Why BMI is a Big Fat Scam


Story at-a-glance

  • Body mass index (BMI), a formula that divides your weight by the square of your height, is one of the most commonly used measures of overweight, obesity, and overall health
  • Initially, BMI was primarily a tool used by insurance companies to set premiums (people with BMIs in the “obese” category may pay 22 percent more for their insurance compared to those in the “normal” category
  • BMI is a flawed measurement tool, in part because it uses weight as a measure of risk, when it is actually a high percentage of body fat that increases your disease risk
  • BMI also tells you nothing about where fat is located in your body, and the location of the fat, particularly if it’s around your stomach (visceral fat), is more important than the absolute amount of fat when it comes to measuring certain health risks
  • Your waist-to-hip ratio is a more reliable indicator of your future disease risk because a higher ratio suggests you have more visceral fat.

 

BY DR. MERCOLA

In 1832, a Belgian mathematician named Adolphe Quetelet developed what is today known as the body mass index (BMI).1The formula divides a person’s weight by the square of his height, and is one of the most commonly used measures of excess weight, obesity, and overall health.

Initially, BMI was primarily a tool used by insurance companies to set premiums (people with BMIs in the “obese” category may pay 22 percent more for their insurance compared to those in the “normal” category2).

Today, however, BMI is an accepted tool used in medical research and in clinical practice. When you have your height and weight recorded at your doctor’s office, it will give him or her an automatic calculation of your BMI, classifying you as underweight if your BMI is below 18.5, normal if it’s 18.5-24.9, overweight if it’s 25-29.9, and obese if it’s 30 or over.

Your doctor may use this number to advise you on your weight, as well as your risk of related conditions like heart disease, high blood pressure, and type 2 diabetes. Unfortunately, BMI is an incredibly flawed tool, and a high BMI doesn’t automatically mean you’re unhealthy, the way many physicians and health insurance companies imply that it does.

The Obesity Paradox: Sometimes Higher BMI Is Healthier

Research involving data from nearly 3 million adults suggests that a having an overweight BMI may be linked to a longer life than one that puts you within a “normal” weight range.

The research, which analyzed 97 studies in all, found that people with BMIs under 30 but above normal (the overweight range) had a 6 percent lower risk of dying from all causes than those who were normal weight, while those whose BMIs fell into the obese range were 18 percent more likely to die of any cause.3

Separate research published in the Journal of the American College of Cardiology, also found that a high BMI was associated with a lower risk of death, a phenomenon known as the “obesity paradox.”4

Indeed, it is quite possible to be overweight and healthy, just as it’s possible to be normal weight and unhealthy. And in some cases, it may, in fact, be healthier to carry a few extra pounds. In a Journal of the American Medical Association (JAMA)editorial, Steven Heymsfield, M.D. and William Cefalu, M.D. explained:5

“The presence of a wasting disease, heart disease, diabetes, renal dialysis, or older age are all associated with an inverse relationship between BMI and mortality rate, an observation termed the obesity paradox or reverse epidemiology. 

The optimal BMI linked with lowest mortality in patients with chronic disease may be within the overweight and obesity range. 

Even in the absence of chronic disease, small excess amounts of adipose tissue may provide needed energy reserves during acute catabolic illnesses, have beneficial mechanical effects with some types of traumatic injuries, and convey other salutary effects that need to be investigated in light of the studies…” 

However, for the vast majority of those who carry around extra pounds, health problems will often result. So why would these studies suggest otherwise? They are likely examples of why BMI is such a flawed tool for measuring your health.

Makers of Weight Loss Drugs Altered BMI Categories, Making 29 Million Americans ‘Overweight’

BMI is used as the measure of national obesity rates, which currently stand at close to 35 percent for adults and 18 percent for kids. However, the cut-off for classifying a person as normal or overweight seems to be quite arbitrary – and at one point was significantly modified by a task force funded, primarily, by companies making weight loss drugs. Mother Jones reported:6

“In 1998, the National Institutes of Health lowered the overweight threshold from 27.8 to 25—branding roughly 29 million Americans as fat overnight—to match international guidelines. 

But critics noted that those guidelines were drafted in part by the International Obesity Task Force, whose two principal funders were companies making weight loss drugs. 

In his recent book ‘Fat Politics: The Real Story Behind America’s Obesity Epidemic,’ political scientist Eric Oliver reports that the chairman of the NIH committee that made the decision, Columbia University professor of medicine Xavier Pi-Sunyer, was consulting for several diet drug manufacturers and Weight Watchers International.”

BMI Uses Weight, Not Body Fat, to Measure Risk

Branding yourself as unhealthy or overweight simply based on your BMI is not recommended (unfortunately, your insurance company probably won’t see it this way). On the other hand, assuming you’re healthy just because your BMI is normal isn’t advised either.

Research suggests BMI may underestimate obesity rates and misclassify up to one-quarter of men and nearly half of women.7 According to researcher Dr. Eric Braverman, president of the nonprofit Path Foundation in New York City:8

“Based on BMI, about one-third of Americans are considered obese, but when other methods of measuring obesity are used, that number may be closer to 60%.”

One of the primary reasons why BMI is such a flawed measurement tool is that it uses weight as a measure of risk, when it is actually a high percentage of body fat that increases your disease risk. Your weight varies according to the density of your bone structure, for instance, so a big-boned person may weigh more, but that certainly doesn’t mean they have more body fat or make them more prone to heart disease, for example.

Athletes and completely out-of-shape people can also have similar BMI scores, or a very muscular person could be classified as “obese” using BMI, when in reality it is mostly lean muscle accounting for their higher-than-average weight. BMI also tells you nothing about where fat is located in your body, and it appears that the location of the fat, particularly if it’s around your stomach, is more important than the absolute amount of fat when it comes to measuring certain health risks, especially heart disease.

Waist-to-Hip Measurement Is Superior to BMI, But Only 10 Percent of Physicians Use It

Your waist-to-hip ratio is a more reliable indicator of your future disease risk because a higher ratio suggests you have more visceral fat. Excess visceral fat—the fat that accumulates around your internal organs — is far more hazardous to your health than subcutaneous fat (the more noticeable fat found just under your skin) – a measure that BMI tells you nothing about. The danger of visceral fat is related to the release of proteins and hormones that can cause inflammation, which in turn can damage arteries and enter your liver, and affect how your body breaks down sugars and fats.

Unfortunately, according to Donna Ryan, a physician who has trained thousands of primary-care doctors in obesity screening, only about 10 percent use waist circumference as a health indicator. She told Mother Jones:9 “Doctors are so pressed for time… And it’s intrusive. You have to put your arms around the patient.” To determine your waist-to-hip ratio, get a tape measure and record your waist and hip circumference. Then divide your waist circumference by your hip circumference. For a more thorough demonstration, please review the video above.

Waist to Hip Ratio Men Women
Ideal 0.8 0.7
Low Risk <0.95 <0.8
Moderate Risk 0.96-0.99 0.81 – 0.84
High Risk >1.0 >0.85

How Much You Exercise Also Predicts Your Disease Risk

Your fitness level is also a far better predictor of mortality than your BMI. One study found that people who rarely exercised had a 70 percent higher risk of premature death than those who exercised regularly, independent of their BMI.10 If you want a simple test to gauge your fitness level, try the abdominal plank test (for a demonstration of how to do a plank, see the video below. If you can hold an abdominal plank position for at least two minutes, you’re off to a good start. If you cannot, you’re likely lacking in core strength, which is important for overall movement stability and strength.

A strong core will also help prevent back pain. Being unable to hold a plank for two minutes may also indicate that you’re carrying too much weight and would benefit from shedding a few pounds. Unfortunately, over 50 percent of American men, and 60 percent of American women, never engage in any vigorous physical activity lasting more than 10 minutes per week.11 This despite a growing body of research clearly showing that “exercise deficiency” threatens your overall health and mental well-being, and shortens your lifespan.

In fact, according to research published in the American Journal of Physiology, the best way to stay young is to simply start exercising, as it triggers mitochondrial biogenesis, a decline of which is common in aging.12 Researchers have also suggested that exercise is “the best preventive drug” for many common ailments, from psychiatric disorders to heart disease, diabetes, and cancer.13 According to Jordan Metzl, a sports-medicine physician at New York City’s Hospital for Special Surgery and author of The Exercise Cure: “Exercise is the best preventive drug we have, and everybody needs to take that medicine.”

So rather than stressing over an arbitrary number like your BMI, you’d be better served by coming up with a comprehensive fitness plan. I recommend incorporating high-intensity interval training (HIIT)strength training (including super slow), core exercises, stretching, and non-exercise activity into your routine. The key is to simply get moving, and work at a high enough intensity with enough variance to keep your muscles adequately challenged.

Every person is different, so there’s not just one “correct” way to exercise. Equally, if not more, important is incorporating regular intermittent movement into your day, as this will help to counteract some of the effects excess sitting has on your body. If you exercise correctly and keep moving throughout your day, and combine it with a healthy eating program, you will optimize your body-fat percentage naturally, and with it gain a predisposition for optimal health.

Belly Fat is Far More Dangerous than Having a Total BMI in Obese Range


A study on belly fat presented at the European Society of Cardiology Congress1, 2 confirms that visceral fat – the type that gathers around your internal organs – is far more dangerous to your health than you might think.

Belly Fat

Story at-a-glance

  • A study on belly fat confirms that visceral fat – the type that gathers around your internal organs – is far more dangerous than having a total BMI in the obese range
  • Cardiovascular deaths in the study were 2.75 times higher for those of normal weight who had big bellies compared to those with both a normal BMI and a normal waist-to-hip ratio
  • Three different measurement techniques are reviewed – all of which are better indicators of disease risk and healthy body size than using BMI, which does not take muscle mass into consideration
  • In his new book, The Fat Switch, Dr. Richard Johnson overturns age old paradigms about diet and obesity by revealing how fructose turns your body into a fat-storage machine – not by way of excess calories but by turning on your “fat switch”

The traditional index of obesity, BMI (body mass index), has been proven to be terribly flawed as having a normal overall BMI and high abdominal obesity was found to be more dangerous than having a total BMI in the obese range.

For example, cardiovascular deaths in the study were 2.75 times higher for those of normal weight who had big bellies compared to those with both a normal BMI and a normal waist-to-hip ratio. It also implies that monitoring one’s belly fat is more important than watching BMI.

According to Medical News Today:3

“Francisco Lopez-Jimenez, M.D., senior author and a cardiologist at Mayo Clinic in Rochestor, explained: ‘We knew from previous research that central obesity is bad, but what is new in this research is that the distribution of the fat is very important even in people with a normal weight.

This group has the highest death rate, even higher than those who are considered obese based on body mass index. From a public health perspective, this is a significant finding.’

…Dr. Lopez-Jimenez wants readers to understand that even though their body mass index might be normal, it doesn’t mean they have a low risk of heart disease. People can determine their risks by getting a waist-to-hip measurement, because where fat is distributed on the body can tell a lot, even if people have normal body weights.”

Your Ideal “Weight” is Not Necessarily Based on Pounds…

There are a number of methods for calculating your ideal body size. The study above used waist-to-hip measurement. This is done by measuring the circumference of your hips at the widest part, across your buttocks. Then measure your waist at the smallest circumference of your natural waist, just above your belly button. Divide your waist measurement by your hip measurement to get the ratio.

The University of Maryland offers a handy online waist-to-hip ratio calculator you can use, which also tells you whether or not you might be at an increased risk for heart disease. The featured study used the following waist-to-hip ratio designations:

  • Normal = 0.85 or below in women, and 0.90 or below in men
  • High = 0.85 or greater in women, and 0.90 or greater in men

Another even simpler method to figure out if you have a weight problem is to measure only your waist circumference (the distance around the smallest area below the rib cage and above your belly button). Waist circumference is the easiest anthropometric measure of total body fat.

Either of these methods are far better than BMI for judging disease risk, as BMI fails to factor in how muscular you are. BMI also cannot give you an indication of your intra-abdominal fat mass.

Waist size, on the other hand, gives a good indication of the amount of fat you’re carrying, particularly around the stomach area. Abdominal fat is considered an important risk factor for cardiovascular diseases such as coronary heart disease and stroke. Your waist size is also a powerful indicator of insulin sensitivity, as studies clearly show that measuring your waist size is one of the most powerful ways to predict your risk for diabetes. If you’re not sure if you have a healthy waist circumference, a general guide is:

  • For men, between 37 and 40 inches is overweight and more than 40 inches is obese
  • For women, between 31.5 and 34.6 inches is overweight, and more than 34.6 inches is obese

Body Fat Percentage – Another Way to Gauge Ideal Body Size

Yet another tool, which many experts are now leaning toward as the most accurate measure of obesity, is body fat percentage. As it sounds, this is simply the percentage of fat your body contains, and it can be a powerful indicator of your health.

  • Too much body fat is linked to chronic health problems like high blood pressure, high cholesterol, heart disease, diabetes, and cancer.
  • Too little body fat is also problematic and can cause your body to enter a catabolic state, where muscle protein is used as fuel.

A general guideline from the American Council on Exercise is as follows:

Classification Women (percent fat) Men (percent fat)
Essential Fat 10-13 percent 2-5 percent
Athletes 14-20 percent 6-13 percent
Fitness 21-24 percent 14-17 percent
Acceptable 25-31 percent 18-24 percent
Obese 32 percent and higher 25 percent and higher

 

Body fat calipers are one of the most trusted and most accurate ways to measure body fat. A body fat or skinfold caliper is a lightweight, hand-held device that quickly and easily measures the thickness of a fold of your skin with its underlying layer of fat. Taken at three very specific locations on your body, these readings can help you estimate the total percent of body fat within your entire body.

You can also use a digital scale that determines body fat, which is what I use personally. I use an Eat Smart Precision GetFit Body Fat Scale that I picked up from Amazon for around $50. Although many body fat measurements can be inaccurate, they are nearly all more accurate than BMI, and are particularly useful to determine whether you are gaining or losing fat. Although the absolute value may be off, the direction you are going (whether your body fat is going up or down) will be very accurate, and this is an incredibly useful measure of whether you’re nearing your health goals or not.

Remember that it is FAR better to monitor your body fat percentage than it is your total weight, as the body fat percentage is what dictates metabolic health or dysfunction – not your total weight.

 

Does Reducing Fructose Intake Matter If You Want to Lose Weight?

A recent study published in the Nutrition Journal4 has brought questions about the health impact of high fructose corn syrup versus sugar back to the fore. The authors claim their findings indicate there’s no difference between regular sugar and high fructose corn syrup on weight loss. Dr. Richard Johnson, author of The Sugar Fix, and The Fat Switch (which I’ll discuss in a moment), sent me the following rebuttal to share with you.

A recent study from James Rippe’s group reported in the Nutrition Journal that low calorie diets caused equivalent weight loss regardless of the content of sugar or high fructose corn syrup. The study involved randomizing 267 overweight adults to receive low calorie diets containing either:

  • 10 percent of the calories as sugar (sucrose)
  • 20 percent as sugar (sucrose)
  • 10 percent as high fructose corn syrup, or
  • 20 percent high fructose corn syrup

Each group was given a diet calculated to reduce total calorie intake by 500 calories, and all groups were enrolled in an exercise program. At the end of 12 weeks all low-calorie groups showed similar decreases in weight. The authors concluded that the key aspect for weight loss is caloric restriction and not the content of fructose in the food. They also said that diets containing sucrose and high fructose corn syrup acted no differently from each other.

Why the Fructose Content of Food Counts

Let us address two issues that this study raises. The first question is whether it matters to reduce the intake of added sugars when you go on a diet. The second question is whether there is any real difference between table sugar (sucrose) and high fructose corn syrup.

    1. Does reducing sugar content matter? It is true that weight is largely governed by the law of thermodynamics, and that to lose weight the most effective way is to reduce food intake. This is why any diet that reduces calories will be effective at weight loss. However, reducing intake of added sugars, such as from table sugar (sucrose) or high fructose corn syrup (HFCS), does matter. These sugars contain fructose, and fructose has been shown to encourage weight gain because fructose can induce resistance to leptin, a hormone that controls appetite.

When fructose is fed to animals, they lose their ability to control their appetite. Restricting fructose intake can lead to a recovery of leptin sensitivity. This may be one reason low carb diets encourage weight loss, as they are essentially low fructose diets.

However, the problem with the study by Rippe is that all four diets consisted of an equivalent reduction in calories – so the benefit of reducing fructose on weight would have been largely obscured. However, we can see trends of a benefit – in that the two diets that contained 10 percent sucrose or HFCS showed a 3.3 and 4.15 kg weight loss, whereas the two diets that contained 20 percent HFCS or sucrose only had a 2.4 and 1.9 kg weight loss. This is likely because the diets lower in fructose were able to satisfy the appetite more effectively and likely did lead to some differences in energy intake.

Of greater concern is not weight, but the effects of fructose on body composition, fatty liver and insulin resistance. Fructose can rapidly induce metabolic syndrome and fatty liver that is not observed in animals fed the same number of calories as glucose or starch.

Weight gain is driven more by calories, but fatty liver and insulin resistance are driven more by fructose. In this study, the authors did not look at fatty liver or insulin resistance as outcomes. However, they did measure changes in fat percentage – again we see similar trends, with a reduction of 1.5 to 2.4 percent of fat in the 10 percent sucrose and HFCS groups, and a reduction of 1.1 to 1.3 percent of fat in the 20 percent sucrose and HFCS groups.

Thus, these studies suggest that reducing calories may reduce weight, but the content of fructose does matter.

Indeed, it is a shame that the authors did not include a hypocaloric diet with high sugar content. For example, some adolescents are ingesting 30 percent of their diet as added sugars. We found that laboratory rats given a diet of 40 percent sugar developed frank diabetes and fatty liver even when they were calorically restricted. We therefore need to rethink about the question of whether calories are just calories. Calories are important when it comes to weight, but the type of calorie can make a big difference on how it affects our risk for fat accumulation and diabetes.

    1. Are there differences between sugar and HFCS? The study by Rippe’s group also implies that HFCS and sugar are relatively equivalent in their effects. For sure, both contain fructose and can induce metabolic syndrome and weight gain in animals. However, there are several differences that suggest that HFCS may be slightly worse.

First, soft drinks containing HFCS do contain more fructose than soft drinks with the equivalent amount of sucrose, in part because of the higher fructose content in HFCS. Our group found that this translates into higher blood fructose levels and higher blood pressure following ingestion. More recently, Michael Goran’s group found that the percentage of fructose in HFCS-containing drinks is often higher than labeled, and may contain as much as 65 percent fructose.

Second, there may also be differences in how the fructose is absorbed between the two drinks. Thus, HFCS may result in faster absorption of the fructose since the fructose is not bound, whereas sucrose must first be degraded to glucose and fructose in the gut before it is absorbed. Our group found that mixtures of fructose and glucose led to worse fatty liver in laboratory animals than equivalent amounts of sucrose. Clearly more studies are needed, but the evidence does suggest that there are likely biological differences in these two added sugars.

In summary, we would recommend reducing intake of added sugars, both from sucrose and from HFCS, in any dietary plan. Reducing natural fruit intake is less necessary for while these fruits also contain fructose, they also contain many excellent nutrients that help combat the effects of fructose. More studies are needed to determine if the biological differences between HFCS and sucrose are clinically important.

‘Fat Switch’ May be Key to Turning Off Obesity

If you have ever struggled losing weight and keeping it off, you already know what a challenge that can be. Dr. Johnson’s new book, The Fat Switch, presents a groundbreaking approach to preventing and reversing obesity. Dr. Johnson asked me to publish his book to help spread the word and we hope to do just that. It’s the first book we’ve published that I did not write, because I felt it shared a powerful message on a very important topic that is central to the work we teach on this site.

I firmly believe that understanding how fructose influences your fat metabolism by activating your “fat switch” is key for achieving optimal weight and health. According to Dr. Johnson, based on his decades of research:

“Those of us who are obese eat more because of a faulty ‘switch’ and exercise less because of a low energy state. If you can learn how to control the specific ‘switch’ located in the powerhouse of each of your cells – the mitochondria – you hold the key to fighting obesity.”

I highly recommend picking up a copy of this book, which has been described as the “Holy Grail” for those struggling with their weight. In it, Dr. Johnson explains the details behind these five basic truths:

  1. Large portions of food and too little exercise are not solely responsible for why you are gaining weight
  2. Metabolic Syndrome is a normal condition that animals undergo to store fat
  3. Uric acid is increased by specific foods and causally contributes to obesity and insulin resistance
  4. Fructose-containing sugars cause obesity not by calories, but by turning on the fat switch
  5. Effective treatment of obesity requires turning off your fat switch and improving the function of your cells’ mitochondria

How Biological Survival Mechanisms Influence Your Weight

While Dr. Johnson is a kidney expert, his research has led him into areas the typical nephrologist will never delve into. In The Fat Switch, he explains how biological survival mechanisms influence body weight in previously unsuspected ways. In the first official review of the book, published in the University of Colorado Hospital magazine, The Insider, Todd Neff writes:

“Uric acid is best known for causing gout, a type of arthritis caused by buildup of uric acid crystals in joints. But the more Johnson and his team looked at uric acid, the more havoc the acid appeared to wreak. In research pending publication, Miguel Lanaspa and Johnson have fingered uric acid as a culprit in obesity.

Uric acid comes from the breakdown of the cellular fuel ATP (produced by the mitochondria) as well as the breakdown of DNA and RNA, primarily from foods. But this breakdown doesn’t have to yield uric acid, Johnson and Lanaspa found. There’s a fork in the metabolic road, with only one of the paths leading to uric acid.

It’s a rocky path. Uric acid stresses mitochondria, which leads mitochondria to boost fat synthesis while burning less energy, Johnson and colleagues have found. The implication is that the same amount of food builds fat into – and saps energy from – people on the uric acid pathway, Johnson and colleagues found.

‘Too much food intake plus too little exercise equals Fat,’ Johnson wrote. ‘However, our work suggests the interpretation is different. Obesity is not from gluttony and idleness, but rather because we have activated the same program all animals use to increase fat stores.'”

How is this biological “fat-storage program” activated? In short: fructose consumption.

Fructose, regardless of its source (although in the modern diet, the vast majority of it comes from processed foods and beverages), is acted on by the enzyme fructokinase in your cells. This enzyme is needed for your body to extract the energy from the fructose. But before getting to that energy, the fructokinase uses up ATP – the fuel in your cells – which activates the fat-storing uric acid metabolic pathway.

So while diet and exercise are still important factors, consumption of fructose appears to have an overriding impact on whether or not your body will hold on to and keep adding to its fat stores or not – despite your best efforts at eating well and exercising.

Watch the video discussion. URL:

How Biological Survival Mechanisms Influence Your Weight

While Dr. Johnson is a kidney expert, his research has led him into areas the typical nephrologist will never delve into. In The Fat Switch, he explains how biological survival mechanisms influence body weight in previously unsuspected ways. In the first official review of the book, published in the University of Colorado Hospital magazine, The Insider, Todd Neff writes:

“Uric acid is best known for causing gout, a type of arthritis caused by buildup of uric acid crystals in joints. But the more Johnson and his team looked at uric acid, the more havoc the acid appeared to wreak. In research pending publication, Miguel Lanaspa and Johnson have fingered uric acid as a culprit in obesity.

Uric acid comes from the breakdown of the cellular fuel ATP (produced by the mitochondria) as well as the breakdown of DNA and RNA, primarily from foods. But this breakdown doesn’t have to yield uric acid, Johnson and Lanaspa found. There’s a fork in the metabolic road, with only one of the paths leading to uric acid.

It’s a rocky path. Uric acid stresses mitochondria, which leads mitochondria to boost fat synthesis while burning less energy, Johnson and colleagues have found. The implication is that the same amount of food builds fat into – and saps energy from – people on the uric acid pathway, Johnson and colleagues found.

‘Too much food intake plus too little exercise equals Fat,’ Johnson wrote. ‘However, our work suggests the interpretation is different. Obesity is not from gluttony and idleness, but rather because we have activated the same program all animals use to increase fat stores.'”

How is this biological “fat-storage program” activated? In short: fructose consumption.

Fructose, regardless of its source (although in the modern diet, the vast majority of it comes from processed foods and beverages), is acted on by the enzyme fructokinase in your cells. This enzyme is needed for your body to extract the energy from the fructose. But before getting to that energy, the fructokinase uses up ATP – the fuel in your cells – which activates the fat-storing uric acid metabolic pathway.

So while diet and exercise are still important factors, consumption of fructose appears to have an overriding impact on whether or not your body will hold on to and keep adding to its fat stores or not – despite your best efforts at eating well and exercising.

Watch the video discussion. URL:https://youtu.be/3W2zSN0JOa8

Decision to deny surgery to obese patients is like ‘racial discrimination’


Bariatric surgeon Shaw Somers said move by local NHS in Vale of York amounts to discrimination because obesity is an illness

An overweight man sitting on the edge of a wall.
Anyone classified as obese – with a BMI of over 30 – will have to wait a year for surgery in the Vale of York.
The decision by an NHS body to restrict obese patients’ access to elective surgery until they lose weight is comparable with racial or religious discrimination, a surgeon has said.

The Vale of York clinical commissioning group (CCG) will make people wait for up to a year for treatment for non-life-threatening conditions such as hip and knee replacements if their body mass index is 30 or higher.

The group said it had taken the decision because it was the “best way of achieving maximum value from the limited resources available”.

Shaw Somers, a bariatric surgeon from Portsmouth, said the move was a logical step and could save money, but amounted to discrimination because obesity was an illness.

“They [the patients] are trying to lose weight in the vast majority of cases and to deny them treatment that they need on the basis of their weight, without then offering them effective help to help them lose weight is rather like discriminating [against] a segment of the population on the basis of their colour or religious persuasion,” he told BBC Radio 4’s Today programme.

“Just saying you can’t have surgery and there is no access to alternative treatments really doesn’t help anyone.”

Chris Hopson, the head of NHS Providers – which represents acute care, ambulance and community services – said the move amounted to “rationing care to save money”.

He told Today that the health service was being asked to deliver too much for the funding available. Rather than commissioning groups making “piecemeal decisions”, Hopson said there should be a national debate about the future of the UK’s healthcare system involving not only politicians, NHS leaders and clinicians – but the public as well, given that tax revenues funded it.

Demand for healthcare was “about to go through the roof” as baby boomers neared the end of their lives, he said. There had been a 6% increase in emergency admissions in the first quarter of this year.

The Royal College of Surgeons (RCS) said that it was a dangerous move that ranked among the “most severe the modern NHS has ever seen”.

She added: “As the true scale of financial pressure on NHS trusts has become clear over the summer, we are fast finding ourselves in a situation where CCGs are introducing draconian commissioning policies, often flouting Nice [National Institute for Health and Care Excellence] or other clinical guidance, in order to balance the books.

A spokesman for NHS England said: “Major surgery poses much higher risks for severely overweight patients who smoke. So local GP-led clinicalcommissioning groups are entirely right to ensure these patients first get support to lose weight and try and stop smoking before their hip or knee operation. Reducing obesity and cutting smoking not only benefits patients but saves the NHS and taxpayers millions of pounds.

“This does not and cannot mean blanket bans on particular patients such as smokers getting operations, which would be inconsistent with the NHS constitution.

“Vale of York CCG is currently under special measures legal direction, and NHS England is today asking it to review its proposed approach before it takes effect to ensure it is proportionate, clinically reasonable, and consistent with applicable national clinical guidelines.”

Portion-size preference does not determine BMI


Adults with overweight do not choose larger food portions than their normal-weight peers, according to recent findings.

“Large portions of food are often blamed for rising rates of obesity,” Natalie M.Reily, a researcher in the school of psychology at The University of New South Wales in Australia, and colleagues wrote. “We tested the possibility that people who are heavier may tend to select or prefer larger portions than do people who are lighter.”

The researchers conducted four studies based on four separate online questionnaires. In study 1, 128 women (mean BMI, 25.35 kg/m2) were asked to choose between images of small and large portions of pasta for a hypothetical meal. In study 2, 293 women (mean BMI, 25.47 kg/m2) were asked to choose between images of small and large portions, images of small and large portions with corresponding labels, and “small” and “large” labels. In an effort to provide more portion-size options, 104 women in study 3 (mean BMI, 24.74 kg/m2) were asked to select their preferred portion size in 28 pairs, which consisted of randomized options of eight different portions sizes. Study 4 had the same design as study 1 with 273 male participants (mean, BMI, 26.25 kg/m2).

In all four studies, researchers found that a somewhat greater percentage of participants with overweight than with normal weight chose larger portions, but the difference was not statistically significant. Researchers concluded that participants with a higher BMI did not select larger portions than those with a lower BMI, although in the forced-choice situations there was a slight tendency for heavier female participants to select the larger portion over the smaller one when compared with the lighter female participants.

“If portion size affects food intake to more or less the same degrees across BMI, and if there are no differences in portion-size preference among people who are heavier and people who are lighter (as observed in the present studies), then other factors need to be considered in attempting to explain the connection between portion size and obesity,” researchers wrote. “For example, rather than ordering larger portions, people with higher BMIs might eat more of what they order than do people with lower BMIs.”

Researchers report the hypothetical nature of all of the studies as a limitation, as well as the sole option of pasta. – by Cassie Homer

Later bedtime in adolescents, young adults tied to increased BMI


A later than average bedtime on weekdays is associated with an increase in BMI over time in adolescents and young adults regardless of sleep duration, according to research in Sleep.

In an observational study investigating the longitudinal relationship between bedtime and BMI, researchers found that each additional hour of delayed bedtime was associated with an increase in BMI of 2.1 kg/m² during the 15-year study period.

Lauren Asarnow

Lauren D. Asarnow

“We found that, in a sample of over 3,000 individuals, going to bed later between the ages of 13 and 32 was associated with weight gain over that same time period above and beyond what’s typical for that developmental period,” Lauren D. Asarnow, MS, of the University of California, Berkeley, told Endocrine Today.

Asarnow and colleagues analyzed data from 3,342 adolescents participating in the National Longitudinal Study of Adolescent Health, a study containing health and behavior data on U.S. adolescents aged 13 to 18 years in the first two waves (1994 to 1996), and again at age 18 to 32 years in the third and fourth waves (2001 to 2002 and 2008 to 2009). Sleep time and sleep duration were self-reported in all waves of the study; sleep diaries were not used. Researchers measured height and weight at each wave; BMI was converted to a z score. Questions assessing fast food consumption, screen time and physical activity were included as potential partial mediators. Researchers used hierarchal linear models using a two-level, random intercept and slopes model to test whether later bedtimes would be associated with an increase in BMI.

A later average workday bedtime was associated with an increase in BMI after controlling for baseline BMI, pubertal status, welfare status and sex. The association persisted after controlling for sleep duration, exercise frequency and screen time (P < .05), but fast food consumption was recognized as a significant partial mediator on bedtime and BMI longitudinally, according to researchers.

“Another interesting point, which was surprising to us, is this was true regardless of how much sleep you were getting,” Asarnow said. “Going to bed at 2 a.m., for example, even if you were getting 8 hours of sleep and waking up at 10 a.m., was associated with weight gain.

“We see this as potentially very good news,” she said. “Bedtime is a highly modifiable behavior. Dr. Allison Harvey and her research team in the Golden Bear Sleep and Mood Research Clinic are currently conducting a study, funded by the National Institute of Child Health and Human Development, to see whether changing sleep habits effect weight gain, eating behavior and other outcomes like emotional health and academic performance. We are anxiously awaiting our results.” by Regina Schaffer

How Early Should Obesity Prevention Start?


Obesity has pervaded the United States and is spreading throughout the world. Following in its wake is type 2 diabetes, which will affect at least half a billion people worldwide by 2030. A majority of U.S. women of childbearing age are overweight or obese (as defined by a body-mass index [BMI, the weight in kilograms divided by the square of the height in meters] >25). These women are likely to gain excessive weight when they’re pregnant, making it harder for them to return to their prepregnancy weight after delivery. Postpartum weight retention not only portends increased lifelong risks for obesity-related complications but also an increased BMI at the inception of future pregnancies. During pregnancy, excessive weight gain, along with other risk factors such as gestational diabetes, can alter fetal growth and metabolism, leading to higher adiposity in the offspring. If the child is female, grows up obese, and becomes pregnant, the cycle begins again. It is time to interrupt this vicious cycle to prevent obesity and chronic diseases in mothers and children.

Once obesity is present, it is challenging to treat because of multiple physiological, behavioral, and cultural feedback loops. The good news is that the prenatal period and the first postnatal year hold critical clues that may lead to interventions to reduce obesity in women and prevent it in children. In a range of animal models (from rodents to nonhuman primates), dietary, hormonal, mechanical, and other perturbations that occur prenatally and during infancy induce lifelong, often irreversible derangements in the offspring’s adiposity and metabolism. These changes involve the environmental alteration of genetic expression, in part through epigenetic mechanisms, rather than changes in the genome itself. Thus, timely intervention during the early, plastic phases of development — unlike corrective efforts made later in life — may lead to improved lifelong health trajectories.

Because of challenges in measuring fetal exposures and the long latency between initial determinants and salient health outcomes, however, it is difficult to translate such proofs of principle in animals to human populations. The first generation of developmental-origins studies in humans linked birth weight to adult obesity-related morbidity and mortality. We now recognize that birth weight and each of its components, gestational duration and fetal growth, are low-resolution, momentary markers for myriad prenatal and perinatal influences. In the past decade, many such influences have been identified and quantified in epidemiologic studies that have involved the period before birth, used modern methods to mitigate confounding, and incorporated biomarkers. These studies have identified prenatal risk factors for obesity ranging from lifestyle factors such as the mother’s smoking status to psychosocial factors including antepartum depression, medical conditions such as gestational diabetes, physiological stress as reflected by fetal exposure to glucocorticoids, and epigenetic markers such as gene-specific DNA methylation levels in umbilical-cord tissue.

After birth, rapid weight gain in the first 3 to 6 months of life is a potent predictor of later obesity and cardiometabolic risk. Lactation cannot be the entire explanation, because breast-fed babies tend to gain more weight than formula-fed babies in the first few months of life. The perinatal hormonal milieu may very well be a contributing factor. In one study, higher leptin levels in umbilical-cord blood, chiefly reflecting placental production, were associated with slower gain in infant weight-for-length and lower adiposity at the ages of 3 years and 7 years. In contrast, higher leptin levels at 3 years of age were associated with faster gains in BMI from 3 to 7 years, suggesting that leptin resistance develops between birth and 3 years of age.1 These findings are consistent with studies in animals showing a critical period of perinatal leptin exposure that allows normal maturation of appetite-regulating neurons in the hypothalamus. Features of infant feeding other than breast versus bottle may also play a role. Among formula-fed infants, the introduction of solids before 4 months was associated with a sixfold increase in the odds of obesity 3 years later.2

Emerging risk factors for obesity include exposure to endocrine disruptors, which appear to do the most damage during times of maximum developmental plasticity, and the gut microbiota. Our bodies contain about 1013 cells but as many as 1014 microorganisms. Certain modifications in the number and type of microorganisms during infancy are associated with excess weight gain, at least in rodents. The infant gut is normally colonized during transit through the birth canal, which could be one reason why children delivered by cesarean section appear to be at elevated risk for obesity.3

Given obesity’s numerous developmental determinants, it is logical that effective prevention would target multiple modifiable factors. In combination, two well-studied prenatal risk factors, excessive gestational weight gain and maternal smoking during pregnancy, and two postnatal factors, fewer months of breast-feeding and a shorter duration of daily sleep during infancy, are associated with wide variation in childhood obesity. In one study, preschool-age children whose mothers did not smoke or gain excessive weight during pregnancy and who were breast-fed for at least 12 months and slept for at least 12 hours per day during infancy had a predicted obesity prevalence of 6%, as compared with 29% among children for whom the opposite was true for all four risk factors4; the rates were similar (4% and 28%, respectively) when the children reached 7 to 10 years of age (see graphPredicted Probability of Obesity at 7 to 10 Years of Age for 16 Combinations of Four Modifiable Prenatal and Postnatal Risk Factors.). These observational data raise the possibility that avoiding some or all of these risk factors could substantially reduce the proportion of childhood obesity.

Preventing racial and ethnic disparities in obesity risk will also require a developmental approach. By school age, rates of obesity among black and Hispanic children in the United States are higher than the rates among white children, even after adjustment for socioeconomic circumstances. Many of the risk factors during pregnancy and early childhood are more prevalent among nonwhite persons, and they explain a substantial proportion of racial and ethnic differences in obesity in mid-childhood.5

Several features of pregnancy and infancy make the prenatal and postnatal periods conducive to behavior change to reduce the risk of obesity and its complications. First, women appear especially willing to modify their behavior during these periods to benefit their children. Second, since pregnant women and infants receive frequent routine medical care, interventions involving improved health care delivery have great potential. Third, these periods are relatively brief, and we know that behavior-change interventions are typically most successful in the short term. Fourth, if effective interventions begun during pregnancy are maintained after birth, they will reduce the risk of maternal obesity for future pregnancies and thus help to interrupt the intergenerational cycle.

Ongoing intervention studies promise to inform medical practice and public health. Many current trials target excessive gestational weight gain, including seven randomized, controlled trials funded by the National Institutes of Health that will together include more than 1000 overweight or obese women and follow infants through at least 1 year of age. It remains to be proven, however, that reducing gestational weight gain reduces the obesity risk in offspring. An alternative approach focuses on dietary quality, independent of calorie content, to ameliorate maternal insulin resistance and excessive placental nutrient transfer. Pilot studies have suggested that a multiple-risk-factor approach during infancy, targeting mothers as conduits for changes in their infants, can improve sleep duration and delay the introduction of solid foods.

But even as we await the results of obesity-prevention trials, some recommendations are warranted because of their beneficial effects on other health outcomes. Pregnant women should not smoke. Treatment of gestational diabetes reduces macrosomia at birth, although such treatment hasn’t been proven to prevent obesity. U.S. rates of elective cesarean sections have apparently leveled off, but reducing these rates, especially of cesarean sections performed before 39 weeks of gestation, is a public health goal. Simple sleep-hygiene measures are worth trying, even in early infancy. The ideal age, in terms of allergy prevention, for introducing solid foods appears to be 4 to 6 months, and further research may show that the same is true in terms of obesity prevention.

 

Source: NEJM

BMI may be most vital determinant of basal metabolic rate in PCOS.


The BMI of patients with polycystic ovary syndrome appeared to be the most important factor in basal metabolic rate, independent of the polycystic ovary syndrome phenotype and insulin resistance, according to Margareta D. Pisarska, MD, who presented the data at the conjoint meeting of the International Federation of Fertility Societies and the American Society for Reproductive Medicine.

“Based on our study — since we do think obesity does play a significant role — we believe it is important for endocrinologists to help counsel these women in a fashion similar to those who are obese by emphasizing that weight loss and lowering BMI are important,” Pisarska, director of the division of reproductive endocrinology and infertility; director of the Fertility and Reproductive Medicine Center at Cedars-Sinai Medical Center; associate professor at Cedars-Sinai Medical Center and the David Geffen School of Medicine at UCLA, told Endocrine Today.

 

The researchers conducted the case-control study examining the metabolic changes (ie, lean body mass, body fat mass, body fat percentage, skeletal muscle mass, BMI and basal metabolic rate) in 128 patients with PCOS (mean age, 28.1 years) and 72 eumenorrheic, non-hirsute controls (mean age, 32.9 years).

In terms of hormonal profile, patients with PCOS had greater testosterone, dehydroepiandrosterone sulfate (DHEA-sulfate), fasting insulin and homeostasis model assessment of insulin resistance (HOMA-IR) levels compared with controls.

After controlling for age and BMI differences, there was no difference in body composition parameters between patients with PCOS and controls. There were no significant results regarding changes to the basal metabolic rate (P=.0162), lean body mass (P=.0153) or skeletal muscle mass (P=.0169), she said.

However, differences in fasting insulin and HOMA-IR remained significant. When looking at insulin resistance in women with PCOS as a potential factor affecting body composition and metabolic rates, there was also no difference between these groups.

“It is not necessarily PCOS; BMI and age are probably the more important determinants of basal metabolic rate, regardless of PCOS phenotype and insulin resistance,” Pisarska said.

BMI may be most vital determinant of basal metabolic rate in PCOS.


The BMI of patients with polycystic ovary syndrome appeared to be the most important factor in basal metabolic rate, independent of the polycystic ovary syndrome phenotype and insulin resistance, according to Margareta D. Pisarska, MD, who presented the data at the conjoint meeting of the International Federation of Fertility Societies and the American Society for Reproductive Medicine.

“Based on our study — since we do think obesity does play a significant role — we believe it is important for endocrinologists to help counsel these women in a fashion similar to those who are obese by emphasizing that weight loss and lowering BMI are important,” Pisarska, director of the division of reproductive endocrinology and infertility; director of the Fertility and Reproductive Medicine Center at Cedars-Sinai Medical Center; associate professor at Cedars-Sinai Medical Center and the David Geffen School of Medicine at UCLA, told Endocrine Today.

The researchers conducted the case-control study examining the metabolic changes (ie, lean body mass, body fat mass, body fat percentage, skeletal muscle mass, BMI and basal metabolic rate) in 128 patients with PCOS (mean age, 28.1 years) and 72 eumenorrheic, non-hirsute controls (mean age, 32.9 years).

In terms of hormonal profile, patients with PCOS had greater testosterone, dehydroepiandrosterone sulfate (DHEA-sulfate), fasting insulin and homeostasis model assessment of insulin resistance (HOMA-IR) levels compared with controls.

After controlling for age and BMI differences, there was no difference in body composition parameters between patients with PCOS and controls. There were no significant results regarding changes to the basal metabolic rate (P=.0162), lean body mass (P=.0153) or skeletal muscle mass (P=.0169), she said.

However, differences in fasting insulin and HOMA-IR remained significant. When looking at insulin resistance in women with PCOS as a potential factor affecting body composition and metabolic rates, there was also no difference between these groups.

“It is not necessarily PCOS; BMI and age are probably the more important determinants of basal metabolic rate, regardless of PCOS phenotype and insulin resistance,” Pisarska said.

Influence of Body Mass Index on Survival in Veterans With Multiple Myeloma.


Abstract

Purpose. We investigated the association between body mass index (BMI) at the time of multiple myeloma (MM) diagnosis and overall survival in a cohort of patients within the Veterans Health Administration system. We also evaluated the association between weight loss in the year prior to diagnosis and survival.

Patients and Methods. Prospective analysis was performed on a retrospectively assembled cohort of 2,968 U.S. veterans diagnosed and treated for MM between September 1, 1999, and September 30, 2009, with follow-up information through October 22, 2011. Cox modeling controlling for patient- and disease-related prognostic variables was used to analyze the data.

Results. Underweight patients (BMI <18.5 kg/m2) had increased mortality, whereas patients who were overweight (BMI 25–29.9 kg/m2) and obese (BMI ≥30 kg/m2) had lower mortality compared with healthy-weight patients (BMI 18.5–24.9 kg/m2). Weight loss ≥10% of baseline in the year before diagnosis was also associated with increased mortality and made the association between increased BMI and survival nonsignificant.

Conclusion. Disease-related weight loss may be an important and heretofore unknown indicator of poor prognosis in MM. Assessment of weight loss prior to MM diagnosis should become a standard component of the clinical history in patients with newly diagnosed MM. Further research may identify relationships between disease-related weight loss and currently used prognostic factors in MM, further defining the role of this clinical factor in prognostic stratification.

 

Source: The Oncologist.

Sexual abuse linked to obesity in children, teens with mental illnesses.


Researchers reported that a history of sexual abuse increased the risk for obesity among children and adolescents who had significant psychiatric illnesses.

“Considering that children with mental illness are already at risk for weight problems and will continue to be at increased risk as they move toward adulthood, recognition of this association is important to consider when clinicians are developing appropriate treatment plans or are evaluating potential adverse effects from current treatment regimens,” Brooks R. KeeshinMD, with the Mayerson Center for Safe and Healthy Children at Cincinnati Children’s Hospital Medical Center, said in an interview.

Keeshin and colleagues analyzed medical charts of 1,434 youth admitted to a Midwestern inpatient psychiatric facility during a 10-month period. The researchers compared rates of physical and sexual abuse in youth with a normal BMI percentile and youth whose BMI percentiles were greater than 85, which in the study was considered to be overweight or obese.

Of the entire cohort, 14.7% reported physical abuse, 16.6% reported sexual abuse and 5.4% reported both.

Controlling for age, race, gender and antipsychotic treatment, Keeshin and colleagues found that youth who reported a history of sexual abuse were at greater odds of being overweight/obese (BMI percentiles 85 to 99) than having a healthy BMI (adjusted OR=1.41; 95% CI, 1.01-1.98). Physical abuse was not associated with an increase in BMI percentile.

Female gender and antipsychotic use were associated with overweight/obesity, although fewer girls (29.2%) than boys (38.6%) were prescribed antipsychotic medication. The researchers said being prescribed antipsychotics was the only significant predictor of “significant obesity,” defined as a BMI percentile greater than 99 (aOR=2.59; 95% CI, 1.57-4.28).

“These data suggest that, in youth with a significant mental illness, sexual abuse is significantly and independently associated with obesity, a finding that may prompt increased attention to weight gain by pediatricians who care for youth with a history of sexual abuse and suffer from mental illness,” the researchers concluded.

Source: Endocrine Today