I think that there is a lot more to this story- it's not just the mother that determines the health of the baby. I've done a lot of research and there is nothing in the literature that says that excessive iodine consumption will lead to any sort of birth defect. If anyone has found anything to support that hypothesis, please inform. Transient hypo or hyperthyroidism, sure.
I'm NOT saying that this is impossible, folks, so please refrain from jumping all over me. I just find this particular cause/effect to be unprovable.
MH is not considering other factors which may have played a part in this. He's had severe exposure to toxic heavy metals. Lead, for instance.
.The father's health or lack thereof and exposure to heavy metals such as lead affects sperm production and health. The longer one works with these toxins the more one's health and the health/viability of the sperm is impacted...infertilty can be the end result. Here's just one example:
The present study showed deterioration in sperm density and motility in the lead exposed pigment factory workers with high prevalence of sperm head abnormality in comparison with the nonoccupationally exposed matched control subjects of same socio-economic status. This observation was in corroboration with the earlier observations of Roy Chowdhury et al., These pigment factory workers exposed to lead fumes and dust during their work, which caused adverse effects on sperm morphology and density.,, Morphological abnormalities of spermatozoa were also depended on the duration and nature of exposure.,
Fructose is the main energy source for spermatozoa motility  and sperm velocity is the average velocity of all spermatozoa in one sample, therefore, both are related with sperm motility grade leading to sperm activity. Lowering of sperm velocity, gross motility, and FP with concomitant rise of SM were prevalent in the lead exposed pigment factory workers of high seminal plasma fructose level, which indicated retarded sperm activity might be due to lead induced alteration of normal fructolysis. This observation showed similarities with the earlier findings. ,,The present finding was also in corroboration with the previous observation by showing diminution of sperm ATPase activity after occupational lead exposure leading to low sperm motility.
As increase amount of free amino acid depends on the degradation of protein present in the system, therefore, lowering of seminal plasma total protein with concomitant rise of free amino acid in pigment factory workers with respect to control subjects indicated that lead may alter the protein metabolism and subsequently increase the amino acid level, suggesting disturbance in cellular nutritional status, necessary for cell survival, and proper function.
Low volume, viscosity, prolonged liquefaction time, and deviation of the seminal fructose, cholesterol, and protein content among the lead exposed pigment factory workers in the present study indicated the alteration of normal secretary activity of seminal vesicle and prostate after occupational lead exposure. Previous study reported that 95% of ejaculatory volume comes from these two accessory sex glands and alteration of normal liquefaction associated with low viscosity, indicating deficiency of liquefying agent due to low prostatic secretary activity. Thus the present study suggesting probable dysfunction of accessory gland seminal vesicle and prostate after toxic insult of lead at work place.
The present study showed significant decline in human sperm quality and fertility (40% workers have fertility problem) without affecting the serum FSH, LH, and testosterone level, which are in corroboration with the previous finding, ,, but at the same time contradictory to others results. ,,
In our study deterioration of sperm quality and fertility potential of the subjects were associated with high lead concentration in whole blood and semen of the workers in respect of duration of exposure. Xuezhi showed that lead exposure caused prolonged liquefaction time, low volume, sperm count, viability, and retarded sperm activity in male workers with high blood lead level, which is similar to the observation of Apostoli et al. and Kasperczyk et al. Semen lead was higher in the infertile men than the fertile group and low semen lead level was the indicator of low industrial exposure. Moderate lead exposure also caused reduction in sperm characteristics among the factory workers.
Therefore, in conclusion it can be pointed out that lead may cross the blood testis barrier and affect spermatozoa of the exposed population leading to accessory gland dysfunction, morphological abnormality, high seminal fructose in oligospermic exposed workers, , disturbance in cellular nutritional status, and energy-dependant processes like sperm production and motility leading to reduced sperm count, retarded sperm activity, and infertility. Smoking habits, addiction to alcohol, gutkha, etc. may be the added factors in lead toxicity, whereas minor electric shock, typhoid, gastritis, pox, and the age of the subjects did not show any correlation after exposure.