers of Mazola Corn Oil to the Popes of Cardiology assured us that virtually anyone could ward off heart disease by lowering their cholesterol, why didn’t more of our doctors raise an eyebrow and warn us : “Actually, that’s not what the research shows” ? … SNIP