Vitamins for the Lungs

There's nothing quite so scary as seeing someone labor to breathe.  I think it goes without saying that lifestyle can have a signicant impact on lung disease when it comes to obesity, smoking cessation, exercise, and nutrition.  But for those suffering with asthma, chronic bronchitis, emphysema, or COPD and doing the necessary things to take care of themselves, here's a peak at some key supplements to take consistently to prevent or lessen further lung decline.  The aging lung will naturally morph without our permission and lung health for the long haul needs to be addressed ASAP before the years pass and it's too late.  Get aggressive with your health care (in all areas) before disease strikes.  If you have a problem breather in the home, get some supplements started TODAY!

There's a stepwise approach to airway management which includes short and long acting bronchodilators, antihistamines, steroids, meds such as Singular or Theophylline, which will hopefully prevent a trip to the Emergency Room.  I'm not advocating that you stop using what is necessary to breathe, but what should a person take as a vitamin regimen to help their lungs function better on a continual basis? 

Here's a great list to follow:

1.  Nutrient levels and lung function have been studied.  Higher levels of antioxidant vitamins (A,C, and E) along with selenium were associated with higher lung function values.  In fact, low intake of Vitamin C and to a lesser extent Vitamin A were associated with increased asthma risk.

2.  Omega-3 fatty acids, Vitamin C, and Zinc on pulmonary function tests and inflammatory markers in children demonstrated beneficial effects. 

3.  A 2009 article examining the role of Vitamin D in COPD concluded there was a dose-dependent association with improved pulmonary function. A multivitamin with Vitamin D is a great idea, or take it as a separate supplement as I do.

4.  A study appearing in late 2008 showed that glutathione, N-acetyl cysteine as well as dietary phenols (curcumin, resveratol, and green tea/quercetin) reduced free radicals and halted inflammation.  Halting inflammation in every way possible is a core strategy in preventing asthma episodes. 

5.  Low levels of hormones have been connected to patients with COPD.  A recent study in 2009 demonstrated that testosterone and DHEA levels were low in COPD patients and were related to lower FEV1, pO2, and PaCO2.  Estrogen and Progesterone use have been associated with improved pulmonary function in premenopausal females. 

6.  Stress and a poor immune system can make one susceptible to colds and breathing difficulties.  Boosting the immune system with great vitamins, adrenal support products, and key sleep supplements can improve more than just the lungs.  If you or one of your children are getting recurrent respiratory symptoms, you should seriously consider a good vitamin regimen.  For adults, you should also consider testing hormones and adrenal function to restore peak performance.


If you, a friend, or family member are suffering with breathing problems, get started on a great vitamin regimen.  And please make sure that you include these key supplements on a daily basis. I promote only pharmaceutical grade and high quality products for these types of needs.

To your good health,
Dr. Sonja

Need To Know Information:Asparatame and The Brain

K. Paul Stoller, M.D., FAAP

ABSTRACT

The artificial sweetener aspartame (6-methyl-1,2,3-oathiazine-4[3H]—one-2,2-dioxide salt of Lphenlalanyl-

2-methl-L-alpha-aspartic acid), is consumed, primarily in beverages, by a very large number

of Americans, causing significant elevations in plasma and brain phenylalanine levels. It is very likely that

aspartame, which was once considered a new chemical warfare agent by the US military has resulted in

an enormous toll in illness, disability, and death. The failure of the medical profession and many

governmental and other public health agencies to concern themselves with this ignored epidemic

parallels what has taken place with the use of Thimerosal in vaccines.

As with Thimerosal, the most grievous offense of the illegal approval and continued use of

aspartame pertain to the damage that this chemical can induce in infants and children. Moreover,

aspartame could affect subsequent generations born to mothers who were misled about the safety of this

and related chemicals. This paper will discuss the role of both aspartame and Thimersol in the pathology

of neurodegenerative disease.

INTRODUCTION

The chemicals we ingest may affect more than our own health.

They affect the health and vitality of future generations.

The danger is that many of these chemicals may not harm us

but will do silent violence to our children.

Senator Abraham S. Ribicoff (l971)

The artificial sweetener aspartame (6-methyl-1,2,3-oathiazine-4[3H]—one-2,2-dioxide salt of Lphenlalanyl-

2-methl-L-alpha-aspartic acid), is consumed, primarily in beverages, by a very large number

of Americans, causing significant elevations in plasma and brain phenylalanine levels. It is very likely that

aspartame, which was once considered a new chemical warfare agent by the US military has resulted in

an enormous toll in illness, disability, and death. The failure of the medical profession and many

governmental and other public health agencies to concern themselves with this ignored epidemic

parallels what has taken place with the use of Thimerosal in vaccines.As with Thimerosal, the most grievous offense of

 

the illegal approval and continued use of aspartame pertain to the damage that this chemical can induce in infants and

 

children. Moreover, aspartame could affect subsequent generations born to mothers who were misled about the safety of

 

this and related chemicals.

THE HISTORY OF ASPARTAME

In October 1980 the Public Board of Inquiry (PBOI) impaneled by the FDA to evaluate aspartame

safety found that the chemical caused an unacceptable level of brain tumors in animal testing. Based on

this fact, the PBOI ruled that aspartame should not be added to the food supply.

This ruling culminated 15 years of regulatory ineptitude, chicanery, and deception by the FDA and

the Searle drug company, aspartame’s discoverer and manufacturer (acquired by Monsanto in 1985), and

then started the ball rolling on two additional decades of maneuvering, manipulating, and dissembling by

the FDA, Searle, and Monsanto.

In 1965, a Searle scientist licked some of a new ulcer drug from his fingers and discovered the

sweet taste of aspartame. Searle’s early tests showed that aspartame produced microscopic holes and

tumors in the brains of experimental mice, epileptic seizures in monkeys, and was converted into

formaldehyde.

Despite of the information in its files, in 1974 the FDA approved aspartame as a dry-foods

additive. The renowned brain researcher, John Olney from Washington University in St. Louis reviewed

the available data and discovered two studies showing brain tumors in rats and petitioned the FDA for a

public hearing. Dr. Olney had already shown that aspartic acid (part of the aspartame molecule) caused

holes in the brains of rats. Aspartame also is one part phenylalanine, and one part methyl (or wood)

alcohol.

The FDA prevailed on Searle to refrain from marketing aspartame until after completion of the

hearing. In 1975, an FDA Special Commissioner’s Task Force reported serious problems with Searle’s

research that was conducted in a manner so flawed as to raise doubts about aspartame safety and create

the possibility of serious criminal intent. The FDA asked the US Attorney for Chicago to seek a grand jury

review of the monkey seizure study, but he let the statute of limitations run out, then (along with two

aides) proceeded to join Searle’s law firm.

In October 1980, the PBOI blocked aspartame marketing until the tumor studies could be

explained, and unless the commissioner overruled the board, the matter was closed. In November 1980,

Ronald Reagan was elected President and Donald Rumsfeld, president of Searle, joined the Reagan

White House. In January 1981, Rumsfeld told a sales meeting that he would call in his chips and get

aspartame approved – Dr. Arthur Hull Hayes, Jr. a pharmacologist and Defense Department contract

researcher became FDA commissioner and his first decision was to defy FDA advisors and approve

aspartame for dry foods. His last decision, before leaving his post because of improprieties (taking gifts

from Pharmaceutical companies) was to approve aspartame for soft drinks in 1983. He immediately

became senior medical advisor to Searle’s public relations firm for $1000/day. Rumsfeld received a $12

million bonus.

As soon as soft drinks with Nutrasweet began to be consumed, complaints began to arrive at the

FDA – dizziness, blurred vision, headaches, and seizures. The complaints were more serious than the

FDA has ever received on any food additive. In 1985, the FDA asked the Centers for Disease Control

(CDC) to review the first 650 complaints (there are now tens-of-thousands). The CDC found that the

symptoms in approximately 25% of cases stopped and then restarted with discontinuing the use of

aspartame and then restarting its use. The day the FDA released the CDC report, which they discounted,

Pepsi Cola announced its switch to aspartame with a worldwide media blitz.

At the same time, human brain tumors rose 10% and previously benign tumors turned virulent. An

FDA deputy commissioner said the data posed no problem; he then became Vice President of clinical

research for Searle.

Four hundred aspartame studies were done between 1985 and 1995. All of the studies Searle

paid for found no problem, but 100% of the studies paid for by non-industry sources raised questions.

NEUROTOXINS AS A FOOD ADDITIVE

The manifestations of aspartame disease in young children are myriad. They include severe

headache, convulsions, unexplained visual loss, rashes, asthma, gastrointestinal problems, obesity,

marked weight loss, hypoglycemia, diabetes, addiction (probably largely due to the methyl alcohol),

hyperthyroidism, and a host of neuropsychiatric features. The latter include extreme fatigue, irritability,

hyperactivity, depression, antisocial behavior (including suicide), poor school performance, the

deterioration of intelligence, and brain tumors.

An average aspartame-sweetened beverage would have a conservative aspartame content of

about 555 mg/liter, and therefore, a methanol equivalent of 56 mg/liter (56 ppm). For example, if a 25 kg

child consumed on a warm day, after exercising, two-thirds of a two-liter bottle of soft drink sweetened

with aspartame, that child would be consuming over 732 mg of aspartame (29 mg/kg). This alone

exceeds what the FDA considers the 99+-percentile daily consumption level of aspartame. The child

would also absorb over 70mg of methanol from that soft drink. This is almost ten times the Environmental

Protection Agency's recommended daily limit of consumption for methanol.

To look at the issue from another perspective, the literature reveals death from consumption of

the equivalent of 6 gm of methanol. It would take 200 12 oz. cans of soda to yield the lethal equivalent of

6 gm of methanol. According to FDA regulations, compounds added to foods that are found to cause

some adverse health effect at a particular usage level are actually permitted in foods only at much lower

levels. The FDA has established these requirements so that an adequate margin of safety exists to

protect particularly sensitive people and heavy consumers of the chemical. Section 170.22 of Title 21 of

the Code of Federal Regulations mandates that this margin of safety is 100-fold below the "highest noeffect"

level. If death has been caused by the methanol equivalent of 200 12 oz. cans of aspartame

sweetened soda, one hundredth of that level would be two cans of soda. The relationship of the lethal

dose to the "highest no effect" level has tragically not been determined for methanol but assuming very

conservatively that the level is one hundredth of the lethal dose, the FDA regulations should have limited

consumption to approximately 24 ounces of aspartame-sweetened soft drink per day.

The high ethanol/methanol ratio of alcoholic beverages must have a very significant protective

effect given that ethanol antidotes methanol, so ignore the argument that methanol already exists in

alcoholic beverages without untoward effects. This is absurd given that alcoholics have a much higher

incidence of cancer and other degenerative diseases, none of which can be attributed to ethanol alone. In

aspartame, the methanol is released, once in the body, unfettered by ethanol to be a pure poison.

The FDA allows a lower safety margin only when "evidence is submitted which justifies use of a

different safety factor." (21.C.F.R.170.22) No such evidence has been submitted to the FDA for methanol.

Thus, not only have the FDA's requirements for acute toxicity not been met, but also, no demonstration of

chronic safety has been made. The fact that methyl alcohol appears in other natural food products does

not exonerate its presence in aspartame, but increases greatly the danger of chronic toxicity developing

by adding another unnatural source of this dangerous cumulative toxin to the food system.

Since the amino acid phenylalanine can be neurotoxic, and can affect the synthesis of inhibitory

monoamine neurotransmitters, the phenylalanine in aspartame can mediate neurologic effects.

Chemicals and compounds that affect physiological systems are classified as drugs by the Food

and Drug Administration (FDA), and are subject to considerably more demanding regulatory procedures

than food constituents. Moreover, because food additives must be shown to be physiologically inert in

order to win initial FDA approval, once they have obtained this approval they are exempt from the

requirement, imposed on all drugs, that their safety be continuously monitored. Companies that

manufacture and use approved food additives are not obligated to monitor adverse reactions associated

with consumption of their product, nor to submit to the FDA reports of such adverse reactions; they are

also not required to carry out further government-mandated research programs to affirm their product's

safety.

However, the consumption of a number of food additives can cause physiological effects, which

include, for some, modification of the chemical composition and functional activities of the nervous

system.

1, 2 Moreover, in the case of aspartame these neural effects were largely unexplored prior to the

compound's addition to the food supply, and were not a factor in calculating the quantities that individuals

can safely consume (the ADI, or acceptable daily intake, currently set for aspartame at 50 mg/kg).

3 The effects of aspartame, and of certain other food additives, like caffeine, involve subtler biochemical

changes, as well as functional consequences that are demonstrable only in specially treated animals

4 (and possibly, by extrapolation, only in especially vulnerable people).

Although these physiological effects are unrelated to the reason that aspartame was placed in

food, they have important health implications given the very large number of people who consume

aspartame. If only 1% of the 100,000,000 Americans thought to consume aspartame ever exceed the

sweetener's ADI, and if only 1% of this group happen coincidentally to have an underlying disease that

makes their brains vulnerable to the effects of an aspartame-induced rise in brain phenylalanine levels,

then the number of people who might manifest adverse brain reactions attributable to aspartame would

still be about 10,000, a number on the same order as the number of neurologically related consumer

complaints already registered with the FDA and other federal agencies.

5, 6

Doses of aspartame, which are within the range actually consumed by some people can affect

the chemical composition of the brain, and thereby contribute to particular CNS sidle effects, including

headaches,

7 inappropriate behavior responses,8, 9 and seizures.10, 11

The major bio-chemical effect of aspartame, in humans, is to raise blood and, presumably, brain

phenylalanine levels

12; in contrast, its main effect in rodents is to raise blood (and brain) tyrosine levels,13,

14

and tyrosine is often the antidote to phenylalanine's effects on the brain. This species difference makes

questionable the extrapolation of much of the rodent literature to humans.

The existence of this major metabolic difference between rodents and people underscores the

point that only large-scale human studies could determine whether or not aspartame is risk-free. But

aspartame cannot be shown to be risk-free, and its regulatory classification should be changed, for

example, to that of a drug.

The Effect of Aspartame on Brain Phenylalanine Levels

The consumption of an aspartame-laden food or beverage contributes to the plasma the three

natural compounds contained within the aspartame molecule: the amino acids phenylalanine and aspartic

acid, and the alcohol methanol,

15 as well as various peptides (like B-aspartame or the aspartylphenylalanine

diketopoperazine that are formed from it spontaneously, on the shelf, or enzymatically,

after its consumption).

Plasma phenylalanine levels are not regulated by any known homeostatic mechanism. At any

particular time plasma levels simply reflect the amounts of phenylalanine being absorbed from the foods

most recently eaten.

16, 17 Consumption of the ADI aspartame dose is thus able to elevate plasma

phenylalanine levels about threefold.

18

Consumption of dietary phenylalanine in the usual way, as a constituent of protein, does not

elevate brain phenylalanine levels.

19 This is because the protein elevates plasma levels of the other large

neutral amino acids (LNAA) (valine, leucine, isoleucine, tryptophan, tyrosine) more than those of

phenylalanine. These other amino acids are considerably more abundant than phenylalanine in the

protein, and the branched-chain amino acids, unlike phenylalanine, are largely unmetabolized when they

pass through the portal circulation.

20

In contrast, consumption of phenylalanine in the form of aspartame, with the other LNAA, that are

always present in proteins, elevates plasma phenylalanine levels without elevating those of the other

LNAA, this causes marked elevations in the plasma phenylalanine ratio (the ratio of the plasma

phenylalanine concentration to the summed concentrations of the other LNAA).

13 Aspartame is the only known phenylalanine-containing food that elevates this ratio.

An elevation in the plasma phenylalanine ratio causes a parallel rise in brain phenylalanine levels,

since a single transport macromolecule within the endothelial cells lining the brain's capillaries mediates

the uptake of all of the LNAA; this macromolecule is unsaturated at normal plasma LNAA levels; and

each of the LNAA's compete for attachment to it, their success depending on their relative affinities for it

and their plasma concentration relative to those of its competitor.

4, 21 The elevation in the plasma phenylalanine ratio also tends to reduce the corresponding ratios for the LNAA, thus decreasing their brain uptakes and tending to lower their brain levels.

13 [Aspartame fails to lower brain tyrosine levels in the rat because the rat's liver hydroxylates dietary phenylalanine so rapidly that plasma tyrosine levels rise even more than those of plasma phenylalanine.

13, 14 However, in humans dietary aspartame probably reduces brain tyrosine uptake.]

If an aspartame-containing beverage is consumed along with, for example, a carbohydrate-rich,

protein-poor dessert food, its effect on brain phenylalanine is doubled.

13 This is because the insulin secretion elicited by the carbohydrate selectively lowers plasma levels of the branched-chain amino acids (by facilitating their uptake into skeletal muscle), without having much of an effect on plasma phenylalanine; this increases the effect of the aspartame on the plasma phenylalanine ratio.

17 A similar doubling may occur if the eater happens to be one of the perhaps 10 million Americans who are, without

knowing it, heterozygous for the phenylketonuria (PKU) gene.

22

Once within brain, neurons producing certain neurotransmitters, such as dopaminergic

nigrostriatal cells, the excess phenylalanine can inhibit enzymes (like tyrosine hydroxylase) needed to

synthesize the neurotransmitters. Excess circulating phenylalanine can also diminish the production of

brain catecholamines and serotonin by competing with their precursor amino acids for transport across

the blood-brain barrier. Hence, physiological processes that depend on the sustained release of

adequate quantities of these transmitters can be affected. One such process creates greater sensitivity to seizures.

23 In humans, aspartame, regardless of dose, causes greater increases in plasma (and brain) phenylalanine than tyrosine. (As shown below,sufficiently high aspartame doses, which transiently exceed the liver's capacity to hydroxylate

phenylalanine, can also potentiate seizures in rodents, whether these seizures are generated by drugs, electroshock, or inhalation of fluorothyl.)All of these relationships have now been demonstrated; most recently, the ability of phenylalanine to suppress dopamine release.

24

Aspartame and Seizure Susceptibility

To determine whether aspartame intake could modify seizure susceptibility, perhaps by

increasing plasma and brain phenylalanine levels, one of our group has examined its effects on the

incidence of seizures, their speed of onset, and the amount of convulsant required to produce the

seizures among mice given treatments known to be epileptogenic.25 In general, animals received various

aspartame doses 1 hr before a CD50 dose of the seizure-inducing treatment, or a fixed aspartame dose 1

hr before various doses of the treatment. The number of animals in each treatment group exhibiting

seizures in the next 60 minutes were counted (when the treatment was pentylenetetrazole), or the time

passing until a given animal had a seizure (when the treatment was inhaled fluorothyl or electroshock).

The aspartame doses used were those shown, in the mice, to cause blood phenylalanine levels to rise

by at least as much as blood tyrosine, i.e., doses of 1000 mg/kg or greater.

Aspartame administration produced a dose-dependent increase in seizure frequency among

animals subsequently receiving the CD50 dose of pentylenetetrazole (PTZ) (65 mg/kg) (Fig. 2). At the

1000 and 2000 mg/kg aspartame doses, 78 and 100% of the animals experienced seizures, compared

with 50% in the water-pretreated group. Other mice pretreated with a fixed dose (1000 mg/kg) of

aspartame, or with water, and given various doses (50-75 mg/kg) of PTZ an hour later exhibited a

significant leftward shift of the PTZ dose response curve (Fig. 3). Enhanced susceptibility to PTZ-induced

seizures was also observed among mice pretreated with phenylalanine (in doses equimolar to effective

aspartame doses), but not among animals pre-treated with aspartic acid or methanol. Co-administration

with aspartame of the LNAA valine, which competes with phenylalanine for passage across the bloodbrain

barrier,4, 21 protected mice from the seizure-promoting effects of the sweetener; in contrast,

alanine, an amino acid which does not compete with phenylalanine for brain uptake, failed to attenuate

aspartame's effect on PTZ-induced seizures.

The evidence does not indicate that aspartame itself causes seizures; but rather that it promotes

seizures in animals that are already at risk (that is, animals treated with PTZ, fluorothyl, or electroshock).

In a similar manner, it is possible that doses of the sweetener that cause a sufficient increase in brain

phenylalanine might increase seizure frequency among susceptible humans, or might allow seizures to

occur in people who are vulnerable but without prior episodes.

It is unfortunate but perhaps not surprising that questions about aspartame's phenylalaninemediated

neurological effects arose after the sweetener was added to the food supply. New clinical data

and the development of new hypotheses, based on laboratory research, can raise questions about any

relatively new compound, even after that compound has passed all of the safety tests required at the time

of its approval. What was and continues to be lacking is a process, free of political influence, for

monitoring possible adverse reactions after food and drug additives are placed in the market.

Government-mandated safety research does not exist for politically protected chemicals and

compounds, such as Thimerosal and aspartame.

REFERENCES

1. Hattan DG, Henry SH, Montgomery SB, Bleiberg MJ, Rulis AM, Bolger PM. Role of the Food and

Drug Administration in regulation of neuroeffective food additives. In: Wurtman RJ, Wurtman JJ, eds.

Nutrition and the Brain.

Vol. 6. New York, NY: Raven Press; 1983: 31-99.

2. Anonymous. Food additives permitted for direct addition to food for human consumption; aspartame;

denial of requests for hearing. Final rule, Federal Register 49, 6672-6682 (1984).

3. Pardridge WM. Potential effects of the dipeptide sweetener aspartame on the brain. In: Wurtman RJ,

Wurtman JJ, eds.

Nutrition and the Brain. Vol. 7. New York, NY: Raven Press; 1996: 199-241.

4. Bradstock MK, Serdular MK, Marks JS, Barmard RJ, Crane NT, Remmington PL, Trowbridge FL.

Evaluation of reactions to food additives: The aspartame experience.

Am J Clin Nutr. 1986;43:464-

469.

5. Department of Health and Human Services.

Quarterly Report on Adverse Reactions Associated with

Aspartame Ingestion

. DHHS, Washington, DC, Oct. 1, 1986.

6. Johns DR. Migraine provoked by aspartame.

N Engl J Med. 1986;315-456.

7. Ferguson JM. Interaction of aspartame and carbohydrates in an eating-disorder patient.

Am J

Psychiatry

. 1985;142:271.

8. Drake ME. Panic attacks and excessive aspartame ingestion. Lancetii: 631 (1986)

9. Wurtman RJ. Aspartame: Possible effect on seizure susceptibility. Lancet ii: 1060 (1985).

10. Watson RG. Seizure and mania after high intake of aspartame.

Psychosomatics. 1986;27:218-220.

11. Stegink L.D, Filer LJ Jr., Baker GL. Effect of aspartame and aspartame loading upon plasma and

erythrocyte free amino acid levels in normal adult volunteers.

J Nutr. 1977;107:1837-1845.

12. Yokogoshi H, Roberts CH, Caballero B, Wurtman RJ. Effects of aspartame and glucose

administration on brain and plasma levels of large neutral amino acids and brain 5-hydroxyindoles.

Am J Clin Nutr.

1984;40:1-7.

13. Fernstrom JD, Fernstrom MH, Gillis MA. Acute effects of aspartame on large neutral amino acids and

monoamines in rat brain.

Life Sci. 1983;32:1651-1658.

14. Ranney RE, Opperrnann JA, Muldoon E, McMahon FG. Comparative metabolism of aspartame in

experimental animals and humans.

J Toxicol Environ Health. 1976;2:441-451.

15. Fernstrom JD, Wurtman RJ, Hammarstrom-Wilkund B, Rand WM, Munro HN, Davidson CS. Diurnal

variation in plasma concentrations of tryptophan, tyrosine, and other neutral amino acids: Effect of

dietary protein intake.

Am J Clin Nutr. 1979;32:1912-1922.

16. Maher TJ, Glaeser BS, Wurtman RJ. Diurnal variations in plasma concentrations of basic and neutral

amino acids and in red cell concentrations of aspartate and glutamate: Effects of dietary protein.

Am J

Clin Nutr.

1984;39:722-729.

17. Stegink LD, Filer LJ Jr., Baker GL., McDonnell JE. Effect of an abuse dose of aspartame upon

plasma and erythrocyte levels of amino acids in phenylketonuric heterozygous and normal adults.

J

Nutr

. 1980;110: 2216-2224.

364

18. Fernstrom JD, Faller DV. Neutral amino acids in the brain: Changes in response to food ingestion.

J

Neurochem

. 1978;30:1531-1538.

19. Elwyn DH, Parikh HC, Shoemaker WC. Amino acid movements between gut, liver and periphery in

unanesthetized dogs. Am J Physiol. 1968;215:1260-1275.

20. Oldendorf WH. Brain uptake of radiolabeled amino acids, amines, and hexoses after arterial injection.

Am J Physiol

. 1971;221:1629-1639.

21. Levy HL, Waisbren SE. Effects of untreated maternal phenylketonuria and hyperphenylalanemia on

the fetus.

N Engl J Med. 1983;309:1269-1274.

22. Jobe PC, Dailey JW, Reigel CE. Noradrenergic and serotonergic determinants of seizure

susceptibility and severity in genetically epilepsy-prone rates.

Life Sci. 1986;39:775-782.

23. Milner JD, Irie K, Wurtman RJ. Effects of phenylalanine on the release of endogenous dopamine from

rat striatal slices.

J Neurochem. 1986;47:1444-1448.

24. Reinhard JF, Reinhard JF Jr. Experimental evaluation of anticonvulsants. In: Vida JA, ed.

Anticonvulsants

. New York, NY: Academic Press; 1972: 58-110.

25. Olney JW, Farber NB, Spitznagel E, Robins LN. Increasing brain tumor rates: is there a link to

aspartame?

Journal of Neuropathology and Experimental Neurology. 1996;55: 1115-1123.

ABOUT THE AUTHOR

Dr. K. Paul Stoller is Medical Director of the Hyperbaric Medical Center of New Mexico, President

of the International Hyperbaric Medical Association, a Fellow of the American Academy of Pediatrics, a

Diplomat of the American Board of Pediatrics, a Diplomat of the American Board of Hyperbaric Medicine,

and a member of the American College for Hyperbaric Medicine. He was University of California

President's Undergraduate Fellow in the UCLA Medical Center's Department of Anesthesiology, and a

former Clinical Assistant Professor of Pediatrics, UNM School of Medicine. Dr. Stoller is also part of the

Divers Alert Network Physician Referral Network. Dr. Stoller is a founding board member of the

International Hyperbaric Medical Association, and its current President. He was also a founding board

member of the

Humane Farming Association, Science Editor of the Animals' Voice Magazine where he

was nominated for a

Maggie. His Op-Ed pieces have appeared in several newspapers and periodicals

from

The Atlanta Constitution, Los Angeles Times, Abq Tribune to The Scientist. He has served on both

the Injury Prevention Committee and the Environmental Hazards Committee of the American Academy of

Pediatrics.

Iodine Deficiency: The Connection to IQ, ADD, Breast Cancer, Thyroid Disease, and More

I've read so many articles throughout the years and there's nothing more disappointing than to read the statement, "The cause of this disease (or problem) is unknown."  Come on.....I mean seriously, that's why we're reading the article in the first place right?  This is always such a let down for me personally because I'm such a "fix-it" personality type.   But, I read a published article recently by a physician who specializes in iodine therapy for hypothyroidism and fibrocystic breast disease. He is  also dedicated to hormonal therapy, fibromyalgia, chronic fatigue, and immune dysfunction in his practice.  On the iodine side of things however, he has performed over 20,000 tests for what I'm getting ready to share with you in this blog today.  That's pretty solid in terms of numbers for someone experienced in this area, and wow, what I learned from his writings was fascinating.  I'm just sharing some of that with you today in this blog.

Iodine is a member of the halogen family and was discovered back in 1811.  It has been used throughout history for the treatment of goiter, but interestingly, there are doctors today that believe iodine causes goiter, and will discourage it's use. 

The body utilizes iodine throughout it's glandular system, in the white blood cells, and especially in the thyroid gland.  Iodine is also concentrated in the breast tissue, salivary glands, pancreas, cerebrospinal fluid, brain, stomach, etc.  You can see from this that  iodine is a key regulator of many body systems and the absence of iodine is known to be a promotor of cancer.  Studies show that.

Now, there's sometimes questions about iodine and iodide.  Iodide is a salt.  Breast tissue, prostate tissue and stomach prefer iodine, but the thyroid, the salivary glands, and the skin prefer iodide.  The body needs both types in order for it to function properly which is often why you see physicians treating their patients with Lugol's solution.  It contains both. 

Iodine is essential for the normal growth and development of children and especially the central nervous system.  Some experts say that a baby's IQ is set by the age of two, and iodine is what sets the IQ.  A deficiency in iodine can result in mental deficiencies, deafness, delayed physical and intellectual development and attention deficit disorder.  The amount of iodine in a mother's diet when she gets pregnant could be one of the most important things to assess in the information we are discovering today. 

Here's some comparison data:
In Japan, an average person eats 13.8mg of iodine per day in their diet.  In America, we eat around 168mcg (notice the difference from mg to mcg).  Here's some compelling evidence of the importance of iodine in our diet.  In the U.S. we have the highest incidence of breast cancer in the world, but Japan has the lowest.  In the U.S. we have 7 deaths under age 1 per 1000 live births.  In Japan it is 3.5 (HALF ours) and the lowest in the world.  We have known for years that people who develop goiter have an inceased risk of developing various cancers.  Do you remember all of the places that iodine exists in our bodies? Those are the same places cancers tend to arise.   In the 1900's goiter was very common among people living in the Great Lakes region (approx 40% of school age children). In 1924 in Akron, Ohio, 56% of the population had goiter.  This is when researchers began to study iodized salt and it's prevention of goiter and when the government began to iodize salt. 

Data now shows that we are headed toward a deficiency again.  Why? We are taking iodine out of bread, milk, and our salt.  Half of cooking salt now contains no iodine.  And for those with high blood pressure, the first thing they will be told to do is to eliminate as much salt as possible from their diet.  In 1997, approximately 11.4% of our population had a severe iodine deficiency and now studies from 2004 to 2006 indicate approximately 17.6% of our population is deficient. Within the last five to six years, the incidence of attention deficit disorder in the U.S. has gone up by almost 500%, and iodine deficiency is certainly a suspicious reason.  I can't help but remember a conference I went to last year where Dr. David Browstein (thyroid specialist, author, speaker) was lecturing. He showed a spelling test of a child who had failed miserably before clinical assessment of thyroid disorder.  He also sketched martians and weird drawings at the side of the paper showing he was not focused well at all.  The physician realized through lab work and physical assessments that the childs thyroid was not functioning properly.  He used appropriate treatments and the child was reissued the same exam within a couple of weeks and scored a 100%...with no martians involved. :) No Ritalin.  No stimulants.  Just a balanced thyroid is all that was needed.

Iodine deficiency results in fibrocystic breast disease.  Iodine treatment is accompanied by decreased breast size and a reduction of pain within a few weeks of therapy and continued use will show scar tissue significantly minimized on mammogram comparisons.  But even further in the scheme of things, are we paying attention to the iodine status of patients with cancer?  I'm afraid the answer is no, but I think we should definitely be encouraging this in our medical evaluations when these conditions exist.

Now please don't just rush out and buy Lugol's solution without the advice of your medical provider.  The message in this is that other reasons may exist for the conditions I have highlighted in this blog.  Assessments and physical exams are very important in determining if this is the right thing for you. But before accepting a certain diagnosis or not looking at all reasonable options, bring this subject up with your doctor.  After reading this and studying further,  I would definitely encourage iodine testing in pregnant women, those with cancer, those with attention deficit disorders, and those with thyroid related symptoms.  The numbers are showing too much of a connection not to pay attention to this.   Please continue to do your own research on this and see what you come up with. 

Here's a simple way to test. http://youtu.be/07yM29WmKFQ

To your good health,
Dr. Sonja