The war on obesity is a war on the poor

`It's the poor wot gets the blame.' That was a popular refrain during the First World War, but it could just as easily be a rousing chorus from the trenches of the War on Obesity. Today there is an assumption that behind every flabby child waddling down the road there are parents who are as thick as mince, with barely enough money to send their overweight offspring to the chip shop for their dinner on the way back from fetching mum and dad's fags. However, two recent pieces of research give the lie to this sketch, suggesting that the middle classes are just as prone to eating crap food and having fat children as the poor.

Just over a week ago, the UK Food Standards Agency (FSA) published research which showed that the poor, far from having a nutrition-lite diet of fat and sugar, actually ate much the same kinds of foods as everyone else (1). In a detailed survey of the eating habits of 3,278 people from households in the most materially deprived sections of the population, the FSA found that the most significant differences in eating habits were related to age, not social class. Younger people, regardless of social class, tended to consume more low-fibre, high-fat, high-sugar and processed foods than older generations. Poor people were no more likely to be overweight or obese than the better-off.

Then, last Sunday, the UK Independent on Sunday declared that `the nation's higher-paid working mothers bear much of the responsibility for the country's ticking obesity time bomb, and not the poorer working-class families who are usually blamed.' (2) Another study, carried out by University College London and Great Ormond Street Hospital, found that children growing up in households with incomes greater than œ33,000 per year were more likely to be obese than those in homes with the lowest incomes. Apparently, middle-class households where the mother works are particularly affected: `Long hours of maternal employment, rather than lack of money, may impede young children's access to healthy foods and physical activity.'

The news that middle-class kids get fat too shouldn't be a shock to anyone. It became frontpage news over the past week only because the problem of obesity has, until now, been readily blamed on the ignorance and moral failings of the working classes; that these `middle classes get fat!' findings have been treated as stunning is testament to the extent to which obesity has been associated with moral turpitude amongst the lower classes. And yet, at the same time as these latest studies seem to have exhonerated the poor, they have also found a new enemy in the War on Obesity: working mothers.

Women who hold down a job, run a home and raise children have got enough on their plates already. Now, apparently, they have to bear responsibility for their children's ill-health, too. As Dr Colin Waine, chairman of the National Obesity Forum, told the Independent on Sunday: `I do not wish to condemn these women but I do think the priority has to be the health of the child and its continued health into adulthood. We are in danger of raising a generation of young people with a much shorter life expectancy than previous generations.' (3) Unfortunately, Dr Waine sounds a bit like those people who say `I'm not a racist, but.' No doubt he will assure us that some of his best friends are working mothers.

Whether being a working mother really is going to make your children fat or not (and we shouldn't leap to conclusions on the basis on one study), the question really should be: does it matter? The fact is, the relationship between ill-health and obesity is a complicated one. It certainly appears to be the case that the very overweight have a lower life expectancy than those who are lighter. But whether this is strictly to do with how much fat they have round their waists is another matter. It is not only the amount of body fat they have that makes the very overweight different to slimmer individuals. For example, obese people tend to take less exercise and there's good evidence that exercise (which in this case means walking regularly rather than running marathons) can offset most of the risks of heart disease, type-II diabetes and so on that are associated with being fat. Moreover, somebody who is capable of being really fat (most people wouldn't get really fat even if they stuffed their faces) may have other physiological problems that increase their propensity for chronic diseases. But for the rest of us - from those of `ideal' weight to the mildly obese - the risk of an early death is pretty much the same across the board.

Nor can we predict an individual's adult health from his or her size as a child. As a thought-provoking new paper by the Australian academic Michael Gard bluntly notes, `no study in the history of medical science has ever established a causal link between childhood fatness and adult ill-health or premature death' (4). So, why all the attention given to obesity in general, and childhood obesity in particular? It's not as if obsessing about our weight has made us any happier (or thinner). For Gard, obesity has become a morality play for those who would like to intervene in our lives: `Unfortunately, many commentators talk about the war on obesity as a war between good and evil; good food versus bad food, wholesome physical activity versus evil technology; and responsible versus irresponsible parenting. If we then factor in the inconvenient fact that obesity research has not produced a "smoking gun" which implicates anyone in particular, the stage is set perfectly for protracted and unhelpful arguments about what research does or does not say about the causes of obesity.' (5)

As the American commentator Paul Campos has noted, the best way to win the War on Obesity is to stop fighting it. But the War on the Poor will carry on regardless of the results of studies into eating habits - after all, it's a war that's been raging for well over a century and serves to confirm the innate superiority of those with a bob or two in their pockets. This extract from a popular English Victorian magazine could have been the product of many a modern-day hack: `The Bethnal Green poor. are a caste apart, a race of whom we know nothing, whose lives are of quite different complexion from ours, persons with whom we have no point of contact.' (6)

Such an explicit statement of the idea that some people are simply of better `stock' than others would be unacceptable today. Nonetheless, the same idea is implicit in the logic of modern thinking on poverty and obesity. Wealthy people who cook decent meals with fresh ingredients are seen as being morally superior - they care about their health and their children's health, and they care for the planet, too. Poorer people, who apparently only eat microwaveable meals or pizzas biked to their homes during an episode of EastEnders, are looked upon as sinful and slothful - they are, in Jamie Oliver's immortal words, `white trash' and `tossers' who allegedly care little for their own wellbeing or that of their families. Today, the sense of a divide between rich and poor is articulated most frequently through issues of health and diet.

The search for some form of moral superiority, rather than a real concern with health, is the driving force behind the authorities' War on Obesity. That is why a campaign ostensibly against fatness can easily shift its attention from feckless `chavs' to working mothers: because it is underpinned by moralistic judgements about our lifestyle choices rather than hard scientific facts about our eating habits. First `white trash' families and now mums who dare to work - the War on Obesity is a war against those who make the `wrong' choices, who refuse to play by the rules laid down by the new elite, and who instead do things their own way. In this sense, the demand that we `eat healthily' and have the correct body shape (whatever that might be) is at root a demand that we conform.

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Attack on HIV broadening

HIV laboratories around the world are humming. New discoveries and treatments are tumbling out of the research pipeline at a remarkable pace, one that promises HIV patients a longer, healthier life. This, for a disease that was a death sentence when it was first identified 26 years ago.

Little wonder that when nearly 6000 experts on HIV and AIDS from 133 nations gathered in Sydney this week for the fourth International AIDS Society Conference on HIV Pathogenesis, Treatment and Prevention, they buzzed. "This is an enormously exciting time," says John Kaldor, deputy director of the National Centre in HIV Epidemiology and Clinical Research at the University of NSW. "Over the past two years people have made striking improvements in therapy, especially for people in whom several regimens have already failed. People have also made significant developments in what are considered biomedical tools -- like microbicides -- to help break the cycle of transmission."

Much, too, has been learned about how the insidious human immunodeficiency virus infects its victims, wreaks such damage and is so hard to beat. According to long-time HIV-AIDS researcher Anthony Fauci, director of the US National Institute of Allergy and Infectious Diseases in Bethesda, Maryland, new insights into the mechanisms by which HIV harms humans have underpinned development of over 25 anti-HIV drugs. "These medications have had an enormous impact in reducing mortality wherever they have been used," says Fauci who, as a clinically and scientifically trained infectious diseases and immunology specialist, was one of the first experts in the world to see, treat and attempt to unravel HIV infection. "Patients I followed 25 years ago would die within months of getting seriously ill. Now I'm following patients for 10, 15 years. They're doing just fine. The triumph has been great."

Entire new classes of drugs promise to keep the triumphs coming, particularly for patients who are developing resistance to the various combinations of existing drugs. To the outsider they sound baffling, but these classes -- integrase inhibitors, fusion inhibitors, CCR5 antagonists and maturation inhibitors -- promise to bring the biggest improvement in HIV treatment since the discovery in the mid-1990s that combined drug treatment, called Highly Active Anti-Retroviral Therapy (HAART), greatly improved viral suppression.

To get a feel for what such drugs are and do, it's necessary to understand why HIV is such a knotty scientific problem. Firstly, as Fauci explains, it attacks the immune system: "Virtually all of the viruses that have been scourges of mankind -- or even viruses that have been trivial -- are viruses that come in and affect the lung, or the skin, or the brain, or the gastrointestinal tract and the immune system is intact and is able to fight the particular virus," he says.

Not so HIV. It targets the immune system itself, perversely destroying the very mechanism the body entrusts with its own defence. Moreover, it's a retrovirus, a virus that has the ability to insert itself directly into its victim's genetic material. It can hide out there. HIV also replicates quickly. That quick turnover enables the virus to mutate, to change its appearance so fast that even when it does stick its viral head over the parapet, the immune system cannot effectively respond. It's a triple whammy. HIV infects the immune system. It's a retrovirus. It mutates rapidly. "You put those three things together and you have a real problem," Fauci concludes.

Still, researchers did target the culprit and have built weapons to fight it. The first anti-HIV drug, AZT, was licensed in 1987, and works by inhibiting the HIV enzyme reverse transcriptase which the virus uses to convert its single strand of RNA into double-stranded DNA, a necessary first step prior to splicing itself into the host cell's genome.

AZT was hailed as a wonder drug, but the euphoria soon faded when it became apparent that HIV's high rate of mutation quickly allowed resistance to the drug to develop. Later, other "anti-retroviral" drugs were developed, and these are generally now combined into triple or even quadruple drug cocktails to prevent drug resistance developing. Among the most successful antiretrovirals now are Lamivudine, Viread and Ziagen.

US infectious diseases specialist Joseph Eron says the most exciting prospects among the new drugs about to become available are integrase inhibitors. These work by blocking another enzyme, integrase, which HIV uses to insert its genetic material into the host cell's DNA. Two such drugs are in development and one, raltegravir, is already available on a trial basis in Australia.

More are on the way. Last week several biotech companies reported on laboratory, or early trials of even newer drugs. "There is now an opportunity for even our most treatment-experienced (resistant) patients to get their viral load (down) to undetectable levels," claims Eron, from the University of North Carolina. He predicts some of these drugs will be options for first-line therapy.

Southern California-based molecular biologist John Rossi goes further. Last week his group at the City of Hope Beckman Research Institute began the first of two trials of a treatment combining genetically engineered HIV with the healing power of blood stem cells.

So far, the method involves removing HIV-infected stem cells from a patient's bone marrow, growing new versions tweaked to fight HIV, and then returning the rejigged cells to the patient. "As long as these cells persist in the patient we will have resistance to HIV infection, with the goal that there would be reduced viral load," said Rossi, who believes the treatment could eventually be given as a shot or pill and combined with conventional treatment.Meanwhile, scientists such as Perth-based Simon Mallal are giving older drugs a new lease on life. On Wednesday he announced that by using high-tech DNA screening techniques, he and his colleagues at the new $20 million Institute for Immunology and Infectious Diseases, to be built at Murdoch University, have developed and trialled a test to determine if a patient will develop life-threatening reactions to abacavir, a drug sold under the brand name Ziagen, and as combination pills that combine it with AZT or other drugs (one such combination pill being Trizivir). "We've entered the era of personalised medicine," says Mallal.

As Fauci's long-lived patients attest, all these advances in HIV research are working. In fact, treatment is so successful that at the conference British expert Brian Gazzard raised a new conundrum facing HIV clinicians: geriatric AIDS.

According to Gazzard, chairman of the British HIV Association, it's becoming clear that HIV infection increases the risk of suffering any of the "geriatric giants": heart disease, dementia and cancers. What's more, increasing numbers of people are becoming infected with HIV later in life.

Research has also revealed that HIV infection is the cause of serious organ damage that, until now, was blamed on the toxic effect of anti-retroviral cocktails. The finding has triggered a scientific rethink of when HIV people should begin drug therapy.

Usually, patients don't start therapy until the level in their blood of a type of immune cell called CD4 cells drops below a certain point. Fauci says experts now want to conduct trials to test the emerging notion that earlier treatment is better. He also wants more data on another treatment question: to treat or not to treat. "I've been convinced as the years go by that you many not necessarily treat someone who has a trivial level of virus and whose CD4 count is really very good," he observes. After all, a "trivial" level of HIV is the goal of researchers struggling to design a vaccine against HIV. A vaccine, says John Kaldor, is the holy grail of HIV prevention. "From the very early days of HIV we've been hunting for a vaccine," he says. "But a vaccine is considered a huge (scientific) problem and will be one for a long time."

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Just some problems with the "Obesity" war:

1). It tries to impose behavior change on everybody -- when most of those targeted are not obese and hence have no reason to change their behaviour. It is a form of punishing the innocent and the guilty alike. (It is also typical of Leftist thinking: Scorning the individual and capable of dealing with large groups only).

2). The longevity research all leads to the conclusion that it is people of MIDDLING weight who live longest -- not slim people. So the "epidemic" of obesity is in fact largely an "epidemic" of living longer.

3). It is total calorie intake that makes you fat -- not where you get your calories. Policies that attack only the source of the calories (e.g. "junk food") without addressing total calorie intake are hence pissing into the wind. People involuntarily deprived of their preferred calorie intake from one source are highly likely to seek and find their calories elsewhere.

4). So-called junk food is perfectly nutritious. A big Mac meal comprises meat, bread, salad and potatoes -- which is a mainstream Western diet. If that is bad then we are all in big trouble.

5). Food warriors demonize salt and fat. But we need a daily salt intake to counter salt-loss through perspiration and the research shows that people on salt-restricted diets die SOONER. And Eskimos eat huge amounts of fat with no apparent ill-effects. And the average home-cooked roast dinner has LOTS of fat. Will we ban roast dinners?

6). The foods restricted are often no more calorific than those permitted -- such as milk and fruit-juice drinks.

7). Tendency to weight is mostly genetic and is therefore not readily susceptible to voluntary behaviour change.

8). And when are we going to ban cheese? Cheese is a concentrated calorie bomb and has lots of that wicked animal fat in it too. Wouldn't we all be better off without it? And what about butter and margarine? They are just about pure fat. Surely they should be treated as contraband in kids' lunchboxes! [/sarcasm].

Trans fats:

For one summary of the weak science behind the "trans-fat" hysteria, see here. Trans fats have only a temporary effect on blood chemistry and the evidence of lasting harm from them is dubious. By taking extreme groups in trans fats intake, some weak association with coronary heart disease has at times been shown in some sub-populations but extreme group studies are inherently at risk of confounding with other factors and are intrinsically of little interest to the average person.

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