Why do smells make some people sick?

Do you get a headache from the perfume of the lady next to you at the table? Do cleaning solutions at work make your nose itch? If you have symptoms prompted by everyday smells, it does not necessarily mean you are allergic but rather that you suffer from chemical intolerance. According to Linus Andersson at Umeå University, this hypersensitivity can be the result of an inability to get used to smells.

Normally your smell perceptions diminish rapidly, as when you enter a friend’s apartment. Even though you clearly notice smells just inside the door, you don’t think about them for long. For people with chemical intolerance, on the other hand, smells seem always to be present. Psychology researcher Linus Andersson has exposed both intolerant and non-intolerant individuals to smells and compared their reactions.

“The hypersensitive individuals felt that the smell was getting stronger even though its concentration had not changed. Their brain activity images also differed from those in the other group,” he says.

The results were observed using methods based on both electroencephalography (EEG) and functional brain imaging technology (fMRI). The EEG method involved placing electrodes on the heads of trial subjects and registering the minute changes in tension in the brain that arise following exposure to smells. Unlike the people in the normal group, Linus Andersson explains, the intolerant people did not evince a lessening of brain activity during the period of more than an hour they were exposed to a smell. The inability to grow accustomed to smells is thus matched by unchanging brain activity over time.

“These individuals also have a different pattern in the blood flow in their brains, compared with those who perceive that a smell diminishes. A similar change can be found in patients with pain disorders, for example.”

Sensitivity to smell impacts the entire body. A further finding in the dissertation is that chemical intolerant people also react strongly to substances that irritate the mucous linings of their nose and mouth. People who cough more when they inhale capsaicin, the hot compound in chili peppers, also have heightened reactions in the brain to other smells. Besides the fact that intolerant individuals perceive that smells grow stronger, effects are also seen in mucous linings and in the brain.

Chemical intolerance is surprisingly common – up to ten percent of the Swedish population report they are bothered by everyday smells, whereas roughly two percent experience severe symptoms. Yet, in contrast to the situation regarding allergies and asthma, there is very little research about what causes this condition. Linus Andersson maintains that if it were possible to identify what characterizes this hypersensitivity then it would be possible to develop methods for diagnosis and treatment. But research can also provide new knowledge about how we should think about our work and everyday environments.

“Some co-workers are bothered more than others by the smell of the printer — what should we do to make our working conditions acceptable to as many people as possible?”

Author:

UMEA University, Why do smells make some people sick?, 20. Januar 2012 Expertanswer (Expertsvar in Swedish

Linus Andersson, Sick of smells: Empirical findings and a theoretical framework for chemical intolerance, Umeå, 2011-12-02

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New Research Shows Two of the Leading Killers in America Might be Linked

“We know there’s a link,” says Heather Snyder, senior associate director of Medical and Scientific Relations for the Alzheimer’s Association. “What we’re trying to find out is the why.”

Snyder is speaking of two of this country’s worst scourges: Alzheimer’s disease and diabetes. Both are major killers. According to the Centers for Disease Control and Prevention, they are, respectively, the sixth and seventh leading causes of death in the U.S.

Now, research has begun to suggest that they share something else besides a capacity for death—namely, a common organic thread. For that reason, research into one may lead to successful means of dealing with the other.

To begin with, 26 million people in the U.S. have diabetes, 7 million of whom don’t even know they are affected, according to the National Institute of Diabetes and Digestive and Kidney Disease. But regardless of awareness, diabetes remains a condition whereby too much sugar builds up in the bloodstream because the body cannot use insulin effectively. That is, the body stops producing sufficient insulin to help cells absorb sugar and turn it into energy.

Certain segments of the population have a disproportionate rate of diabetes, including Hispanic, African, Asian and Native Americans. According to the National Institutes of Health, 8.3 percent of the U.S. population have diabetes, but more than 16.1 percent of the adult population of American Indians and Alaska Natives have been diagnosed with it. The rates of diabetes vary by region, with American Indians in southern Arizona suffering the highest rates in the country at 33.5 percent.

Diabetes and Alzheimer’s have several links. For example, insulin resistance and type 2 diabetes increase the risk of both heart disease and stroke. Damaged blood vessels can result from either of these conditions, and researchers believe that damaged vessels in the brain may well contribute to Alzheimer’s.

Further, our brain cells use a high level of energy, which can be affected by diabetes because the disease retards the body’s ability to absorb sugar to generate the necessary energy. Healthy brain function also depends on a symphony of many different chemicals working in concert. Too much insulin can throw off the balance of these chemicals and potentially trigger Alzheimer’s. Finally, high blood sugar causes inflammation, which could damage brain cells and help Alzheimer’s develop.

Tackling the connection between diabetes and Alzheimer’s disease may ultimately involve a better understanding of vascular dementia, a disease with the same symptoms as Alzheimer’s. But as Snyder puts it, “Of the top 10 causes of death in the United States, Alzheimer’s is the only one without any way to prevent, cure or slow its progression.” Vascular dementia, by contrast, can be prevented or managed through many of the same healthy habits that can also reduce the risk of diabetes.

“[Vascular dementia] results from hypertension, a high-fat diet, smoking and uncontrolled diabetes,” says Carson Henderson, associate director of Two Hawk Institute, an Indian-owned and -operated corporation focused on health education, training and research in Indian country. “If you exercise, eat right, and don’t smoke, you might be able to prevent vascular dementia as you age.”

Vascular dementia is caused by low blood flow to the brain, often as the result of a stroke or series of strokes. “With vascular dementia, your brain cells are dying, because small, tiny blood vessels in the brain are being blocked, and the cells below are not receiving blood or oxygen,” explains Carson Henderson’s husband, Neil Henderson, Oklahoma Choctaw, who directs the American Indian Diabetes Prevention Center at the University of Oklahoma Health Sciences Center’s College of Public Health. “Vascular dementia looks a lot like Alzheimer’s disease, but it is not the same causation. You still get memory loss and confused thinking.”

The latest link between diabetes and dementia was established by a recent study undertaken by Kyushu University in Japan. Researchers analyzed “1,017 community-dwelling dementia-free subjects” over the course of 15 years and found that Alzheimer’s disease and vascular dementia “were significantly higher in subjects with diabetes then in those with normal glucose tolerance.”

Snyder puts the significance of the finding this way: “Diabetes affects your heart, and there are links between cardiovascular health and brain health. The brain uses 25 percent of the oxygen in blood for its functions, if the heart isn’t healthy, the brain won’t be healthy, either.”

So the ties between diabetes and heart disease and stroke continue to be uncovered. Now, with the possibility that diabetes might be among the causes of one of America’s most lethal diseases, organizations like the Alzheimer’s Association are doing everything they can to spread awareness—and prevention.

Source: A Deadly Duo: New Research Shows Two of the Leading Killers in America Might be Linked
By ICTMN Staff December 14, 2011

“We know there’s a link,” says Heather Snyder, senior associate director of Medical and Scientific Relations for the Alzheimer’s Association. “What we’re trying to find out is the why.”

Snyder is speaking of two of this country’s worst scourges: Alzheimer’s disease and diabetes. Both are major killers. According to the Centers for Disease Control and Prevention, they are, respectively, the sixth and seventh leading causes of death in the U.S.

Now, research has begun to suggest that they share something else besides a capacity for death—namely, a common organic thread. For that reason, research into one may lead to successful means of dealing with the other.

To begin with, 26 million people in the U.S. have diabetes, 7 million of whom don’t even know they are affected, according to the National Institute of Diabetes and Digestive and Kidney Disease. But regardless of awareness, diabetes remains a condition whereby too much sugar builds up in the bloodstream because the body cannot use insulin effectively. That is, the body stops producing sufficient insulin to help cells absorb sugar and turn it into energy.

Certain segments of the population have a disproportionate rate of diabetes, including Hispanic, African, Asian and Native Americans. According to the National Institutes of Health, 8.3 percent of the U.S. population have diabetes, but more than 16.1 percent of the adult population of American Indians and Alaska Natives have been diagnosed with it. The rates of diabetes vary by region, with American Indians in southern Arizona suffering the highest rates in the country at 33.5 percent.

Diabetes and Alzheimer’s have several links. For example, insulin resistance and type 2 diabetes increase the risk of both heart disease and stroke. Damaged blood vessels can result from either of these conditions, and researchers believe that damaged vessels in the brain may well contribute to Alzheimer’s.

Further, our brain cells use a high level of energy, which can be affected by diabetes because the disease retards the body’s ability to absorb sugar to generate the necessary energy. Healthy brain function also depends on a symphony of many different chemicals working in concert. Too much insulin can throw off the balance of these chemicals and potentially trigger Alzheimer’s. Finally, high blood sugar causes inflammation, which could damage brain cells and help Alzheimer’s develop.

Tackling the connection between diabetes and Alzheimer’s disease may ultimately involve a better understanding of vascular dementia, a disease with the same symptoms as Alzheimer’s. But as Snyder puts it, “Of the top 10 causes of death in the United States, Alzheimer’s is the only one without any way to prevent, cure or slow its progression.” Vascular dementia, by contrast, can be prevented or managed through many of the same healthy habits that can also reduce the risk of diabetes.

“[Vascular dementia] results from hypertension, a high-fat diet, smoking and uncontrolled diabetes,” says Carson Henderson, associate director of Two Hawk Institute, an Indian-owned and -operated corporation focused on health education, training and research in Indian country. “If you exercise, eat right, and don’t smoke, you might be able to prevent vascular dementia as you age.”

Vascular dementia is caused by low blood flow to the brain, often as the result of a stroke or series of strokes. “With vascular dementia, your brain cells are dying, because small, tiny blood vessels in the brain are being blocked, and the cells below are not receiving blood or oxygen,” explains Carson Henderson’s husband, Neil Henderson, Oklahoma Choctaw, who directs the American Indian Diabetes Prevention Center at the University of Oklahoma Health Sciences Center’s College of Public Health. “Vascular dementia looks a lot like Alzheimer’s disease, but it is not the same causation. You still get memory loss and confused thinking.”

The latest link between diabetes and dementia was established by a recent study undertaken by Kyushu University in Japan. Researchers analyzed “1,017 community-dwelling dementia-free subjects” over the course of 15 years and found that Alzheimer’s disease and vascular dementia “were significantly higher in subjects with diabetes then in those with normal glucose tolerance.”

Snyder puts the significance of the finding this way: “Diabetes affects your heart, and there are links between cardiovascular health and brain health. The brain uses 25 percent of the oxygen in blood for its functions, if the heart isn’t healthy, the brain won’t be healthy, either.”

So the ties between diabetes and heart disease and stroke continue to be uncovered. Now, with the possibility that diabetes might be among the causes of one of America’s most lethal diseases, organizations like the Alzheimer’s Association are doing everything they can to spread awareness—and prevention.

Authors: ICTMN Staff December 14, 2011

Republished by courtesy of Indian Country Today Media Network
Original Source: A Deadly Duo: New Research Shows Two of the Leading Killers in America Might be Linked
Twitter: Indian Country

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Children in rural communities get a “double-dose” of the pesticide chlorpyrifos from food and drift from neighboring fields

Washington, DC — As children settle into the new school year, health professionals are demanding that the Environmental Protection Agency (EPA) ban the neurotoxic chemical chlorpyrifos, a pesticide used on farms throughout the country and the same chemical that the agency banned some ten years ago for use in homes.

In a letter to be submitted to EPA tomorrow, over two dozen health professionals cite new science showing the health impacts of chlorpyrifos, including lowering IQs and increasing the risk of ADHD and learning disabilities among children.

“EPA should follow the science and take this brain toxin completely off the market” said Dr. David Carpenter, MD, Director Institute for Health & The Environment, University at Albany. “Chlorpyrifos poses serious threats to children’s health and doesn’t belong in our homes, on our farms, or on our cafeteria trays.”

The recent studies show that exposure to chlorpyrifos in the womb and in early childhood, during critical development “windows,” can lead to lasting effects on the brain. Researchers now say that as many as 25% of all U.S. children may have IQs several points lower due to eating foods treated with chlorpyrifos and similar pesticides.

“Fruits and vegetables are essential for healthy children but shouldn’t be grown with chlorpyrifos,”said Ted Schettler, MD, MPH, Science Director of the Science and Environmental Health Network, and one of the letter’s signatories. “Children in rural communities face a double dose of this brain poison. They are exposed to chlorpyrifos drifting from neighboring fields, and again when the pesticide is on their food.”

Chlorpyrifos was banned for use in homes over ten years ago because of it’s potential harm to children. But ten million pounds of chlorpyrifos are still used on agricultural fields each year. Air monitoring, biomonitoringand poisoning data confirm that extensive human exposure to chlorpyrifos is linked to its continued use in agriculture. According to data from the Centers for Disease Control,the vast majority of us — including children — carry breakdown products of the chemical in our bodies.

Children living in farm communities are at especially high risk. In addition to exposure from food they may also be breathing in particles that drift into their classrooms and homes from nearby farms. Farmworker children are exposed even more, as parents sometimes carry residues of the pesticide home at the end of the day on clothing and shoes.

“Chlorpyrifos drift poses serious threats to communities like mine,” said Luis Medellin, of the community organization El Quinto Sol de America. Luis grew up in homes next to farms using chlorpyrifos in California’s San Joaquin Valley. “The realities on the ground show that this brain toxin can’t be used safely and should not be used in the fields.”

At age 17, Luis began using Pesticide Action Network’s Drift Catcher to document chemical drift from neighboring citrus fields, finding that a majority of samples contained chlorpyrifos. Residents also sampled chlorpyrifos in their urine, and all but one had levels above what EPA considers “acceptable.”

In their letter to EPA (pdf), health professionals are demanding that EPA ban all uses of chlorpyrifos. In their letter they state:

We urge EPA to act now on the weight of scientific evidence of health harms of chlorpyrifos for children and fetuses. It is time that EPA take action to protect the public health and provide a healthy legacy for our children and for future generations. We call on EPA to cancel all uses of pesticide chlorpyrifos.

Other letters with a similar demand were delivered to EPA from environmental health groups nationwide, including a petition signed by more than 6,000 concerned citizens across the country.

Author:

PAN, Toxic Brain Chemical Must Be Banned: Health Professionals Demand EPA Take Action, October 5, 2011

Related articles:

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Finding removes the idea once and for all that IBS symptoms are not real and are “only psychological”

A large academic study has demonstrated structural changes in specific brain regions in female patients with irritable bowel syndrome (IBS), a condition that causes pain and discomfort in the abdomen, along with diarrhea, constipation or both.

A collaborative effort between UCLA and Canada’s McGill University, the study appears in the July issue of the journal Gastroenterology.

The findings show that IBS is associated with both decreases and increases in grey matter density in key areas of the brain involved in attention, emotion regulation, pain inhibition and the processing of visceral information.

IBS affects approximately 15 percent of the U.S. population, primarily women. Currently, the condition is considered by the medical field to be a “functional” syndrome of the digestive tract not working properly rather than an “organic” disorder with structural organ changes. Efforts to identify structural or biochemical alterations in the gut have largely been unsuccessful. Even though the pathophysiology is not completely understood, it is generally agreed that IBS represents an alteration in brain-gut interactions.

These study findings, however, show actual structural changes to the brain, which places IBS in the category of other pain disorders, such as lower back pain, temporomandibular joint disorder, migraines and hip pain — conditions in which some of the same anatomical brain changes have been observed, as well as other changes. A recent, smaller study suggested structural brain changes in IBS, but a larger definitive study hadn’t been completed until now.

“Discovering structural changes in the brain, whether they are primary or secondary to the gastrointestinal symptoms, demonstrates an ‘organic’ component to IBS and supports the concept of a brain-gut disorder,” said study author Dr. Emeran Mayer, professor of medicine, physiology and psychiatry at the David Geffen School of Medicine at UCLA. “Also, the finding removes the idea once and for all that IBS symptoms are not real and are ‘only psychological.’ The findings will give us more insight into better understanding IBS.”

Researchers employed imaging techniques to examine and analyze brain anatomical differences between 55 female IBS patients and 48 female control subjects. Patients had moderate IBS severity, with disease duration from one to 34 years (average 11 years). The average age of the participants was 31.

Investigators found both increases and decreases of brain grey matter in specific cortical brain regions.

Even after accounting for additional factors such as anxiety and depression, researchers still discovered differences between IBS patients and control subjects in areas of the brain involved in cognitive and evaluative functions, including the prefrontal and posterior parietal cortices, and in the posterior insula, which represents the primary viscerosensory cortex receiving sensory information from the gastrointestinal tract.

“The grey-matter changes in the posterior insula are particularly interesting since they may play a role in central pain amplification for IBS patients,” said study author David A. Seminowicz, Ph.D., of the Alan Edwards Centre for Research on Pain at McGill University. “This particular finding may point to a specific brain difference or abnormality that plays a role in heightening pain signals that reach the brain from the gut.”

Decreases in grey matter in IBS patients occurred in several regions involved in attentional brain processes, which decide what the body should pay attention to. The thalamus and midbrain also showed reductions, including a region — the periaqueductal grey — that plays a major role in suppressing pain.

“Reductions of grey matter in these key areas may demonstrate an inability of the brain to effectively inhibit pain responses,” Seminowicz said.

The observed decreases in brain grey matter were consistent across IBS patient sub-groups, such as those experiencing more diarrhea-like symptoms than constipation.

“We noticed that the structural brain changes varied between patients who characterized their symptoms primarily as pain, rather than non-painful discomfort,” said Mayer, director of the UCLA Center for Neurobiology of Stress. “In contrast, the length of time a patient has had IBS was not related to these structural brain changes.”

Mayer added that the next steps in the research will include exploring whether genes can be identified that are related to these structural brain changes. In addition, there is a need to increase the study sample size to address male-female differences and to determine if these brain changes are a cause or consequence of having IBS.

Literature:

University of California, Study finds structural brain alterations in patients with irritable bowel syndrome, Los Angeles, July 22, 2010.

Photo: UCLA

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The University of Rochester Medical Center-led study is published in the International Journal of Andrology.

Because testosterone produces the masculine brain, researchers are concerned that fetal exposure to anti-androgens such as phthalates “which are pervasive in the environment“ has the potential to alter masculine brain development, said lead author Shanna H. Swan, Ph.D., professor of Obstetrics and Gynecology, director of the URMC Center for Reproductive Epidemiology, and an expert in phthalates.

“Our results need to be confirmed, but are intriguing on several fronts,” Swan said. “Not only are they consistent with our prior findings that link phthalates to altered male genital development, but they also are compatible with current knowledge about how hormones mold sex differences in the brain, and thus behavior. We have more work to do, but the implications are potentially profound.”

Phthalates are chemicals used to soften plastics. Recent studies have shown that the major source of human exposure to the two phthalates of most concern (DEHP and DBP) is through food. These phthalates are used primarily in polyvinyl chloride (PVC), so any steps in the processing, packaging, storage, or heating of food that use PVC-containing products can introduce them into the food chain.

Phthalates are also found in vinyl and plastic tubing, household products, and many personal care products such as soaps and lotions. Phthalates are becoming more controversial as scientific research increasingly associates them with genital defects, metabolic abnormalities, and reduced testosterone in babies and adults. A federal law passed in 2008 banned six phthalates from use in toys such as teethers, play bath items, soft books, dolls and plastic figures.

In Swan’s study, higher concentrations of metabolites of two phthalates, di(2-ethylhexyl) phthalate (DEHP), and dibutyl phthalate (DBP), were associated with less male-typical behavior in boys on a standard play questionnaire. No other phthalate metabolites measured in-utero was linked to the less-masculine behavior. Girls’ play behavior was not associated with phthalate levels in their mothers, the study concluded.

Swan’s interest in phthalates stems from an investigation into the environmental causes of reproductive health problems. Since 1998 she has led the federally funded, multi-center Study for Future Families (SFF), which established a large database from which to explore various scientific questions about toxins.

The current study focused on a small sample of SFF mothers who delivered children between 2000 and 2003. The mothers provided urine samples around the 28th week of pregnancy. The urine was analyzed for phthalate metabolites by the Centers for Disease Control and Prevention (CDC).

Swan hypothesized that phthalates may lower fetal testosterone production during a critical window of development – somewhere within eight to 24 weeks gestation, when the testes begin to function – thereby altering brain sexual differentiation.

To explore the question, researchers reconnected with mothers from the SFF sample and asked them to complete a standard research questionnaire, called the Preschool Activities Inventory (PSAI), for their children ages 3 1/2 to 6 1/2 years.

The PSAI is designed to discriminate play behavior within and between the sexes, and in the past has been shown to reflect the endocrine-disrupting properties of other toxins, such as PCBs and dioxins. The PSAI addressed three aspects of play: types of toys children choose (trucks versus dolls), activities (rough-and-tumble play, for example), and child characteristics.

However, researchers were concerned about how the choice of toys available in any given household might skew results, so in addition they asked about parental views toward atypical play. For example, the survey asked, “What would you do if you had a boy who preferred toys that girls usually play with?” The possible answers included “strongly encourage” (him to play this way) to “strongly discourage.”

The final survey scores are designed to reflect sex-typical play. Higher scores meant more male-typical play and lower scores meant more female-typical play.

Researchers then examined boys play-behavior scores in relation to the concentration of phthalate metabolites in their mothers’ prenatal urine samples, finding that higher concentrations of DEHP and DBP metabolites were associated with less masculine play behavior scores.

Earlier studies by Swan and others have shown that phthalate exposure during pregnancy might affect the development of genitals of both male rodents and baby boys. Scientists refer to this cluster of genital alterations as the “phthalate syndrome,” and research suggests that in rodent pups, the syndrome can have adverse consequences for later sexual development.

If endocrine disrupters such as phthalates can impair genital development and hormone levels in the body, the play-behavior study noted, then a deeper examination of how these chemicals impact the brain is warranted.

Reference: University of Rochester Medical Center, Pilot study relates phthalate exposure to less-masculine play by boys, Nov. 16, 2009

Increased prevalence of the autism spectrum disorders (ASD) and the failure to find genetic explanations has pushed the hunt for environmental causes. These disorders are defined clinically but lack objective characterization.

 To meet this need, we measured neurobehavioral and pulmonary functions in eight ASD boys aged 8 to 19 years diagnosed clinically and compared them to 145 unaffected children from a community with no known chemical exposures. As 6 of 35 consecutive mold/ mycotoxin (mold)-exposed children aged 5 to 13 years had ASD, we compared them to the 29 non-ASD mold-exposed children, and to the eight ASD boys. Comparisons were adjusted for age, height, weight, and grade attained in school. 

The eight ASD boys averaged 6.8 abnormalities compared to 1.0 in community control boys. The six mold-exposed ASD children averaged 12.2 abnormalities. The most frequent abnormality in both groups was balance, followed by visual field quadrants, and then prolonged blink reflex latency. 

Neuropsychological abnormalities were more frequent in mold-exposed than in terbutaline-exposed children and included digit symbol substitution, peg placement, fingertip number writing errors, and picture completion. Profile of mood status scores averaged 26.8 in terbutaline-exposed, 52 in mold exposed, and 26 in unexposed. The mean frequencies of 35 symptoms were 4.7 in terbutaline, 5.4 in mold/ mycotoxins exposed and 1.7 in community controls. 

Reference:   Kilburn KH, Thrasher JD, Immers NB., Do terbutaline- and mold-associated impairments of the brain and lung relate to autism?, Toxicol Ind Health. 2009 Sep 30.

Neuroimaging studies done by means of magnetic resonance imaging (MRI) have provided important insights into the neurobiological basis for autism. The aim of this article is to review the current state of knowledge regarding brain abnormalities in autism. Results of structural MRI studies dealing with total brain volume, the volume of the cerebellum, caudate nucleus, thalamus, amygdala and the area of the corpus callosum are summarised. In the past 5 years also new MRI applications as functional MRI and diffusion tensor imaging brought considerable new insights in the pathophysiological mechanisms of autism. Dysfunctional activation in key areas of verbal and non-verbal communication, social interaction, and executive functions are revised. Finally, we also discuss white matter alterations in important communication pathways in the brain of autistic patients. 

Reference: Verhoeven JS, De Cock P, Lagae L, Sunaert S., Neuroimaging of autism, Neuroradiology. 2009 Sep 15.