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Hypothyroidism: Should we screen all pregnant women?

2012-02-19T01:51:00.000-08:00

What are the practical implications of recent studies linking maternal thyroid deficiency with impaired growth, adverse neurologic outcomes, and fetal death?

SHRAGA BLAZER, MD; ETAN Z. ZIMMER, MD

Dr. Blazer is director, neonatal unit, and Dr. Zimmer is director, obstetrics unit, Rambam Medical Center and Faculty of Medicine, Technion-Israel Institute of Technology, Haifa, Israel.

Emerging research indicates that thyroid hormones play a key role in fetal brain development, and asymptomatic hypothyroidism during pregnancy may have an adverse effect on fetal growth and neurologic development. Findings published in the past year call our attention to the importance of identifying and adequately treating thyroid-deficient gravidas:

Maternal free thyroxine (FT4) concentration below the 10th percentile at 12 weeks is associated with significant impairment of psychomotor development at ages 1 and 2 years.¹
The average serum thyroid-stimulating hormone (TSH) and FT4 levels of neonates born to hypothyroid mothers were significantly higher than those of controls; birth weight and head circumference were significantly lower.²

But given the paucity of data on how maternal hypothyroidism affects the offspring, is universal screening justified? We review the evidence to date, present the current positions of 3 organizations, and offer recommendations for current clinical practice.

MATERNAL THYROID STATUS IS IMPORTANT THROUGHOUT GESTATION

The fetal thyroid gland begins to develop at 3 weeks’ gestation; it concentrates iodine and synthesizes thyroid hormone after 10 to 12 weeks.

Prior to this, the mother provides the thyroid hormones through placental diffusion (see “How thyroid needs change during pregnancy”). Indeed, thyroid hormones have been detected in human coelomic and amniotic fluids as early as 8 weeks’ gestation, before the fetal thyroid starts to function.³

New perspective on role of maternal thyroid function. It was previously believed that the mother’s thyroid hormone supply to the fetus was irrelevant after 10 to 12 weeks. However, Vulsma et al⁴ demonstrated that substantial amounts of thyroxine (T4) are transferred from mother to fetus during late gestation. They discovered T4 in the cord blood of fetuses at term who were unable to synthesize T4 due to organification defects or thyroid agenesis. The T4 in these cases (noted at concentrations 25% to 50% of normal) was obviously of maternal origin.

How thyroid hormone needs change during pregnancy

Thyroid hormone requirement increases during pregnancy in normal women, to provide for the added maternal and fetal needs. Thyroxine (T4) requirement also may grow as a result of placental degradation and increased maternal T4 clearance.²⁰

Thyroid hormone turnover is altered during pregnancy, mainly in association with:

lowered iodide availability to the maternal thyroid gland,
increased serum thyroid-binding globulin (TBG) concentration, and
increased production of thyroid-stimulating factors by the placenta.

Maternal serum inorganic iodide levels decrease during pregnancy, possibly due to increased renal clearance of iodide—which stems from increased glomerular filtration rate, and transplacental transfer of iodide and iodothyronines.^8,21 The reduced circulating concentration of iodide leads to decreased availability of iodide to the thyroid gland, and results in a 10% to 20% increase of thyroid volume.²¹ This iodide loss has no clinical importance where iodine intake is sufficient, but may lead to hypothyroidism and goiter in regions of overt iodine deficiency.
The increase in the TBG serum concentration in pregnancy results from estrogen-induced increased synthesis and reduced hepatic clearance of TBG.
Serum TBG starts to rise after conception and reaches a plateau at midgestation, leading to an increase in total T4 and total triiodothyronine (T3) levels. In addition, the placenta produces human chorionic gonadotropin (hCG), which has thyroid-stimulating hormone (TSH)-like bioactivity and stimulates T4 production by the thyroid gland. Placental production of hCG is maximal during the first trimester.
Thus, total T4 and total T3 levels rise during the first trimester to a peak in midgestation. However, only a small amount of these hormones is unbound: The increase in free T4 during this trimester is mild, and coincides with a mild transient decrease in TSH levels that subsequently return to normal.

Most pregnant women are euthyroid by laboratory evaluation, and their TSH, free T4, and free T3 levels remain within normal values.

THYROID HORMONES: IMPORTANT TO BRAIN DIFFERENTIATION AND DEVELOPMENT

In the mammalian embryo, thyroid hormones appear to regulate processes of neuronal proliferation, migration, synaptogenesis and myelination, though the precise mechanism is not fully understood.

Unlike T4, triiodothyronine (T3, the most potent thyroid hormone) does not readily penetrate the brain. Indeed, most brain T3 is produced locally from T4, after which it binds to nuclear thyroid hormone receptors. These in turn bind to specific DNA sequences in the regulatory region of target genes.⁵ A sufficient level of such receptors has been observed in the human fetus as early as 9 weeks’ gestation.

Information comes mostly from animal models, mainly rats. We must thus remain aware that the transfer of thyroid hormones from mother to embryo or fetus may differ between species,⁶ as may the stages of brain development before and after birth.

HYPOTHYROIDISM DURING PREGNANCY

The frequency of thyroid deficiency in pregnancy varies from 0.19% in Japan⁷ to 2.2% in Belgium⁸ and 2.5% in the United States.⁹

Hypothyroidism in pregnancy may be due to preexisting illness or a disease that evolves during pregnancy; in developed nations, the most common causes are Hashimoto’s thyroiditis, subacute thyroiditis, and surgical or radioactive ablation of the thyroid gland.

The hypothyroid state may be subclinical and can remain undiagnosed throughout pregnancy. The clinical manifestations of hypothyroidism (fatigue, sensitivity to cold, muscle irritability, cramps, constipation, paresthesia of the distal portion of the extremities, dry skin, and hair loss) may be masked in gestation as symptoms of pregnancy. Gestational hypothyroidism can be classified as overt (low FT4 values and elevated TSH) or subclinical (normal FT4 values and elevated TSH).

The IQ scores of children of hypothyroid women averaged 4 points lower than those of controls at age 7 to 9 years.

Increased rates of fetal death have also been associated with subclinical disorder (see “The importance of adequate supplementation: 2 case studies”).¹⁰

Monitoring thyroid hormone levels in hypothyroid women is performed several times during gestation (every 4 to 6 weeks), and the dosage of T4 supplementation adjusted as needed. Mandel et al, who studied women with primary hypothyroidism, noted that the replacement dosage had to be increased by 45% during pregnancy.¹¹ This trend was apparent in the first trimester and persisted throughout gestation.

The importance of adequate supplementation: 2 case studies

The following cases underscore the importance of:

knowledge of maternal thyroid status during periconception,
thyroid hormone supplementation for subclinical hypothyroidism, and
close follow-up and appropriate adjustment of replacement therapy throughout pregnancy.

Case 1

Elevated TSH discovered after successive pregnancy losses

A woman suffered 2 consecutive pregnancy losses. Subsequent work-up revealed subclinical hypothyroidism: Her thyroid-stimulating hormone (TSH) value was moderately elevated and free thyroxine (FT4) was normal. Thyroid hormone supplementation was initiated.

Four months later the patient conceived spontaneously. Levothyroxine therapy in the prepregnant dosage was continued. The mother’s general physician monitored her levels during gestation.

TSH value was normal at 5 weeks but elevated again at 9 weeks. The dosage of thyroid hormone supplementation was increased and the TSH value returned to normal—and remained so in all subsequent studies, every 4 to 6 weeks until labor.

The child was born at 40 weeks’ gestation, with a birth weight of 3,680 g, a head circumference of 36 cm, and normal neonatal thyroid functions. Presently 7 years old, he is healthy and well developed.

Case 2

The perils of unmonitored supplementation

A year after her thyroid function was found to be normal, a woman became pregnant. At the 5th gestational week, fatigue and constipation prompted reexamination of her thyroid function. TSH values were elevated; FT4 was borderline low.

According to her endocrinologist she was given levothyroxine 100 μg daily throughout pregnancy, but no follow-up was conducted. At 39 weeks’ gestation the patient delivered a male newborn weighing 2,890 g with a head circumference of 33.7 cm. Neonatal thyroid function was:

at 52 hours of age, TSH = 14.3 μIU/mL, FT4 = 37.4 pmol/L;
at 132 hours of age, TSH = 8.0 μIU/mL, FT4 = 31.5 pmol/L.

Spontaneous normalization of the pituitary-thyroid axis was evident at age 17 days. The child, now 9 years old, displays problems with fine motor coordination and mild learning impairment.

HOW DOES MATERNAL THYROID STATUS AFFECT FETAL BRAIN DEVELOPMENT?

Data on the impact of maternal hypothyroidism on the offspring’s mental development come from interventional experimental studies in animals, and, in humans, from observational studies only.

Animal studies show permanent cortical changes. Hypothyroidism in rats causes a reduction in brain size of the newborn pups and a lower total body mass of the embryos.¹²

Lavado-Autric et al¹³ recently reported that subtle T4 insufficiency in the pregnant rat disrupts migration of neurons in the fetal cortex and hippocampus, leading to the presence of neurons in aberrant locations in the adult offspring’s brain and “blurring” of cortical layers. These alterations in cortical cytoarchitecture seem to be permanent, not simply a reflection of delayed maturation.

Recent human studies point to neurologic impairment. It is well recognized that severe iodine deficiency during pregnancy may be associated with impaired psycho-neuro-intellectual outcome in progeny. However, since thyroid hormone deficiency can occur in both mother and fetus, it is difficultto determine whether any mental retardation is caused by maternal or fetal hypothyroidism, or both.

Elevated maternal TSH associated with lower child IQ scores. Man and Jones¹⁴ first suggested in 1969 that mild maternal hypothyroidism with no iodine deficiency was associated with lower infant IQ scores.
More recently, Haddow et al¹⁵ also found that maternal hypothyroxinemia is associated with adverse neurologic outcome of the offspring. They measured TSH in stored serum samples collected from 25,216 pregnant women. The children of 62 women who had elevated TSH (above the 98th percentile) in combination with low T4 levels were compared to 124 children of matched control mothers.
The children of hypothyroid women performed slightly worse than controls in a battery of 15 neuropsychological tests at the age of 7 to 9 years; their full-scale IQ averaged 4 points lower (P = .06).
Thyroid supplementation not associated with improved IQ. Of the 62 women with overt disease, only 14 were treated for hypothyroidism during pregnancy. The full-scale IQ score of the children born to untreated women averaged 7 points lower (P = .005) than that of matched controls. Interestingly, there was no significant difference in mean IQ between the children born to treated and untreated hypothyroid mothers, suggesting therapy had no significant protective effect on IQ.
However, since the 14 treated mothers still had high TSH levels, it is possible that they actually received suboptimal treatment.
First trimester hypothyroidism linked to impaired psychomotor development. A 2003 study by Pop et al¹ investigated the relationship between maternal hypothyroxinemia in the first trimester and neurodevelopment of the offspring. They showed that low maternal FT4 (below the 10th percentile) with normal TSH at 12 weeks’ gestation was associated with significant impairment of the child’s psychomotor development at 1 and 2 years of age.
However, children whose mothers’ FT4 concentrations increased later in pregnancy (24 and 32 weeks’ gestation) did not demonstrate significant delay of mental and motor function at age 1 or 2.
This study is limited by small numbers in the subgroups (63 cases and 62 controls at 1 year; 57 cases and 58 controls at 2 years). Further research is required to evaluate results.
Alterations in the pituitary-thyroid axis noted in the early neonatal period. Recently, we prospectively compared thyroid function in 2 groups of full-term newborns: 259 infants born to 250 hypothyroid mothers who received thyroid replacement therapy during pregnancy, and 139 healthy newborns of women who had at least 2 normal thyroid function tests during their pregnancy.² Maternal thyroid function tests were assessed 2.3±0.7 (mean±standard deviation) times during pregnancy.
The neonates’ average serum TSH and FT4 levels, measured 25 to 120 hours after birth, were significantly higher among a substantial subset of the intervention-group newborns (44.4%, P<.001) than among control-group newborns. Serum FT4 correlated positively with TSH in controls but not in study newborns, suggesting autonomous hyperfunction of the thyroid gland in the latter group.
Birth weight (study, 3,295±446 g versus control, 3,454±413 g; P <.001) and head circumference (study, 34.6±1.4 cm versus control, 35.1±1.0 cm; P <.001) were significantly lower in the study group.
We assume that the impaired intrauterine growth and unduly elevated serum TSH and FT4 values observed in the study newborns might reflect insufficient hormone replacement of their mothers during pregnancy.

OFFICIAL GUIDELINES ARE UNCLEAR

Considering the adverse effects that maternal hypothyroidism, even subclinical, can have on the offspring, the question arises: Is universal periconceptional screening for thyroid dysfunction appropriate? The current recommendations on this subject are unclear:

The Endocrine Society in 1999 called for a cost-effective screening program for hypothyroidism in all women before conception or in early pregnancy.¹⁶

The American Association of Clinical Endocrinologists recommended in 2002 that routine TSH measurement be performed before pregnancy or during the first trimester in all women.¹⁷

The American College of Obstetricians and Gynecologists, in contrast, stated in 2002 that data are insufficient to warrant routine screening of asymptomatic pregnant women; thyroid function tests should be performed only in gravidas with symptoms or a personal history of thyroid disease.¹⁸

WHY ROUTINE SCREENING IS NOT YET JUSTIFIED

In view of the findings of adverse events associated with maternal hypothyroidism, a universal screening program appears warranted for timely initiation of therapy. However, data on the efficacy of T4 replacement in averting such effects is insufficient. Thus, it is premature to implement routine screening for thyroid function of all women contemplating pregnancy or early in gestation.

Well-designed clinical trials are needed to determine method and timing of testing, precise diagnostic criteria for maternal hypothyroidism, and ways to assure the adequacy and efficacy of therapy.

A randomized controlled antenatal screening study¹⁹ underway in South Wales aims to recruit 22,000 pregnant women.

IS CURRENT TREATMENT INADEQUATE?

These observations call into question the adequacy of current therapeutic regimens:

no significant differences were seen in the IQ scores of children of untreated and treated hypothyroid mothers,¹⁵ and
infants of treated hypothyroid women demonstrated restricted intrauterine growth and abnormal neonatal thyroid function.²

Take-home message. Although findings indicate hypothyroidism during pregnancy may have an adverse effect on fetal growth and neurodevelopment, evidence is insufficient to justify universal screening. Still, what we have learned to date enables us to formulate a reasonable monitoring and follow-up protocol (see “Clinical recommendations”).

CLINICAL RECOMMENDATIONS

In the general population, thyroid function testing—specifically, thyroid-stimulating hormone (TSH) and free thyroxine (FT4) studies—prior to conception or in early pregnancy is reasonable, but the decision should be left to the individual patient and her physician.
TSH and FT4 testing should be performed prior to conception and during pregnancy in women with a family history of thyroid disease, symptoms of thyroid disease, or an immune disorder.
For women with a personal history of hypothyroidism who are taking thyroxine (T4) replacement, serum TSH should be closely monitored in early pregnancy. Most of these patients will become hypothyroid as detected by a rise in TSH unless the T4 dose is increased in early pregnancy.
For pregnant women found to be hypothyroid, close monitoring (4 to 6 week intervals) of TSH and FT4 throughout pregnancy and careful adjustment of the thyroid supplementation dosage are warranted.

The authors report no financial relationships relevant to this article.

REFERENCES

1. Pop VJ, Brouwers EP, Vader HL, Vulsma T, van Baar AL, de Vijlder JJ. Maternal hypothyroxinaemia during early pregnancy and subsequent child development: a 3-year follow-up study. Clin Endocrinol(Oxf). 2003;59:282–288.

2. Blazer S, Moreh-Waterman Y, Miller-Lotan R, Tamir A, Hochberg Z. Maternal hypothyroidism may affect fetal growth and neonatal thyroid function. Obstet Gynecol. 2003;102:232–241.

3. Contempre B, Jauniaux E, Calvo R, Jurkovic D, Campbell S, de Escobar GM. Detection of thyroid hormones in human embryonic cavities during the first trimester of pregnancy. J Clin Endocrinol Metab. 1993;77:1719–1722.

4. Vulsma T, Gons MH, de Vijlder JJ. Maternal-fetal transfer of thyroxine in congenital hypothyroidism due to total organification defect or thyroid agenesis. N Engl J Med. 1989;321:13–16.

5. Oppenheimer JH, Schwartz HL. Molecular basis of thyroid hormone-dependent brain development. Endocr Rev. 1997;18:462–475.

6. Morreale De Escobar G, Obregon MJ, Escobar del Rey F. Is neurodevelopment related to maternal hypothyroidism or to maternal hypothyroxinemia? J Clin Endocrinol Metab. 2000;85:3975–3987.

7. Kamijo K, Saito T, Sato M, et al. Transient subclinical hypothyroidism in early pregnancy. Endocrinol Jpn. 1990;37:397–403.

8. Glinoer D. The regulation of thyroid function in pregnancy: pathways of endocrine adaptation from physiology to pathology. Endocr Rev. 1997;18:404–433.

9. Utiger RD. Maternal hypothyroidism and fetal development. N Engl J Med. 1999;341:601–602.

10. Allan WC, Haddow JE, Palomaki GE, et al. Maternal thyroid deficiency and pregnancy complications: implications for population screening. J Med Screen. 2000;7:127–130.

11. Mandel SJ, Larsen PR, Seely EW, Brent GA. Increased need for thyroxine during pregnancy in women with primary hypothyroidism. N Engl J Med. 1990;323:91–96.

12. Usenko V, Lepekhin E, Lyzogubov V, Kornilovska I, Ushakova G, Witt M. The influence of low doses 131I-induced maternal hypothyroidism on the development of rat embryos. Exp Toxicol Pathol. 1999;51:223–227.

13. Lavado-Autric R, Auso E, Garcia-Velasco JV, et al. Early maternal hypothyroxinemia alters histogenesis and cerebral cortex cytoarchitecture of the progeny. J Clin Invest. 2003;111:1073–1082.

14. Man EB, Jones WS. Thyroid function in human pregnancy. V. Incidence of maternal serum low butanol-extractable iodines and of normal gestational TBG and TBPA capacities; retardation of 8-month-old infants. Am J Obstet Gynecol. 1969;104:898–908.

15. Haddow JE, Palomaki GE, Allan WC, et al. Maternal thyroid deficiency during pregnancy and subsequent neuropsychological development of the child. N Engl J Med. 1999;341:549–555.

16. The Endocrine Society. The Endocrine Society issues recommendations in response to major hypothyroidism study. August 1999. Available at:www.endosociety.org/pubrelations/pressreleases/archives/1999/hypothyroid.cfm. Accessed March 26, 2004.

17. AACE Thyroid Task Force. American Association of Clinical Endocrinologists medical guidelines for clinical practice for the evaluation and treatment of hyperthyroidism and hypothyroidism. Endocr Pract. 2002;8:457–469.

18. American College of Obstetricians and Gynecologists. Thyroid disease in pregnancy. Clinical management guidelines for obstetrician-gynecologists. ACOG practice bulletin No. 37. Obstet Gynecol. 2002;100:387–396.

19. Lazarus JH, Wald NJ, Angele C, et al. The controlled antenatal thyroid screening study (CATS): first observations. Endocrine Abstracts. 2003;5:P262.

20. Brent GA. Maternal thyroid function: interpretation of thyroid function tests in pregnancy. Clin Obstet Gynecol. 1997;40:3–15.

21. Burrow GN, Fisher DA, Larsen PR. Maternal and fetal thyroid function. N Engl J Med. 1994;311:1072–1078.

Het gevaar van maagzuurremmers

2012-02-09T01:49:00.000-08:00

Danger of Antacid Medications

The U.S. Food and Drug Administration (FDA) announced a safety alert for proton pump inhibitors (PPIs). PPIs are a class of medications commonly used to treat stomach and duodenal ulcers, reflux esophagitis, and other gastric problems. PPIs include:
• AcipHex (rabeprazole sodium)
• Dexilant (dexlansoprazole)
• Nexium (esomeprazole magnesium)
• Omeprazole (omeprazole) Over-the-Counter (OTC)
• Prevacid (lansoprazole) and OTC Prevacid 24hr
• Prilosec (omeprazole) and OTC
• Protonix (pantoprazole sodium)
• Vimovo (esomeprazole magnesium and naproxen)
• Zegerid (omeprazole and Sodium bicarbonate) and OTC

The FDA stated, “…the use of stomach acid drugs known as proton pump inhibitors (PPIs) may be associated with an increased risk of Clostridium difficile–associated diarrhea (CDAD). A diagnosis of CDAD should be considered for patients taking PPIs who develop diarrhea that does not improve.”(1)

C. difficile is a bacterium that can infect the colon and cause severe, life-threatening diarrhea. It causes over three million cases of diarrhea per year in the U.S. Approximately 1-4% of patients with C. difficile die from the illness.

Those who read my books don't have to wait years for the FDA to act. Three years ago in Drugs That Don’t Work and Natural Therapies That Do, I wrote about the consequences of long-term use of PPIs. I stated, “The reason we are seeing such a dramatic increase in C. difficile infections is clear; it is due to the overuse of powerful antacid medications.”

What can you do? If you are prescribed a PPI, you should take it for the shortest possible time period. If possible, long-term use of this class of medications should be avoided. Also, taking a healthy probiotic along with a PPI can help avoid problems like C. difficile.

More information about PPIs and how to use a holistic approach to overcome stomach and esophageal problems can be found in my book, Drugs That Don’t Work and Natural Therapies That Do.

(1)http://www.fda.gov/Safety/MedWatch/SafetyInformation/SafetyAlertsforHumanMedicalProducts/ucm290838.htm

De Kritieke Rol van Tarwe bij Menselijke Ziekte

2012-02-07T02:25:00.000-08:00

Dr. Mercola

Lectine bestaat uit Wheat Germ Agglutinin (WGA) of wel Tarwekiem Agglutinine en glycoproteïne. Door duizenden jaren selectief tarwe te kweken op steeds toenemende hoeveelheden eiwit is de concentratie van WGA lectine proportioneel toegenomen.

WGA is grotendeels verantwoordelijk voor de vele indringende slechte effecten.

En wat is erger, WGA wordt in de hoogste concentraties gevonden in "volkoren tarwe" inclusief de veronderstelde superieure gekiemde vorm.

Wat uniek is van WGA glycoproteïne is dat het directe schade kan aanbrengen aan je meeste weefsels in je lichaam zonder dat het een specifieke set genetische vatbaarheden of immuun gemedieerde articulaties nodig heeft.

Dit zou kunnen verklaren waarom chronische onstekings- en degeneratieve aandoeningen endemisch zijn bij tarwe consumerende bevolkingsgroepen.

WGA lectine is een uitzonderlijk sterke tegenstander omdat het geformeerd is uit dezelfde disulfide verbindingen die gevulkaniseerd rubber een menselijk haar zo sterk, buigzaam en duurzaam maken.

Zoals door de mens gemaakte pesticiden zijn lectines extreem klein en resistent tegen afbraak door levende systemen en hebben ze de neiging om te accumuleren en geïncorporeerd te worden in de weefsels waar ze normale biologische processen verstoren.

Bij extreem kleine concentraties stimuleert WGA de synthese van pro-inflammatoire chemische boodschapperstoffen. WGA veroorzaakt thymusatrofie in ratten. WGA kan de bloed- hersenbarrière passeren. Het hindert waarschijnlijk ook genexpressie en verstoort de endocriene functie.

Bronnen:

GreenMedInfo 2009

Commentaar Dr. Mercola:

Ik heb lang verteld over de gevaren van het eten van alle types granen, inclusief de verondersteld gezonde volkoren tarwe en gekiemde varianten.

Het schuld van het "gevaar" wordt meestal aan gluten, een eiwit dat in het algemeen gevonden wordt in tarwe, rogge en gerst. Coeliaki, ook wel tarwe- of glutenintolerantie, treedt op wanneer je lichaam geen gluten kan verteren.

De onverteerde gluten brengt vervolgens je immuunsysteem om de bekleding van de dunne darm hetgeen symptomen als diarree of verstopping, misselijkheid en buikpijn kan veroorzaken.

Na verloop van tijd raakt de dunne darm steeds meer beschadigd en minder in staat om nutriënten zoals ijzer en calcium te absorberen. Dit kan weer tot anemie, osteoporose en andere problemen leiden.

Dit is echter maar één probleem dat met het eten van tarwe in verband gebracht wordt en het is misschien niet het meest ernstige probleem. Die eer zou wel eens naar tarwelectine kunnen gaan.

Wat is Tarwelectine?

Lectine is een verdedigingsmechanisme voor de tarweplant, ervoor bestemd om natuurlijke vijanden zoals schimmels en insecten af te weren. Ongelukkigerwijs is dit eiwit ook erg bestand tegen afbraak door levende systemen en het accumuleert gemakkelijk in weefsels waar het normale biologische processen hindert en als antinutriënt werkt.

Kiemen, fermenteren of verteren kan over het algemeen een paar van de negatieve effecten van zulke antinutriënten oplossen (zoals in het geval van het fermenteren van soja, dat veel van zijn antinutriënt eigenschappen verwijdert). Lectines zijn echter resistent tegen deze types van bewerking.

Om deze reden bestaan lectines zelfs in "gezond" gekiemd brood en waarschijnlijk in hun hoogste concentraties in volkoren tarwe variaties.

Dr. Del Thiessen verklaarde de gevaren zeer goed in het artikel "The Awful Truth About Eating Grains". Als je een paar minuten hebt stel ik voor dat je dit artikel in zijn geheel leest.

Maar om het in het kort samen te vatten schrijft Dr. Thiessen:

"Lectines, die eiwitten zijn die overal in het plantenkoninkrijk voorkomen, worden erkend als de voornaamste antinutriënten in voedsel. Lectines in granen zijn tarwekiem agglutinine (WGA). Het kan verterings/absorptie activiteiten verstoren en het kan de balans van de bacteriële flora veranderen hetgeen problemen kan veroorzaken met normaal darmmetabolisme. Het potentieel om de menselijke gezondheid te verstoren is groot."

De Gevaren van Tarwelectine

Wat is precies het potentieel van lectines om je gezondheid te ontwrichten? Hier zijn voorbeelden van de gevaren waarover je hier meer uitgebeid kunt lezen :

- Pro-Inflammatoir: WGA lectine stimuleert de synthese van pro-inflammatoire chemische boodschapstoffen, zelfs bij kleine concentraties.

- Immunotoxisch: WGA lectine kan binden met witte bloedcellen en ze activeren.

- Neurotoxisch: WGA lectine kan de bloed-hersenbarrière passeren en zich hechten aan de beschermende coating om je zenuwen die de myeline schede heet. Het is ook in staat om zenuwgroeifactor te remmen die belangrijk is voor de groei, het onderhoud en het overleven van bepaalde target neuronen.

- Cytotoxisch (Toxisch voor cellen): WGA lectine veroorzaakt mogelijk geprogrammeerde celdood.

Verder laat de wetenschap zien dat WGA lectine zelfs:

- Genexpressie kan verstoren-· Endocriene functie kan verstoren

- De maag-darmfunctie negatief kan aantasten

- Vergelijkbare eigenschappen met bepaalde virussen kan delen

WGA lectine is in staat om de celmembranen van je darmen te passeren en zo je lichaam binnen kunnen komen. Verder, als je slijmvliesbarrière aangetast is door bijvoorbeeld het gebruik van bepaalde medicijnen zoals aspirine en ibuprofen, kan lectine nog problematischer worden.

Onthoud dat lecitine niet alleen in tarwe voorkomt. Alle zaden van de grasfamilie (rijst, tarwe, spelt, rogge, etc.) hebben hoge levels lectine.

Dr. Peter 'D Adamo van het bloedgroependieet geeft in zijn site lijsten van voedingsmiddelen waarbij hij ook de lectinecontent bij ieder product aangeeft:

http://www.dadamo.com/typebase4/typeindexer.htm

Tarwegluten Kan Ook Je Gezondheid Beschadigen

Zoals ik eerder zei treedt coeliaki op wanneer je lichaam geen gluten kan verteren die in tarwe gevonden wordt (gluten komt ook voor in rogge, gerst, haver en spelt).

Volgens statistieken van de Universiteit van Chicago Celiac Disease Center, lijdt gemiddeld 1 uit de 133 anderszins gezonde mensen aan deze spijsverteringsziekte.

Voorgaande studies hebben ontdekt dat dit aantal zou wel eens zo hoog als 1 uit 33 kunnen zijn in risicobevolkingsgroepen.

“Gluten” komt uit het Latijnse woord voor lijm en zijn plakkende eigenschappen houdt brood en cake bij elkaar. Maar diezelfde eigenschappen verstoren de afbraak en absorptie van nutriënten uit ander voedsel in dezelfde maaltijd.

Het resultaat is een samengeplakte constiperende klomp in je darm in plaats van een voedzaam, gemakkelijk verteerde maaltijd.

De onverteerde gluten "triggert" dan je immuunsysteem om de bekleding van je dunne darm aan te vallen hetgeen symptomen als diarree of constipatie, misselijkheid en buikpijn kan veroorzaken.

Na verloop van tijd raakt je dunnen darm steeds meer beschadigd en minder in staat om nutriënten zoals ijzer en calcium op te nemen.Dit kan weer tot anemie, osteoporose en andere problemen leiden.

De snelle toename van coeliaki en mildere vormen van glutenintolerantie in geen verassing gezien het moderne westerse dieet dat voor een groot deel uit koolhydraten uit granen bestaat.

Daar komt bij dat de moderne tarwe heel verschillend is van de tarwe die je voorouders aten. De verhouding van gluteneiwit in tarwe is enorm toegenomen als een resultaat van kruisen.

Tot de 19^e eeuw werd tarwe in het algemeen ook gemengd mat andere granen, bonen en noten; puur tarwemeel wordt pas de laatste 200 jaar gemalen tot geraffineerd wit meel.

Het resulterende hooggluten, geraffineerd graandieet dat de meesten van jullie gegeten hebben sinds je kindertijd was gewoonweg niet een deel van het dieet van eerdere generaties.

Om de zaken nog gecompliceerder te maken blijft coeliaki vaak jarenlang onopgemerkt omdat symptomen niet altijd aanwezig zijn. En omdat coeliaki tot voor kort gezien werd als zeldzame ziekte blijft het vaak niet gediagnosticeerd of mis gediagnosticeerd als IBS of lactose intolerantie.

Als je coeliaki hebt - een bloedtest kan het duidelijk maken - is het absoluut noodzakelijk dat je geen gluten eet om niet je gezondheid nog meer schade toe te brengen.

Wees je er alsjeblieft bewust van dat gluten is veel voedingsmiddelen verborgen kan zitten inclusief soepen, sojasaus, snoepjes, vleeswaren en in verschillende vetarme en vetloze producten dus je moet er zeker van zijn dat je de etiketten gelezen hebt voordat je ze eet. Kijk ook uit met mout, zetmeel, hydrolyzed vegetable protein (HVP), texturized vegetable protein (TVP) en natuurlijke smaakmakers. Sommige farmaceutische producten en alcohol kunnen ook gluten bevatten.

Moet Je Granen Opgeven?

In mijn ervaring heeft zon 75-80% van ALLE mensen baat bij het vermijden van granen, zelfs van gekiemde volkoren granen. Dit geldt of je nu een glutenintolerantie hebt of niet. Dat is omdat, behalve de problemen met antinutriënten zoals lectine en eiwit zoals gluten, granen snel tot suikers afgebroken worden in het lichaam, hetgeen verhoogde insulinelevels veroorzaakt die gezondheidsproblemen verergeren zoals:

- Overgewicht

- Hoog cholesterol

- Hoge bloeddruk

- Type 2 diabetes

- Kanker

De enige consistente uitzonderingen zouden diegenen zijn wiens voedingstype het koolhydraattype is en je niet lijdt aan symptomen van intolerantie.

Gerelateerde Linken:

The Awful Truth About Eating Grains

More Reasons to Avoid Wheat

Why is Wheat Gluten Disorder on the Rise?