Fw: [1MinuteNews] DNA - Disease aren't always real

[Guest guest]

[1MinuteNews] DNA - Disease Links aren't always realThis is from my upline

Presidential in Mannatech, but it is so good I had to pass it on.

Don

 

Over the years we've seen many signposts that genetics have less of a role than

previously thought in the potential for optimal health and well-being. Below is

an article that appeared in the Wall Street Journal and Science Journal this

week I thought you might find interesting. I have also included the 5 Tenets of

Nutrigenomics and attached the UCB article from a few years back that highlights

the potential for food and diet to modulate our genes. Enjoy! Noni

 

Five Tenets of Nutrigenomics: http://nutrigenomics.ucdavis.edu/

.. Under certain circumstances and in some individuals, diet can be a serious

risk factor for a number of diseases.

.. Common dietary chemicals can act on the human genome, either directly or

indirectly, to alter gene expression or structure.

.. The degree to which diet influences the balance between healthy and disease

states may depend on an individual's genetic makeup.

.. Some diet-regulated genes (and their normal, common variants) are likely to

play a role in the onset, incidence, progression, and/or severity of chronic

diseases.

.. Dietary intervention based on knowledge of nutritional requirement,

nutritional status, and genotype (i.e., " personalized nutrition " ) can be used

to prevent, mitigate or cure chronic disease.

 

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SCIENCE JOURNAL

By SHARON BEGLEY

 

DNA-Disease Links

Aren't Always as Real

As They First Appear

January 14, 2005; Page B1

 

For two decades we have been hearing claims that a glitch in one or another gene

raises the risk of diseases from cancer to heart disease, schizophrenia to

depression.

 

Small wonder, then, that we have become genetic fatalists, assuming " my genes

did it. " I regularly hear from physicians who are frustrated that so many

patients believe their medical fate is written indelibly into their DNA and

therefore resist steps that can stave off disease.

 

That is doubly tragic because the percentage of so-called association studies --

linking a genetic variant to a disease -- that are probably wrong is

astonishing. One analysis concluded that fewer than one-third hold up. Another,

by British scientists in 2003, estimated that as many as 95% are " false

positives " -- flat-out wrong.

 

" The field has a very poor record of replicating associations between DNA

variants and disease, " says Sholom Wacholder of the National Cancer Institute.

" We are probably doing something wrong. "

 

You caught a hint of this in last week's news that a widely-cited estimate of

the breast-cancer risk from two particular genes is likely overblown. In that

case, scientists concluded that women with mutations in genes named BRCA1 or

BRCA2 have an 82% chance of developing breast cancer by age 80 (absent the

mutations, the lifetime risk is 12%).

 

Other studies of BRCA had found risks of 36%, 56%, 65%, 73% -- and some of those

could well be an overestimate, too, the researchers concede. Why? By recruiting

volunteers, they were more likely to get women with a family history of breast

cancer, notes Dr. Wacholder. Families share many more DNA variants than just

BRCA. If you find high breast-cancer rates in relatives with a BRCA mutation,

the temptation is to blame BRCA, but other variants may also be at fault.

 

For BRCA, there is no question that mutations raise the risk of breast (and

ovarian) cancer. The argument is over how much. But for other genetic variants

the debate is much more fundamental: Do they or don't they make you more likely

to develop a disease?

 

There is no dispute about diseases that are clearly caused by a mutation in a

single gene -- diseases such as sickle cell and Huntington's. The increasing

skepticism about genetic studies instead focuses on complex but common diseases

that result from the interaction of many, many genes as well as the environment:

cancers, obesity, mental illnesses and heart disease.

 

The list of genes whose link to a disease has not held up is a veritable

alphabet soup. ADD1 and hypertension; APOE and schizophrenia; BLMH and

Alzheimer's; COMT and bipolar disorder; GSTM1 and breast cancer; PON1 and

coronary-artery disease . . . I could go on. For hundreds of other genes, there

seems to be a much weaker link to the disease than first report suggested, with

the genetic variation accounting for a tiny bit of the disease risk.

 

" On a good day, it might explain only 1% or 2% of the variance, " says Irving

Gottesman of the University of Minnesota, an expert on the genetics of

psychiatric illnesses who has long been skeptical of simplistic gene-disease

links.

 

One reason for what Dr. Wacholder calls " this unfortunate situation " is how easy

it has become to analyze genes. Time was, that was so difficult that geneticists

would first identify, based on knowledge of a disease, which genes might play a

role. When they found that a suspect gene indeed raised the disease risk, it

meant something.

 

Now, though, reading genes is so quick, taking a day rather than months, that

scientists can and do scan thousands. By chance alone, some of those will seem

to raise the risk of disease in a statistically significant way, says Joel

Hirschhorn of the Broad Institute at Harvard University and the Massachusetts

Institute of Technology in Cambridge, Mass. " Statistically significant " means

less than a one-in-20 chance that the link was coincidental and not real.

 

" If you test enough different genes for an association with enough different

diseases, you'll automatically get a 'significant' result, " he says. But that

might be only a coincidence: Flipping 10 heads in a row doesn't mean you have a

two-headed coin.

 

Geneticists have been embarrassed at how many claims of gene-disease links fail

to " replicate. " That is, after the initial claim there is either a deafening

silence, with no follow-up studies confirming the association, or an outright

refutation. (Many negative results never see the light of print; journals prefer

papers that find something to those that fail to.) In one comprehensive

analysis, scientists led by Dr. Hirschhorn counted more than 600 reported

associations between a DNA variant and a disease. Only 166 had been studied at

least three times; only six had been consistently replicated.

 

Another source of error is not taking into account how genes cluster by

ethnicity. Say you find a DNA variant that's more common in people with diabetes

than in healthy people. And say you did your study on Finns. Like every ethnic

group, Finns share distinctive genetic variants that others lack. As a result,

says Dr. Hirschhorn, " you might have found a genetic marker of ancestry and not

for diabetes at all. [such effects] can completely fake you out. " It's a lesson

geneticists have been slow to learn.

 

.. You can e-mail me at sciencejournal.