Month: December 2005

…there is no clear evidence that schools are contributing to the growth in obesity.  The obesity-related complaints about school lunches, vending machines, and physical education are based largely on the assumption that these factors are causing our kids to get fat.  Yet, I find little evidence to support this claim.  For example, in looking at survey data on the health behavior of middle and high school students, the factor I found that best predicted whether or not a kid was obese was tooth brushing [emphasis added].  More important than how much junk food they ate, soda they drank, or physical education they received was whether or not they brushed their teeth.  Among fourteen- to seventeen-year-olds, only 16 percent of kids who brushed their teeth more than once a day were overweight compared to 24 percent who brushed less than once a day.  Of course, other factors were important as well — teenagers who play more computer games, eat more fast-food, and drink less whole milk were also more likely to be obese — but these factors were tiny in comparison with tooth brushing.  Meanwhile school policies, such as whether the kid was in physical education or ate school lunches, had no predictive power for whether or not a child was obese.

Now obviously the act of brushing one’s teeth plays little direct role in a child’s weight, but it is a good indicator of something else — in what type of household the child lives.  Children who brush their teeth more often are more likely to come from homes where health and hygiene are a priority…In other words, outside of genetics, the biggest factor predicting a child’s weight is what type of parenting they receive [emphasis added].

That is from J. Eric Oliver’s Fat Politics: The Real Story Behind America’s Obesity Epidemic.  Here is my previous post on the book; the comments are open.

Here is a defense of using those rat tests to judge what will cause cancer in humans:

The "junk science" they are referring to is the long-standing and
well-confirmed practice of identifying chemicals likely to cause cancer
in humans by testing them in animals. The animals (rodents) are a
standard model for biological processes of relevance to humans (which
is why drug companies and medical researchers have been using them for
a century). They are well understood and are the only sentinels for
detecting carcinogenicity of any use to public health. Since chemically
induced cancer has a latency period of decades (typically 20 years or
more), waiting for it to appear in human populations would meant that
once detected, even if exposure would cease instantly (which can never
happen), it would take another 20 or more years to eliminate the
cancers from exposure (all the cancers induced in the 20 years exposure
prior to detection). But even then, the chances of detecting any but
the most powerful carcinogens in human populations (via epidemiology)
is small. Epidemiology is a very insensitive tool. I say this with some
authority, as I am a cancer epidemiologist specializing in chemical
exposures and have authored numerous peer reviewed studies in that area
over many years.

The main rhetorical lever ACSH employs is the
use of high doses in the animal studies, doses that are much higher
than usually faced by humans. But as ACSH knows well (but didn’t
divulge) there is a technical requirement for using these doses. If one
were to use doses in animals predicted to cause cancer at a rate we
would consider a public health hazard, we would need tens of thousands
of animals to test a single dose, mode of exposure and rodent species
or strain. This makes using those doses infeasible. Thus a Maximum
Tolerated Dose is used, one that causes no other pathology except
possibly cancer and doesn’t result in more than a 10% weight loss. The
assumption here is that something that causes cancer at high doses in
these animals will also do so at low doses. This is biologically
reasonable. It is a (surprising) fact, that most chemicals, given in no
matter how high a dose, won’t cause the very unusual and specific
biological effect of turning an animal cell cancerous. Cancer cells are
not "damaged" cells in the individual sense but "super cells," capable
of out competing normal cells. It is only in the context of the whole
organism that there is a problem. It is not surprising, then, that very
few chemicals would have be ability to turn a normal cell into a
biological super cell of this type. Estimates are that is far less than
10%, perhaps only 1% of all chemicals that have this ability. Thus
western industrial civilization doesn’t have to come to a screeching
halt if we eliminate industrial chemical carcinogens from our
environment.

We know of no false negatives with this process.
Every chemical we know that causes cancer in humans also does so in
rodents (with the possible exception of inorganic trivalent arsenic,
which is equivocal).

Here is the full post.  I’m not close to having the expertise to evaluate these claims, but two points.  First, the author is highly qualified; as a blogger he is anonymous but I can vouch for his credentials.  Second, it should be the self-appointed task of bloggers to pass along arguments which either struck them or which might shake up their readers.