Mice fed at the ‘wrong’ time gained twice as much weight even though they ate the same amount

By Larry Hobbs
Tuesday, September 08, 2009

Mice fed at the “wrong” time gained more than twice as much weight as those fed at the “right” time even though their calorie intake and level of activity was the same.

This according to a study from researchers at Northwestern University in Evanston, Illinois.

The strain of mice they used are “nocturnal, being more active and consuming most of their calories (80%) during the dark phase”.

Right Time Feeding

Mice fed at the wrong time gained 20%

When they were fed during the 12 hours that they normally eat, that is, the “right” time, the mice gained roughly 20% of their body weight during the 6-week study, going from roughly 22.5 grams to 27 grams (data guessed at from Figure 1 in the paper).

Wrong Time Feeding

Mice fed at the right time gained 45%

However, when mice were fed during the 12 hours that they do not normally eat, that is, the “wrong” time, the mice gained roughly 45% of their body weight, going from roughly 22 grams to 32 grams (data guessed at from Figure 1 in the paper).

Mice and Diet

Mice were 9-weeks-old and fed a 60% high-fat diet

The mice were 9-weeks-old when the study began and were fed a 60% high-fat diet.

Sleep

No difference in sleep between mice

“Sleep restriction or poor sleep quality could also be leading to weight gain, although our preliminary data indicate no overall sleep differences between light- and dark-fed mice,” the authors noted.

Other Research

Non-breakfast eaters and those with night-eating syndrome tend to be heavier

Other research shows that “non-breakfast eaters or patients with night-eating syndrome” tend to be heavier the paper also notes.

Studies have also found that people who circadian rhythms are interrupted have higher blood sugar and insulin levels.

Conclusion

Eating at the ‘wrong’ time can lead to weight gain

“These findings, taken together with the present results indicate that the synchrony between circadian and metabolic processes plays an important role in the regulation of energy balance and body weight control,” the authors concluded.

“Importantly, this study is the first to show causal evidence that feeding at the ‘wrong’ time can lead to weight gain.”

REFERENCE

Arble D, Bass J, Laposky A, Vitaterna M, Turek F. Circadian timing of food intake contributes to weight gain. Obesity (Silver Spring). 2009 Sep 3, published early on-line.

AUTHOR’S CONTACT INFORMATION

Fred W. Turek, PhD
Center for Sleep and Circadian Biology
Northwestern University
Evanston, Illinois, USA
(847) 491.2865 phone
(847) 491.5211 fax
http://www.northwestern.edu/neurobiology/faculty/turek.html
fturek@northwestern.edu

Charles & Emma Morrison Professor
Director of the Center for Circadian Biology & Medicine
Faculty, Dept. of Psychiatry & Neurology, Feinberg School of Medicine

Richard Moore, MD, PhD on How Drug Companies Have Changed

By Larry Hobbs
Friday, September 11, 2009

This is an excerpt from a letter by Richard Moore, MD, PhD dated August 31, 2009 on how drug companies have changed.

Excerpt from Dr. Moore’s Letter

Excerpt from Dr. Moore’s Letter: Dr. Moore on how drug companies have changed

“During the summer of 1956, between my junior and senior year in medical school, I was fortunate to work in the research laboratories of Eli Lilly.”

“It was a wonderful experience.”

“All of the scientists there were first rate and dedicated to finding the truth and to helping people.”

“And the intellectual atmosphere was first class especially since six of the scientists had been awarded positions in which for the rest of their lives, they could do research on any problem that interested them even if it was not conceivably related to a potential drug.”

“All decisions about whether a given compound should be considered a beneficial drug and go to market were made exclusively by the scientists.”

“The businessmen had no say in this.”

“In those days, Eli Lilly was an exemplary company dedicated more to helping people than to profits.”

Drug Companies Now Run by MBA, Not Scientists

Drug Companies Went From Being Run by Scientists to Being Run by MBA

“Fast forward to 2006.”

“I was on an airliner flying to Indiana to visit my alma mater, Purdue University.”

“I got into a conversation with the person sitting next to me and discovered that she was the head of research at Lilly.”

“I told her that 50 years earlier I had worked in the Lilly research labs and loved it.”

“I asked her how she liked working there.”

“She replied that at first, she had loved it also but now she had 435 days before she could take early retirement.”

“I asked what went so wrong that she was counting the days before she could get out.”

“She said that some years ago, the leaders who were scientists had been replaced by M.D.’s.”

“That wasn’t so bad; they didn’t understand the science, but they knew some of the terms and the M.D.’s could usually be talked into doing the right thing.”

“Then the M.D.’s were replaced by finance people – people with MBA’s.”

“And MBA’s have NO concept of science or of natural laws as I can testify from being a former college professor.”

“The straw that broke the camel’s back was when her research group discovered a previously unknown enzyme that is present in high amounts in three vital organs: heart, liver, and kidney.”

“So far, they didn’t know what this enzyme does.”

“However, her boss, who was an MBA, had told her that her research group had one year to find an inhibitor of that enzyme so Lilly could market it as a drug.”

“And, as she pointed out, since no one yet knew what that enzyme does, inhibiting it might be the last thing one would ever want to do.”

“Perhaps you’ve noticed that, especially a couple years ago, one drug after another was being taken off the market.”

“That ought to tell you something!”

“Because my first publication (when working at Lilly) was about a compound that decreases absorption of cholesterol, I maintained a casual interest in drugs used to lower blood cholesterol levels.”

“Several years ago, a cholesterol-lowering drug was quietly removed from the market because they finally realized the mechanism whereby this drug lowered blood cholesterol was to drive cholesterol into the arteries!”

Contact Information

Dr. Moore’s Contact Information

Here is contact information for Dr. Moore.

Richard D. Moore, MD, PhD
4 Calle Sabina
Placitus, NM 87043
thehbpsolution.com
richardbigsky@comcast.net
(505) 771-8615 phone
(505) 615-8020 cell

About Dr. Moore

Dr. Moore has been teaching a researching biophysics for more than 40 years

Dr. Moore’s received his M.D. from Indiana University, and his Ph.D. in biophysics from Purdue University.

Starting in 1963, Dr. Moore spent 40 years as a college professor and research scientist teaching and researching cellular biophysics.

Dr. Moore’s Discoveries

Dr. Moore research group discovered key findings about insulin

Dr. Moore’s research group research group discovered that insulin regulates the activity of the mechanism that exchanges potassium for sodium in live cells.

Dr. Moore’s group also also discovered that, connected with this, insulin elevates the pH inside cells.

Dr. Moore’s and the ratio of potassium to sodium

Dr. Moore recognized how the imbalance of potassium to sodium causes hypertension and other diseases

This research and that of others then led to insights in how our dietary imbalance between potassium and sodium cause hypertension and other diseases.

Trying to Educate the Public Since 1983

Dr. Moore has been trying to educate the public about the importance of the dietary ratio of potassium-to-sodium for since 1983

“Since recognizing the critical importance of the dietary ratio of potassium-to-sodium (in 1983), I have been trying to educate the public about this issue primarily by writing books.”

Author of Several Books

Dr. Moore is the author of several books

Dr. Moore is the author of several books including “The High Blood Pressure Solution”.

Dr. Moore is the also co-author of “The Salt Solution”.

This book discusses how an imbalance of potassium and sodium not only affects:
– stroke
– hypertension
but also how it affects:
– osteoporosis
– stomach cancer
– asthma
– kidney disease

Comments from Larry Hobbs

Comments from Larry Hobbs Dr. Moore is the author of several books

Dr. Moore’s point about the drug that lowered cholesterol, which people assume must be good, but it turned out it was bad because it was doing this by driving cholesterol into the arteriesis the same point I’ve made in several videos.

That is, the amount that a drug lowers your cholesterol or blood pressure or blood sugaris irrelevant!

The only thing that matters is whether or not a drug lowers your total risk of death.

Do not be fooled into thinking that just because a drug lowers your blood pressure or blood sugar or cholesterol, that it must be good for you.

This may or may not be true.

The only way to know if it the drug is doing any good is to look at the TOTAL risk of death.

For example…

Cholesterol-lowering drugs known as statins dramatically lower LDL levels, but increase the risk of death.

Julian Whitaker, MD, has noted that while oral diabetes drugs lower blood sugar levels, they cause more problems than they solve.

Dr. Whitaker has stated that this has been known since at least 1973, when a paper came out showing this while he was doing his residency at Emory University.

Dr. Whitaker has also said that when this paper came out in 1973, the doctor he was training under stopped using all oral diabetes drugs.

Dr. Whitaker has said that he does not use any oral diabetes drugs to this day.

Dr. Whitaker is the author of several books including “Reversing Diabetes”.

A blood pressure study by Sylvia Smoeller (2004) shows that, in older women with hypertension without a history of cardiovascular disease, 7 out of 8 blood pressure drugs or drug combinations, although they lowered blood pressure, they increased the risk of dying from cardiovascular disease compared with those taking no drugs.

So, do not be fooled by a number on a piece of paper.

The only way to know if a drug is doing any good is to look at the total risk of death.

Low-dose Qnexa: 3.75 mg Phentermine plus 23 mg Topamax causes weight loss of 5.1% vs 1.6% w/placebo

By Larry Hobbs
Wednesday, September 09, 2009

Morbidly obese patients given the lowest dose of Qnexa, containing 3.75 mg of phentermine plus 23 mg of Topamax (topiramate), lost an average weight loss of 18 pounds versus 6 pounds with placebo after one year, or 5.1 percent of body weight versus 1.6 percent with placebo according to a press release from press release from Vivus, Inc, the company developing the drug.

Weight Loss for Those Who Completed the Study

Weight Loss for Those Who Completed the Study : 7% vs 2.5%

Forty-seven percent (47 percent) of those given the low-dose Qnexa completed the entire one-year study.

The average weight loss for these patients was 7 percent of body weight versus 2.5 percent of those given the placebo who completed the study.

Subjects

Subjects: 1267 morbidly obese patients

The study, which was called the EQUIP (OB-302) study, involved “1,267 morbidly obese patients (1,050 females and 217 males) across 93 centers in the United States” the press release notes.

The number on each dose of the drug was as follows:

• 498 on placebo
• 234 on Low Dose Qnexa (3.75 mg phentermine / 23 mg controlled release topiramate (Topamax))

BMI

Starting BMI: 42

The average starting body mass index (BMI) was 42.1.

Dose

Dose slowly increased over one month

The dose was slowly increased (titrated) over four weeks.

Diet

Diet: Patients suggested to reduce calorie intake by 500 calories per day

Patients were asked to follow a diet that was reduced by 500 calories per day.

Conclusion

Conclusion: Weight loss with drug combination exceeds other agents

“The weight loss observed with Qnexa in these two one-year, double-blind, randomized trials far exceeds the weight loss observed for other agents reported in literature,” said Kishore Gadde, MD, director of obesity clinical trials at Duke University and a lead investigator.

REFERENCE

Vivus. Vivus announces positive results from two phase 3 studies; obese patients on qnexa achieve average weight loss up to 14.7% and significant improvements in co-morbidities.

Press Release from Vivus Inc. 2009 Sept 09, http://ir.vivus.com/releasedetail.cfm?ReleaseID=407933.

High-dose Qnexa: 15 mg Phentermine plus 92 mg Topamax causes weight loss of 10.4% vs 1.8% w/placebo

By Larry Hobbs
Fatnews, Wednesday, September 09, 2009

Overweight and obese patients given the highest dose of Qnexa, containing 15 mg of phentermine plus 92 mg of Topamax (topiramate), lost an average weight loss of roughly 24 pounds versus 5 pounds with placebo after one year, or 10.4 percent of body weight versus 1.8 percent with placebo according to a press release from press release from Vivus, Inc, the company developing the drug.

Weight Loss for Those Who Completed the Study : 13.2% vs 2.4%

Sixty-four percent (64 percent) of those given the high-dose Qnexa completed the entire one-year study.

The average weight loss for the “completers” was 30 pounds or 13.2 percent of body weight versus 6 pounds or 2.4 percent of those given the placebo.

Subjects

Subjects: 2487 overweight and obese patients

“The CONQUER study included 2,487 overweight and obese patients (1,737 females and 750 males) with high blood pressure, high cholesterol or type 2 diabetes across 93 centers in the United States” the press release notes.

The number on each dose of the drug was as follows:

• 979 on placebo
• 981 on Low Dose Qnexa (15 mg phentermine / 92 mg controlled release topiramate (Topamax))

Body Weight

Starting body weight: 227 lbs

The average starting body weight was 227 pounds.

BMI

Starting BMI: 36.6

The average starting body mass index (BMI) was 36.6.

Dose

Dose slowly increased over one month

The dose was slowly increased (titrated) over four weeks.

Diet

Diet: Patients suggested to reduce calorie intake by 500 calories per day

Patients were asked to follow a diet that was reduced by 500 calories per day.

Conclusion

Conclusion: Weight loss with drug combination exceeds other agents

“The weight loss observed with Qnexa in these two one-year, double-blind, randomized trials far exceeds the weight loss observed for other agents reported in literature,” said Kishore Gadde, MD, director of obesity clinical trials at Duke University and a lead investigator.

REFERENCE

Vivus. Vivus announces positive results from two phase 3 studies; obese patients on qnexa achieve average weight loss up to 14.7% and significant improvements in co-morbidities. Press Release from Vivus Inc. 2009 Sept 09, http://ir.vivus.com/releasedetail.cfm?ReleaseID=407933.

Drug company salesman had Xanax withdrawal symptoms for 6 months

by Larry Hobbs
Monday, August 03, 2009

Gwen Olsen, author of “Confessions of an RX Drug Pusher”, who worked as a sales representative for the drug companies for 15 years calling on doctors, tells how she was addicted to the anti-anxiety drug Xanax (alprazolam) for 10 years.

She also says that after stopping Xanax, she experienced withdrawal symptoms for 6 months.

She says that all psychiatric drugs can be addictive.

She notes that withdrawal symptoms with any psychiatric drug can be 10 times worse than the initial symptoms.

She notes that psychiatric drugs—antidepressants, anti-anxiety drugs, etc—should NEVER be stopped quickly, but must be withdrawn very, very slowly.

More information about Gwen Olsen can be found on her website:

http://gwenolsen.com/

Book: Confessions of an Rx Drug Pusher

Pictured: Electric lollipop that allows blind people to ‘see’ using their tongue

By Daily Mail Reporter
02nd September 2009

An electric lollipop that allows the blind to ‘see’ using their tongue has been developed by scientists. The extraordinary device converts images captured by a tiny camera into a series of electrical tingles, which can be felt on the tongue. Nerves then send these messages to the brain, which turn the tingles back into pictures.

Tests show that nerves in the tongue can send messages to the brain which can form pictures

After only a day’s practice, those using the machine were able to make out shapes, movement and read signs. Some were even able to interpret objects after just 15 minutes of training. One blind man, who was testing the device, is reported to have cried when he read his first letter. The BrainPort device, which is expected to go on sale later this year, is unlikely to replace guide dogs or walking sticks, but could dramatically improve the lives of those with sight problems. Dr William Seiple, of vision healthcare and research organisation Lighthouse International, which has been testing the device, said four blind volunteers had quickly learned how to find doorways and the buttons on a lift, pick out knives and forks, and read letters and numbers.

Helping the blind see: The component parts of the Brainport Vision Device

They were also able to pick out cups and forks at the dinner table without having to fumble. Dr Seiple said: ‘At first, I was amazed at what the device could do. One guy started to cry when he saw his first letter.’ Robert Beckman, of Wicab, which is developing the BrainPort, said: ‘It enables blind people to gain perception-of their surroundings, displayedon their tongue. ‘It enables them to identify objects, like a ball or distinguish letters of the alphabet. They cannot necessarily read a book but they can read a sign.’

The BrainPort is made up of an inch-long video camera hidden in a pair of sunglasses, which the user wears. Signals from the camera are sent along a cable to a handheld control unit, about the size of a mobile phone, and then to a lollipop shaped stick, which is placed on the tongue. The control unit converts the image into a low resolution black, white and grey picture, which is then recreated as a square grid of 400 electrodes  –  around the size of a postage stamp  –  on the lollipop. Each of the electrodes pulses according to how much light is in that area of the picture. White areas have a strong pulse, grey areas have a weak pulse while black areas give no signal.

The control unit allows the user to zoom in and out, and adjust the contrast of the picture and intensity of the tingle. Although users initially ‘feel’ the image on their tongue, with practice the signals activate the ‘visual’ parts of the brain for some people. Aimee Arnoldussen, a neuroscientist with Wicab, said: ‘It becomes a task of learning, no different than learning to ride a bike. It’s similar to how a baby learns to see.’ Wicab, based in Middleton, Wisconsin, is submitting the BrainPort to the U.S. Food and Drug Administration for approval this month.

It could be approved for sale in America by the end of the year and will cost about £6,000. If the tests are a success, it could be on sale in Britain next year.

Wonder drug in development to let dieters eat whatever they want – without gaining a single pound

By Fiona Macrae
04th September 2009

A pill that allows dieters to gorge on junk food without putting on a pound is being developed by scientists. The couch potato’s dream, it would allow people to eat all their favourite foods without worrying about their waistline. The wonder drug would also protect against diabetes, liver disease and other debilitating conditions associated with unhealthy eating habits. The breakthrough hinges on the discovery of a metabolism ‘masterswitch’ – a gene key to weight control. Mice lacking the gene, known as IKKE, stay slim despite being fed a lard-based diet. The ‘knock-out’ mice also free of the liver problems associated with a junk food diet and appear to be protected against diabetes, the journal Cell reports.

Researcher Alan Saltiel said: ‘We’ve studied other genes associated with obesity – we call them “obesogenes” – but this is the first one we’ve found that, when deleted, stops the animal from gaining weight. ‘The fact that you can disrupt all the effects of the high fat diet by deleting this one gene in mice is pretty interesting and surprising.’ It is thought that the gene makes enzymes called kinases that help regulate metabolism. Removing the gene – and the kinases – speeds up metabolism, leading to more calories being burnt.

Dr Saltiel said: ‘Perhaps most interestingly, the mice burn more calories even though they aren’t eating any less or exercising any more.’

The drug would allow people to eat fatty foods without putting on weight.

In the case of people, a drug that cuts kinase levels could allow people to eat  fatty and sugary foods without putting on weight. It would also enable them to stay trim without going to the gym. The researchers, from the University of Michigan in the US, are now hunting for such a pill and predict that many others will join the search.

They said: ‘The specificity of the apparent actions of IKKE, the nature of the enzyme, and the profound resistance of the knock-out mice to the high-fat diet, make it an especially appealing drug target for the treatment of metabolic disease.’ If they do find the right formula, the drug could be on the market within a decade. But with suggestions that such a drug could increase vulnerability to infection, there are many hurdles to be crossed. The rising tide of obesity has inspired a worldwide search for new weight loss drugs. Scientists at the Salk Institute in California are researching ‘exercise in a pill’ – drug that gives the benefits of exercise without leaving the sofa.

Search: The rise in overweight and obese people has led to a hunt for new weight loss drugs

In experiments, a medicine being developed to help heart bypass patients, boosted fat burning and stamina in inactive mice. The drug fooled the muscles into thinking they have exercised long and hard, rapidly burning fat and boosting fitness. Others are trying to capitalise on the health benefits of red wine to create a fat-burning pill that protects against diabetes. But obesity experts caution people against pinning their hopes on a quick fix, saying diet and exercise are key in the battle of the bulge.

Scientists find evidence some forms of prostate cancer ‘may be caused by virus’

Some forms of prostate cancer may be caused by a virus, raising the possibility of a vaccine being developed to combat it, say scientists. Researchers examined more than 300 tumours and found the infection, known as XMRV, in almost a third of them. It could lead to the creation of antiviral drugs to stave off prostate cancer, or screening programmes to discover who is at risk of developing the condition.

The finding gives hope to men suffering from prostate cancer

Experts welcomed the findings, but pointed out that it was far too early to say for certain whether the virus was the cause of these tumours, as their presence could simply be a coincidence. Prostate cancer is Britain’s most common cancer among men and the second highest killer, after lung cancer. A total of 35,000 men are diagnosed with cancer of the prostate every year. Some 10,000 of these are found to have the aggressive ‘tiger’ form, with most dying within 18 months. The scientists behind the study, from Utah University in the U.S., said the xenotropic murine leukaemia virus (XMRV) was more likely to be present in men who had aggressive cancers  –  raising the hope of new treatments for them.

It also suggests the virus could be sexually-transmitted  –  just like the human papilthatloma virus (HPV) which causes 70 per cent of all cervical cancer cases.

A nationwide HPV vaccination programme has just begun, which it is hoped will save the lives of hundreds of women. Professor Ila Singh, who led the study, said he hoped a similar vaccine could be developed for prostate cancer, which claims 12,000 victims every year. ‘The recognition human papilloma viruses most often initiate cervical carcinomas has focused efforts on viral detection for early diagnosis and on preventive vaccination,’ he said. ‘Similarly, a determination that a retrovirus can cause prostate cancer would focus efforts on preventing transmission, antiviral therapy, and vaccine development.

‘The pharmacological inhibition of viral replication, as achieved with HPV-1, could dramatically limit the pathological consequences of chronic viral infection.’

Certain viruses are known to cause cancer of the liver. This has prompted scientists to question whether infections may also play a role, alongside genetic and environmental factors, in causing breast and stomach tumours. The findings, published in the Proceedings of the National Academy of Sciences, follow a 2006 study that linked XMRV to a specific genetic mutation which was common among men with prostate cancer. But Prof Singh says the infection occurs independently of the gene variation  –  meaning it could prove to be a trigger of tumours.

He said: ‘Our observations provide evidence for an association of XMRV with malignant cells and with more aggressive tumours.’

Dr Helen Rippon, of the Prostate Cancer Charity, said: ‘The findings of this new study into the XMRV virus are intriguing, but do pose several key questions about the role the infection has to play in prostate cancer. ‘Most significantly, the researchers are yet to discover whether the virus is a cause, an effect or simply an innocent bystander in the development of the disease. ‘It will still be some time until it is understood whether the XMRV virus is a potential cause of prostate cancer in men.

‘We look forward to the results of further studies examining this.

‘Around the world, extensive work is being undertaken to identify risk factors for prostate cancer which will enable treatments and tests for the disease to be refined.’

Fortify bread with selenium to fight off cancer, urge experts

By Fiona Macrae
09th September 2009

Britons could lead longer, healthier lives if our wheat and bread was fortified with selenium, scientists believe. The mineral has been linked to a host of health benefits from boosting resistance against flu and fighting off cancer, to being more fertile and living longer. It may also help keep people mentally sharp into old age. But British soil is not naturally rich in selenium and most people eat just half amount the need each day.

Adding small amounts of it to the fertiliser used for the wheat that goes into bread production could quickly boost levels, the British Science Festival heard. In fact, adding just three to four slices of selenium-enriched bread a day into a normal diet would give men their recommended 75micrograms of selenium a day. Women would obtain the advised 60, studies at the Government-funded Rothamsted agricultural research institute suggest.

Researcher Professor Steve Mcgrath said that enriching the soil, rather than the flour itself, would not require any new regulations, although a nationwide drive would need Government input. He said: ‘It may not reach all sectors, it may be niche parts of the market, but it would be better for public health to have it more widespread.

‘The use of trace amounts of selenium-containing fertiliser to biofortifiy UK wheat could easily restore daily dietary intake of selenium to recommended levels, which should be of benefit to human health.’ Supplements are expensive and easy to forget to take each day, while selenium-rich foods such as Brazil nuts, kidney and shellfish  which can be hard to work into the diet. Professor Margaret Rayman, a selenium expert from Surrey University, said: ‘There are lots of people who just never eat these foods.

‘Everybody eats cereals, so that’s the more sensible approach.’

Found, the chemical that could spell an end to ADHD

By Jenny Hope
09th September 2009

Breakthrough: Children with ADHD have low levels of a brain chemical vital for making them pay attention in return for rewards (posed by model)

Hyperactive children have low levels of a brain chemical vital for causing them to pay attention in return for rewards, claim researchers. It is the first objective evidence that deficiencies in the brain’s system for reward and motivation are linked to the disorder affecting thousands of children. Brain imaging tests run by US researchers show a lack of dopamine – a chemical messenger – in children with attention deficit hyperactivity disorder (ADHD).

The chemical is essential for helping trigger behaviour involving motivation and reward, which results in reduced levels of attention and behavioural problems. Up to 100,000 British children with ADHD are given the drug Ritalin, which appears to act by releasing dopamine to improve concentration. Around three to seven per cent of children are believed to have ADHD, with many continuing to experience problems as adults.

Lead researcher Nora Volkow, of the Brookhaven Laboratory, New York, said it was the first definitive evidence that patients suffering from ADHD have lower-than-normal levels of proteins essential for activating the brain’s reward system. She said ‘These deficits in the brain’s reward system may help explain the clinical symptoms of ADHD, including inattention and reduced motivation, as well as the propensity for complications such as dug abuse and obesity among ADHD patients.’

Results from previous studies had been less conclusive because in many cases patients had undergone treatment or underlying conditions that may have affected the functioning of the dopamine system, she said. The latest study looked at 53 adults with ADHD who had never received treatment and 44 healthy people. The researchers used a PET (positron emission tomography) scanner to measure two markers of the dopamine system. Lying in a PET scanner, each patient was injected with a tiny amount of a ‘radiotracer’ compound designed to bind to dopamine receptors and transporters in a bid to track their activity levels. The results ‘clearly showed’ that ADHD had lower levels of dopamine active in the areas of brain important for processing motivation and reward, compared with healthy people. The measurements of dopamine markers correlated with clinical symptoms such as reduced levels of attention, said a report in the Journal of the American Medical Association.

Funding for the study came from US National Institutes on Mental Health, Alcohol and Drug Abuse. Dr Volkow said the results meant current use of medication such as Ritalin was justified because it would be compensating for poor dopamine levels in ADHD students. She said ‘Our findings imply that these deficits in the dopamine reward pathway play a role in symptoms of inattention in ADHD and could underlie these patients’ abnormal responses to reward. ‘This pathway plays a key role in reinforcement, motivation, and in learning how to associate various stimuli with rewards.

‘Its involvement in ADHD supports the use of interventions to enhance the appeal and relevance of school and work tasks to improve performance.

‘Our results also support the continued use of stimulant medications – the most common pharmacological treatment for ADHD – which have been shown to increase attention to cognitive tasks by elevating brain dopamine.’ Co-author Gene-Jack Wang, chairman of Brookhaven’s medical department, said: ‘Other studies from our group suggest that patients who abuse drugs or overate may be unconsciously attempting to compensate for a deficient reward system by boosting their dopamine levels.

‘Finding ways to address the underlying reward-system deficit could improve the direct clinical outcome of ADHD,’ he added.