German scientists said on Sunday they had shown how a gene long associated with obesity might make people fat, a finding that could lead to new drugs to help control weight.Mice without the FTO gene did not become obese and had less fat tissue overall because they burned off more calories even though they moved less and ate more, according to the study published in the journal Nature.

FTO has been long linked to obesity. Studies have shown people with two copies of the “obese” version of the gene on average weigh nearly 7 lbs (3 kg) more and are about 70 percent more likely to be obese than those with other versions.

People and mice are similar genetically.

“So, this work provides a crucial piece of evidence supporting the notion that the FTO gene itself is likely to be involved in the effects of common human genetic variants on body fat,” Stephen O’Rahilly of the University of Cambridge, who was not involved in the study, said in a statement.

“This finding will promote research into the development of drugs that modulate FTO activity.”

Obesity, which raises the risk of diseases such as type 2 diabetes and heart problems, has increasingly become a global problem with people exercising less and leading more sedentary lifestyles.

The World Health Organization classifies about 400 million people around the world as obese, and the numbers are increasing.

In their study, Ulrich Ruther and colleagues at the University of Dusseldorf in Germany took a group of mice and knocked out, or inactivated, the FTO gene to see if they could figure out why the gene might make animals, and people, fat.

Animals lacking the gene were thin because they spontaneously burned off many calories, suggesting FTO plays a direct role in controlling metabolism, they reported.

“The human FTO gene has previously been shown to be linked to human obesity, however, this research helps unlock the complex interplay between factors expressed in the brain that control both appetite and metabolism,” said David Cameron-Smith, an obesity expert at Deakin University in Australia.

“A cure, genetic or pharmaceutical, for human obesity is many years away, although any new knowledge on how the brain controls hunger and growth will help solve the complex disease.”

Scientists have found a role for the GABA neurotransmitter, one of the master communicators among neurons, in the much complicated weight-control puzzle.

Headed by scientists at Beth Israel Deaconess Medical Center (BIDMC), the study may help in forming a clearer picture of the numerous events that lead to weight gain and weight loss.

“Body weight maintenance is made up of three basic stages. In the first stage, the brain receives sensory input from the body [including information provided by circulating hormones such as leptin and ghrelin and from fuels such as glucose and fatty acids,” Nature magazine quoted the paper’s senior author, Dr. Bradford Lowell, a Professor of Medicine at Harvard Medical School, as saying.

He said that in the second stage, the brain combine this sensory information with environmental cues (such as aromas and other enticements), as well as information gathered from the organism’s emotional state.

Finally, in the last stage, the brain’s neurocircuitry plays a major role by enabling the brain to make appropriate alterations in food intake and energy expenditure in order to maintain energy balance, and in turn avert weight gain and obesity.

Earlier scientists focused on identifying the neuropeptides involved in this process, which often proves essential to maintaining energy balance - but not always.

“It is well known that AgRP [Agouti-related protein] neurons play a critical role in feeding and energy balance regulation. However, the deletion of AgRP and NPY [two neuropeptides released from the AgRP neurons] produces little metabolic effect,” explained Qingchun Tong, PhD, a postdoctoral fellow in the Lowell laboratory and the study’s first author.

In an alternate theory, the scientists suggested that release of the GABA neurotransmitter was mediating the function of AgRP neurons.

The researchers generated a group of mice with disrupted release of GABA specifically from the AgRP neurons, and it was confirmed that genetically altered mice exhibited profound metabolic changes.

“The mice with AgRP neuron-specific disruption of GABA release were lean, had higher energy expenditure and showed resistance to diet-induced obesity. We also found that these animals showed reduced food intake response to the hormone ghrelin. This suggests to us that the neurocircuit engaging GABA release from the AgRP neurons mediates at least part of ghrelin’s appetite-stimulating action,” said Tong.

He added: “As these new findings demonstrate, GABA release is an important component that mediates the function of AgRP neurons. Discoveries such as this will ultimately help us to design an efficient strategy to tackle the current epidemic of obesity and metabolic disease.”

The study is published in the latest on-line issue of Nature Neuroscience.

A drug which blocks the urge to eat can help dieters shed pounds and inches, a study suggests. Belgian researchers writing in the Lancet said people taking rimonabant lost an average of 8.6 kilograms (18.9 pounds) in a year.

They also lost an average of 8.5 centimetres (over three inches) from their waists.

UK experts commented that rimonabant might help people lose weight - but could not replace eating healthily.

In the UK, it is estimated that one in five men and a quarter of women are obese.

Hunger

The researchers from Antwerp University Hospital studied 1,507 people from Europe and the US who were obese or overweight.

This drug doesn’t offer an easier way of losing weight but it appears to help you do it more successfully Dr David Haslam, National Obesity Forum

They were either assigned to take 5mg or 20mg of rimonabant or a dummy pill each day.

All those taking part in the study were also advised to cut 600 calories from their daily intake.

Nine hundred and twenty people completed the year-long study.

Just over 39% of those who took the higher dose of rimonabant lost more than 10% of their bodyweight.

People on the higher dose of the drug lost an average of five kilograms (11 pounds) more than those taking the dummy pill.

They also cut their waist measurement by an average of seven centimetres (just under three inches) more than those on the dummy pill.

Carrying weight around the abdomen has been shown to put people at high risk of heart disease and diabetes.

A separate study by Karolinska Institute researchers in Sweden, published in the British Medical Journal on Friday, showed people with a waist measurement of more than a metre, equivalent to 39.4 inches, were at highest risk.

The Dutch team taking the higher dose of rimonabant showed improvements in cardiovascular risk factors such as cholesterol levels, insulin resistance and metabolic syndrome, a condition which can increase the risk of heart disease.

However, they also showed the highest level of side effects such as nausea, dizziness and diarrhoea.

Rimonabant works by blocking the endocannabinoid system in the brain which regulates hunger.

‘Encouraging’

Dr Luc Van Gaal, who carried out the study, said: “Treatment with rimonabant over one year led to sustained, clinically meaningful weight loss, reduction in waist circumference and associated improvements in several cardiovascular and metabolic risk factors.”

UK experts said the drug was effective - but only in conjunction with dieting.

Dr David Haslam of the National Obesity Forum, said: “This drug appears to be very successful.

“This drug doesn’t offer an easier way of losing weight. But it appears to help you do it more successfully.”

Nilami Sritharan, a nutritionist with the Medical Research Council, said: “These are very encouraging results. But it’s important to remember drugs such as these are only an adjunct to improving your diet and lifestyle.”

Professor Steve Bloom, an obesity specialist at Imperial College and Hammersmith Hospitals, said: “This drug is a helpful addition. But one would need more clinical studies to make sure it is safe.”

A pill that helps you lose weight and quit smoking? That was amazing enough to capture headlines last week. But scientists say the experimental drug might be even more versatile, providing a new tool to help people stop abusing drugs and alcohol, too.It’s called rimonabant, or Acomplia, and last week researchers reported it could help people not only lose weight but keep it off for two years.

That burnished the drug’s reputation after two studies in March, which suggested it could fight both obesity and smoking, two of humanity’s biggest killers.

The French pharmaceutical firm Sanofi-Aventis plans to seek federal approval for rimonabant next year.But the drug’s benefits may go beyond just smokers and obese people, researchers say.

“I think it’s going to have a big impact on the treatment of addiction,” said Dr. Charles O’Brien, an addiction expert at the University of Pennsylvania and the Philadelphia Veterans Affairs Medical Center.

Animal studies suggest rimonabant can block the effects of marijuana and fight relapse in alcohol and cocaine abuse, he said. Once it is approved for treating obesity or smoking, “we’ll be free to study it in these other areas and I’ll try to get my hands on it as quickly as possible,” O’Brien said.

He’s not alone in his enthusiasm.

Halting the brain’s reward system
The National Institute on Alcohol Abuse and Alcoholism is interested in seeing whether rimonabant can help treat heavy drinkers, said Dr. George Kunos of the institute. No human test results for rimonabant in alcohol abuse have yet been published, he said.

But researchers at the National Institute on Drug Abuse reported in 2001 that a single dose of the drug could block the effects of smoked marijuana in people, not just animals. That suggests the drug could be useful in treating marijuana dependence, said Marilyn Huestis, principal investigator of the study. The institute is now pursuing follow-up research, said Huestis, acting chief for chemistry and drug metabolism research at NIDA.

Rimonabant’s versatility traces back to its effects on the brain’s reward system, circuitry that tells you to keep on doing something. Basically, it appears to help break the connection between an activity like smoking and the rewarding feeling it causes in the brain.

The body has its own marijuana-like substances called endocannabinoids, and they activate certain brain cells that in turn can lead to stimulation of the brain’s reward system. Pleasurable things like drinking alcohol are thought to activate a feeling of reward by acting through the endocannabinoid system.

“We think that the (endocannabinoid) system is overactivated by chronic smoking, or perhaps even excessive overeating,” said Dr. Robert Anthenelli of the University of Cincinnati College of Medicine and the Cincinnati Veterans Affairs Medical Center. He’s on the advisory board of Sanofi-Aventis.

Rimonabant blocks the effect of the natural endocannabinoids by keeping them from latching onto the brain cells they normally stimulate, he said. In smokers, for example, that seems to restore the natural balance of the brain reward circuitry, he said.

What makes us fat? A generation ago, the answer was simple — eating more than we needed to.

That may still be true, but researchers investigating the genetics behind appetite, metabolism and weight gain have learned that putting on pounds is much more complicated than a simple equation of calories. They’re finding certain genes allow some people to pig out and not gain weight, while others put on pounds after a slight overindulgence. Other research has shed light on genes that may play a role in how much we crave food.

But can these findings lead to surefire treatments to tackle this country’s growing weight problem? A consensus among scientists is surprisingly optimistic.

“I truly believe that the discovery of obesity susceptibility genes will identify new molecules and pathways that will lead to effective new medications and other interventions,” said Dr. Alan Shuldiner, head of endocrinology, diabetes and nutrition research at the University of Maryland’s School of Medicine. Shuldiner adds, however, “I do not think this will occur in the near future.”

Still, Andrew Greenberg, director of obesity and metabolism studies at Tufts University, pointed out that obesity research has accelerated in recent years, and that’s bound to help scientists find cures sooner.

“The Internet has changed science,” he said. “It has changed the pace at which we learn about each other’s research and then build on it. Advances are happening faster than ever before.”

An Anti-Obesity Wonder Drug?

In fact, the introduction of new treatments has already begun. In the coming year, the French pharmaceutical giant Sanofi-Aventis plans to release what many believe could be one of the first truly effective anti-obesity drugs. Preliminary data from large trials have suggested that weight loss is much greater than with any current drugs on the market.

The drug, rimonabant, targets receptors of cannabinoid 1, which stimulates appetite and other cravings (including nicotine) in the brain. By blocking cannabinoid 1’s receptors, rimonabant helps people beat their cravings and lose weight.

Shuldiner said so far the trials for rimonabant have been “very impressive. “I believe it will be a very useful agent for weight loss. But not the end-all.”

While a drug like rimonabant is designed to help any person beat cravings and lose weight, part of finding “end-all” treatments may lie in figuring out how people’s genetics vary and tailoring drugs to match.

A recent study in Spain has offered insight into one such variation. The research, published in the Journal of Clinical Endocrinology & Metabolism, examined the role of a gene that may lie behind a phenomenon that so many find frustrating — you cut back calories but still don’t lose weight at the same pace as your thinner friends. Jose Ordovas, director of nutrition and genomics research at Tufts University, said those frustrated dieters may share a variation in a gene called perilipin.

Targeting a Fat Guardian

Perilipin, he explained, creates a protein that settles around fat droplets and protects the fat from being destroyed.

“That may sound funny these days,” Ordovas said. “But in old times, fat was difficult to hold on to, so this protein protected it.”

Some versions of the perilipin gene (originally identified by Greenberg and colleagues) make this fat bodyguard stronger, while other mutations make it weaker.

“This means we have identified one of probably many genetic variations that help us distinguish between those who will and won’t respond to diet,” said Ordovas. “Some people think that patients don’t lose weight because they don’t follow the recommendations. But in some cases, their bodies may just be more thrifty with the fat.”

Figuring out how people’s genes react differently when it comes to weight loss might also help prevent dangerous side effects to obesity-fighting drugs as they emerge on the market.

Many may remember the controversy over phen-fen, a once popular obesity-fighting combination of drugs that was recalled in 1997 after some studies and reports showed it caused heart problems in some patients. By tailoring drugs to people with specific genomes, drug manufacturers may be able to avoid such fallouts in the future.

“Sometimes side effects only affect a minority of people,” said Ordovas. “In the future, we can identify drugs and supplements and target them to people with specific genetic profiles.”

The pace at which scientists identify new obesity-related genes has stepped up in the past few years as genetic research gains momentum. But Greenberg cautions that not every new discovery means new cures are on the way.

“We’ve come a long way in understanding obesity,” he said. “But every study has to be carefully replicated. And exercise and diet will always form the cornerstone of any obesity treatment.”

Acomplia (rimonabant) currently being sold in Europe has been seen by many patients struggling with obesity as a “miracle pill.”

Many studies have shown that this medication helps patients loose weight when compared to a placebo. Most of the weight reduction results from patients limiting the number of calories they consume on a daily basis. Acomplia helps to control appetite– something that for many patients involved in weight reduction programs is a major obstacle to success.

Even though the safety of the medication is being monitored, no major problems have yet been reported. There are some mild side effects that people should be aware of, including nausea, dizziness, anxiety and depression.

Many Europeans have accepted the efficacy of this medication. Sweden, for example, has approved reimbursement of the drug through their public service program.

How does it work? It controls the urge to eat. Many are calling this the “anti munchie effect.” Acomplia works in the central nervous system by affecting the cannabioids receptors in the brain. Yes, the same receptors that give people the urge to eat when exposed to marijuana.

The point of all the hype around accomplia is that it has been a long time since we have seen a medication so effective in controlling appetite. The FDA is considering approval of this drug in the U.S., but there is no clear indication as to when it will happen. In the mean time, other pharmaceutical companies are working on similar typed of drugs.

Why? Because the world is severely overweight and obesity is creating pockets of epidemic proportions of diabetes and heart disease.

Of course, a simple pill is not the answer to an unhealthy lifestyle. But hopefully, this “miracle drug” will be the miracle we all need to start focusing in eating right and exercising.

A drug which treats obesity by reducing the desire to eat has been launched in the UK. But NHS chiefs warned people not to expect it to become widely available straight away as the cost-effectiveness of the pill needed to be assessed.

Rimonabant is the first drug to target factors governing the body’s appetite, metabolism and energy use. Trials showed it can reduce weight by a tenth.

UK experts said it could not replace healthy food and regular exercise.

In the UK, it is estimated that one in five men and a quarter of women are obese.

Cost

But at a cost of over £55 for a month’s treatment, it could end up costing the NHS billions of pounds of money.

The drug still has to be assessed by NHS advisers the National Institute for Health and Clinical Excellence.

The review is not expected for another two years and NHS bosses warned the public not to expect its widespread use immediately.

Gill Morgan, chief executive of the NHS Confederation, said primary care trusts may be reluctant to prescribe the drug ahead of NICE guidance.

“PCTs receive a fixed allocation of money to deliver all the services for their local community and have to take difficult decisions on competing priorities.”

And she added weight loss was “predominantly about diet and exercise”.

Preventative measures aren’t enough on their own Dr David Haslam, of the National Obesity Forum

The drug’s manufacturer, Sanofi Aventis, has argued the drug represents good value for money when set against the £7bn per year cost of tacking obesity.

Other anti-obesity drugs are already available, but rimonabant is the only one to target the endocannabinoid system, which governs the body’s appetite.

In a series of trials involving more than 6,000 patients in the US and Europe, a quarter lost more than 10% of their initial body weight after a year. About half lost more than 5%.

Side effects in some patients included nausea, dizziness and anxiety.

Significant improvements in measures of glucose control, cholesterol and triglyceride blood fats were also seen.

Smoking

Rimonabant, sold under the brand name Acomplia, is currently licensed for the treatment of obese patients, or overweight patients with associated risk factors such as type 2 diabetes or poor cholesterol and triglyceride readings.

But there are also trial data suggesting that the drug can help people give up smoking by overcoming their cravings.

However at present it is only being marketed to tackle obesity.

Dr David Haslam, clinical director of the National Obesity Forum, said the drug offered a real opportunity to get to grips with the obesity crisis.

“Preventative measures aren’t enough on their own. It brings into focus the priority that should be given to treatment as well as prevention.

“The launch of rimonabant is important news for patients who are overweight, with type 2 diabetes, or low HDL cholesterol or high triglycerides.”

Food cravings and drug addiction affected the brain similarly in studies, suggesting new weight- loss medicines may help treat recovering addicts.

Brain scans of 18 cocaine addicts found that when they thought about drugs they exhibited higher levels of dopamine, a chemical tied to feelings of reward and pleasure, in a brain region that’s also activated by food deprivation. Other studies showed reduced sensitivity in the reward circuits of both addicts and obese people, possibly leading them to compensate with drugs or overeating.

The data is to presented Friday at a meeting in San Francisco. Pfizer Inc., Sanofi-Aventis SA and Bristol-Myers Squibb Co. are developing new types of diet pills that work by blocking hunger signals in the brain. Some U.S. health officials hope to capitalize on the drugmakers’ research by testing the compounds on smoking, alcoholism and other substance abuse.

“The moment that you can show that there is in fact feasibility that these compounds are useful, then I think that there will be more openness” for companies to develop them for drug addiction, said Nora Volkow, director of the National Institute on Drug Abuse, in a telephone interview this week.

While drugmakers are racing to gain a piece of the market for treating the two-thirds of Americans who are overweight, companies so far have been reluctant to invest in new addiction treatments. Volkow said drugmakers are wary of the stigma tied to substance abuse and the uncertainty of pricing because few insurers cover treatment for drug addiction.

Her staff has been working with Paris-based Sanofi to see if its experimental fat-fighting pill, Acomplia, can block drug cravings in animals. Acomplia, which was introduced in Europe in July, suffered its third delay in U.S. approval this week. Until medicines are cleared for sale by the Food and Drug Administration, scientists need the backing of companies to gain access to test their compounds.

Volkow and other researchers will discuss their findings on weight-loss drugs and substance abuse at the Brookhaven National Laboratory Addiction Symposium, part of the annual meeting of the American Association for the Advancement of Science.

There’s a scene in last year’s The Devil Wears Prada, the comedy about life as an underling at a high-fashion magazine helmed by the devilish Meryl Streep, in which new girl Anne Hathaway tries to choke down lunch before she’s due back at her desk.

“So none of the girls here eat anything?” she asks a more seasoned employee.
“Not since 2 became the new 4 and 0 became the new 2,” he says.”Well, I’m a 6,” Anne replies.

“Which is the new 14.”

Yeah, that pretty much sums it up.

Always thin, models have become a breed of Incredible Shrinking Women.

Last August at a fashion show in Uruguay, Luisel Ramos, 22, suffered a heart attack, believed to be the result of anorexia.

Last September at the New York shows, the gaunt figures of the girls disturbed many observers. At the time, Allure magazine editor Linda Wells told The New York Times she could hear fellow audience members gasp at the sight of the frail models. “What becomes alarming is when you see bones and start counting ribs,” she said.

Later that month, Madrid Fashion Week banned underweight models, and by year’s end Italian designers began requiring that models submit proof that they don’t suffer from eating disorders.

And in November, a model named Ana Carolina Reston, 21, died of complications because of anorexia nervosa and bulimia. The 5-foot-7 Brazilian weighed 88 pounds.

In January, Spanish clothing chains Mango and Zara announced that over the next few years they would replace their skinny window mannequins with dummies more reflective of the average woman’s size.

Some naturally skinny

By the time New York Fashion Week rolled around in early February, the Council of Fashion Designers of America (CFDA) had formed a health committee whose members include experts on nutrition, fitness and eating disorders. And one morning during Fashion Week, they held a panel discussion about their new recommendations, which include:

• Educating the industry about the early warning signs of eating disorders.

• Not hiring models under the age of 16 for runway shows and not allowing models under 18 to work past midnight at fittings and photo shoots.

• Supplying healthy snacks backstage and at shoots, and providing nutrition and fitness education.

If only industry-wide change were as easy as slipping a model out of one halter gown and into another.

The day of the panel discussion, Women’s Wear Daily ran a story about modeling’s newest faces — one of the featured girls was 15 years old.

And there was the unfortunate inclusion of diet pills in Fashion Week giveaway bags.

And the girls on the runway this season? Skinny as ever.

That probably didn’t surprise designer Michael Kors, who visited Palm Beach before Fashion Week and said he didn’t expect a sea change in the super-thin aesthetic.

“I don’t think we’re going to suddenly see the bodacious, curvy model reappear on the runway, and I don’t think she’s ever really been part of a runway season,” he said. “But I do think we’ll hopefully not see a lot of unhealthy girls out there.”

The thing is, Kors said, many models come by their extreme skinniness naturally.

“I think the public is perhaps not aware of how young some of these models are,” he said. “The reality is, when I was 16 years old I was super-skinny with not much effort. And a lot of these models are 16 and 15 years old. I think the problem is, if there’s no one around who’s responsible for them and they kind of step over the line and stop taking care of themselves…

“Let’s be honest. At 16, how many people are aware of what to eat and how to take care of themselves?” he said, noting that a lot of models come from poorer countries, like the Ukraine. “We have very few American models on the runway. In our entire casting of almost 35 women, we had two.”

At the CFDA’s panel discussion, Calvin Klein model Natalia Vodianova, 24, talked about how her poor childhood in Russia did not prepare her for the pressures of modeling.

When she moved to Paris to pursue modeling at the age of 17, she began comparing herself with other models and becoming consumed with thoughts about diet and exercise. As her weight plummeted, her hair fell out, and she said she was unusually edgy. “It was happening to me before I even realized it.”

And yet, her career took off.

But when the 5-foot-9 model got married and got back up to 115 pounds, some fashion houses called her agency and questioned her weight gain.

“You arrive (in the modeling business) as a healthy person,” Vodianova said. “I wasn’t aware that anything was wrong with me. I thought it was normal.”

Also at the CFDA breakfast, designer Donna Karan said most of the responsibility lies with a model’s family and agent: “The agency is the mother of the model or the father of the model.”

‘Supermodel’ size better

But it’s not up to agents, says Olympia Devine, a former model who has owned three modeling agencies and now produces Palm Beach Fashion Week.

“It’s easy enough for a designer to say that, but the industry itself dictates size. You have the designers producing sample collections that are one standard size,” she says. “Those sample collections are arriving like that from Europe and New York, and the sizing then becomes the agency’s responsibility to fill with the right models. It’s not the other way around.

“It’s almost a biological challenge to find that many girls that skinny, that height.”

At Bill Blass, creative director Michael Vollbracht fits on a model who’s a size 6 — “and a size 6 is not a regular woman, I’m sorry” — but scales down to a size 2 for the models who walk the Blass runway.

When he visited Palm Beach last month, he had already cast his show for New York Fashion Week. “And I said to my casting director, ‘Make sure this one has a hamburger before she comes,’ because we didn’t use certain girls last season because of their weight.”

Vollbracht, whose muses have included va-va-voomy Brigitte Bardot and petite but not painfully thin Jane Fonda, says he’d like to see “girls with a little more weight on them.”

He misses the glory days of the supermodels — “Cindy Crawford and Claudia Schiffer and Linda Evangelista and Christy Turlington, who were a little bit bigger girls, and they were wonderful.”

Why thin is in: Follow the money

Thin has always been in, designers say.

Well, not exactly.

Before the proliferation of highly processed foods and an increasingly sedentary lifestyle, it was prestigious to be plump, explains Nancy Etcoff in Survival of the Prettiest: The Science of Beauty.

But when poor women began piling on the pounds because eating junk food is cheaper in the short run than eating whole foods, it became a sign of status to be thin.

“Extreme thinness is a fashion, a fashion set by the highest social classes, as most fashions are,” Etcoff writes.

Models in the latter half of the 20th century “have always been skinny — don’t forget Twiggy and don’t forget Kate Moss,” says designer Carolina Herrera. “If you show the clothes on skinny girls that look very good, everything looks good. There is a fantasy for women sitting in the audience dreaming that she’s going to look like them if she wears the clothes.”

Even though more than half of American women wear a size 14 or larger.

“We do live in a society where 60 percent of our society is obese,” says Johanna Kandel, founder and executive director of the West Palm Beach-based Alliance for Eating Disorders Awareness. “It’s about getting rid of the extremes and living in the normal range.”

Kandel applauds fashion for addressing the issue.

“We shouldn’t only be pointing the finger at fashion. It’s pretty much our society that perpetuates this unrealistic standard of beauty….

“There’s a lot of adolescent females that look at these runway shows and the magazines. For me it’s just great that we’re starting with one specific aspect and hopefully it’ll continue.”

The central issue is one of health, Kors says.

“I don’t want to look at someone who’s big and unhealthy, and I don’t want to look at anyone who’s skinny and unhealthy. That’s the most important thing to kind of get out of this whole thing.”

And pressure to be thin doesn’t entirely emanate from Seventh Avenue, Kors says. “Listen, I think we have Hollywood, we have the New York social world… the front row is sometimes thinner than the runway.”