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Vitamin D & The Brain

Vitamin D DeficiencyVitamin D deficiency has hit an epidemic level. Not only are intakes devastatingly low, but also exposure to the sun has become increasingly limited for fear of contracting skin cancer. In his June 23, 1011, newsletter at Newsmax Health, Dr.Russell Blaylock educates his readers when he states that vitamin D3 is actually a hormone rather than a vitamin, and that a deficit of this compound may result in undesirable consequences in the brain, including depression.

Dr.Blaylock is a renowned neurosurgeon with a keen desire for people to take some control over their own health.  He implies that supplemental vitamin D3, “…lowers risk of infections, which would reduce the incidence of brain inflammation.”   He adds that research can place behavioral disorders in the lap of vitamin D deficiency, and  suggests that all of us get a vitamin D blood-level test to find out where we stand, noting that current accepted values are too low to be any benefit.   About the conditions, Dr. Blaylock says, “…depression, anxiety, panic attacks, obsessive-compulsive disorder, suicide risk, and even criminal behavior…can be traced to chronic brain inflammation.”  The good doctor would like to see blood vitamin D levels between 70 and 100 nanograms per milliliter.  That means that most of us need to take at least 2000 IU of vitamin D3 a day, with as much as 10,000 IU for severe deficiency.

The body needs cholesterol to make vitamin D from the sun’s ultra-violet radiation.  When the resulting chemical mix gets to the liver it becomes vitamin D3, the active form of the hormone, which the body uses to help maintain bone integrity, to increase neuromuscular function, and to modulate the immune system.  There has been considerable support over the past decade for the role of vitamin D in brain development and function.  It was noted by Kesby and colleagues at Australia’s Queensland Brain Institute that, “…this vitamin is actually a neuroactive steroid that acts on brain development, leading to alterations in brain neurochemistry and adult brain function.”  (Kesby. 2011)  Deficiencies have been related to depression, as well as to Parkinson’s disease and cognitive decline.

Of particular interest to American researchers at the U. of South Carolina is the relationship of vitamin D deficit to postpartum depression as one of the several mood disorders studied in 2010.  Using a moderate sample size at the outset, scientists found that low levels of vitamin D are associated with increased postpartum depression, as measured by evaluation on the Edinburgh Postpartum Depression Scale. (Murphy. 2010)  Even though larger studies are encouraged, the outcomes are likely to be the similar.

When the immune system abandons its competence because of nutritional deficit, inflammation ensues, often with a mighty wrath.  Such is the case with deficit of vitamin D in various maladies that include diabetes and multiple sclerosis, as well as depression.  Depression is a family affair characterized by feelings of hopelessness, despair, anxiety, irritability and restlessness.  Depression understandably accompanies degenerative disease, in part by the hopelessness is may engender.  If vitamin D is able to address depression, might it also be able to help get a handle on these conditions?   Whatever the cause of vitamin D deficiency, levels lower than 30 nanograms per milliliter have been associated with heart disease, type 2 diabetes, infectious diseases, autoimmune disorders, and neurological conditions. (Nimitphong. 2011)

References

MAIN ABSTRACT
Dr. Blaylock
Up Vitamin D3 for Your Brain
Thursday, June 23, 2011 10:11 AM

SUPPORTING ABSTRACTS
Mol Cell Endocrinol. 2011 Jun 1. [Epub ahead of print]
The effects of vitamin D on brain development and adult brain function.
Kesby JP, Eyles DW, Burne TH, McGrath JJ.

Source Queensland Brain Institute, University of Queensland, St. Lucia, Qld 4076, Australia.

J Am Psychiatr Nurses Assoc. 2010 May;16(3):170-7.
An exploratory study of postpartum depression and vitamin d.
Murphy PK, Mueller M, Hulsey TC, Ebeling MD, Wagner CL.

SourceMedical University of South Carolina, Charleston, SC, USA, [email protected]

Curr Opin Clin Nutr Metab Care. 2011 Jan;14(1):7-14.
Vitamin D, neurocognitive functioning and immunocompetence.
Nimitphong H, Holick MF.

SourceSection of Endocrinology, Diabetes, Nutrition, Department of Medicine, Boston University Medical Center, Boston, Massachusetts, USA.

Acta Psychiatr Scand. 2011 Apr 12. doi: 10.1111/j.1600-0447.2011.01705.x. [Epub ahead of print]
D’ for depression: any role for vitamin D?: ‘Food for Thought’ II.
Parker G, Brotchie H.

SourceSchool of Psychiatry, University of New South Wales, and Black Dog Institute, Randwick, Sydney, NSW, Australia.

Psychopharmacology (Berl). 2011 Jun;215(4):733-7. Epub 2011 Jan 29.
Exploring the relationship between vitamin D and basic personality traits.
Ubbenhorst A, Striebich S, Lang F, Lang UE.

SourceDepartment of Physiology, University of Tuebingen, Gmelinstr. 5, 72076, Tuebingen, Germany.

FASEB J. 2008 Apr;22(4):982-1001. Epub 2007 Dec 4.
Is there convincing biological or behavioral evidence linking vitamin D deficiency to brain dysfunction?
McCann JC, Ames BN.

*These statements have not been evaluated by the FDA.
These products are not intended to treat, diagnose, cure, or prevent any disease.

Brain Fog

red-bow-on-fingerThere is a relationship between central nervous system missteps and markers of inflammation. Age doesn’t matter; it happens across the board. If the occasional bout of forgetfulness strikes you, you might recoil in fear of early-onset dementia, especially if the “occasions” are too close together. Is there anything you can do about this? Could it be something you ate? Maybe it’s something you didn’t eat.

Inflammation is a protective response to injury or destruction of tissue that tries to rid the body of the detrimental agent. The process elevates blood markers that are useful in predicting the onset of chronic conditions, such as diabetes or cardiovascular disease. One of these markers is called homocysteine, an amino acid made from methionine that degrades arterial architecture.  But what of mental lapses?  “Epidemiological studies show a positive, dose-dependent relationship between mild-to-moderate increases in plasma total homocysteine concentrations (Hcy) and the risk of neurodegenerative diseases, such as…cognitive impairment…”  (Herrmann.  2011)  Cognitive impairment is not necessarily a sign of impending dementia or Alzheimer’s disease, but elevated homocysteine is “…a surrogate marker for B vitamin deficiency (folate, B12, B6) and a neurotoxic agent.”  (Ibid.)

If you can provide details about your forgetfulness, you don’t have dementia. If you can recall what you read yesterday about the local political scene, you don’t have dementia. If you forgot where you put the car keys, join the crowd.  Nonetheless, you could have homocysteine levels that are too high for your own good.  It’s recognized that taking classes, doing word puzzles, playing chess, and generally challenging the mind can preserve memory.  But these activities won’t necessarily influence renegade body chemistry. Though conjectural, it has been suggested that inflammation disrupts the integrity of the blood-brain barrier, the highly selective membrane that protects the brain from pathogens in the blood, as well as regulates which molecules can pass between the blood and the cerebral spinal fluid. Inflammation compromises the function of the membrane, allowing large molecules access to the brain, resulting in neuronal damage.  (Stolp. 2009).

Herrmann and Obeid (2011) admit that the prospect of improving any degree of neurological distortion caused by homocysteine can be realized with B vitamins. Parallel independent investigation revealed that women with cognitive abasement had higher Hcy values than women without such a burden, and that the folate (a B vitamin also called B9) levels of the affected cohort were measurably lower.  (Faux. 2011)

Homocysteine can be changed back to methionine under the right conditions, namely in the presence of a methylation molecule, such as folic acid (called folate in food). Folate insufficiency, or outright inadequacy, can initiate mental lapses that could balloon into more serious conditions if deficit is prolonged. Therapeutically, folic acid is able to reduce Hcy and the occurrence of neural tube defects in neonates. A side benefit was observed to be the prevention of cervical dysplasia and protection against neoplasm formation in ulcerative colitis.  (Kelly.  1998) Geriatric scientists had indicted homocysteine as causative of neurobehavioral anomalies across a wide range of cognitive domains (Jyme. 2005), and later identified vitamin B12, vitamin B6, and folate (or folic acid) as ameliorative agents.  (Selhub. 2010)

Homocysteine levels do not always increase because of something we did or ate, but because of something we didn’t eat. That would be the foods providing ample supplies of B12, B6, and folic acid.  Certain chronic and contagious diseases that evoke an inflammatory response, even the flu or seasonal allergies, can bring on a foggy mind. Relieving the cause should bring physical relief, and changing the body chemistry should eliminate the fog. All you need is a cue to help you remember that your sunglasses are sitting above your eyebrows.

References

Herrmann W, Obeid R.
Homocysteine: a biomarker in neurodegenerative diseases.
Clin Chem Lab Med. 2011 Mar;49(3):435-41.

Stolp HB, Dziegielewska KM.
Review: Role of developmental inflammation and blood-brain barrier dysfunction in neurodevelopmental and neurodegenerative diseases.
Neuropathol Appl Neurobiol. 2009 Apr;35(2):132-46.

Faux NG, Ellis KA, Porter L, Fowler CJ, Laws SM, Martins RN, Pertile KK, Rembach A, et al
Homocysteine, Vitamin B12, and Folic Acid Levels in Alzheimer’s Disease, Mild Cognitive Impairment, and Healthy Elderly: Baseline Characteristics in Subjects of the Australian Imaging Biomarker Lifestyle Study.
J Alzheimers Dis. 2011 Sep 2.

Kelly GS
Folates: supplemental forms and therapeutic applications.
Altern Med Rev. 1998 Jun;3(3):208-20.

Jyme H. Schafer, MD, MPH; Thomas A. Glass, PhD; Karen I. Bolla, PhD; Margaret Mintz, MS; Anne E. Jedlicka, MS; Brian S. Schwartz, MD, MS
Homocysteine and Cognitive Function in a Population-based Study of Older Adults
J Am Geriatr Soc. 2005;53(3):381-388

Selhub J, Troen A, Rosenberg IH.
B vitamins and the aging brain.
Nutr Rev. 2010 Dec;68 Suppl 2:S112-8.

Schulz RJ.
Homocysteine as a biomarker for cognitive dysfunction in the elderly
Curr Opin Clin Nutr Metab Care. 2007 Nov;10(6):718-23.

Aron M. Troen, Melissa Shea-Budgell, Barbara Shukitt-Hale, Donald E. Smith, Jacob Selhub, and Irwin H. Rosenberg
B-vitamin deficiency causes hyperhomocysteinemia and vascular cognitive impairment in mice
PNAS August 26, 2008 vol. 105 no. 34 12474-12479

Roberts RO, Geda YE, Knopman DS, Boeve BF, Christianson TJ, Pankratz VS, Kullo IJ, Tangalos EG, Ivnik RJ, Petersen RC.
Association of C-reactive protein with mild cognitive impairment.
Alzheimers Dement. 2009 Sep;5(5):398-405.

Mancinella A, Mancinella M, Carpinteri G, Bellomo A, Fossati C, Gianturco V, Iori A, Ettorre E, Troisi G, Marigliano V.
Is there a relationship between high C-reactive protein (CRP) levels and dementia?
Arch Gerontol Geriatr. 2009;49 Suppl 1:185-94.

Herrmann W
Significance of hyperhomocysteinemia.
Clin Lab. 2006;52(7-8):367-74.

*These statements have not been evaluated by the FDA.
These products are not intended to treat, diagnose, cure, or prevent any disease.

Cell Phone Radio Frequency And Child Behavior

Radiation-Cell-phoneUntil we’ve mastered the art of telepathy as a means of universal communication, we’re stuck with the cell phone and all that it brings to the table, some of which can be anticipated, like the bill at the end of the month, and some that can’t be expected, like the radio frequency radiation that is alleged to change your unborn child from Mother Teresa to Attila the Hun. Funny thing about science, there’s a study for everything, except for why the eye of a needle is not at the other end.

It has been assumed that using a cell phone in front of your unborn child will render cerebral changes in him/her that will eventuate into attention deficit and hyperactivity. Such is the conclusion of a group of Yale School of Medicine researchers who worked with mice. The authors of this study noted an increase of neurobehavioral disorders in children and decided to look for a cause. To be fair to researchers, mice are used in the laboratory because some of their metabolic characteristics parallel those of humans, and because they mature quickly enough to track their development in a reasonable time span. They also share 99% of their genes with humans.

In this experiment, pregnant mice were exposed to an activated, but muted, cell phone suspended above their cage, while a pregnant control group was exposed to a deactivated phone. As adults, those mice subjected to cell phone radiation as fetuses tended to be more hyperactive and had reduced memory capacity compared to the controls. The outcome was attributed to dose-responsive impaired glutamatergic synaptic transmission onto layer V pyramidal neurons of the prefrontal cortex. Got it?  Not exactly a topic at your next cocktail party, this scientific crooning means that the neurological wires in the front part of the brain don’t develop the right way. This is the section of the brain in charge of complex cognitive behaviors, personality expression, decision making and social behavior.  Like other pronouncements in the research world, “further experiments are needed…to determine the risk of exposure during pregnancy.”  (Aldad, 2012)

Rodent pregnancies typically last fewer than three weeks, and the brains of newborn mice are far less developed than those of human babies. Despite the findings, potential risks in humans might not be similar. However, in human studies done in Germany, scientists found that about 6% of children who were exposed to radio-frequency electromagnetic fields at any time in their existence exhibited “abnormal mental behavior.”  Here, too, “more studies…are warranted…”  (Thomas, 2010)

If a definitive case can be made for the hazard of cell phone radiation, it’ll certainly be a major public health concern. But a trend in this direction might have been established in a Danish study that recruited the cell-phone-using mothers of more than 13,000 children. The mothers were enrolled early in their pregnancies, and seven years later were asked to submit a subjective questionnaire regarding the current health and behavior status of their school-aged children. Those children who had prenatal or postnatal exposure to cell phone use demonstrated greater association with behavioral difficulties and hyperactivity. (Divan, 2008)  Other, confounding, factors may have come into play, though, including diet, lifestyle and permissiveness, exposure to environmental contaminants such as heavy metals, and genetics. Cognitive and language development seem not to be affected by cell phones, as evidenced in a subsequent study by the same research team. (Divan, 2011)

Repeatability is characteristic of a well-constructed study. To ascertain the results of their 2008 report, Divan and colleagues duplicated that work, but with more than twice the number of subjects and the consideration of the confounders. The findings were the same:  prenatal and postnatal cell phone use is associated with behavior problems in school-aged children. (Divan, 2010)  To confuse the issue, Spanish researchers found little evidence of abnormal neurodevelopment in a prenatal group exposed to cell phone radiation when tested at 14-months of age and compared to a group of nonusers. (Vrijheid, 2010)  What seems to be needed is a longitudinal study, one that tracks the development of, and tests, the same group of users and nonusers over a period of time, maybe ten or more years.

If the results of a ten-year study were absolutely definitive of cell phone culpability, it’s unlikely that patterns of cell phone use would change, despite a risk of uncomfortable child behavior. Returning to the dark ages of landlines is unthinkable. Besides, in a few years the problem will belong to somebody else. What self-respecting parent would sacrifice immediate convenience for the future?

References

Divan HA, Kheifets L, Obel C, Olsen J.
Prenatal and postnatal exposure to cell phone use and behavioral problems in children.
Epidemiology. 2008 Jul;19(4):523-9.

Divan HA, Kheifets L, Obel C, Olsen J.
Cell phone use and behavioural problems in young children.
J Epidemiol Community Health. 2010 Dec 7. [Epub ahead of print]

Divan HA, Kheifets L, Olsen J.
Prenatal cell phone use and developmental milestone delays among infants.
Scand J Work Environ Health. 2011 Jul;37(4):341-8. doi: 10.5271/sjweh.3157. Epub 2011 Mar 14.

Tamir S. Aldad, Geliang Gan, Xiao-Bing Gao, & Hugh S. Taylor
Fetal Radiofrequency Radiation Exposure From 800-1900 Mhz-Rated Cellular Telephones Affects Neurodevelopment and Behavior in Mice
Scientific Reports. Volume:2 ,Article number:312  doi:10.1038/srep00312  15 March 2012

Thomas S, Heinrich S, von Kries R, Radon K.
Exposure to radio-frequency electromagnetic fields and behavioural problems in Bavarian children and adolescents.
Eur J Epidemiol. 2010 Feb;25(2):135-41. Epub 2009 Dec 4.

Vrijheid M, Martinez D, Forns J, Guxens M, Julvez J, Ferrer M, Sunyer J.
Prenatal exposure to cell phone use and neurodevelopment at 14 months.
Epidemiology. 2010 Mar;21(2):259-62.

*These statements have not been evaluated by the FDA.
These products are not intended to treat, diagnose, cure, or prevent any disease.

Lead And Violent Behavior

police-lineWhat’s This?

Childhood exposure to lead dust has been associated with enduring physical and behavioral effects.  Recent exploration into this public health menace has revealed that leaded gasoline, used to reduce engine knocking and to modify octane levels from the 1920’s to the 1970’s, is no less involved in the damage than the lead from paint and water supply lines (either from solder or from lead pipes).  The city air that was contaminated by vehicle exhaust decades ago has been linked to increased violent crime.  You might wonder how lead would stay in the air for decades.  It usually doesn’t, but lead particles land on the lawn, the sidewalk, the playground, and waft into your front door, alighting on the carpet and furniture.

Recent research by Tulane toxicologist Howard W. Mielke and demographer Sammy Zahran, from Colorado State University’s Center for Disaster and Risk Analysis, compared the amount of lead released in six American cities:  Atlanta, Chicago, Indianapolis, Minneapolis, New Orleans, and San Diego, covering the span from 1950 to 1985.  The changes in lead values during those years were matched by parallel ups and downs of aggravated assaults, as garnered from FBI records.  The analysis of data revealed that for each one percent increase in airborne lead dust exposure there was a related increase in aggravated assault by a half percent (Mielke and Zahran, 2012).

Lead has been used for thousands of years, poisoning people along the way.  The complete picture of lead’s toxicity was barely realized until the second half of the 20th century, when it was finally admitted that there is no safe threshold for lead exposure—there is no known amount of lead too small to do damage.

Developing fetuses are susceptible to the lead contamination of their mothers, and are likely to be premature or of low birth weight, especially for first delivery (Torres-Sanchez, 1999) (Cleveland, 2008).  Because their bodies are smaller and in a constant state of growth and development, children are more at risk for lead poisoning.   They absorb it faster, suffering more physical harm than an adult, and because they spend time on the floor learning to crawl and walk, their exposure is pronounced.  It’s common to see slow development of expected childhood milestones, such as talking and combining words, in cases such as this, which often eventuate to loss of appetite, abdominal distress and vomiting, weight loss, constipation, anemia, kidney failure, irritability, lethargy, failure to thrive, learning disabilities and behavioral problems (Landrigan, 2002).  Early lead exposure is decidedly prophetic of later neurological abnormalities (Nie, 2011), reduced IQ among them.  Blood lead concentrations that peak at age two are thought to lower IQ scores at ages 4 to 6, when IQ becomes sufficiently stable to measure (Chen, 2005).

How Did It Get There?

By this time you might think this is more an urban concern than a suburban or rural one.  Depending on the age of the domicile, you’re partly right.  Regardless of location, many, if not most, homes built prior to 1978 were slathered with lead paint inside and out.  Because lead tastes sweet, flakes of it found their way into the mouths of toddlers, not only from walls and trim, but also from furniture and toys.  The rail of a crib often served as a teething ring.  Urban environs are more likely to house factories and industries that either produce lead-related goods, including batteries, wire and pipes, some medical equipment, ceramic glazes, ammunition, and circuit boards, or that recycle such commodities.  That would increase the odds of lead exposure by a substantial margin.  And the plumbing use of lead in solder and pipe joining was ubiquitous until the advent of plastics.  On the rural side of this coin sit lead-tainted pesticides and exhaust particles from agricultural equipment and contaminated ground water from airborne lead sources miles away.  Not many people eat game harvested with lead ammunition, so that source is not worth the mention.  Ingesting a bullet or a piece of lead shot is a remote probability.

Attitude Adjustment

Lead exposure is not limited to the United States, but is problematic wherever there is cultural and industrial development.  The birth-to-twenty cohort recently studied in South Africa, comprising more than a thousand adolescents, demonstrated a relationship of lead exposure to rule breaking and aggressive behavior (Naicker, 2012).  To explain this behavioral anomaly, scientists looked for a neuroanatomical commonality, discovering decreases in brain volume associated with childhood lead levels.  In this inquiry they found that total brain gray matter is inversely associated with blood lead concentration, particularly in the area of the brain responsible for relaying nerve signals between the right and left hemispheres, a spot that controls rational cognitive functions as well as autonomic functions such as the regulation of blood pressure, digestion and respiration (Cecil, 2008).  Gray matter volume loss was more obvious in males than in females.  The result is that lead affects the prefrontal cortex so dramatically that executive function and decision-making suffer, leading to persistent antisocial behavior (Tiihonen, 2008).

Society has associated underprivileged life with increased odds of criminal activity, but was heretofore unable to put a finger on causality.  Acceptable lead levels for children have been 10 micrograms per deciliter.  This was to have been lowered to 5 mcg/dL by 2012.  Adult levels have been established at 25 mcg/dL.  In children, an increase from 10 to 20 mcg is associated with almost a three point drop in IQ (Schwartz, 1994), affecting levels of GABA, which slows down the activity of nerve cells in the brain, and of NMDA, which is an amino acid derivative labeled as an excitotoxin that wires up neuronal circuits (Watkins, 2006).  Lead exposure crosses socio-economic lines and thus becomes an equal opportunity toxicant that is related even to ADD/ADHD disorders (Nigg, 2010).  A staggering declaration made by the National Center for Healthy Housing, after analyzing reports from The USA, Britain, Canada, Australia, France, Italy, West Germany, and New Zealand, suggests that murder could be associated with more severe cases of childhood lead poisoning, (Nevin, 2007).  The urban underprivileged may have been exposed to more lead residue (Cleveland, 2008) from gasoline, paint, and food can solder than their rural counterparts, so much so that traces of lead have been found in the enamel of their teeth (Cleymaet, 1991) (Uryu, 2003), levels of which tripled from 1930’s to the mid 60’s.

As of 2002, more than a million housing units offered shelter to low-income families (earning < $30 K yearly) with children under age six.  Of those, 17% of government-subsidized units had hazards.  Thirty-five percent of all low-income families had hazards.  For families with modestly higher earnings, it’s 19%.  Understandably, the greatest risks appear in dwellings that are antiquated, often also having high lead concentrations in the soil.  Housing in the Northeast had twice the danger of the rest of the country.

What To Do?

Removal of heavy metals, notably lead, mercury and cadmium, is important to body function at the cellular level.  The traditional medical approach to chelation, the process whereby the chelator binds to the metal and carries it away from the body, might use succimer, which is an analogue of dimercaprol, a toxic substance with a small therapeutic range and many adverse side effects.  In a succimer trial sponsored by the National Institute of Environmental Health Sciences that enrolled almost eight hundred children with blood lead levels from 20-40 mcg/dL, the lead values of the study group decreased with succimer, but also did their IQ’s by a single point, which seems insignificant.  But what is significant is that their behavior worsened, as reported on a parent assessment scale, leading investigators to infer that this treatment may not be ideal for children with lead levels in the particular range, citing accompanying decline in tests of cognition and psychological function (Rogan, 2001).  Later study at the University of Cincinnati that followed a like protocol also noted a decrease in blood lead levels, but, too, a lack of benefit for cognitive, learning/memory, attention, and neuromotor skills, drawing researchers to the same conclusion (Dietrich, 2004).

As a chelator, chlorella vulgaris has been found to reduce damage by lead exposure and to maintain the integrity of bone marrow (Queiroz, 2003), while reducing lead levels in blood and tissues and restoring liver function (Queiroz, 2008).  Later study found chlorella to restore the activity of natural killer cells and to reverse the zinc loss caused by lead exposure (Queiroz, 2011).  Ascorbic acid, vitamin C, has been known to handle lead problems since the late 1930’s, when scientists found lead-exposed factory workers to respond to daily doses of vitamin C and to excrete lead in their urine (Holmes, 1939).  Sixty years later, investigators saw lead levels decline as ascorbic acid levels increased in the general population having baseline lead values of 15 mcg/dL or higher (Simon, 1999).  Though both these modalities were shown to reduce lead levels, no commentary about cognitive or behavioral character is retrieved from these studies.  Sadly, lead stored in bone can leach into the blood even after chelation is deemed successful.

Where lead levels are high, trace mineral levels may be low, and probably are.  The earnest and judicious use of minerals that belong in the body may be able to push out those that do not belong and, by virtue of their own properties, rescue the mental and physical domains transgressed upon by lead and other heavy metals.

References

Bakhireva LN, Rowland AS, Young BN, Cano S, Phelan ST, Artyushkova K, Rayburn WF, Lewis J.
Sources of Potential Lead Exposure Among Pregnant Women in New Mexico.
Matern Child Health J. 2012 Feb 24. [Epub ahead of print]

Bellinger DC.
Lead.
Pediatrics. 2004 Apr;113(4 Suppl):1016-22

Bouchard MF, Bellinger DC, Weuve J, Matthews-Bellinger J, Gilman SE, Wright RO, Schwartz J, Weisskopf MG.
Blood lead levels and major depressive disorder, panic disorder, and generalized anxiety disorder in US young adults.
Arch Gen Psychiatry. 2009 Dec;66(12):1313-9.

Carpenter DO, Nevin R.
Environmental causes of violence.
Physiol Behav. 2010 Feb 9;99(2):260-8. Epub 2009 Sep 14.

Cecil KM, Brubaker CJ, Adler CM, Dietrich KN, Altaye M, Egelhoff JC, Wessel S, Elangovan I, Hornung R, Jarvis K, Lanphear BP.
Decreased brain volume in adults with childhood lead exposure.
PLoS Med. 2008 May 27;5(5):e112.

Chen A, Dietrich KN, Ware JH, Radcliffe J, Rogan WJ.
IQ and blood lead from 2 to 7 years of age: are the effects in older children the residual of high blood lead concentrations in 2-year-olds?
Environ Health Perspect. 2005 May;113(5):597-601.

Aimin Chen, MD, PhD
Improving Behavior of Lead-Exposed Children: Micronutrient Supplementation, Chelation, or Prevention
The Journal of Pediatrics.  Volume 147, Issue 5 , Pages 570-571, November 2005

Chen A, Cai B, Dietrich KN, Radcliffe J, Rogan WJ.
Lead exposure, IQ, and behavior in urban 5- to 7-year-olds: does lead affect behavior only by lowering IQ?
Pediatrics. 2007 Mar;119(3):e650-8

Cleveland LM, Minter ML, Cobb KA, Scott AA, German VF.
Lead hazards for pregnant women and children: part 1: immigrants and the poor shoulder most of the burden of lead exposure in this country. Part 1 of a two-part article details how exposure happens, whom it affects, and the harm it can do.
Am J Nurs. 2008 Oct;108(10):40-9; quiz 50.

Cleymaet R, Collys K, Retief DH, Michotte Y, Slop D, Taghon E, Maex W, Coomans D.
Relation between lead in surface tooth enamel, blood, and saliva from children residing in the vicinity of a non-ferrous metal plant in Belgium.
Br J Ind Med. 1991 Oct;48(10):702-9.

Dietrich KN, Ware JH, Salganik M, Radcliffe J, Rogan WJ, Rhoads GG, Fay ME, Davoli CT, Denckla MB, Bornschein RL, Schwarz D, Dockery DW, Adubato S, Jones RL; Treatment of Lead-Exposed Children Clinical Trial Group.
Effect of chelation therapy on the neuropsychological and behavioral development of lead-exposed children after school entry.
Pediatrics. 2004 Jul;114(1):19-26.

Holmes HN, Amberg EJ, Campbell K.
VITAMIN C TREATMENT IN LEAD POISONING.
Science. 1939 Apr 7;89(2310):322-3.
http://www.seanet.com/~alexs/ascorbate/193x/holmes-hn-etal_j_lab_clin_med-1939-v23-n11-p1119.html

Houston DK, Johnson MA.
Does vitamin C intake protect against lead toxicity?
Nutr Rev. 2000 Mar;58(3 Pt 1):73-5.

Howard W. Mielke, Sammy Zahran
The urban rise and fall of air lead (Pb) and the latent surge and retreat of societal violence
Environment International. Volume 43, August 2012, Pages 48–55

Jacobs DE, Clickner RP, Zhou JY, Viet SM, Marker DA, Rogers JW, Zeldin DC, Broene P, Friedman W.
The prevalence of lead-based paint hazards in U.S. housing.
Environ Health Perspect. 2002 Oct;110(10):A599-606.

Koike S.
[Low-level lead exposure and children’s intelligence from recent epidemiological studies in the U.S.A. and other countries to progress in reducing lead exposure and screening in the U.S.A].
Nihon Eiseigaku Zasshi. 1997 Oct;52(3):552-61.

Kordas K, Stoltzfus RJ, López P, Rico JA, Rosado JL.
Iron and zinc supplementation does not improve parent or teacher ratings of behavior in first grade Mexican children exposed to lead.
J Pediatr. 2005 Nov;147(5):632-9.

Landrigan PJ, Schechter CB, Lipton JM, Fahs MC, Schwartz J.
Environmental pollutants and disease in American children: estimates of morbidity, mortality, and costs for lead poisoning, asthma, cancer, and developmental disabilities.
Environ Health Perspect. 2002 Jul;110(7):721-8.

Naicker N, Richter L, Mathee A, Becker P, Norris SA.
Environmental lead exposure and socio-behavioural adjustment in the early teens: the birth to twenty cohort.
Sci Total Environ. 2012 Jan 1;414:120-5. Epub 2011 Dec 3.

Nevin R.
How lead exposure relates to temporal changes in IQ, violent crime, and unwed pregnancy.
Environ Res. 2000 May;83(1):1-22.

Nevin R.
Understanding international crime trends: the legacy of preschool lead exposure.
Environ Res. 2007 Jul;104(3):315-36. Epub 2007 Apr 23.

Nie LH, Wright RO, Bellinger DC, Hussain J, Amarasiriwardena C, Chettle DR, Pejović-Milić A, Woolf A, Shannon M.
Blood lead levels and cumulative blood lead index (CBLI) as predictors of late neurodevelopment in lead poisoned children.
Biomarkers. 2011 Sep;16(6):517-24. doi: 10.3109/1354750X.2011.604133. Epub 2011 Aug 9.

Nigg JT, Nikolas M, Mark Knottnerus G, Cavanagh K, Friderici K.
Confirmation and extension of association of blood lead with attention-deficit/hyperactivity disorder (ADHD) and ADHD symptom domains at population-typical exposure levels.
J Child Psychol Psychiatry. 2010 Jan;51(1):58-65. Epub 2009 Nov 23.

Queiroz ML, Rodrigues AP, Bincoletto C, Figueirêdo CA, Malacrida S.
Protective effects of Chlorella vulgaris in lead-exposed mice infected with Listeria monocytogenes.
Int Immunopharmacol. 2003 Jun;3(6):889-900.

Queiroz ML, Torello CO, Perhs SM, Rocha MC, Bechara EJ, Morgano MA, Valadares MC, Rodrigues AP, Ramos AL, Soares CO.
Chlorella vulgaris up-modulation of myelossupression induced by lead: the role of stromal cells.
Food Chem Toxicol. 2008 Sep;46(9):3147-54. Epub 2008 Jul 19.

Queiroz ML, da Rocha MC, Torello CO, de Souza Queiroz J, Bincoletto C, Morgano MA, Romano MR, Paredes-Gamero EJ, Barbosa CM, Calgarotto AK.
Chlorella vulgaris restores bone marrow cellularity and cytokine production in lead-exposed mice.
Food Chem Toxicol. 2011 Nov;49(11):2934-41. Epub 2011 Jul 26.

Rogan WJ, Dietrich KN, Ware JH, Dockery DW, Salganik M, Radcliffe J, Jones RL, Ragan NB, Chisolm JJ Jr, Rhoads GG; Treatment of Lead-Exposed Children Trial Group.
The effect of chelation therapy with succimer on neuropsychological development in children exposed to lead.
N Engl J Med. 2001 May 10;344(19):1421-6.

Schwartz J.
Low-level lead exposure and children’s IQ: a meta-analysis and search for a threshold.
Environ Res. 1994 Apr;65(1):42-55.

Simon JA, Hudes ES.
Relationship of ascorbic acid to blood lead levels.
JAMA. 1999 Jun 23-30;281(24):2289-93.

Tiihonen J, Rossi R, Laakso MP, Hodgins S, Testa C, Perez J, Repo-Tiihonen E, Vaurio O, Soininen H, Aronen HJ, Könönen M, Thompson PM, Frisoni GB.
Brain anatomy of persistent violent offenders: more rather than less.
Psychiatry Res. 2008 Aug 30;163(3):201-12. Epub 2008 Jul 26.

Luisa E. Torres-Sánchez, Gertrud Berkowitz, Lizbeth López-Carrillo, Laura Torres-Arreola, et al
Intrauterine LeadExposure and Preterm Birth
Environmental Research. Volume 81, Issue 4, November 1999, Pages 297–301

Uryu T, Yoshinaga J, Yanagisawa Y, Endo M, Takahashi J.
Analysis of lead in tooth enamel by laser ablation-inductively coupled plasma-mass spectrometry
Anal Sci. 2003 Oct;19(10):1413-6.

Watkins JC, Jane DE.
The glutamate story.
Br J Pharmacol. 2006 Jan;147 Suppl 1:S100-8.

Wright JP, Dietrich KN, Ris MD, Hornung RW, Wessel SD, Lanphear BP, Ho M, Rae MN.
Association of prenatal and childhood blood lead concentrations with criminal arrests in early adulthood.
PLoS Med. 2008 May 27;5(5):e101.

*These statements have not been evaluated by the FDA.
These products are not intended to treat, diagnose, cure, or prevent any disease.

Electromagnetic Headaches

emf-headachesWhen it blows in the wind, we try to find out where it’s coming from. Once in a while, though, there’s so much stench we can’t identify the source. Such is the case with electromagnetic fields—EMF’s— and related wavy things. There’s so much hullabaloo about the good and the bad that we can’t decide if EMF’s are, well, good or bad. They’ve been around forever, so exposure to them is nothing new. Man-made EMF’s, from the generation of electricity, household appliances, industrial equipment and, of course, telecommunications and broadcasting, add to the apparent physiological burden already begun by the simplicity of human metabolism and Earth’s magnetic properties. Is it really a big deal?

Tiny electric currents exist in the body because of the chemistry that allows it to work, even in the absence of external electrical fields. Nerves, for example, send signals by transmitting electrical impulses. All our biochemical reactions follow the rearrangement of charged particles. Your heart responds to an electrocardiogram, right? The concern is that low-frequency electrical fields affect the human body just as they affect anything else made from charged particles. These exogenous fields, if large enough, can cause changes inside the body by stimulating nerves or muscles…or organs. Lucky for us, most exogenous currents are too small to have any ill effect, even directly beneath a high voltage transmission line. On the other hand, the biological effect of radiofrequency fields is heating, and this is the reason for scientific intervention in the placement of sources, such as phone towers.

Biological effects are measurable responses to a stimulus or to a change in the environment. Most of these are harmless, like listening to music or exercising. Changes that are irreversible or that persist for a long time might not be harmless. Electromagnetic fields above a certain level present a concern. That is understandable, and measures are taken to limit exposure, even internationally. Lower levels, over the long term, are suspected of causing unwanted biological responses, including headaches, to which some people are more or less sensitive. Cases of hypersensitivity to EMF’s have been reported for a few decades. Some researchers group them with the condition known as multiple chemical sensitivity illness. Oddly, a plethora of those reporting such sensitivity seem to fall into categories that defy characterization (Levallois, 2002). In polls and surveys, people will express a concern about the ill effects of EMF’s in the absence of personal symptoms, worrying that their cell phones may eventually cause sleep disturbances and headaches (Schreier, 2006) (Hillert, 2002).

Cell phones emit waves as long as they’re turned on and are looking for a signal from the tower. Wi-Fi, not necessarily related to wireless fidelity, contains that technology which connects electronic devices to each other and to the internet using radio waves. Some investigators claim that both can interfere with a child’s ability to learn and remember, while others feel that autistic spectrum conditions are likewise related (Herbert, 2013, parts 1 and 2). If the pharmaceutical powers control a considerable part of the economy, they deserve credit for telling us in their TV spiels that the side effects of their products are worse than the diseases they purport to treat. Powerful industrial entities have an interest in leading the unsuspecting public to believe their EMF’s are completely harmless, since they cannot be perceived by the senses, including pain receptors. If, as suspected, DNA damage actually results from EMF-induced oxidative stress, physiologic consequences can be expected and headaches to be the presentation (Wolf, 2005). Children are exposed to EMF’s at home, on the school bus, in the classroom, at the doctor’s office, and probably everywhere else, with few exceptions, if any. Cell phone standards, by the way, were established years ago and have not been revisited. We are unsure of their effects on developing brains, but, by looking at students’ academic orientation, we can guess. Most European nations forbid the sale of cell phones to those under eighteen.

Cause-effect situations are more definitive than associations or relations. Pathologies that may be associated with EMF’s are not definitely caused by them. Therefore, compared to other disease vectors, little is being done to address possibilities of EMF involvement. Some reports indicate the blood-brain barrier to become more permeable after exposure to EMF’s (Leszczynski, 2002), even from fellow riders in a public conveyance (Kato, 2012). That we are constantly bombarded with radiation is a concern of WHO and the children’s health expert panel (WHO, 2011) (ICNIRP, 2009), (IEEE, 2005). But that concern is magnified because mobile phones work close to the head, causing the distribution of energy to be direct. This raises the question of relationships/associations to glioma and neuroma (Hours, 2007) (Schüz, 2006) naturally requiring closer inspection. Because of subjectivity, no determination is possible (Cardis, 2010), although hints are numerous (Cardis, 2011).

Cancer aside, the headache issue is a global topic. In many countries, about a fourth of cell phone users polled associate headache with EMF (Thamire, 2004) (Meg, 2005) (Al-Khlaiwi, 2004) (Genius, 2012) (Kato, 2012) (Schreier, 2006). Yet, until asked, none relates the two. Talking on a mobile phone for one hour a day incurs the cumulative effect that upsets homeostasis, allowing for exposure to ten thousand watts of accrued radiation. A microwave oven emits only 2 milliwatts at two inches distance; a hundredth of that at twenty inches (FDA, 2011).

We all know that lifestyle can’t be dictated. Smokers smoke and drinkers drink.Second-hand smoke is a health matter. There is no such thing as second-hand drinkingexcept to a fetus. But there is such a thing as second-hand radiation. We seemto prefer first-hand.

References

Al-Khlaiwi T, Meo SA.
Association of mobile phone radiation with fatigue, headache, dizziness, tension and sleep disturbance in Saudi population.
Saudi Med J. 2004 Jun;25(6):732-6.

Augner C, Hacker GW.
Are people living next to mobile phone base stations more strained? Relationship of health concerns, self-estimated distance to base station, and psychological parameters.
Indian J Occup Environ Med. 2009 Dec;13(3):141-5.

Belyaev IY, Hillert L, Protopopova M, Tamm C, Malmgren LO, Persson BR, Selivanova G, Harms-Ringdahl M.
915 MHz microwaves and 50 Hz magnetic field affect chromatin conformation and 53BP1 foci in human lymphocytes from hypersensitive and healthy persons.
Bioelectromagnetics. 26(3):173-184, 2005.

Belyaev IY, Markovà E, Hillert L, Malmgren LO, Persson BR.
Microwaves from UMTS/GSM mobile phones induce long-lasting inhibition of 53BP1/gamma-H2AX DNA repair foci in human lymphocytes.
Bioelectromagnetics. 2008 Oct 6. [Epub ahead of print]

Cardis E, Deltour I, Vrijheid M, Combalot E, Moissonnier M, Tardy H, Armstrong B, et al
INTERPHONE Study Group.
Brain tumour risk in relation to mobile telephone use: results of the INTERPHONE international case-control study.
Int J Epidemiol. 2010 Jun;39(3):675-94.

Cardis E, Armstrong BK, Bowman JD, Giles GG, Hours M, Krewski D, McBride M, Parent ME, et al
Risk of brain tumours in relation to estimated RF dose from mobile phones: results from five Interphone countries.
Occup Environ Med. 2011 Sep;68(9):631-40.

Dahmen N, Ghezel-Ahmadi D, Engel A.
Blood laboratory findings in patients suffering from self-perceived electromagnetic hypersensitivity (EHS). Bioelectromagnetics. 30(4):299-306, 2009.

Eltiti S, Wallace D, Ridgewell A, Zougkou K, Russo R, Sepulveda F, Mirshekar-Syahkal D, Rasor P, Deeble R, Fox E.
Does short-term exposure to mobile phone base station signals increase symptoms in individuals who report sensitivity to electromagnetic fields? A double-blind randomized provocation study.
Environ Health Perspect. 2007 Nov;115(11):1603-8.

FDA. 2011
Microwave Oven Radiation
http://www.fda.gov/radiation-emittingproducts/resourcesforyouradiationemittingproducts/ucm252762.htm

Furubayashi T, Ushiyama A, Terao Y, Mizuno Y, Shirasawa K, Pongpaibool P, Simba AY, et al.
Effects of short-term W-CDMA mobile phone base station exposure on women with or without mobile phone related symptoms.
Bioelectromagnetics. 30(2):100-113, 2009.

Genuis SJ, Lipp CT.
Electromagnetic hypersensitivity: fact or fiction?
Sci Total Environ. 2012 Jan 1;414:103-12.

Herbert MR, Sage C.
Autism and EMF? Plausibility of a pathophysiological link – Part I.
Pathophysiology. 2013 Jun;20(3):191-209.

Herbert MR, Sage C
Autism and EMF? Plausibility of a pathophysiological link part II.
Pathophysiology. 2013 Jun;20(3):211-34.

Hietanen M, Hämäläinen A-M, Husman T.
Hypersensitivity symptoms associated with exposure to cellular telephones: No causal link. Bioelectromagnetics 23:264-270, 2002.

Hillert L, Berglind N, Arnetz BB, Bellander T.
Prevalence of self-reported hypersensitivity to electric or magnetic fields in a population-based questionnaire survey.
Scand J Work Environ Health. 2002 Feb;28(1):33-41.

Hours M, Bernard M, Montestrucq L, Arslan M, Bergeret A, Deltour I, Cardis E.
Cell Phones and Risk of brain and acoustic nerve tumours: the French INTERPHONE case-control study.
Rev Epidemiol Sante Publique. 2007 Oct;55(5):321-32.

Institute of Electrical and Electronics Engineers (IEEE).
IEEE standard for safety levels with respect to human exposure to radio frequency electromagnetic fields, 3 kHz to 300 GHz, IEEE Std C95.1, 2005.

International Commission on Non-Ionizing Radiation Protection (ICNIRP).
Statement on the “Guidelines for limiting exposure to time-varying electric, magnetic and electromagetic fields (up to 300 GHz)”, 2009.

Johansson A, Nordin S, Heiden M, Sandström M.
Symptoms, personality traits, and stress in people with mobile phone-related symptoms and electromagnetic hypersensitivity.
J Psychosom Res. 68(1):37-45, 2010.

Kato Y, Johansson O.
Reported functional impairments of electrohypersensitive Japanese: A questionnaire survey.
Pathophysiology. 2012 Apr;19(2):95-100.

Kim DW, Lee JH, Ji HC, Kim SC, Nam KC, Cha EJ.
Physiological effects of RF exposure on hypersensitive people by a cell phone.
Conf Proc IEEE Eng Med Biol Soc. 2008;1:2322-2325.

Landgrebe M, Hauser S, Langguth B, Frick U, Hajak G, Eichhammer P.
Altered cortical excitability in subjectively electrosensitive patients: results of a pilot study.
J Psychosom Res. 62(3):283-288, 2007.

Landgrebe M, Frick U, Hauser S, Langguth B, Rosner R, Hajak G, Eichhammer P.
Cognitive and neurobiological alterations in electromagnetic hypersensitive patients: results of a case-control study.
Psychol Med. 38(12):1781-1791, 2008.

Dariusz Leszczynski
EFFECT OF GSM MOBILE PHONE RADIATION ON BLOOD-BRAIN BARRIER (2002)
http://www.ursi.org/Proceedings/ProcGA02/papers/p1043.pdf

Levallois P, Neutra R, Lee G, Hristova L.
Study of self-reported hypersensitivity to electromagnetic fields in California.
Environ Health Perspect. 2002 Aug;110 Suppl 4:619-23.

Markova E, Hillert L, Malmgren L, Persson BR, Belyaev IY.
Microwaves from GSM Mobile Telephones Affect 53BP1 and gamma-H2AX Foci in Human Lymphocytes from Hypersensitive and Healthy Persons.
Environ Health Perspect. 113(9):1172-1177, 2005.

McCarty DE, Carrubba S, Chesson AL, Frilot C, Gonzalez-Toledo E, Marino AA.
Electromagnetic hypersensitivity: evidence for a novel neurological syndrome.
Int J Neurosci. 2011 Dec;121(12):670-6.

Meo SA, Al-Drees AM.
Mobile phone related-hazards and subjective hearing and vision symptoms in the Saudi population.
Int J Occup Med Environ Health. 2005;18(1):53-7.

Nieto-Hernandez R, Rubin GJ, Cleare AJ, Weinman JA, Wessely S.
Can evidence change belief? Reported mobile phone sensitivity following individual feedback of an inability to discriminate active from sham signals.
J Psychosom Res. 65(5):453-460, 2008.

Schreier N, Huss A, Röösli M.
The prevalence of symptoms attributed to electromagnetic field exposure: a cross-sectional representative survey in Switzerland.
Soz Praventivmed. 2006;51(4):202-9.

Schuz J, Böhler E, Berg G, Schlehofer B, Hettinger I, Schlaefer K, Wahrendorf J, Kunna-Grass K, Blettner M.
Cellular phones, cordless phones, and the risks of glioma and meningioma (Interphone Study Group, Germany).
Am J Epidemiol. 2006 Mar 15;163(6):512-20.

Simkó M, Mattsson MO.
Extremely low frequency electromagnetic fields as effectors of cellular responses in vitro: possible immune cell activation.
J Cell Biochem. 2004 Sep 1;93(1):83-92.

Thamire  Al-Khlaiwit,  Sultane A Meoos
Association of mobile phone radiation with fatigue, headache, dizziness, tension and sleep disturbance in Saudi population
Saudi Medical Journal 2004; Vol. (6): 732-736

WHO
Electromagnetic fields and public health: mobile phones
Fact sheet N°193. June 2011
http://www.who.int/mediacentre/factsheets/fs193/en/

Wolf FI, Torsello A, Tedesco B, Fasanella S, Boninsegna A, D’Ascenzo M, Grassi C, Azzena GB, Cittadini A.
50-Hz extremely low frequency electromagnetic fields enhance cell proliferation and DNA damage: possible involvement of a redox mechanism.
Biochim Biophys Acta. 2005 Mar 22;1743(1-2):120-9.

Yokus B, Cakir DU, Akdag MZ, Sert C, Mete N.
Oxidative DNA damage in rats exposed to extremely low frequency electro magnetic fields.
Free Radic Res. 2005 Mar;39(3):317-23.

*These statements have not been evaluated by the FDA.
These products are not intended to treat, diagnose, cure, or prevent any disease.