Over cooking, carcinogens and AGEs

cookingAll About Cooking & Carcinogens

By Ryan Andrews

Higher cooking temperatures can create chemical reactions among amino acids, creatines, and sugars — reactions that may produce dangerous compounds that can damage our DNA.

We know that cooking food has some benefits:

  • It can make food safer
  • It can concentrate tastes and flavors
  • It can reduce spoilage
  • It can soften tough foods
  • It increases the amount of energy our bodies can get from food
  • It breaks starch molecules into more digestible fragments
  • It denatures protein molecules

But before we get too excited about cooking, the modern diet can be overwhelmingly heat-processed. Higher cooking temperatures can create chemical reactions among amino acids, creatines, and sugars — reactions that may produce dangerous carcinogens and mutagens (compounds that can damage our DNA).

Now suddenly we have “unhealthy” compounds created in otherwise “healthy” foods — stuff like potatoes, fish, whole grains, etc.

Don’t freak out and throw your barbecue grill off the balcony just yet. Let’s start by learning more about what these compounds are, and how they work.

Cooking creates chemical compounds

Heat plus food molecules can create several products in the process of chemical conversion known as cooking. (And you thought you were just slapping a burger on the grill! Now you can say “I am chemically converting proteins!” Fancy.)

Some of the most notable end products include:

  • Heterocyclic amines and polycyclic aromatic hydrocarbons
  • Advanced glycation end products
  • Acrylamide

Let’s look at each of these in more depth.

Heterocyclic amines (HCAs) and polycyclic aromatic hydrocarbons (PAHs)

What are they and where do they come from?

HCAs are made when creatines and amino acids (both found in meats) react together with heat. PAHs include over 100 different compounds formed by the incomplete burning of organic matter (e.g., oil, gas, coal, food, etc.) at temperatures in excess of 392 degrees F (200 C).

heat

Thus, raw foods don’t have HCAs nor PAHs. Indeed, more than 90% of our exposure to HCAs and PAHs comes from cooked food.


 

Protection against loss of innate defenses in adulthood by low advanced glycation end products (AGE) intake: role of the antiinflammatory AGE receptor-1.

Increased oxidant stress and inflammation (OS/infl) are linked to both aging-related diseases and advanced glycation end products (AGEs). Whereas AGE receptor-1 (AGER1) reduces OS/infl in animals, this has not been assessed in normal humans.

OBJECTIVE:

The objectives of the study were to determine whether AGER1 correlates with AGEs and OS/infl and a reduction of dietary AGEs (dAGEs) lowers OS/infl in healthy adults and chronic kidney disease (CKD-3) patients.

DESIGN:

This study was cross-sectional with 2-yr follow-up studies of healthy adults and CKD-3 patients, a subset of which received a reduced AGE or regular diet.

SETTING:

The study was conducted at general community and renal clinics.

PARTICIPANTS:

Participants included 325 healthy adults (18-45 and >60 yr old) and 66 CKD-3 patients.

INTERVENTION:

An isocaloric low-AGE (30-50% reduction) or regular diet was given to 40 healthy subjects for 4 months and to nine CKD-3 patients for 4 wk.

MAIN OUTCOME:

Relationships between age, dAGEs, serum AGEs, peripheral mononuclear cell AGE-receptors, and OS/Infl before and after reduction of dAGE intake were measured.

RESULTS:

AGEs, oxidant stress, receptor for AGE, and TNFalpha were reduced in normal and CKD-3 patients after the low-AGE diet, independently of age. AGER1 levels in CKD-3 patients on the low-AGE diet resembled 18- to 45-yr-old normal subjects. Dietary, serum, and urine AGEs correlated positively with peripheral mononuclear cell AGER1 levels in healthy participants. AGER1 was suppressed in CKD-3 subjects, whereas receptor for AGE and TNFalpha were increased.

CONCLUSIONS:

Reduction of AGEs in normal diets may lower oxidant stress/inflammation and restore levels of AGER1, an antioxidant, in healthy and aging subjects and CKD-3 patients. AGE intake has implications for health outcomes and costs and warrants further testing.

Signs and symptoms of autoimmune disease

  • Rheumatoid arthritis

    Rheumatoid arthritis affects joint linings, causing painful swelling. Over long periods of time, the inflammation associated with rheumatoid arthritis can cause bone erosion and joint deformity.
  • Lupus

    Symptoms vary but can include fatigue, joint pain, rash, and fever. These can periodically get worse (flare-up) and then improve.
  • Celiac disease

    The classic symptom is diarrhea. Other symptoms include bloating, gas, fatigue, low blood count (anemia), and osteoporosis. Many people have no symptoms.
  • Sjögren’s syndrome

    The main symptoms are dry mouth and dry eyes.
  • Polymyalgia rheumatica

    Symptoms usually develop quickly and include aching of the shoulders, neck, or hips
  • Multiple sclerosis

    Multiple sclerosis causes many different symptoms, including vision loss, pain, fatigue, and impaired coordination. The symptoms, severity, and duration can vary from person to person. Some people may be symptom free most of their lives, while others can have severe chronic symptoms that never go away.
  • Ankylosing spondylitis

    Symptoms typically appear in early adulthood and include reduced flexibility in the spine. This reduced flexibility eventually results in a hunched-forward posture. Pain in the back and joints is also common.
  • Type 1 diabetes

    Symptoms include increased thirst, frequent urination, hunger, fatigue, and blurred vision.
  • Alopecia areata

    The main symptom is hair loss.
  • Vasculitis

    Symptoms include fever, fatigue, weight loss, and muscle and joint pain.
  • Temporal arteritis

    Symptoms include headaches, jaw pain, vision loss, fever, and fatigue. Diagnosis usually requires biopsy of the temporal artery.

The Molecular Roots of Alzheimer’s

Summary: Findings may help to shed light on how Alzheimer’s and other neurodegenerative diseases develop.

Source: WUSTL.

Cellular ‘housekeeping’ molecule’s structure linked to neurodegeneration

Scientists at Washington University School of Medicine in St. Louis have detailed the structure of a molecule that has been implicated in Alzheimer’s disease. Knowing the shape of the molecule — and how that shape may be disrupted by certain genetic mutations — can help in understanding how Alzheimer’s and other neurodegenerative diseases develop and how to prevent and treat them.

The study is published Dec. 20 in the journal eLife.

The idea that the molecule TREM2 is involved in cognitive decline — the hallmark of neurodegenerative diseases, including Alzheimer’s — has gained considerable support in recent years. Past studies have demonstrated that certain mutations that alter the structure of TREM2 are associated with an increased risk of developing late-onset Alzheimer’s, frontal temporal dementia, Parkinson’s disease and sporadic amyotrophic lateral sclerosis (ALS). Other TREM2 mutations are linked to Nasu-Hakola disease, a rare inherited condition that causes progressive dementia and death in most patients by age 50.

“We don’t know exactly what dysfunctional TREM2 does to contribute to neurodegeneration, but we know inflammation is the common thread in all these conditions,” said senior author Thomas J. Brett, PhD, an assistant professor of medicine. “Our study looked at these mutations in TREM2 and asked what they do to the structure of the protein itself, and how that might impact its function. If we can understand that, we can begin to look for ways to correct it.”

The analysis of TREM2 structure, completed by first author, Daniel L. Kober, a doctoral student in Brett’s lab, revealed that the mutations associated with Alzheimer’s alter the surface of the protein, while those linked to Nasu-Hakola influence the “guts” of the protein. The difference in location could explain the severity of Nasu-Hakula, in which signs of dementia begin in young adulthood. The internal mutations totally disrupt the structure of TREM2, resulting in fewer TREM2 molecules. The surface mutations, in contrast, leave TREM2 intact but likely make it harder for the molecule to connect to proteins or send signals as normal TREM2 molecules would.

Image shows the structure of TREM2.

TREM2 lies on the surface of immune cells called microglia, which are thought to be important “housekeeping” cells. Via a process called phagocytosis, such cells are responsible for engulfing and cleaning up cellular waste, including the amyloid beta that is known to accumulate in Alzheimer’s disease. If the microglia lack TREM2, or the TREM2 that is present doesn’t function properly, the cellular housekeepers can’t perform their cleanup tasks.

“Exactly what TREM2 does is still an open question,” Brett said. “We know mice without TREM2 have defects in microglia, which are important in maintaining healthy brain biology. Now that we have these structures, we can study how TREM2 works, or doesn’t work, in these neurodegenerative diseases.”

TREM2 also has been implicated in other inflammatory conditions, including chronic obstructive pulmonary disease and stroke, making the structure of TREM2 important for understanding chronic and degenerative diseases throughout the body, he added.

ABOUT THIS ALZHEIMER’S DISEASE RESEARCH ARTICLE

Funding: This work was supported by the National Institutes of Health (NIH), grant numbers R01-HL119813, R01-AG044546, R01-AG051485, R01-HL120153, R01-HL121791, K01-AG046374, T32-GM007067, K08-HL121168, and P50-AG005681-30.1; the Burroughs-Wellcome Fund; the Alzheimer’s Association, grant number AARG-16-441560; and the American Heart Association, grant number PRE22110004. Results were derived from work performed at Argonne National Laboratory (ANL) Structural Biology Center. ANL is operated by U. Chicago Argonne, LLC, for the U.S. DOE, Office of Biological and Environmental Research, supported by grant number DE-AC02-06CH11357.

Source: Diane Duke Williams – WUSTL
Image Source: NeuroscienceNews.com image is credited to Daniel L. Kober.
Original Research: Full open access research “Neurodegenerative disease mutations in TREM2 reveal a functional surface and distinct loss-of-function mechanisms” by Daniel L Kober, Jennifer M Alexander-Brett, Celeste M Karch, Carlos Cruchaga, Marco Colonna, Michael J Holtzman, and Thomas J Brett in eLife. Published online December 20 2016 doi:10.7554/eLife.20391


Abstract

Neurodegenerative disease mutations in TREM2 reveal a functional surface and distinct loss-of-function mechanisms

Genetic variations in the myeloid immune receptor TREM2 are linked to several neurodegenerative diseases. To determine how TREM2 variants contribute to these diseases, we performed structural and functional studies of wild-type and variant proteins. Our 3.1 Å TREM2 crystal structure revealed that mutations found in Nasu-Hakola disease are buried whereas Alzheimer’s disease risk variants are found on the surface, suggesting that these mutations have distinct effects on TREM2 function. Biophysical and cellular methods indicate that Nasu-Hakola mutations impact protein stability and decrease folded TREM2 surface expression, whereas Alzheimer’s risk variants impact binding to a TREM2 ligand. Additionally, the Alzheimer’s risk variants appear to epitope map a functional surface on TREM2 that is unique within the larger TREM family. These findings provide a guide to structural and functional differences among genetic variants of TREM2, indicating that therapies targeting the TREM2 pathway should be tailored to these genetic and functional differences with patient-specific medicine approaches for neurodegenerative disorders.

“Neurodegenerative disease mutations in TREM2 reveal a functional surface and distinct loss-of-function mechanisms” by Daniel L Kober, Jennifer M Alexander-Brett, Celeste M Karch, Carlos Cruchaga, Marco Colonna, Michael J Holtzman, and Thomas J Brett in eLife. Published online December 20 2016 doi:10.7554/eLife.20391

MRI Scans Detect “Brain Rust” in Schizophrenia

Summary: According to a new study, the brain blocks the ability for creating new memories shortly after waking in order to prevent the disruption of the stabilization of memory consolidation that occurs during sleep.

Source: ACNP.

A damaging chemical imbalance in the brain may contribute to schizophrenia, according to research presented at the American College of Neuropsychopharmacology Annual Meeting in Hollywood, Florida.

Using a new kind of MRI measurement, neuroscientists reported higher levels of oxidative stress in patients with schizophrenia, when compared both to healthy individuals and those with bipolar disorder.

“Intensive energy demands on brain cells leads to accumulation of highly reactive oxygen species, such as free radicals and hydrogen peroxide,” according to the study’s lead investigator, Dr. Fei Du, an Assistant Professor of Psychiatry at Harvard Medical School. In schizophrenia, excessive oxidation – which involves the same type of chemical reaction that causes metal to corrode into rust – is widely thought to cause inflammation and cellular damage. However, measuring this process in the living human brain has remained challenging.

Du and colleagues at McLean Hospital measured oxidative stress using a novel magnetic resonance spectroscopy technique. This technique uses MRI scanners to non-invasively measure brain concentrations of two molecules, NAD+ and NADH, that give a readout of how well the brain is able to buffer out excessive oxidants.

Image shows a brain model.

Among 21 patients with chronic schizophrenia, Du observed a 53% elevation in NADH compared to healthy individuals of similar age. A similar degree of NADH elevation was seen in newly diagnosed schizophrenia, suggesting that oxidation imbalance is present even in the early stages of illness. More modest NADH increases were also seen in bipolar disorder, which shares some genetic and clinical overlap with schizophrenia.

In addition to offering new insights into the biology of schizophrenia, this finding also provides a potential way to test the effectiveness of new interventions. “We hope this work will lead to new strategies to protect the brain from oxidative stress and improve brain function in schizophrenia,” Du concludes.

ABOUT THIS SCHIZOPHRENIA RESEARCH ARTICLE

Funding: This work was supported by grants from MH092704 (F.D.); NARSAD (F.D.); NARSAD (D.O.); MH094594 (D.O.); MH104449 (D.O.); Shervert Frazier Research Institute (B.M.C.).

Source: Erin Colladay – ACNP
Image Source: NeuroscienceNews.com image is in the public domain.
Original Research: The study will be presented at the 55th Annual Meeting of the American College of Neuropsychopharmacology.

Metal toxins and MTHFR gene mutations

Heavy metals can be found everywhere in our environment. They become problematic for people when they accumulate at high concentrations in the human body. Unfortunately some people have a genetic predisposition to toxicity from heavy metals. As with other toxins, people with unaddressed MTHFR mutations have trouble clearing metals from their systems. This can lead to behavioral, structural and functional abnormalities in the human body depending on which metals have built up.

The most common metals are aluminum, antimony (found in flame retardant materials), arsenic (found in chicken and the water supply), beryllium, bismuth, cadmium, lead (found in paint), mercury, nickel, platinum, thallium, thorium, tin, tungsten and uranium. Unfortunately it is next to impossible to avoid many of these in the environment. Even if you are not exposed to industrial areas, you can still pick up metals in your drinking water, from vaccinations, tattoo ink, mercury amalgam fillings, pre-1978 houses, cigarette smoke (including secondhand smoke) and contaminated food sources.

Symptoms of chronic toxic metal exposure can be subtle, often overlapping with those of other illnesses. Fatigue, digestive issues, joint pain, depression, blood sugar issues and female reproductive problems can all be caused by heavy metals. According to Dr. Kendal Stewart, metals are not water soluble and therefore can’t be regulated. They compete with other minerals that we need. In a normal person, the body acts as its own chelator by utilizing its own glutathione. Cysteine-rich proteins bind to the heavy metals and keep them out of the fat cells where they like to congregate, helping the person to eliminate them. Unfortunately people with methylation gene defects can’t excrete metals due to impaired cysteine metabolism and reduced glutathione. These people can’t properly regulate good minerals either.

Testing for heavy metals can be tricky as they like to hide in tissues. Blood tests are woefully inaccurate so an advised approach is to test via a combination of methods such as hair, feces and urine (see the link for pros and cons of each type of test). If you have a heavy metal burden it is important to work with an experienced practitioner to clear your system. Ideally this will include a complete assessment of the bodily pathways that are dysfunctional and a correction so that the build-up does not continue to happen. Chelation must be done carefully because, as Dr. Stewart explains, chelation can block hormones, other minerals and disrupt other processes in the body. It must be balanced without overwhelming the body. Chelation also presents opportunities for infections like yeast and viruses. The form of treatment must be appropriate to other issues the patient is experiencing.

Dr. Mercola provides a number of tips for reducing your body’s heavy metal burden. Unfortunately for those with MTHFR, avoidance may not be enough. You have to work actively to improve your methylation and detoxification processes.

https://clubalthea.com/2014/08/10/detox-your-lungs-from-air-pollution-and-metal-toxins/

https://clubalthea.com/2016/10/11/neck-pain-and-mthfr-gene-folate-methionine/

Email motherhealth@gmail.com for exome or complete DNA sequence test.

A Host of Common Chemicals Endanger Child Brain Development, Report Says

Summary: A new report calls for renewed attention to the growing evidence that many common and widely available chemicals endanger neurodevelopment in fetuses and children of all ages.

Source: University of Illinois.

In a new report, dozens of scientists, health practitioners and children’s health advocates are calling for renewed attention to the growing evidence that many common and widely available chemicals endanger neurodevelopment in fetuses and children of all ages.

The chemicals that are of most concern include lead and mercury; organophosphate pesticides used in agriculture and home gardens; phthalates, found in pharmaceuticals, plastics and personal care products; flame retardants known as polybrominated diphenyl ethers; and air pollutants produced by the combustion of wood and fossil fuels, said University of Illinois comparative biosciences professor Susan Schantz, one of dozens of individual signatories to the consensus statement.

Polychlorinated biphenyls, once used as coolants and lubricants in transformers and other electrical equipment, also are of concern. PCBs were banned in the U.S. in 1977, but can persist in the environment for decades, she said.

The new report, “Project TENDR: Targeting Environmental NeuroDevelopment Risks,” appears in the journal Environmental Health Perspectives.

“These chemicals are pervasive, not only in air and water, but in everyday consumer products that we use on our bodies and in our homes,” Schantz said. “Reducing exposures to toxic chemicals can be done, and is urgently needed to protect today’s and tomorrow’s children.”

Schantz is a faculty member in the College of Veterinary Medicine and in the Beckman Institute for Advanced Science and Technology at the U. of I.

“The human brain develops over a very long period of time, starting in gestation and continuing during childhood and even into early adulthood,” Schantz said. “But the biggest amount of growth occurs during prenatal development. The neurons are forming and migrating and maturing and differentiating. And if you disrupt this process, you’re likely to have permanent effects.”

Some of the chemicals of concern, such as phthalates and PBDEs, are known to interfere with normal hormone activity. For example, most pregnant women in the U.S. will test positive for exposure to phthalates and PBDEs, both of which disrupt thyroid hormone function.

Image shows an infographic.

“Thyroid hormone is involved in almost every aspect of brain development, from formation of the neurons to cell division, to the proper migration of cells and myelination of the axons after the cells are differentiated,” said Schantz. “It regulates many of the genes involved in nervous system development.”

Schantz and her colleagues at Illinois are studying infants and their mothers to determine whether prenatal exposure to phthalates and other endocrine disruptors leads to changes in the brain or behavior. This research, along with parallel studies in older children and animals, is a primary focus of the Children’s Environmental Health Research Center at Illinois, which Schantz directs.

Phthalates also interfere with steroid hormone activity. Studies link exposure to certain phthalates with attention deficits, lower IQ and conduct disorders in children. “Phthalates are everywhere; they’re in all kinds of different products. We’re exposed to them every day,” Schantz said.

The report criticizes current regulatory lapses that allow chemicals to be introduced into people’s lives with little or no review of their effects on fetal and child health.

“For most chemicals, we have no idea what they’re doing to children’s neurodevelopment,” Schantz said. “They just haven’t been studied.

“And if it looks like something is a risk, we feel policymakers should be willing to make a decision that this or that chemical could be a bad actor and we need to stop its production or limit its use,” she said. “We shouldn’t have to wait 10 or 15 years — allowing countless children to be exposed to it in the meantime — until we’re positive it’s a bad actor.”

ABOUT THIS NEURODEVELOPMENT RESEARCH ARTICLE

Funding: The National Institute of Environmental Health Sciences at the National Institutes of Health and the U.S. Environmental Protection Agency fund the Children’s Environmental Health Research Center at the University of Illinois.

Source: Diana Yates – University of Illinois
Image Source: This NeuroscienceNews.com image is credited to Julie McMahon.
Video Source: The video is credited to Beckman Institute.
Original Research: Full open access research for “Project TENDR: Targeting Environmental Neuro-Developmental Risks. The TENDR Consensus Statement” by Bennett D, Bellinger DC, Birnbaum LS, Bradman A, Chen A, Cory-Slechta DA, Engel SM, Fallin MD, Halladay A, Hauser R, Hertz-Picciotto I, Kwiatkowski CF, Lanphear BP, Marquez E, Marty M, McPartland J, Newschaffer CJ, Payne-Sturges D, Patisaul HB, Perera FP, Ritz B, Sass J, Schantz SL, Webster TF, Whyatt RM, Woodruff TJ, Zoeller RT, Anderko L, Campbell C, Conry JA, DeNicola N, Gould RM, Hirtz D, Huffling K, Landrigan PJ, Lavin A, Miller M, Mitchell MA, Rubin L, Schettler T, Tran HL, Acosta A, Brody C, Miller E, Miller P, Swanson M, and Witherspoon NO. in Environmental Health Perspectives. Published online July 2016 doi:10.1289/EHP358

Chemicals Banned 40 Years Ago Linked to Increased Autism Risk Today

Summary: Despite being banned in the late 1970’s, organochlorine chemical exposure during pregnancy increases the risk for autism in offspring, a new study reports.

Source: Drexel University.

Chemicals used in certain pesticides and as insulating material banned in the 1970s may still be haunting us, according to new research that suggests links between higher levels of exposure during pregnancy and significantly increased odds of autism spectrum disorder in children.

According to the research, children born after being exposed to the highest levels of certain compounds of the chemicals, called organochlorine chemicals, during their mother’s pregnancy were roughly 80 percent more likely to be diagnosed with autism when compared to individuals with the very lowest levels of these chemicals. That also includes those who were completely unexposed.

Although production of organochlorine chemicals was banned in the United States in 1977, these compounds can remain in the environment and become absorbed in the fat of animals that humans eat, leading to exposure.

With that in mind, Kristen Lyall, ScD, assistant professor in Drexel University’s A.J. Drexel Autism Institute, and her collaborators, decided to look at organochlorine chemicals during pregnancy since they can cross through the placenta and affect the fetus’ neurodevelopment.

“There’s a fair amount of research examining exposure to these chemicals during pregnancy in association with other outcomes, like birth weight — but little research on autism, specifically,” Lyall said. “To examine the role of environmental exposures in risk of autism, it is important that samples are collected during time frames with evidence for susceptibility for autism — termed ‘critical windows’ in neurodevelopment. Fetal development is one of those critical windows.”

Their paper describing this study was titled, “Prenatal Organochlorine Chemicals and Autism,” and published in Environmental Health Perspectives. Now a researcher in the A.J. Drexel Autism Institute’s Modifiable Risk Factors Program, Lyall was with the California Department of Public Health when she began the work. She teamed with researchers from the department, including Gayle Windham, PhD, and Martin Kharrazi, PhD, members of the Kaiser Permanente Division of Research (which includes the study’s principal investigator, Lisa Croen, PhD), as well as an expert on measuring organochlorine chemicals, Andreas Sjodin, PhD, of the Division of Laboratory Sciences of the National Center for Environmental Health.

The team looked at a population sample of 1,144 children born in Southern California between 2000 and 2003. Data was accrued from mothers who had enrolled in California’s Expanded Alphafetoprotein Prenatal Screening Program, which is dedicated to detecting birth defects during pregnancy.

Participants’ children were separated into three groups: 545 who were diagnosed with autism spectrum disorder, 181 with intellectual disabilities but no autism diagnosis, and 418 with a diagnosis of neither.

Blood tests taken from the second trimester of the children’s mothers were used to determine the level of exposure to two different classes of organochlorine chemicals: Polychlorinated biphenyls (PCBs, which were used as lubricants, coolants and insulators in consumer and electrical products) and organochlorine pesticides (OCPs, which include chemicals like DDT).

“Exposure to PCBs and OCPs is ubiquitous,” Lyall said. “Work from the National Health and Nutrition Examination Survey, which includes pregnant women, shows that people in the U.S. generally still have measurable levels of these chemicals in their bodies.”

However, Lyall emphasized that exposure levels were key in determining risk.

“Adverse effects are related to levels of exposure, not just presence or absence of detectable levels,” she said. “In our Southern California study population, we found evidence for modestly increased risk for individuals in the highest 25th percentile of exposure to some of these chemicals.”

It was determined that two compounds in particular — PCB 138/158 and PCB 153 — stood out as being significantly linked with autism risk. Children with the highest in utero levels (exposure during their mother’s pregnancy) of these two forms of PCBs were between 79 and 82 percent more likely to have an autism diagnosis than those found to be exposed to the lowest levels. High levels of two other compounds, PCB 170 and PCB 180, were also associated with children being approximately 50 percent more likely to be diagnosed — again, this is relative to children with the lowest prenatal exposure to these PCBs.

Image shows a girl holding up a sign with autism written on it.

None of the OCPs appeared to show an association with higher autism diagnosis risk.

In children with intellectual disabilities but not autism, the highest exposure to PCBs appeared to double the risk of a diagnosis when compared to those with the lowest exposure. Mid-range (rather than high) OCP exposure was also associated with an increased level of intellectual disability diagnosis when measured against children with the lowest exposure levels.

“The results suggest that prenatal exposure to these chemicals above a certain level may influence neurodevelopment in adverse ways,” Lyall said.

These results are a first step to suggest these compounds may increase risk of development of autism, and Lyall and her colleagues are eyeing up more work in the field.

“We are definitely doing more research to build on this — including work examining genetics, as well as mixtures of chemicals,” Lyall said. “This investigation draws from a rich dataset and we need more studies like this in autism research.”

ABOUT THIS AUTISM RESEARCH ARTICLE

Source: Frank Otto – Drexel University
Image Source: This NeuroscienceNews.com image is in the public domain.
Original Research: Abstract for “Polychlorinated Biphenyl and Organochlorine Pesticide Concentrations in Maternal Mid-Pregnancy Serum Samples: Association with Autism Spectrum Disorder and Intellectual Disability” by Kristen Lyall, Lisa.A. Croen, Andreas Sjödin, Cathleen K. Yoshida, Ousseny Zerbo, Martin Kharrazi, and Gayle C. Windham in Environmental Health Perspectives. Published online August 2016 doi:10.1289/EHP277

CITE THIS NEUROSCIENCENEWS.COM ARTICLE
Drexel University. “Chemicals Banned 40 Years Ago Linked to Increased Autism Risk Today.” NeuroscienceNews. NeuroscienceNews, 23 August 2016.
<http://neurosciencenews.com/organochlorine-autism-neuroscience-4890/&gt;.

Abstract

Polychlorinated Biphenyl and Organochlorine Pesticide Concentrations in Maternal Mid-Pregnancy Serum Samples: Association with Autism Spectrum Disorder and Intellectual Disability

Background: Polychlorinated biphenyls (PCBs) and organochlorine pesticides (OCPs) are neurodevelopmental toxicants, but few studies have examined associations with autism spectrum disorder (ASD).

Objectives: To determine whether prenatal exposure to PCBs and OCPs influences offspring risk of ASD and intellectual disability without autism (ID).

Methods:
We conducted a population-based case-control study among Southern California births, including children with ASD (N=545) meeting Diagnostic and Statistical Manual of Mental Disorders (DSM)-IV-TR criteria, ID (N=181), and general population (GP) controls (N=418). Concentrations of 11 PCB congeners and 2 OCPs measured in banked second trimester serum samples were compared between the diagnostic groups. Logistic regression was used to calculate crude and adjusted odds ratios (AOR) for associations with ASD, and separately for ID, compared to GP controls, by quartiles of analyte concentrations in primary analyses.

Results: Geometric mean levels of several PCB congeners were higher in the ASD group compared to ID and GP groups. ASD risk was elevated for a number of PCB congeners, particularly for the highest vs. lowest quartile of PCB138/158 (AOR=1.79, 95% CI 1.10, 2.71) and PCB153 (AOR=1.82, 95% CI 1.10, 3.02), and for highest deciles of other congeners in secondary analyses. PCB138/158 was also associated with increased ID (AOR=2.41, 95% CI 1.18, 4.91), though no trend was suggested. OCPs were not associated with increased risk of ASD in primary analyses, while non-monotonic increases in risk of ID were found with p,p’-DDE.

Conclusions: Our results suggest higher levels of some organochlorine compounds during pregnancy are associated with ASD and ID.

“Polychlorinated Biphenyl and Organochlorine Pesticide Concentrations in Maternal Mid-Pregnancy Serum Samples: Association with Autism Spectrum Disorder and Intellectual Disability” by Kristen Lyall, Lisa.A. Croen, Andreas Sjödin, Cathleen K. Yoshida, Ousseny Zerbo, Martin Kharrazi, and Gayle C. Windham in Environmental Health Perspectives. Published online August 2016 doi:10.1289/EHP277