Wednesday, May 29, 2013

Scientists Crack HIV Coding, Leading To Possible AIDS Cure
Posted By News Talk Florida On May 29, 2013 @ 1:07 pm In 1060 Breaking News,1060 Featured,1190 Breaking News,1190 Featured,1470 Breaking News,1470 Featured,820 Breaking News,820 Featured,Breaking News,Featured,Legacy | No Comments
[1]Scientists have completely mapped the structure of the protein that encases HIV’s critical genetic information, a development that could eventually lead to new drugs to fight AIDS.
A research team from the University of Pittsburgh School of Medicine was able to use a supercomputer from the University of Illinois known as “Blue Waters” to reveal “seams” in the HIV’s capsid, the protein casing of a virus that holds its DNA. In order to be effective, the capsid has to be strong enough to protect the virus’ DNA while it is outside of a host cell, but malleable enough to break open once a virus infects a cell, allowing the virus to reprogram its host.
Scientists have long tried to develop therapies that attack HIV’s capsid, but it’s so far proved too tough to crack. Its chemical makeup had never been completely described before the University of Pittsburgh study, published Wednesday in Nature.
“HIV’s capsid is stable enough to protect the virus’ essential components, but it also has to disassociate once it enters the cell,” says Peijun Zhang, one of the authors of the study. “Understanding the interface by which it disassociates is important to developing new therapies.”
Read more on this story at [2]

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Sunday, May 26, 2013

A breath of salty air for patients with cystic fibrosis

How surfers in Australia inspired the development a new device that taps the benefits of salt water mist to treat cystic fibrosis patients.

The innovative nebulizer turns salt water into deep-penetrating aerosol mist.
(Credit: Cambridge Consultants)
In a seemingly random but nevertheless important discovery, scientists watching surfers with cystic fibrosis in Australia several years ago found that inhaling sea water mist reduced lung problems associated with the inherited disease.
So Cambridge Consultants in the U.K. paired with pharma firm Parion to develop and design a type of aerosol delivery systemt, called trans-nasal pulmonary aerosol delivery (tPAD), that brings the benefits of salt water treatment to the comfort of patients' homes, working overnight while they sleep.
The big deal about this device? Its long cannula that keeps droplets small enough to travel deep into the lungs.
"We immediately recognised the potential of this project to transform the lives of CF patients," said Matthew Allen, programme director at Cambridge Consultants, in a news release. "The challenge was to build an aerosol nebulizer system that could be comfortably used by patients overnight -- with the saline mist traveling down a long cannula to the sleeping patient without forming the large droplets that often occur in a standard nebuliser system. The size of the saline droplets is crucial to the success of the treatment as they need to be small enough to penetrate deep into the lungs."
Cystic fibrosis is a chronic disease affecting more than 70,000 people worldwide, and while there is no cure, inhaling a super salty solution -- twice as salty as water in the Atlantic Ocean -- can bring great relief by rehydrating the layer of unusually sticky mucus lining their lungs. The new nebulizer delivers the aerosol mist through the nose for eight hours and is safe and effective in children as well as adults.

Wednesday, May 22, 2013

How Likely Is Prostate Cancer to Kill?

Older, sicker men with non-aggressive prostate cancer had a significantly greater risk of dying of causes other than prostate cancer, a risk that increased with age at diagnosis and comorbidities, data from a large cohort study affirmed.
During 14 years of follow-up, other-cause mortality ranged from 24% for men with no comorbid conditions at diagnosis to 57% for men with three or more comorbidities. For men who were 65 at diagnosis, the mortality hazard versus no baseline comorbidities increased with the number of comorbid conditions from 1.2 to 2.6.
The impact of comorbidity burden on other-cause mortality increased with age ranges from younger than 60 to older than 75 at diagnosis but was greater in older ages, as reported online inAnnals of Internal Medicine.
Yet use of aggressive therapy predominated, regardless of comorbidity burden, including for 60% of men with three or more comorbidities, David F. Penson, MD, of Vanderbilt University in Nashville, Tenn., and co-authors concluded.
"Our data provide a framework to which all patients can apply their attitudes and assess their likelihood of treatment-related benefit on the basis of their age, comorbidity, and disease characteristics," the authors wrote.
"Our data show that men ages 60 years or older with three or more comorbid conditions approach 50% mortality at 10 years after diagnosis," they continued. "Therefore, given the low likelihood of short-term prostate cancer mortality and the high likelihood of other-cause mortality, older men with more than three major comorbid conditions who are choosing primary treatment should strongly weigh the risk of death from other causes before realizing any potential survival benefit from aggressive therapy."
Although estimated life expectancy should figure prominently in treatment decisions, available data suggest physician skill in this area is lacking, often leading to inappropriate treatment. One recent retrospective study showed that men with Charlson morbidity scores of 3 or greater receive aggressive treatment in the form of surgery or radiation in a majority of cases, despite a 70% risk of dying of other causes within 8 years of prostate cancer diagnosis (Cancer 2011;117:2058-2066).
Several factors may contribute to inappropriate treatment, the authors continued. Available data on other-cause mortality associated with comorbidity have come from single-institution case series or have involved only one type of treatment or treatment option. Instruments for determining the risk of other-cause mortality are "prohibitively cumbersome" for use in clinical practice.
In an effort to inform on clinical decision making specific to prostate cancer, Penson and colleagues queried the Prostate Cancer Outcomes Study (PCOS) database, a population-based cohort study of men with newly diagnosed prostate cancer. The cohort was derived from a subset of patients in the NCI Surveillance, Epidemiology, and End Results (SEER) program.
The PCOS cohort included men with nonmetastatic prostate cancer diagnosed from Oct. 1, 1994 through Oct. 31, 1995. All participants completed a baseline survey within 6 months of diagnosis, and each patient's medical record was reviewed 1 and 5 years after diagnosis.
Penson and colleagues stratified the PCOS cohort by clinical and pathologic characteristics, using D'Amico criteria: diagnostic PSA, Gleason score, and clinical stage at diagnosis.
The analysis comprised 3,183 men: 1,221 with no comorbidities, 1,020 with one, 523 with two, and 419 with three or more. In general, aggressive treatment was employed less often in men with a greater comorbidity burden. Even so, the investigators found that 256 of 419 (61%) of men with three or more comorbid conditions received aggressive therapy.
During the 14 years of follow-up, estimated other-cause (non-prostate cancer) mortality was 24% among men with no comorbidities at baseline, 33% for men with one comorbidity, 46% for men with two comorbidities, and 57% for men with three or more comorbid conditions.
After adjustment for age, race, SEER geographic area, tumor risk, and type of treatment, the hazard ratios for other-cause mortality versus men with no comorbidities were 1.2, 1.7, and 2.4 for men with one, two, or three or more comorbidities.
Advancing age added to the other-cause mortality hazard conferred by comorbidity burden. For example, men with three or more comorbidities had an estimated 10-year other-cause mortality of 26% if they were younger than 60 at diagnosis. The mortality increased to 40% for men 61 to 74 and to 71% for men 75 or older.
The investigators found that 29% of men with no comorbidities received nonaggressive treatment (androgen deprivation or watchful waiting), as did 33% of men with one comorbidity, 18% of men with two comorbidities, and 20% of men with three or more comorbid conditions.
The author of an accompanying editorial emphasized the complexities of integrating comorbidity and life expectancy into clinical decision making.
"Patients should be aware that the cumulative incidence of prostate cancer mortality and other-cause mortality in men aged 70 years or older is similar for those with three or more comorbid conditions and those at high risk for tumor aggressiveness," Lazzaro Repetto, MD, of Sanremo Hospital in Italy and colleagues wrote.
"Furthermore, the study showed that in the overall population, patients with zero or one comorbid condition who were receiving nonaggressive treatment had a statistically significantly higher risk for prostate cancer death than did those treated aggressively."
The data generated by Penson and colleagues make a good case for using age, tumor grade, and comorbidity burden to identify men who are unlikely to benefit from aggressive therapy, they added.
Attitudes toward nonaggressive treatment of prostate cancer have changed in the almost 20 years since men in the Penson study had newly diagnosed prostate cancer, said Edward Messing, MD, of the University of Rochester in New York. So have the patients, such that older men with comorbidities are living longer.
"How urologists are practicing now is a little bit different than how they practiced a few years ago," Messing, who was not involved in the study, told MedPage Today. "A few years ago, most urologists and radiation therapists would treat patients regardless of the severity of the disease and ... regardless of comorbidities."
"That clearly was not a wise approach, and I think both urology and radiation therapy have been appropriately chastised for that. That is not going on now to the same degree."
The study did not address the effect of aggressive treatment on complications, quality of life, or survival, Messing added. Moreover, treatment of prostate cancer has evolved considerably since 1994 and 1995, when the patients in study were treated.
"The message is that you don't have to treat these people and if you are treating them, don't do it," he said. "But it's not clear that they actually presented compelling information that would do that."

Tuesday, May 21, 2013

Should you be taking vitamin B to protect against Alzheimer's?

Research on the effect of B vitamins on mild cognitive impairment was done at Oxford University
Research on the effect of B vitamins on mild cognitive impairment was done at Oxford University
For as long as he can remember, John Hough has suffered from a poor memory. ‘I hated learning poems at school — after a few lines it had all gone,’ says the 83-year-old retired electrical engineer from Banbury. 
His memory only worsened with age. ‘He’s always been forgetful,’ says Kathleen, his 80-year-old wife, who just happens to have a photographic memory. But, increasingly, she was finding herself having to remind him about things. 
‘We have had our differences over memory,’ she adds diplomatically. But both are firmly agreed on one thing: the letter five years ago inviting John to take part in a trial to test whether high doses of several B vitamins could protect his ageing memory was a godsend. 
For although Kathleen, a retired university lecturer in physiology, still has to remind her husband to take his vitamins, she is happy to do so ‘because I really noticed the difference when he stopped taking them’.
This has been reinforced by research published yesterday in the top journal Proceedings of the National Academy of Sciences, which showed that people in the trial who got the B vitamins were almost entirely protected from the brain shrinkage suffered by those who only got a placebo pill.
A rapidly shrinking brain is one of the signs of a raised risk for Alzheimer’s. Those taking the B vitamins had 90 per cent less shrinkage in their brains.
And the research showed the areas of the brain that were protected from damage are almost exactly the same Alzheimer’s typically destroys. This ‘Alzheimer’s footprint’ includes areas that control how we learn, remember and organise our thoughts, precisely those that gradually atrophy as the ghastly disease progresses. 
‘I’ve never seen results from brain scans showing this level of protection,’ says Paul Thompson, professor of neurology and head of the Imaging Genetics Center at UCLA School of Medicine, California.
He’s a leading expert in brain imaging, and his centre has the largest database of brain scans in the world. ‘We study the brain effects of all sorts of lifestyle changes — alcohol reduction, exercising more, learning to handle stress, weight loss — and a good result would be a 25 per cent reduction in shrinkage,’ he says. 
In other words, the 90 per cent reduction seems really impressive. So, could the simple answer to memory problems be to take B vitamins? 

Three pills with startling results

The new research — part funded by the Government’s Medical Research Council — was based on data from the trial in which John took part. This was run for two years by OPTIMA (Oxford Project to Investigate Memory and Ageing) at Oxford University, and involved 271 people with early signs of a fading memory, known as mild cognitive impairment. This can be a precursor to Alzheimer’s.
The study was designed to discover whether giving high doses of three B vitamins — B6, B12 and folic acid — could slow the rate at which the participants’ memory worsened.
As well as giving the participants standard memory and cognitive tests, the researchers scanned some of the volunteers’ brains at the beginning and end of the study to see what effect, if any, there was on the rate these were shrinking. 
We all lose brain cells as we get older, normally about half a per cent a year. If you have mild cognitive impairment, that rises to  1  per cent, and when Alzheimer’s sets in, the atrophy speeds up to 2½ per cent. 

How it slows brain shrinkage

Why do experts think B vitamins might be the answer? The link is that they effectively help keep in check our levels of an amino acid called homocysteine. Normally we don’t have much of this because it is quickly turned into two important brain chemicals, including acetylcholine, which is essential for laying down memories.
There have been lots of studies showing that Alzheimer’s patients have unusually high levels of homocysteine in their bloodstream. They also have low levels of acetylcholine (in fact, the most common Alzheimer’s drug works by boosting acetylcholine). 
Some people with mild cognitive impairment will go on to develop Alzheimer's, a neuroscience expert claims
Some people with mild cognitive impairment will go on to develop Alzheimer's, a neuroscience expert claims
So it seems that the usual conversion of homocysteine into acetylcholine is going wrong. And that’s where the  B vitamins are thought to come in. 
Older people are particularly likely to be deficient in these nutrients. That’s because, as we age, our bodies become less good at getting it from food, and certain widely-used drugs, such as proton pump inhibitors for acid reflux, make the extraction process even more difficult.
So the thinking is, boost B vitamins and you boost the conversion of homocysteine into acetylcholine. Another theory is that high levels of homocysteine may actually trigger brain shrinkage.
A further reason B vitamins could help is given by Professor Teodoro Bottiglieri Baylor, at the Institute of Metabolic Disease in Dallas, Texas. ‘The link between brain deterioration — memory loss, cognitive deficits — and B vitamin deficiency is standard neurology textbook stuff,’ he says. 
‘You get it with various disorders that prevent B vitamins functioning properly, such as severe alcoholism and pernicious anaemia.’
However, the Oxford trial was the first time the vitamin B theory had been tested in a proper trial. When the initial results were published in the leading journal PLoS ONE in 2010, two findings attracted a lot of attention. 
First, the vitamins appeared to halve shrinkage across the whole brain compared with the brains of the people taking the placebo pill. But second, and very  significantly, the vitamins only benefited people who had a high homocysteine level — over 13 (a healthy level is said to be between about seven and ten).
‘It was a useful finding,’ says David Smith, professor emeritus of pharmacology at Oxford, and lead researcher on the trial. ‘It showed you’ll only benefit from the vitamins if your homocysteine level is high, but it also told us that when it rises above a healthy level it can damage brain cells.’ 
But the trial didn’t answer an important question: Does brain shrinkage make you lose your memory? It sounds very plausible that it should, and tests showed that the memory of people getting the vitamins stopped getting worse. However, the researchers couldn’t say for certain this was because their brains weren’t shrinking as quickly.
That’s where the latest study comes in. It involved a much more sophisticated analysis of the brain scans from the first study, by a new team from the Functional Magnetic Resonance Imaging Centre at Oxford. 
This analysis showed that the protection against shrinkage was even more effective than reported  previously — not just halving it, but reducing it by 90 per cent. 
The old study had looked at the whole brain; this one only looked at the effect in the Alzheimer’s footprint and found that in there, just where help was needed, the vitamins had an even greater impact. 
The new study also made the connection between less shrinkage and greater cognitive improvement. 
A new statistical analysis established that slowing the rate of brain  atrophy was directly responsible for slowing the rate at which the memory deteriorates. 

Who’s likely to benefit?

The studies make a clear connection between too much homocysteine and poorer memory. The next step might be for homocysteine to be a new biomarker for Alzheimer’s risk, tested for and lowered if necessary. 
‘The study needs to be repeated because there’s a lot to learn about why homocysteine is damaging and whether lowering it can stop people with memory problems progressing to Alzheimer’s,’ says Professor Thompson. ‘But if the results survive retesting, homocysteine level could be a useful biomarker for Alzheimer’s risk.’
So could B vitamins stop you developing Alzheimer’s? ‘We can’t tell from this research because it didn’t go on long enough,’ says Professor Smith. ‘It would cost about £6 million to do the study to prove it, but we haven’t been able to get the funding. Surely it would be well worth it.’
Dr Gwenaelle Douaud, an imaging and neuroscience expert and leader of the new study, says: ‘Slowing the progression is the Holy Grail of Alzheimer’s research. 
‘We know some people with mild cognitive impairment will go on to develop Alzheimer’s and the best marker of raised risk at the moment is the amount of shrinkage in an area called the medial temporal lobe. This is right in the middle of the Alzheimer’s footprint — the area B vitamins protect.’
how much vitamin b is too much

There are a number of theories about how high homocysteine harms the brain. ‘There is some evidence that it stimulates the growth of the “tangles” of protein in the brain that are one sign of Alzheimer’s,’ says Dr Douaud.
‘Another possibility is it could be stopping the growth of new brain cells in the hippocampus, a crucial region for making memories.’
The impressive results from this latest study raise questions that need more research. They do suggest that it might be worth having your homocysteine level tested to see if it is too high. But it is not an easy test to get done.

What about side-effects?

‘Most GPs are not very familiar with homocysteine risks, and it’s not a standard test, although you can get it done privately,’ says Dr Siobhain Quinn, a psychiatrist specialising in older mental patients at St Peter’s Hospital, in Chertsey, Surrey.
‘However, testing for B12 is quite common in the elderly and it is standard practice to give tablets or injections if it is too low. So that could be a way of getting treatment, but probably not in the high doses used in the Oxford trial.’
Professor David Smith believes it would be wrong not to offer high-dose vitamins to someone with memory problems and raised homocysteine. His published papers state that he is named as an inventor on two patents held by the University of Oxford on the use of folic acid to treat Alzheimer’s disease.
But Robin Jacoby, emeritus professor of old-age psychiatry at Oxford, who was also involved in the first study, cautions: ‘As a medical scientist I wouldn’t advise anyone to take high doses of B vitamins yet to protect their brain without first consulting their GP.. 
‘There is a link between high levels of folic acid and cancer, although the risk is low.’ 
Dr Eric Karran, director of research at Alzheimer’s Research UK, also doesn’t think the evidence is good enough yet. ‘Until further trials have confirmed these findings, we would recommend people think about a healthy and balanced diet along with controlling weight and blood pressure, as well as taking exercise,’ he says.
Because this new study depends on results of brain scans, it is worth mentioning a criticism of the original study, published in 2010. 
Researchers said although 271 people had taken part, only 168 had scans. This suggested a large number dropped out or disappeared from final results, which made findings very unreliable. 
Professor Smith explained at the time they weren’t dropouts and he had expected fewer people to have scans and allowed for it. ‘Everyone was asked if they were prepared to have two scans and quite a number said they weren’t. So we knew who was going to be scanned and we randomised them to vitamins or placebo, making the results perfectly valid.’
As for the Houghs, they need little convincing. ‘I dread to think what I’d be like now without my daily pill,’ John remarked when he heard about the latest study. 
After the trial finished, he stopped taking the vitamins for six months, and he and Kathleen said the difference was obvious and he started taking them again.
Although he also regularly forgets where he’s put his ‘blooming’ walking stick, John’s very clear about other things. 
‘The memory clinic just sent me an appointment for May 27,’ he says. Without consulting his diary, he adds: ‘That’s a Bank Holiday. I’ll have to check it with them.’

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Thursday, May 16, 2013

Just a spoonful of sugary drink confusion

SugarAre sugary drinks to blame for obesity and diabetes or have they been simply served up by the media, politicians, and even some scientists as a scapegoat for all of society’s ills?
In recent months, the question has sparked harsh words, flared tempers, op-eds, demonization, and even talk of creating policy that would ban or limit consumption of sugar-sweetened beverages like sodas. But what does the scientific evidence really show once emotion and exaggeration are removed from the equation?
With the intent of setting the scientific record straight, respected academics and nutrition researchers came together to discuss the issues in Boston on Tuesday, April 23, at Experimental Biology 2013. The symposium, organized by the American Society for Nutrition, would be the second of its kind over two years at the conference to evaluate sugar and how it relates to health. The event was sponsored by the Corn Refiner’s Association (CRA) and endorsed by the Medical Nutrition Council.
Exaggerated and “emotion-raising” statements
Biostatistician David Allison, MD, a professor at University of Alabama at Birmingham, addressed how misinformation in the peer-reviewed literature and the media about sugar and sugary drinks has spread confusing messages to the public. He called out several examples of how studies with an epidemiological design have reported their findings in exaggerated ways. Many of these trials have found only ecological correlations linking sugary drink consumption to rising obesity numbers. Correlations are the weakest form of evidence and don’t establish causation. There are also correlations linking the rise in bottled water consumption and obesity, for example, he said.
However, despite discovering only weak associations in their data along with inconsistencies, many of these studies are titled in ways that inflate their findings and they use language that suggests causality. Examples he gave include “Sugary beverages represent a threat to global health” (Popkin),”Public health: The toxic truth about sugar (Lustig), and “Fructose: pure, white, and deadly. Fructose, by any other name, is a health hazard.” (Bray). These examples have “emotion-raising” language that leads to further exaggerations and inaccuracies in press releases and in articles by journalists, Dr. Allison said. The most recent example of an article with exaggerated statements, Dr. Allison told me after the event, is one from Bloomberg entitled “Daily Soft Drinks Raise Diabetes Risk by 22%, Study Shows”.
“There’s no surprise that people are confused,” Dr. Allison said. “Imagine you’re a newspaper reporter with no scientific training reading these titles trying to write an article that will inform regulators and the public about sugar-sweetened beverages. You think cause and effect has been demonstrated when in fact it’s only a correlation.”
In addition, as there is a tendency for studies sponsored by industry to show bias, Dr. Allison reminded that there also exists “white hat bias”—a systemic bias among academic scientists that leads to exaggerating findings from their data. “When you look at the peer-reviewed literature, there are multiple demonstrable biases and inappropriate statements that serve to exaggerate,” he said.
The standard for acting or creating policies is subjective and depends on the situation and one’s values and judgments, he said. In contrast, the standard for drawing a conclusion about causation requires randomized controlled trials. Are there any? Yes, Dr. Allison said there do exist several randomized controlled trials that evaluate sugar-sweetened beverages and changes in body weight. Some do show, he concedes, that within the context of additional calories sugary drinks may lead to weight gain.
Dr. Allison makes clear he’s not “advocating” sugary drinks. He agrees that it makes common sense for individuals wishing to lose weight to limit their intake of sugary drinks and other nonessential kilocalories. However, he maintains that the current evidence testing whether reducing sugary drink consumption reduces body weight in consumers has shown only equivocal effects. “As scientists and scholars, we can and should hold ourselves to higher standards,” he said.
Solids versus liquids
Purdue University professor of nutrition science Richard Mattes, Ph.D., believes that sugary drinks do lend to increased risk of weight gain in ways beyond their contribution of calories. He’s not so much concerned with the sugar content of sugar-sweetened beverages; the problem, he said, is the difference in the way those calories are consumed—as liquids versus solids. “When we consume beverages, our bodies are incredibly quick at processing and excreting them. A calorie is not a calorie anymore.”
Citing research from his own lab and that of others, Mattes explained that the evidence suggests that the body’s sensations in response to clear beverages are different in comparison to solid food. For example, when hungry our bodies sense that they want to eat food until full, but our bodies tend to be relatively thirsty all day long. There is a strong “stop” signal and a weak “go” signal when eating solid foods, he suggested. In the case of clear beverages, the opposite is true: there is a weak “stop” signal, and a strong “go” signal.
These sensory signal differences of clear beverages also don’t appear to apply with viscous energy-dense beverages such as soups or liquid meal-replacements. The reason may due to the pattern in which viscous energy-dense beverages are consumed. They are usually consumed in a regimented way, such as at a specific time of day. The dietary pattern that people use to consume clear beverages, on the other hand, is often as frequent as snacking. It’s not because people are eating more food, it’s the change in the way they’re eating their food, Mattes explained.
Frequent sugary drink consumption and the rise of obesity and diabetes in the U.S. has nutritional biologist Kimber Stanhope, Ph.D., an associate project scientist at UC Davis, alarmed despite lack of sufficient evidence establishing causation. She said that while adequately powered clinical trials and longer interventions are needed, she questions why it would be necessary to avoid acting now. “Do we need to wait for these results before we revise the dietary guidelines and start educating the public accordingly?” she asked.
In randomized controlled trials that Stanhope’s lab has produced, sugars—whether as table sugar, high-fructose corn syrup, glucose, and fructose—all comparably increase body fat in subjects when consumed in excess. She also presented data showing that pure glucose versus pure fructose consumed in excess may behave differently in the body. Pure glucose, for example, led to increases of subcutaneous adipose tissue (fat just under the skin) while fructose led to increases of visceral adipose tissue (fat around the organs), which may contribute to increased insulin resistance and cardiovascular risk. Notably, her research also shows that when comparing high-fructose corn syrup and table sugar, these don’t show changes related to body composition suggesting that the metabolism of glucose and fructose behaves differently when consumed together.
Sugar on the brain and addiction
Stanhope also pointed out that glucose and fructose may have different affects on the brain. For example, she cited a recent study published in JAMA (Page et al) that showed glucose consumption promoted appetite suppression in the brain whereas fructose did not. The study has been a source of much speculation regarding whether or not the fructose moiety of sugar and high-fructose corn syrup could be addictive versus other types of carbohydrates.
Nutritional neurologist Miguel Alonso, MD, believes that functional MRIs (fMRIs) as used in the JAMA study and others can indeed be useful for studying brain regions that are involved in decision making and reward aspects of both drugs and food. He also finds interest in the clinical overlap between obesity and drug addiction. For example, there is evidence of a shared vulnerability for the two because of genetic predisposition.
However, Dr. Alonso said that the notion that sugar or any other particular food component is addictive is highly speculative and based on weak and limited evidence. Addiction is highly complex and generally defined by several criteria in an individual that involve tolerance, withdrawal symptoms, lack of control, and interference with daily activities, he said. He also questions what findings can be drawn from fMRI studies that compare fructose versus glucose.
“There is limited and insufficient data in humans on the link between food, obesity and addiction. Brain overlaps do exist, but that does not equal addiction,” Dr. Alonso said. “Recent fMRI data suggest neuroadaptation following repeated intake of palatable food, including sweetened beverages. There is a need to clarify the link, particularly experimental interventions.
Experimental studies are needed to clarify associations found in cross-sectional studies related to the brain, he said. A study by Burger and Stice, for example, found an association between frequent consumption of ice cream and a reduction in sensitivity in regions of the brain related to food reward. These studies lead to questions about how long it takes for neuroadaptations to occur, how specific these changes are, and how they contribute to eating patterns under normal conditions. Dr. Alonso said that while some recent fMRI data suggest different acute brain responses in response to fructose versus glucose, there is still need for research that includes normal conditions of intake and behavioral correlates to better interpret the findings.
Cardiologist Jame Rippe, M.D., founder and director of the Rippe Lifestyle Institute and professor of biomedical sciences at the University of Central Florida, whose organization has participated in funding Dr. Alonso’s pilot research, said that new studies using tools such as functional MRI to study the brain were lending interesting results. But he said that it’s not surprising that areas of “the epicenter of where decisions come to pass” would “light up,” or become active, in response to sugar or any other carbohydrate-containing foods. “It makes all the sense in the world, since the brain relies on glucose,” he said.
However, he said that the speculation about how different sugars—high-fructose corn syrup, sucrose, glucose or fructose—are handled by the brain and talk of addiction feels like, as Yogi Berra once said, “déjà vu all over again.” He reminded of similar arguments he’s made before in previous years as a CRA consultant. It has been a challenge, he said, to educate consumers that the way high-fructose corn syrup and table sugar (sucrose) are treated in the body is the same metabolically, as supported by several randomized controlled trials. And, it’s also been a challenge to help people understand that fructose and glucose are “always consumed together” in a normal diet. One cannot make too much of studies using high amounts of pure glucose or pure fructose whether it be in animals or humans. When consumed together, their absorption and metabolism are different.
What about dose?
Dr. Rippe added that the way sugars are treated in the body has been well studied and regulators and health organizations should take note of that. And he praised the scientists at the event and ASN for coming together to speak out against inaccuracies reported in the peer-reviewed literature and the media.
In addition, Dr. Rippe took issue with the American Heart Association (AHA) for coming out with a statement recommending that sugar be limited to only 150 Kcal per day for men and 100 Kcal for women. The recommendation is only about a third of what has been set by the Institute of Medicine in current Dietary Guidelines for Americans. The IOM dictates, yet does not recommend, that up to 25 percent of kilocalories (Kcal) can be consumed safely from added sugars.
“The AHA has acknowledged that their recommendation wasn’t based on any definitive proof, just their thoughts,” Dr. Rippe said. He added that the IOM recommendations were based on actual evidence from the current literature.
But he said his lab “put the AHA recommendations to the test” anyway. Rippe’s lab conducted a trial that randomized subjects to diets consisting of either 8, 18, or 30 percent of total Kcals from added sugars. Despite consuming roughly four times more than AHA recommendations, the subjects in the group consuming 30 percent added sugars did not show any difference in cardiovascular risk factors as compared to the other groups (including blood lipids, leptin, ghrelin, or fasting insulin). The evidence suggests there are no dangers in consuming sugars up to 25 percent of Kcals within the context of an energy-balanced diet. Some will point out that the study was funded by the CRA and should not be trusted, but Dr. Rippe’s results are corroborated by other randomized controlled trials in the literature.
After the symposium, I spoke to Friedman School professor of nutrition Edward Saltzman, who chaired the event, who said to me that his reaction to the meeting could be summarized as, “I believed every speaker.” That poses a problem, he added, because of from a distance it’s easy to understand why the general public remains more confused due to conflicting evidence on sugar-sweetened beverages. “The issue is far from resolved,” Saltzman said.
Making the medicine to go down
The day after the event, I spoke to professor of nutrition and metabolism David Jenkins, M.D., who told me that he thought more attention should be given to the work of nutrition researcher John Sievenpiper, M.D., of St. Michael’s Hospital, University of Toronto. He said Dr. Sievenpiper “has an army of researchers combing the literature” on sugar and its effects on health.
Dr. Sievenpiper is the lead author of several meta-analyses (of which Dr. Jenkins is often listed as a co-author) comparing sugars on different parameters related to metabolism and body weight. As discussed in my prior interviewwith Dr. Sievenpiper, these meta-analyses found no differences in the effects of fructose, glucose, or other carbohydrates on several parameters on body weight, blood lipids, and blood pressure. In addition, Dr. Sievenpiper’s research suggests a marked benefit from fructose for glycemic control when consumed in amounts normally found in fruit.
Dr. Jenkins said that he did agree with the thrust of some researchers—such as Walter Willet, M.D., and David Ludwig, M.D.—to recommend that the public reduce consumption of sugary drinks in general when they are identified as providing excessive calories in people’s diets. However, the Atwater Lectureship recipient disagrees with attempts to force reduced consumption using warning statements or regulations.
Most well recognized for developing the low-glycemic index concept, Dr. Jenkins also suggested that sugars be used as put by Mary Poppins, “to make the medicine go down.” More to the point, he said people should use sugar strategically in combination with nutrients that would otherwise “taste like cardboard,” like viscous fiber. Present in several vegetables and whole-grain foods, viscous fiber is not often thought of as palatable, however, it is shown in studies to slow down the rate in which sugar and other carbohydrates are absorbed, reduce total and LDL cholesterol, as well as increase satiety (the feeling of fullness). “If I could get people to eat ‘cardboard’ by itself I would, but put a little sugar on it, a little salt, or a little fat, and people will eat it,” he said.
Whether Dr. Jenkins would approve of washing down steel cut oats, asparagus, or Brussels sprouts with a bottle of Mountain Dew or any other brand of soft drink, he didn’t exactly say. But it may be worth a try for those who have a sweet tooth and who wouldn’t include these highly beneficial foods in their diets otherwise.