Anti-Soy Myth?

September 18, 2003

Not sure if this is a myth or not but my wife has hypothyroidism, is on

synthroid, and we eat any and all the soy products we want, and she's

doing fine.

On Thursday, September 18, 2003, at 12:34 AM,

wrote:

> hi cherie,

> i have hypothyroidism too. my dr. said it was ok to

> eat soy occasionally and that when i did eat soy to

> make sure it was several hours after i take the

> thyroid medicine. the same goes for broccoli,

> cauliflower, and cabbage (and some others i can't

> think of right now). i have greatly reduced the

> amount of soy i eat/drink, but haven't reduced the

> veggies. i think the benefits of the veggies outweigh

> the potential harm they might cause.

> susie

>

My unconscious surfaces in fiction and art,

music being the base for these.

--W B Kek, poet

September 18, 2003

My doctor never mentioned this to me at all (but he always told me to research

well, as he could not!) Several of my friends who have hypothyroidism have been

advised by their doctors to avoid soy, as it interferes with the absorption of

the medication. There is an excellent medical treastise on this at :

http://thyroid.about.com/gi/dynamic/offsite.htm?site=http%3A%2F%2Fwww.soyonlines\

ervice.co.nz under the British Food Standards Agencies Committee on Toxicity

Report link.

Here is an eye-opening quote from that report:

Interaction with thyroxine medication

Phytoestrogens could potentially interact with thyroxine medication, which is

given to patients diagnosed with congenital hypothyroidism. As previously

outlined, phytoestrogens could alter TBG concentrations and increase the binding

capacity for thyroxine. If a fixed dose of thyroxine is used in treatment,

ingestion of large amounts of phytoestrogens could lower the amount of thyroxine

available in the free (active) form.

Alterations in the concentration of TBG may not be the only mechanism by which

phytoestrogens could disrupt thyroxine treatment (Chorazy et al, 1995; Jabbar et

al, 1997). Studies in infants with congenital hypothyroidism have found that

those fed soy-based infant formula have an increased requirement for thyroxine

(above expected replacement levels). Indeed, a study by Jabbar et al (1997)

estimated that as much as an 18-25% increase in thyroxine might be required.

This increased requirement disappeared, however, once the soy-based formula was

discontinued. In addition, clinicians and parents of these children noted marked

alterations in bowel habit, which also resolved following removal of the

soy-based formula (Pinchera et al, 1965). This observation led the authors to

speculate that increased removal of thyroxine in the faeces was the most likely

explanation for the reduced thyroxine concentration.

In 1998, following recommendations from the New Zealand Ministry of Health,

clinicians were advised to closely monitor thyroxine levels in infants with

hypothyroidism who were fed soy-based infant formula or high levels of other soy

containing infant foods. It was suggested that in these infants, a higher than

usual level of thyroxine would be required to maintain an euthyroid state (New

Zealand Ministry of Health, 1998).

It is also possible that the use of isoflavone-containing dietary supplements

may interfere with thyroid medication used to maintain a euthyroid state in

hypothyroid individuals. No data are available on estimated intakes of

phytoestrogen from dietary supplements, however dietary exposure levels will

increase very significantly if individuals take these supplements.

Thyroid autoimmunity

A study by Fort et al (1990) primarily investigating diabetes also reported an

increased prevalence in thyroid disease amongst children fed soy-based infant

formula as infants. This was a retrospective telephone recall study comparing

cases of hypo- and hyperthyroidism in children with their siblings and other

non-related controls. Of the infants fed soy-based formula, 31% developed

autoimmune thyroid disease compared to 7% of controls. A cause and effect

relationship was not established. The study itself was limited by a number of

confounding factors including recall bias by patients, which compromises the

accuracy of the information obtained. In addition, the small group numbers do

not allow the results to be adjusted for age, sex, or parental health status and

dietary habits, which may also have contributed to the child's autoimmune