expert commentary: The Daddy Factor | Fathers' pre-conception role in atypical development of the newborn - epigenetics & mutations - paradigms - -McCune

[Guest guest]

Commentary by Betty Mekdeci. Executive Director, Birth Defect Research

for Children

Fwd with permission:

In 1986, one of the special masters representing Judge Weinstein in the

Agent Orange litigation contacted our organization, Birth Defect

Research for Children, regarding the children of Vietnam Veterans and

how best to assist them through the Agent Orange Class Assistance

Program (AOCAP) that had been set up our of the settlement funds. I was

extremely reluctant to become involved having spent ten years in court

against a division of Dow Chemical Company. In addition, I knew that it

was difficult enough to prove that a toxic exposure could cause birth

defects through a maternal exposure. Tackling paternal exposures would

be an awesome and perhaps fruitless undertaking.

The special master persisted and we agreed to collect data on the

numbers and types of disabilities in the children of Vietnam veterans so

we could make recommendations about the types of programs that would be

needed to assist them. This was at the beginning of the development of

our project, the National Birth Defect Registry.

We contacted the New Jersey Agent Orange Commission for assistance and

they helped us with the design of the registry's questionnaire pages

that collected the data on the area and type of the veterans' service.

They also insisted that we add categories for immune, allergic,

endocrine, learning, attention and other conditions that would not

normally be added to a birth defect project.

This was prophetic. >From our first analysis of data on the children of

male veterans, we found a pattern of increases in learning, attention,

immune and endocrine problems. This has been consistent from the first

analysis of 300 cases to future analyses of 2,000 cases. These data are

also consistent with animal, cell culture and epidemiological studies of

dioxin in other environmental exposures.

This was surprising, so we started looking at all the literature we

could find on male-mediated birth defects. There are over 120 different

chemicals that will produce birth defects in the offspring when treated

males are mated with untreated does. There is even a study of

male-mediated toxicity with thalidomide. A lot of information was

provided to us by Friends of the Earth. Male-mediated birth defects had

been one of their key issues, but they had to give it up because they

couldn't get any funding to pursue this issue.

We have presented our Agent Orange data to the National Academy of

Science, the VA, the EPA subcommittee on endocrine disruptors,

congressional veterans' affairs committees and in the national media.

Because of our work on Agent Orange, we were well known to military

organizations and nine months after the first Gulf War, we started

getting calls from veterans who had children with birth defects.

According to the General Accounting Office, Gulf War veterans were

potentially exposed to over 31 different reproductive toxicants. Once

again, we started collecting data and found an increase in a rare

craniofacial syndrome (Goldenhar) in the children of male Gulf War

veterans. We were asked to present our data to the Presidential

Advisory Committee on Gulf War Illnesses. Subsequently the Department

of Defense funded a study that found a tripling of Goldenhar Syndrome in

the children of Gulf War veterans when the children were born in

military hospitals. We are currently using our data for a study with

the University of Texas, SW to look at cases born in both military and

civilian hospitals.

There are now three other government-funded studies that have found

increases in birth defects in the children of Gulf War veterans. Yet,

nothing has been done to assist the children of Gulf War veterans.

The answer to this puzzling indifference may be illustrated by this

anecdote. I was asked to make a presentation on our work at a NIEHS

workshop. I presented our charts on Agent Orange and Gulf War birth

defects. After the presentation, a member of the National Teratology

Society approached me and said " the society " had a meeting and decided

there was no such thing as male-mediated birth defects.

The world is flat...the king has clothes...the sun revolves around the

earth. Why not? It's so because we say it is so.

*/Betty Mekdeci/*

Executive Director

Birth Defect Research for Children

http://www.birthdefects.org

- - - -

*/The Bad Daddy Factor/*

Drinking, smoking, taking prescription meds or failing to eat a balanced

diet can influence the health of men's future children.

http://www.miller-mccune.com/health/the-bad-daddy-factor-25764/

- - - -

[Comment: Kusenda & Sebat thoroughly minimize the possibility that some

and perhaps many mutations found in autism were caused by environmental

pollutants. ~]

*/The role of rare structural variants in the genetics of autism

spectrum disorders/*

M. Kusenda, J. Sebat

Cytogenet Genome Res 123:36--43 (2008)

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2920182/

excerpt:

The prevailing hypothesis for the genetic basis of autism

and other neuropsychiatric disorders has thus been the

'common gene/common disease' hypothesis which posits

that disease results due to the additive or multiplicative effects

of multiple genetic and environmental factors, with

individual genes accounting only for a small increase in the

risk in an individual patient (Lohmueller, 2003). Consequently,

considerable effort has been devoted to the approaches

most suitable to test this hypothesis, which are primarily

linkage analysis and more recently genome-wide association

studies (GWAS). Despite rigorous effort, definitive

identification of autism genes by this approach remains elusive.

Results from early linkage studies of ASD found evidence

for linkage at many different locations throughout

the genome (Risch et al., 1999). Several subsequent linkage

scans produced similar results (Alarcon et al., 2002; Auranen

et al., 2002; IMGSAC, 2001; Liu et al., 2001; Szatmari

et al., 2007), but no individual loci identified therein were

widely replicated. These findings were consistent with the

model that autism is a complex disorder involving a large

number of different genes.