Binge eating caused by faulty gene, sometimes

Barbara Hirsch wrote:
I wrote this study up about a year or so ago when it came out. The
melanocortin-4 receptor IMC4R) mutation is the most common genetic
cause of obesity. The reason for this is that it's dominantly
inherited, i.e., you only need one allele of the gene to have the
mutation expressed. There are many variations of the mutation, and
some result in more obesity than others.

1) It's different mutations within one gene rather than many
variations of the mutation.

2) Some of these mutations are dominant, others are not:
http://www.jci.org/cgi/content/full/106/2/271

3) There are even combinations that predispose carriers to obesity in
the heterozygote state -- one would need two different mutations for
the obesity risk to increase:
http://www.jci.org/cgi/content/full/106/2/185

DZ

In the study researchers found that the subjects with the mutation had
a higher prevalence of binge eating disorder (BED) than those without
the mutation. However, since the researchers were looking for a reason
for the obesity, they did not report data on any subjects with
bulimia. Therefore, it can't be concluded from the article that
bingeing and purging are related to MC4R.

However, just because many people with BED are free of the MC4R
mutation does not mean they don't have another unknown genetic reason
for the behavior. All causes of obesity have an environmental and a
genetic component. In some cases, the genetic component is so
overwhelming that it is all but impossible to control the obesity
(i.e., leptin mutations, leptin receptor mutations) and in others, it
is fairly easy to contain with extra effort.

FWIW,


Barbara Hirsch, Publisher
OBESITY MEDS AND RESEARCH NEWS
The latest in obesity research and weight loss drug development
http://www.obesity-news.com/

On Sat, 07 Aug 2004 20:56:51 GMT, DZ wrote:

mutation expressed. There are many variations of the mutation, and
some result in more obesity than others.

1) It's different mutations within one gene rather than many
variations of the mutation.

Symantics. I didn't say polymorophism, I said variations of the
mutation.

2) Some of these mutations are dominant, others are not:
http://www.jci.org/cgi/content/full/106/2/271

So?

3) There are even combinations that predispose carriers to obesity in
the heterozygote state -- one would need two different mutations for
the obesity risk to increase:
http://www.jci.org/cgi/content/full/106/2/185

Depends on the mutation. Some are more sever than others.


Barbara Hirsch, Publisher
OBESITY MEDS AND RESEARCH NEWS
The latest in obesity research and weight loss drug development
http://www.obesity-news.com/

On Sat, 07 Aug 2004 20:56:51 GMT, DZ wrote:

mutation expressed. There are many variations of the mutation, and
some result in more obesity than others.

1) It's different mutations within one gene rather than many
variations of the mutation.

Symantics. I didn't say polymorophism, I said variations of the
mutation.

2) Some of these mutations are dominant, others are not:
http://www.jci.org/cgi/content/full/106/2/271

So?

3) There are even combinations that predispose carriers to obesity in
the heterozygote state -- one would need two different mutations for
the obesity risk to increase:
http://www.jci.org/cgi/content/full/106/2/185

Depends on the mutation. Some are more sever than others.


Barbara Hirsch, Publisher
OBESITY MEDS AND RESEARCH NEWS
The latest in obesity research and weight loss drug development
http://www.obesity-news.com/

Barbara Hirsch wrote:
On Sat, 07 Aug 2004 20:56:51 GMT, DZ wrote:

mutation expressed. There are many variations of the mutation, and
some result in more obesity than others.

1) It's different mutations within one gene rather than many
variations of the mutation.

Symantics. I didn't say polymorophism, I said variations of the
mutation.

2) Some of these mutations are dominant, others are not:
http://www.jci.org/cgi/content/full/106/2/271

So?

This discussion so far revolved under the assumption that the
mechanism (considering polymorphisms at melanocortin 4 receptor) is
via dominant inheritance. However, some mutations in this gene show
recessive mechanism and there are even situations where two different
mutations are required. It would then be misleading to say that there
is 50% chance for the offspring to have increased obesity
predisposition given that one parent carries one copy of the mutation,
because one would also have to consider the mutation type.

DZ

3) There are even combinations that predispose carriers to obesity in
the heterozygote state -- one would need two different mutations for
the obesity risk to increase:
http://www.jci.org/cgi/content/full/106/2/185

Depends on the mutation. Some are more sever than others.


Barbara Hirsch, Publisher
OBESITY MEDS AND RESEARCH NEWS
The latest in obesity research and weight loss drug development
http://www.obesity-news.com/

Barbara Hirsch wrote:
On Sat, 07 Aug 2004 20:56:51 GMT, DZ wrote:

mutation expressed. There are many variations of the mutation, and
some result in more obesity than others.

1) It's different mutations within one gene rather than many
variations of the mutation.

Symantics. I didn't say polymorophism, I said variations of the
mutation.

2) Some of these mutations are dominant, others are not:
http://www.jci.org/cgi/content/full/106/2/271

So?

This discussion so far revolved under the assumption that the
mechanism (considering polymorphisms at melanocortin 4 receptor) is
via dominant inheritance. However, some mutations in this gene show
recessive mechanism and there are even situations where two different
mutations are required. It would then be misleading to say that there
is 50% chance for the offspring to have increased obesity
predisposition given that one parent carries one copy of the mutation,
because one would also have to consider the mutation type.

DZ

3) There are even combinations that predispose carriers to obesity in
the heterozygote state -- one would need two different mutations for
the obesity risk to increase:
http://www.jci.org/cgi/content/full/106/2/185

Depends on the mutation. Some are more sever than others.


Barbara Hirsch, Publisher
OBESITY MEDS AND RESEARCH NEWS
The latest in obesity research and weight loss drug development
http://www.obesity-news.com/