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Inflammatory Bowel Disease Linked to Prevalence of Neurological Disorder

January 21st, 2011

Inflammatory bowel disease (IBD) has been linked to an increased risk for subsequent neurological disorders, new research suggests.

Initial 2-year results from an ongoing study that will be presented May 1 at the American Academy of Neurology’s 59th Annual Meeting, in Boston, Massachusetts, showed individuals with IBD were 4 times more likely to develop neuromuscular conditions (including carpal tunnel syndrome and small fiber neuropathy) and 6 times more likely to have sensorimotor polyneuropathy (PN) compared with individuals with other types of gastric conditions.

“Based on these initial results, we believe IBD itself is directly related to the neuropathy and that neuropathy in these patients is much more common than we previously thought,” the study’s principal investigator, Francisco De Assis Gondim, MD, PhD, from the Federal University in Ceara, Brazil, told Medscape.

Women at Greater Risk for Neuromuscular Complications

Although the link between IBD and neurologic disease has been reported before, most of the studies have been small, retrospective case series. In 2005 (Gondim FA et al. Brain. 2005;128:867-879), Dr. Gondim and colleagues also reported the association in a case series of 33 patients with IBD and PN as well as a literature analysis, At the time, this was the largest study and provided the most convincing evidence of the link between IBD and peripheral neuropathy to date.

The initial aim of the current cohort study, said Dr. Gondim, was to determine the prevalence of IBD-associated neurologic disease. To do this, investigators compared 103 individuals with IBD

37 with Crohn’s disease (CD) and 66 with ulcerative colitis (UC)

with 51 control subjects who had other gastric disorders, including dyspepsia, gastritis, and irritable bowel syndrome (IBS).

All subjects received a standard neurological evaluation, including vibration assessment, electromyography, screening for common causes of neuropathy, including possible vitamin B12 deficiency, diabetes, glucose intolerance, and hypothyroidism. They also underwent a neurological workup that included neuroimaging.

Headache was the most commonly reported neurological complaint and had a similar prevalence in all 3 study groups

48.6% in CD patients, 56.9% in the UC group, and 56.9% among controls.

However, the investigators report neuromuscular diseases, including parasthesias and SFN, were much more likely to occur in UC and CD patients compared with the control group.

Carpal tunnel syndrome was 4 times more prevalent in the UC group, and SP was more than 6 times more common in IBD patients, affecting 21% of subjects in the UC and CD groups.

In addition, said Dr. Gondim, the study also showed that neuromuscular complications in general and carpal tunnel syndrome in particular were much more common in women.

A Good Start

“Compared with the control group, the IBD group had a much higher prevalence of neuropathy. In spite of the fact that some of the IBD patients had [neuropathy] risk factors, there were a substantial number who did not, which leads us to conclude there is a direct relationship between IBD and neuropathy,” said Dr. Gondim.

Whether this is due to an immune-mediated phenomenon, an undetected vitamin deficiency, or some other mechanism is not clear, he said. However, the link between IBD and neuropathy is something clinicians need to be aware of, since neuromuscular disease is a common IBD complication that is frequently misdiagnosed as a rheumatological disorder.

The investigators intend to follow study participants for at least another 3 years, with the aim of gaining a better understanding of the natural history of neurological complications in IBD patients.

In the future, Dr. Gondim also hopes to launch a larger, long-term, multicenter cohort study in IBD patients who are neurologically competent at study outset to confirm the link between IBD and neuropathy and better characterize patients who are at risk for neurological complications.

“There’s a lot of work still to do, but this is a good start,” he said.

American Academy of Neurology 59th Annual Meeting: Abstract S16.005. April 28

May 5, 2007

Dr. Perlmutter’s comment:

This is breathtaking that this would be considered breaking news. Please see

BrainRecovery.com which I published 7 years ago. Complementary based physicians have long recognized that inflammation, like that in inflammatory bowel disease, is systemic and therefore affects other organ systems like the nervous system. It’s time for gastroenterologists to talk to neurologists.

ADHD Drug Does Stunt Growth

December 16th, 2010

After 3 Years on Ritalin, Kids Are Shorter, Lighter Than Peers

From WebMD.com

After three years on the ADHD drug Ritalin, kids are about an inch shorter and 4.4 pounds lighter than their peers, a major U.S. study shows.

The symptoms of childhood ADHD — attention deficit hyperactivity disorder — usually get dramatically better soon after kids start taking stimulant drugs. But this benefit may come with a cost, says James Swanson, PhD, director of the Child Development Center at the University of California, Irvine.

“Yes, there is a growth suppression effect with stimulant ADHD medications,” Swanson tells WebMD. “It is going to occur at the age of treatment, and over three years it will accumulate.”

Whether these kids eventually grow to normal size remains a question. Kids entered the study in 1999 at ages 7 to 9. The current report is a snapshot taken three years later. The 10-year results — when the kids are at their adult height — won’t be in for two more years.

“The big question now is whether there is any effect on these kids’ ultimate height,” Swanson says. “We don’t know if by the time they are 18 they will regain the height.”

The finding appears to end decades of debate over whether stimulant medications affect children’s growth. Less than 10 years ago, a National Institutes of Health panel concluded that the drugs carried no long-term growth risk.

That opinion was so widely accepted that the study authors — who include most of the leading ADHD researchers in the U.S. — did not warn parents that the study medication might carry this risk.

At the time, researchers thought that any short-term stunting of growth would be made up by a hypothesized “growth spurt” that would occur with continued treatment. But Swanson and colleagues saw no evidence of such a growth spurt.

Another widely accepted theory was that ADHD itself stunted kids’ growth. But in a surprise finding, the study found that ADHD kids who do not take stimulant drugs are much larger than kids without ADHD. And these untreated kids continued to grow much faster than kids taking stimulant drugs.

Swanson says that children who had been taking ADHD drugs before the study began were smaller than kids who had not yet started treatment. Those who first began treatment at the start of the study were normal in size, but grew more slowly than normal kids as the study went on.

After three years, the growth suppression seemed to reach its maximum effect. That’s also when the effect of the ADHD drug used in the study — immediate-release Ritalin three times a day, every day of the year — seemed to wear off.

“We compared the effect of medication relative to just pure behavioral treatment,” Swanson says. “That effect was substantial at 14 months and reduced a bit at 24 months. But at 36 months the relative advantage of ADHD drugs over behavioral treatment is gone.”

Swanson and colleagues note that the study did not test the sustained-release stimulant medications that are now the standard treatment for ADHD.

Omar Khwaja, MD, PhD, a neurologist at Children’s Hospital inBoston, last year analyzed studies of different ADHD drugs and found strong evidence that ADHD drugs do, indeed, stunt children’s growth. In fact, Khwaja and colleagues calculated a growth effect that almost exactly matches the effect seen in the Swanson study.

But Khwaja agrees with Swanson that nobody yet knows what the long-term results of this side effect will be.

“Whether there will be rebound growth at end of puberty, the jury is still out,” Khwaja tells WebMD.

“Parents have to be aware that stimulants are an enormous benefit to a lot of children with ADHD, but there is reason to be cautious with all medicines that affect the brain,” he says.”Growth monitoring should be standard practice for kids taking these medications.”

Swanson and colleagues report their findings in the August issue of the Journal of the American Academy of Child and Adolescent Psychiatry.

Posted in ADD/ADHD, Children & Pregnancy, Drugs & Prescriptions | 2 Comments »

Breast Cancer and Fish
December 10th, 2010

From Organic Consumers.org

Many streams, rivers and lakes already bear warning signs that the fish caught within them may contain dangerously high levels of mercury, which can cause brain damage. But, according to a new study, these fish may also be carrying enough chemicals that mimic the female hormone estrogen to cause breast cancer cells to grow.

“Fish are really a sentinel, just like canaries in the coal mine 100 years ago,” says Conrad Volz, co-director of exposure assessment at the University of Pittsburgh Cancer Institute’s Center for Environmental Ecology. “We need to pay attention to chemicals that are estrogenic in nature, because they find their way back into the water we all use.”

Volz and colleagues, including biochemist Patricia Eagon, took samples from 21 catfish and six white bass donated by local anglers as part of a study presented at the American Association for Cancer Research meeting in Los Angeles this week. The fish were caught in five places: a relatively unpolluted site 36 miles upstream from Pittsburgh on the Allegheny River; an industrial site on the Monongahela River; an Allegheny site downstream from several industries that release toxic chemicals; and the confluence of the Allegheny and Monongahela rivers, where Pittsburgh dumps much of its treated sewage and sewer outflows. “This is the largest concentration of combined sewer outflows in the U.S.,” Volz notes, about the confluence, known as the Point. The researchers also bought several fish at the store as controls.

Using an organic solvent, the researchers created an extract from the skin, flesh and fat of the various fish. They then bathed a breast cancer cell line — known as MCF-7 — in the extract. “We used this cell line because it has estrogen receptors in it, meaning that if estrogens are present it causes this cell line to proliferate,” Volz explains. “If you put something on it and it grows, then it must be stimulating the estrogen receptor.” In addition to responding to pure estrogen applied as a positive control, the extract from two of the white bass and five of the catfish caused the breast cancer cells to thrive.

The highest response came from fish caught in the industrial section of the Monongahela River. “The Monongahela River area is the area in Pittsburgh that was the site of most of the steel production over the last 100 years,” Volz says. “That area is still an industrial beehive.” But the broadest response came from where the sewer outflows and sewage treatment plants flow into the rivers from Pittsburgh; three of the four catfish caught here caused the breast cancer cells to proliferate. “Sewage might be more responsible for putting estrogenic chemicals in the water than the industries alone,” Volz adds. “All of the hormone replacement products that women use go down the drain, along with birth control pills, antibacterial soaps, and many of the plastics we use, like Bisphenol A, have such effects.”

It remains unclear exactly what estrogen-mimicking chemicals were actually present in the fish and what kind of cancer-causing role they might have. But their effects on the fish themselves were clear: the gender of nine of the fish could not be determined. “Increased estrogenic active substances in the water are changing males so that they are indistinguishable from females,” Volz says. “There are eggs in male gonads as well as males are secreting a yolk sac protein. Males aren’t supposed to be making egg stuff.”

And this estrogen burden is widespread. The store-bought white bass caused breast cancer cells to grow like its river-caught counterparts (as well as containing higher levels of mercury, arsenic and other contaminants) after being trucked to Pittsburgh from Lake Erie. “These fish, again, were in waters that were seeing industrial waste as well as possible combined sewer outflows,” Volz notes. “This isn’t just happening in Pittsburgh, this is happening everywhere in the industrialized world.”

Volz says he and his fellow researchers are launching a broader survey this summer that will entail sampling fish all along the Allegheny River. Efforts will be made to determine if it is industrial waste, sewage or agricultural runoff — or all three — that is responsible for the problem. In the meantime, cooking the fat out of fish may be the best defense. “If you broil fish and let the fats drip out that will take most of the contaminants out,” Volz says, though that may not be enough given other exposures to potentially tainted water. “What our study does show us is that there is exposure potential to vast populations that use water from our rivers as their drinking water supply.”

Posted in Ailments, Cancer, Men & Women, Toxins & Harmful Ingredients | No Comments »

Researcher sees link between vitamin D, autism
December 1st, 2010

From AutismToday.com:

The growing prevalence of autism is one of the biggest scientific whodunits in the medical world, with few clues for its rising incidence.

But a U.S. researcher is advancing a controversial hypothesis: that autism is related to vitamin D deficiency during fetal development and early childhood.
Dr. John Cannell, a psychiatrist and prominent vitamin D advocate, says flagging levels of the vitamin in pregnant women and young children could be the elusive factor explaining the rising rate of autism.

The evidence for such a link is circumstantial, and autism experts describe the hypothesis as speculative. But Dr. Cannell, founder of the Vitamin D Council, a non-profit advocacy group, says autism rates have skyrocketed in lockstep with medical advice given to the public since the late 1980s to avoid all exposure to bright sunshine.

“If it’s true, I can’t think of another situation where medical advice was so damaging to such a large number of people,” says Dr. Cannell, who practises at Atascadero State Hospital in California.

The vitamin D link “is an interesting speculation,” says Dr. Wendy Roberts, a professor of pediatrics at the University of Toronto and one of Canada’s leading autism experts.

Because the cause of autism is such an enigma, Dr. Roberts says researchers should investigate vitamin D, but the public should treat the idea more cautiously.

“You like to be able to have something that is firm and clear before you get parents all excited and doing something and then, once again, being disappointed,” she said.

Although Dr. Cannell is something of a maverick in research circles, he has credentials. Last year, he published an important peer-reviewed paper linking low vitamin D levels to an increased susceptibility to influenza, based on research at his hospital.

But for his autism hypothesis, he is now jeopardizing his chances of publication in a scientific journal by e-mailing the Vitamin D Council newsletter outlining the idea to thousands of U.S. autism activists – a possible violation of the rules of publication.

Dr. Cannell said he decided to disseminate his hypothesis now to encourage the public to increase its sun exposure during the warmer part of the year.

“If only 10 pregnant women go outside and sunbathe a little bit, they may be saved a lifetime of misery,” he said.

The idea that vitamin D deficiency may have a link to autism isn’t as farfetched as it once might have seemed because the deficiency is also emerging as a possible cause of many diverse illnesses, ranging from multiple sclerosis to cancer.

Last month, the Canadian Cancer Society recommended adults start taking the sunshine vitamin to reduce their risk of cancer.

Autism refers to a spectrum of conditions that involve repetitive behaviours and difficulty communicating and interacting socially. Autism manifests itself in the first few years of life and is thought to be some kind of neurological disorder affecting brain function.

One discredited theory is that the mercury-containing preservative thimerosal once used in childhood vaccines causes autism. Studies have failed to find any link.

The cause of autism is further clouded because some scientists speculate that part of the apparent increase in incidence – in the United States it is being diagnosed about 10 times more frequently now than in the early 1990s – may reflect improved reporting by doctors more aware of the condition.

The current Canadian estimate is that about 60 children out of every 10,000, or about 1 in 165, have autism and related conditions. Up until the 1990s, the prevalence was thought to be far lower, at only 4 or 5 children in 10,000.

If there is a vitamin D link, incidence rates around the world would probably vary by latitude. Rates would be lower in equatorial areas, where sun exposure is higher, than in northern latitudes, but studies investigating geographical differences in diagnosis haven’t been done.

Dr. Cannell says some of the strongest evidence vitamin D may have a hand in the disorder is that the vitamin is converted in the body to a steroid hormone, which in animal experimentation has been found to influence brain development. If vitamin levels are low, whatever brain development it is linked to will be skewed.

Startling trend
The occurrence of autism spectrum disorders (the most sever of which is autism) has risen sharply during recent years.
Rate per 10,000
UNITED STATES
1980s: 4-5
1990s: 30-60
2000A: 67
CANADA
2001B: 60
SOURCES: ENVIRONMENTAL HEALTH PERSPECTIVES
A- CENTRES FOR DISEASE CONTROL
B-CAIRN

Posted in Brain Health, Autism, Vitamin D | No Comments »

Coenzyme Q10 Does Not Improve Parkinson’s Disease Symptoms
November 24th, 2010

Please see my comment at the end of the article.

Science Daily

Small doses of the antioxidant coenzyme Q10 appear to increase blood levels of this naturally occurring compound in patients with Parkinson’s disease, but does not improve Parkinson’s disease symptoms, according to an article that will appear in the July 2007 print issue of Archives of Neurology, one of the JAMA/Archives journals.

Parkinson’s disease is a neurodegenerative disorder characterized by tremors and difficulty with walking or other movements. The biological mechanisms underlying the condition are not fully understood, but researchers suspect a malfunction of the mitochondria, parts of the cells that help convert food to energy, according to background information in the article.

Coenzyme (CoQ10), an antioxidant sold as a dietary supplement, is also involved in mitochondrial processes. “Because of these functions, CoQ10 has attracted attention concerning neuroprotective actions in neurodegenerative disorders linked to mitochondrial defects or oxidative [oxygen-related] stress, such as Huntington’s disease and Parkinson’s disease,” the authors write. Previous studies indicate that high doses of CoQ10 (1,200 milligrams) may slow the deterioration associated with Parkinson’s disease.

Alexander Storch, M.D., of the Technical University of Dresden, Germany, and colleagues conducted a randomized clinical trial of a 300-milligram dose of CoQ10 in 131 patients with Parkinson’s disease who did not have changes in motor functions and were on stable treatment for their condition. Those assigned to the treatment group took 100 milligrams of CoQ10 three times daily for three months, followed by a two-month “washout” period. The researchers assessed Parkinson’s disease symptoms before treatment began, each month during treatment and again after the washout period. Blood tests were performed at the beginning of the study, after three months of treatment and after the washout period.

A total of 106 patients completed the full three months of the study–55 in the CoQ10 group and 51 in the placebo group. The compound was well tolerated overall, and the percentage of patients who experienced adverse effects–including viral infection, diarrhea and hearing loss–did not differ between the two groups. Blood levels of CoQ10 increased in the treatment group from an average of 0.99 milligrams per liter to an average of 4.46 milligrams per liter after three months.

“Although we demonstrated a significant increase in plasma levels of CoQ10 toward levels observed with high doses of standard CoQ10 formulations in Parkinson’s disease and other disorders, our study failed to show improvement of Parkinson’s disease symptoms and did not meet its primary or secondary end points,” which were changes on scales that measured Parkinson’s disease symptoms and their effects on physical and mental functioning, the authors write. “Our study further demonstrated that 300 milligrams per day of nanoparticular CoQ10 is safe and well tolerated in patients with Parkinson’s disease already taking various antiparkinsonian medications.”

“Since we did not find symptomatic effects of CoQ10 in Parkinson’s disease, our study does not support the hypothesis that restoring the impaired energy metabolism of the diseased dopaminergic neurons leads to symptomatic benefits in Parkinson’s disease,” the authors conclude. “Future studies will need to explore the protective effects of CoQ10 at the highest effective dose (equivalent to about 2,400 milligrams per day of a standard formulation) over a long treatment period and in a large cohort of patients both sufficient to clearly define the protective potential of this compound in Parkinson’s disease.”

Dr. Perlmutter’s comment:

And nobody said it would. We have never expected CoQ10 to affect symptoms of PD. Nevertheless, the studies showing a dramatic slowing of progression are quite sound thank you very much. Again, let’s focus on treating the fire, not just the smoke. Renegade Neurologist

Slowing the Decline in Parkinsons Disease

Posted in Health & Nutrition, Parkinson's Disease | 5 Comments »

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