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Packaged diet foods may spur more weight loss

In a head-to-head comparison with a traditional diet, people who stuck to a diet of portion-controlled packaged foods lost almost twice as much weight as those who only got advice on how to trim calories, according to a new study.

Dr. Michael Dansinger, a nutrition expert at Tufts Medical Center, said having less freedom in choosing meals seems to help people meet their dieting goals.

"When there's less structure, then participants are making more decisions, and I think too often they're making decisions that undermine their goal to stick to a calorie target," said Dansinger, who was not part of the study.

The diet the researchers studied was the Medifast 5 & 1 Plan. It consists of five pre-packaged meals each day, along with one meal of vegetables and protein prepared by the dieter.

Dieters can pick from 70 different packaged foods to create five meals totaling about 1,000 calories a day.

People on the plan can also purchase different levels of support along with the meals, such as access to dieticians and recipes. Typically, the plan costs about $300 a month.

To see how effective the Medifast diet is in helping people lose weight and keep it off, the researchers asked 60 people to join the plan for free.

They compared these dieters to another 60 people who were given advice on how to meet a 1,000 calorie-per-day target, but who continued to buy and prepare their own food.

For everyone in the study, the goal for the first 26 weeks was to lose weight, and during the second half of the study the goal was to maintain weight.

All of the participants were obese, having a body mass index (BMI) - a measure of body size relative to height - between 35 and 50.

A BMI of 35 represents, for example, a person who is 5-feet 8-inches tall and 230 pounds.

By the end of the study, 15 people dropped out of the regular-food group and 10 dropped out of the Medifast group.

After six months, those who stuck with either dieting approach lost weight.

People in the Medifast group shed an average of 16.5 pounds, or 6.7 percent of their starting weight.

Dansinger said such a reduction in weight is modest, but it can have a meaningful impact on people's health.

"That's been demonstrated in numerous studies to be effective for improving blood sugar in people with diabetes or delaying the progression from pre-diabetes to type 2 diabetes and to reduce other heart disease risk factors, including blood pressure, cholesterol and inflammation," he told Reuters Health.

The regular-food group lost an average of 8.4 pounds, or 3.4 percent of their body weight.

The Medifast dieters also had greater reductions in body fat, waist circumference and cholesterol than the other group.

Of the average 16.5 pounds Medifast dieters lost, 14 were fat mass. Regular-food dieters lost an average of 8.14 pounds of fat. The study did not examine the diets' effects on bone and muscle mass.

Medifast users lost an average 2.24 inches around their waists and their total cholesterol dropped an average 8.4 milligrams, compared to 1.46 inches and 1.1 milligrams, respectively, in the regular diet group.

Over time, though, the dieters in both groups tended to rebound somewhat toward their original weights.

After one year in the study, the Medifast group ended up about 10 pounds, or 4.2 percent, lighter than when they started, while the other group was about four pounds, or 1.7 percent, lighter.

James Shikany, the lead author of the study, said the results show that sticking to the Medifast diet makes it harder for dieters to eat more calories than they should.

"It's more of a regimented type of diet, and some people find that's what they need in order to limit their portion intake," said Shikany, who is a professor at the University of Alabama at Birmingham Division of Preventive Medicine.

Dansinger said the weight loss results from the Medifast diet appear to fall in the middle of the pack of other weight loss interventions.

Some approaches, such as weight loss surgery or more extreme diets can have more dramatic results.

But in terms of dietary interventions or FDA-approved weight loss pills, the effect is roughly comparable, he said.

Lisa Davis, the vice president of science and clinical affairs at Medifast, said earlier studies of the diet actually found greater weight reductions.

One explanation she offered is that the current study participants' demographics, such as race, appeared to be different in Shikany's study than in earlier ones.

In particular, Shikany's study included a majority of African Americans whereas other studies had mostly caucasians, Davis said.

"I think that's worth investigating in the future," she told Reuters Health.

Medifast funded the current study, and one of the researchers has been a consultant to Medifast.

Dansinger said that based on this and other studies, he would recommend meal-replacement diets.

"In my opinion, for patients who have had repeated failures with other attempts at sustaining weight loss, the Medifast plan or other similar plans appear to be a good option," he said.

Shikany agreed, but said it's unclear whether cost could be a factor in the diet's appeal.

"If you take (cost) out of the equation, I think it would be a good option for some people, especially for people who need that extra assistance in weight loss efforts as far as determining portions," he said.

Sex and the Superbug: Meet Antibiotic-Resistant Gonorrhea

Here’s a tidbit you probably didn’t know: Gonorrhea is the second-most frequently reported “notifiable” disease, according to the Centers for Disease Control (CDC). (That means that if you have it, your doctor or local health official needs to report it to the federal government so they can track it; gonorrhea is beaten out only by chlamydia.)

Though gonorrhea—being a sexually transmitted disease (STD) and all—doesn’t come up in conversation too often, it's way more prevalent than you probably think. It’s also a superbug, meaning it’s grown resistant to the usual treatments because the gonorrhea bacteria has mutated to become stronger than ever.  In fact, earlier this month you may have seen alarmist headlines (“Sex Superbug Could be ‘Worse Than AIDS,’” said about drug-resistant gonorrhea. The CDC was quick to respond, quelling fears about the bug’s presence in the U.S. Many reports were referring to gonorrhea strain H041, which is very resistant to ceftriaxone—the drug widely recommended for treating gonorrhea. That strain, though, hasn’t ever been reported in the U.S., said the CDC.

Gonorrhea is caused by Neisseria gonorrhoeae, a gram-negative bacterium (which means the cells have a double cell lining). The World Health Organization (WHO) estimates that about 62 million people get gonorrhea every year. To get it, you have to have contact with the mouth, penis, vagina, or anus of an infected sexual partner. Once N. gonorrhoeae bacteria have been transmitted, they infect mucosal surfaces in the genitals and throat.

Symptoms of gonorrhea manifest differently in men and women, and also vary in severity (many people, in fact, are asymptomatic). When symptoms do appear, men may see a urethral discharge, or feel pain in their testicles or scrotum. Complications for guys can result in epididymitis, which is pain and inflammation of the epididymis (for those not into genital anatomy and physiology, that’s part of the testicle that stores sperm; we’re getting up close and personal now). In women, gonorrhea may also cause vaginal discharge or bleeding between periods.

Symptoms of untreated gonorrhea aren’t just uncomfortable and embarrassing, though. There are complications of gonorrhea infections that nobody likes to think about: In women, the STD can spread to the uterus and fallopian tubes, increasing the risk of pelvic inflammatory disease, infertility, and ectopic pregnancy (a dangerous situation in which the embryo implants outside of the uterus). Gonorrhea can be passed from mother to child, and it also increases your risk for HIV. So, in the end, it’s a pretty serious infection.

For a while, gonorrhea could be treated easily with penicillin and sulfa drugs. In the late 1960s, though, studies began showing that gonorrhea was rapidly increasing its resistance to penicillin. It beat the antibiotics by making an enzyme—penicillinase—that made penicillin totally ineffective. Then, in the 1980s, strains of gonorrhea that did not produce penicillinase began showing resistance; they showed up in the U.S. in 1980 during an outbreak in North Carolina. This meant that certain strains of gonorrhea had undergone a genetic mutation: They had picked up a chromosome that allowed them to be resistant in a different way. (As a reminder, antibiotics target certain structural components in bacteria to defeat them. If these structural components change, even just a little bit, this change affects the susceptibility of the bacteria to an antibiotic.) What we learned in the ‘80s was that not only did some strains of gonorrhea produce an enzyme that destroyed penicillin, other strains were shifting so that penicillin couldn’t affect them.

Since 1986, the United States Gonococcal Isolate Surveillance Project (GISP) has been monitoring antibiotic resistance to gonorrhea. According to GISP, by 2010, 27 percent of all of the gonorrhea samples were resistant to penicillin, tetracycline, and ciprofloxacin, or some combination of these drugs.

By 2010, 27 percent of all gonorrhea tested was resistant to three major antibiotics or some combination of these drugs.

Cefixime, an oral cephalosporin antibiotic (cephalosporins are a sub-group of beta-lactam antibiotics, like carbapenems) was the recommended antibiotic for gonorrhea treatment, until gonorrhea began to develop resistance that drug too. In 2012, the CDC  updated its treatment guidelines and now recommends an injectable cephalosporin, called ceftriaxone, along with azithromycin or doxycycline, instead of oral cephalosporins. Combination therapies (meaning more than one antibiotic) provide almost a one-two punch against these bacteria—so the hope is that this remains effective. But cephalosporins are our last line of antibiotic defense against gonorrhea. As authors wrote in 2012 in a piece in the New England Journal of Medicine, it is now “time to sound the alarm.”

Simply put, the outlook is not good. In 2011, doctors from Japan published a case study revealing that gonorrhea was acquiring even more resistance—this time, to injectable ceftriaxone. Since then, samples of ceftriaxone-resistant gonorrhea have been detected in France and Spain, too, reports the CDC.

So what to do? We clearly need new options for treatment, but those don’t seem to be coming any time soon. The best method of protection against gonorrhea is abstinence. But that’s not always the most realistic prevention method. The CDC also strongly recommends the use of latex condoms—and not just for vaginal intercourse, but also for oral sex as well. In his New Yorker piece on antibiotic-resistant gonorrhea, Dr. Jerome Groopman briefly explores condom use in fellatio; through interviews with medical professionals, Groopman explains that the most conventional (and effective) way to transmit gonorrhea is through fellatio, because the urethra can come into contact with the human pharynx (throat). The pharynx is a breeding ground for resistance in gonorrhea.

So while we wait for new antibiotics, the best advice we have when it comes to gonorrhea superbugs is: Don’t forget to use a condom.

Weight Gain May Change Personality

 After gaining a significant amount of weight, people may grow more self-conscious about their choices, while at the same time being weaker in the face of temptation, a new study finds.

Researchers already have an idea about how personality traits contribute to weight gain. For instance, people pleasers tend to eat more at parties, conscientious folk are more likely to have a regular exercise routine, and those with a Type A personality may be at increased risk for health problems like weight gain and heart disease. These are all averages, of course, and every person with a certain personality won't fall into the associated health group.

"What we don't know is whether significant changes in weight are associated with changes in our core personality traits," Angelina Sutin of the Florida State University College of Medicine said in a statement. "Weight can be such an emotional issue, we thought that weight gain may lead to long-term changes in psychological functioning."
[The 7 Biggest Diet Myths Debunked]

Sutin and her colleagues at the National Institutes of Health (NIH) looked at data on the personality traits and weights of more than 1,900 people at two time points, nearly a decade apart.

During that period, those who gained more than 10 percent of their body weight became more impulsive and were more likely to give in to temptations compared with those whose weight remained stable, the researchers found.

At the same time, weight gain was also associated with increased thoughtfulness in decision making. These results held regardless of how much participants weighed, specifically their body mass index (BMI, or a measure of body fatness) at the beginning of the study.

The researchers speculate that people who have put on pounds might feel more self-conscious about their actions because of negative comments they've received about their weight. But they may still have trouble keeping temptations at bay even as they become more aware of their choices, and those effects can snowball, the researchers say.

"The inability to control cravings may reinforce a vicious cycle that weakens the self-control muscle," the researchers wrote on April 29 in the journal Psychological Science. "Yielding to temptation today may reduce the ability to resist cravings tomorrow. Thus, individuals who gain weight may have increased risk for additional weight gain through changes in their personality."

The study drew from NIH's Baltimore Longitudinal Study of Aging, whose participants ranged from middle to older age with an average age of about 59 at the study's start, and the Baltimore Epidemiologic Catchment Area study, whose participants were younger, with an averge age of about 45 at the study's start.

Eating insects could help fight obesity, U.N. says

The thought of eating beetles, caterpillars and ants may give you the creeps, but the authors of a U.N. report published on Monday said the health benefits of consuming nutritious insects could help fight obesity.
More than 1,900 species of insects are eaten around the world, mainly in Africa and Asia, but people in the West generally turn their noses up at the likes of grasshoppers, termites and other crunchy fare.
The authors of the study by the Forestry Department, part of the U.N. Food and Agriculture Organization FAO), said many insects contained the same amount of protein and minerals as meat and more healthy fats doctors recommend in balanced diets.
"In the West we have a cultural bias, and think that because insects come from developing countries, they cannot be good," said scientist Arnold van Huis from Wageningen University in the Netherlands, one of the authors of the report.
Eva Muller of the FAO said restaurants in Europe were starting to offer insect-based dishes, presenting them to diners as exotic delicacies.
Danish restaurant Noma, for example, crowned the world's best for three years running in one poll, is renowned for ingredients including ants and fermented grasshoppers.
As well as helping in the costly battle against obesity, which the World Health Organization estimates has nearly doubled since 1980 and affects around 500 million people, the report said insect farming was likely to be less land-dependent than traditional livestock and produce fewer greenhouse gases.
It would also provide business and export opportunities for poor people in developing countries, especially women, who are often responsible for collecting insects in rural communities.
Van Huis said barriers to enjoying dishes such as bee larvae yoghurt were psychological - in a blind test carried out by his team, nine out of 10 people preferred meatballs made from roughly half meat and half mealworms to those made from meat.

Smoking – health risks


You can eat five portions of fruit or veg a day and exercise regularly – but healthy behaviour means little if you continue to smoke.
The message that 'smoking is bad for you' is an old one, so not everyone gives it their full attention.
Below we list the health risks of smoking.
Why quit smoking?
Most people know that smoking can cause lung cancer, but it can also cause many other cancers and illnesses.
Smoking directly causes over 100,000 deaths in the UK each year and contributes to many more.
Of these deaths, about 42,800 are from smoking-related cancers, 30,600 from cardiovascular disease and 29,100 die slowly from emphysema and other chronic lung diseases.
How do cigarettes damage health?

Cigarettes contain more than 4000 chemical compounds and at least 400 toxic substances.
When you inhale, a cigarette burns at 700°C at the tip and around 60°C in the core. This heat breaks down the tobacco to produce various toxins.
As a cigarette burns, the residues are concentrated towards the butt.
The products that are most damaging are:
tar, a carcinogen (substance that causes cancer)
nicotine is addictive and increases cholesterol levels in your body
carbon monoxide reduces oxygen in the body
components of the gas and particulate phases cause chronic obstructive pulmonary disorder (COPD).
The damage caused by smoking is influenced by:
the number of cigarettes smoked
whether the cigarette has a filter
how the tobacco has been prepared.
Smoking affects how long you live
Research has shown that smoking reduces life expectancy by seven to eight years.

Of the 300 people who die every day in the UK as a result of smoking, many are comparatively young smokers.
The number of people under the age of 70 who die from smoking-related diseases exceeds the total figure for deaths caused by breast cancer, AIDS, traffic accidents and drug addiction.
Non-smokers and ex-smokers can also look forward to a healthier old age than smokers.
Major diseases caused by smoking
Cardiovascular disease
Cardiovascular disease is the main cause of death due to smoking.
Hardening of the arteries is a process that develops over years, when cholesterol and other fats deposit in the arteries, leaving them narrow, blocked or rigid. When the arteries narrow (atherosclerosis), blood clots are likely to form.
Smoking accelerates the hardening and narrowing process in your arteries: it starts earlier and blood clots are two to four times more likely.
Cardiovasular disease can take many forms depending on which blood vessels are involved, and all of them are more common in people who smoke.

Coronary thrombosis: a blood clot in the arteries supplying the heart, which can lead to a heart attack. Around 30 per cent are caused by smoking.
Cerebral thrombosis: the vessels to the brain can become blocked, which can lead to collapse, stroke and paralysis. Damage to the brain's blood supply is also an important cause of dementia.
If the kidney arteries are affected, then high blood pressure or kidney failure results.
Blockage to the vascular supply to the legs may lead to gangrene and amputation.
Smokers tend to develop coronary thrombosis 10 years earlier than non-smokers, and make up 9 out of 10 heart bypass patients.
Smokers are more likely to get cancer than non-smokers. This is particularly true of lung cancer, throat cancer and mouth cancer, which hardly ever affect non-smokers.
The link between smoking and lung cancer is clear.
Ninety percent of lung cancer cases are due to smoking.
If no-one smoked, lung cancer would be a rare diagnosis – only 0.5 per cent of people who've never touched a cigarette develop lung cancer.
One in ten moderate smokers and almost one in five heavy smokers (more than 15 cigarettes a day) will die of lung cancer.
The more cigarettes you smoke in a day, and the longer you've smoked, the higher your risk of lung cancer. Similarly, the risk rises the deeper you inhale and the earlier in life you started smoking.
For ex-smokers, it takes approximately 15 years before the risk of lung cancer drops to the same as that of a non-smoker.
If you smoke, the risk of contracting mouth cancer is four times higher than for a non-smoker. Cancer can start in many areas of the mouth, with the most common being on or underneath the tongue, or on the lips.
Other types of cancer that are more common in smokers are:
bladder cancer
cancer of the oesophagus
cancer of the kidneys
cancer of the pancreas
cervical cancer
Chronic obstructive pulmonary disease (COPD) is a collective term for a group of conditions that block airflow and make breathing more difficult, such as:

emphysema – breathlessness caused by damage to the air sacs (alveoli)
chronic bronchitis – coughing with a lot of mucus that continues for at least three months.
Smoking is the most common cause of COPD and is responsible for 80 per cent of cases.
It's estimated that 94 per cent of 20-a-day smokers have some emphysema when the lungs are examined after death, while more than 90 per cent of non-smokers have little or none.
COPD typically starts between the ages of 35 and 45 when lung function starts to decline anyway.

In smokers, the rate of decline in lung function can be three times the usual rate. As lung function declines, breathlessness begins.
As the condition progresses, severe breathing problems can require hospital care. The final stage is death from slow and progressive breathlessness.
Other risks caused by smoking

Smoking raises blood pressure, which can cause hypertension (high blood pressure) – a risk factor for heart attacks and stroke.
Couples who smoke are more likely to have fertility problems than couples who are non-smokers.
Smoking worsens asthma and counteracts asthma medication by worsening the inflammation of the airways that the medicine tries to ease.
The blood vessels in the eye are sensitive and can be easily damaged by smoke, causing a bloodshot appearance and itchiness.
Heavy smokers are twice as likely to get macular degeneration, resulting in the gradual loss of eyesight.
Smokers run an increased risk of cataracts.
Smokers take 25 per cent more sick days year than non-smokers.
Smoking stains your teeth and gums.
Smoking increases your risk of periodontal disease, which causes swollen gums, bad breath and teeth to fall out.
Smoking causes an acid taste in the mouth and contributes to the development of ulcers.
Smoking also affects your looks: smokers have paler skin and more wrinkles. This is because smoking reduces the blood supply to the skin and lowers levels of vitamin A.
Smoking and impotence
For men in their 30s and 40s, smoking increases the risk of erectile dysfunction (ED) by about 50 per cent.

Erection can't occur unless blood can flow freely into the penis, so these blood vessels have to be in good condition.
Smoking can damage the blood vessels and cause them to degenerate: nicotine narrows the arteries that lead to the penis, reducing blood flow and the pressure of blood in the penis.
This narrowing effect increases over time, so if you haven't got problems now, things could change later.
Erection problems in smokers may be an early warning signal that cigarettes are already damaging other areas of the body – such as the blood vessels that supply the heart.
Smoking and others
There are many health-related reasons to give up cigarettes – not just for smokers, but to protect those around you.
Babies born to mothers who smoke during pregnancy are twice as likely to be born prematurely and with a low birth weight.
Passive smoking
The 'side-stream' smoke that comes off a cigarette between puffs carries a higher risk than directly inhaled smoke.
Children who grow up in a home where one or both of their parents smoke have twice the risk of getting asthma and asthmatic bronchitis. They also have a higher risk of developing allergies.
Infants under two years old are more prone to severe respiratory infections and cot death.
For adults, passive smoking seems to increase the risk of lung cancer, but the evidence for an increased risk of heart disease is not yet conclusive.
Thinking about quitting?
As well as reducing your risk of getting a smoking-related illness, there are other benefits to quitting smoking.
General health improves – tiredness and headaches can be linked to smoking.
Your sense of taste and smell improve.
Your heart will be less strained and work more efficiently.
Stopping smoking is the single biggest thing you can do to improve your health, but it's a difficult task.
Smokers who are trying to kick their habit may be disappointed to find there's no single quit method that guarantees success.
The weight of evidence suggests that smokers should set a date to stop, and do their best to quit completely from this point.
On average it takes four to five attempts to give up, and there are a number of things that can help willpower.
Nicotine replacement treatment (NRT) in the form of gum, skin patches or nasal spray.
Zyban (bupropion) is a medicine that's licensed to help smoking cessation.
Champix (varenicline): a medicine that mimics the effect of nicotine in the body, and so reduces the urge to smoke and also reduces withdrawal symptoms. Varenicline can double your chance of successfully quitting
Behaviour modification programmes.
Alternative therapies such as acupuncture and hypnosis.
Research shows that people who take part in a full 'quit smoking' programme, including behavioural therapies and medication, may increase their chance of successfully quitting from about 3 per cent on willpower alone to over 30 per cent.


For such a complex and often treatment-refractory cancer, acute myeloid leukemia (AML) has a comparatively modest genetic makeup, according to investigators in the Cancer Genome Atlas Research Network.
Foraging into the genomes of both normal and cancerous cells in adults with AML, they have revealed what lead investigator Timothy J. Ley, MD, calls the cancer's "genetic playbook," a finding that could help in the development of better risk models and, ideally, therapies better targeted to each patient's disease subtype.
The report is published online May 1 in the New England Journal of Medicine.
By comparing genomes from normal skin with genomes from the malignant cells of 200 adults with de novo AML, Dr. Ley, from the Genome Institute at Washington University in St. Louis, Missouri, and colleagues found that the AML genomes have, on average, only 13 mutations. Other types of adult cancers that have been sequenced have hundreds of mutations.
Nearly all AML samples tested had at least 1 nonsynonymous mutation — that is, a mutation that is likely to be significant in the development of de novo AML.
"This dataset will provide a framework for future studies that pertain to the molecular classification of patients with AML. The identification of many potentially important relationships among recurrently mutated AML genes and pathways provides a comprehensive foundation for an understanding of the genetic rules of pathogenesis," they write.
"Giving Great Insights"
The investigators found nonsynonymous mutations in each of 9 different gene categories, including mutations in signaling genes (found in 59% of all samples), genes related to DNA methylation (44%), chromatin-modifying genes (30%), and NPM1, the gene encoding nucleophosmin, which is overexpressed, underexpressed, rearranged, or deleted in several types of cancer (27%).
Although chromosomal deletions, segment repeats, and other abnormalities found in some patients with AML are important for diagnosis and risk stratification, about half of all patients with AML have normal karyotypes. Some patients in this intermediate-risk cytogenetic category respond well to consolidation chemotherapy, whereas others do poorly. Identifying which patients might benefit from which therapy has been challenging, so deeper analysis of the genetic and epigenetic basis of AML is needed, the investigators write.
"This is the largest genome-wide analysis of AML ever performed, and it gives us great insight into not only what's going on in this intermediate-risk group, but also in the more complex karyotypes," John F. DiPersio, MD, PhD, who is one of the study investigators, told Medscape Medical News.
Uncomplicated, Yet Intricate
The findings suggest that AML is a "curiously uncomplicated malignancy.... It's associated with a very limited number of mutations, compared with things like lung cancer or melanoma, so there's a possibility that we may figure out what the drivers are, how this disease functions," said Dr. DiPersio, who is chief of the division of oncology at the Washington University School of Medicine.
"This lack of complexity is relative, however," writes David P. Steensma, MD, from the division of hematologic malignancies at the Dana-Farber Cancer Institute and Harvard Medical School in Boston, Massachusetts, in an accompanying editorial.
"The clonal architecture of AML is dazzlingly intricate, especially in cases arising from the myelodysplastic syndromes, with some subclones becoming extinct over time, and others achieving dominance, unpredictably," he writes.
The investigators performed whole-genome sequencing of primary tumor and matched skin samples from 50 patients with de novo AML, and exome capture and sequencing of paired samples from another 150 patients. The study involved 108 men and 92 women; mean age at study entry was 55 years.
The most frequently occurring mutations were in NPM1 (in 27% of samples), FLT3 (28%), DNMT3A(26%), IDH1/IDH2 (20%), NRAS or KRAS (12%), and RUNX1 (10%).
Mutations in FLT3DNMT3A, and NPM1 were more frequently grouped together than would be predicted statistically, and these genes were found less frequently in association with transcription-factor fusions than would otherwise be expected, the investigators report.
"This observation, combined with the strong association between samples having concurrent mutations in NPM1, FLT3, and DNMT3A and distinct clusters in messenger RNA, microRNA, and DNA methylation, suggests that samples with mutations in all 3 genes represent a novel subtype of AML," they write.
Secondary AML a Different Disease
Dr. DiPersio cautioned that the study focused specifically on de novo AML, and should not be used to draw conclusions about treatment-related, or secondary, AML.
"Treatment-related AML is probably a different disease, at least in part; it may be substantially different. The lesson we learned is don't assume that treatment-related AML is exactly like de novo AML," he explained.
Genomic studies of treatment-related AML are in progress, and are likely to reveal "substantial and striking" differences between disease types," he said.
In his editorial, Dr. Steensma contends that most AML secrets have been laid bare.
"It is likely that all the common, recurrent genetic lesions in AML — the molecular equivalent of major causes of death, such as stroke and heart disease — are now described. In individual cases, rare genetic events may occur, akin to uncommon causes of death, such as falling down a well or being struck by space debris," he writes.