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September 2nd, 2001 - Open Knowledge — LiveJournal

Sep. 2nd, 2001

01:10 am - More about Clarence Bass

Having an e-mail discussion with someone about Clarence Bass. Here's
part of my end of the conversation:

CRAN = Calorie Restriction with Adequate Nutrition

Correspondent suggested that Bass's high carbohydrate diet was not
optimal for weight loss, and had little scientific backing.


Thanks for the detailed response! I think that Bass's views are more
nuanced than you suggest. For example, he advocates always eating
some protein and fat with each meal to better achieve the satiety you
mention. He also recommends a "volumetric" diet, in which low-caloric
density foods (high in fiber and water) are substituted for
high-caloric density foods. Low-caloric density foods tend to contain
complex carbohydrates, hence his recommendation. Note, that he would
probably recommend avoiding a lot of pretzels or bagels (traditionally
considered "good" diet foods due to their low fat content) because of
their high energy density.

According to a nutritional analysis of his diet:

complex carbs 58% Protein 29% Fat 12% (Saturated 3%, Polyunsaturated
4%, monounsaturated 4%) simple sugar 1%. daily fiber intake: 58 grams

I also don't think that "...all of the empirical evidence seem to
contradict Bass's claims..." For example, he references Barbara
Rolls' work:



Eur J Clin Nutr 1999 Apr;53:S166-S173

Intake of fat and carbohydrate: role of energy density. Rolls
BJ, Bell EA.

Nutrition Department, Pennsylvania State University, University
Park 16802, USA.

In this review, we consider two hypotheses which could explain
why high-fat foods are overeaten. The first hypothesis is that
fat is overeaten because it affects satiety and satiation less
than carbohydrate. In several studies which have evaluated the
effects of fat on satiety and satiation, fat differed little
from carbohydrate when both the palatability and energy density
of the test foods were matched. Therefore it is unlikely that
the effects of fat on satiety or satiation provide the primary
explanation for why it is overeaten. The second hypothesis is
that the high energy density of fat facilitates its
overconsumption. Support for this view comes from recent
studies in which energy density significantly influenced intake
when both the macronutrient content and palatability of the test
foods were matched. For example, when individuals were fed diets
varying in energy density and could eat as much food as they
liked, they ate the same amount of food (by weight) so energy
intake varied directly with energy density. Furthermore, when
participants consumed foods of low energy density, they felt
satisfied, despite reductions in energy intake. These findings
show that energy density is a key determinant of energy intake
in that cognitive, behavioral, and sensory cues related to the
volume or weight of food consumed can interact with or override
physiological cues associated with food intake.

J Am Diet Assoc 1998 Apr;98(4):408-413


See also this paper:



Persons successful at long-term weight loss and
maintenance continue to consume a low-energy, low-fat diet.

Shick SM, Wing RR, Klem ML, McGuire MT, Hill JO, Seagle H.

Department of Epidemiology, University of Pittsburgh School of
Medicine, PA 15213, USA.

OBJECTIVES: To describe the dietary intakes of persons who
successfully maintained weight loss and to determine if
differences exist between those who lost weight on their own vs
those who received assistance with weight loss (eg, participated
in a commercial or self-help program or were seen individually by
a dietitian). Intakes of selected nutrients were also compared
with data from the third National Health and Nutrition
Examination Survey (NHANES III) and the 1989 Recommended Dietary
Allowances (RDAs). SUBJECTS: Subjects were 355 women and 83 men,
aged 18 years or older, primarily white, who had maintained a
weight loss of at least 13.6 kg for at least 1 year, and were the
initial enrollees in the ongoing National Weight Control
Registry. On average, the participants had lost 30 kg and
maintained the weight loss for 5.1 years. METHODS: A
cross-sectional study in which subjects in the registry completed
demographic and weight history questionnaires as well as the
Health Habits and History Questionnaire developed by Block et
al. Subjects' dietary intake data were compared with that of
similarly aged men and women in the NHANES III cohort and to the
RDAs. Adequacy of the diet was assessed by comparing the intake
of selected nutrients (iron; calcium; and vitamins C, A, and E)
in subjects who lost weight on their own or with
assistance. RESULTS: Successful maintainers of weight loss
reported continued consumption of a low-energy and low-fat
diet. Women in the registry reported eating an average of 1,306
kcal/day (24.3% of energy from fat); men reported consuming 1,685
kcal (23.5% of energy from fat). Subjects in the registry
reported consuming less energy and a lower percentage of energy
from fat than NHANES III subjects did. Subjects who lost weight
on their own did not differ from those who lost weight with
assistance in regards to energy intake, percent of energy from
fat, or intake of selected nutrients (iron; calcium; and vitamins
C, A, and E). In addition, subjects who lost weight on their own
and those who lost weight with assistance met the RDAs for
calcium and vitamins C, A, and E for persons aged 25 years or
older. APPLICATIONS: Because continued consumption of a low-fat,
low-energy diet may be necessary for long-term weight control,
persons who have successfully lost weight should be encouraged to
maintain such a diet.



That said, I agree with you that high-protein isocaloric diets may
also lead to weight loss. My principal concerns with a high protein
and/or high fat diet would be the 1) increased risk of heart disease
and cancer 2) increased risk of kidney disease 3) increased risk of
osteoporosis. For example, according to John McDougall

"....By the eighth decade of life people in affluent societies
commonly lose about 30 percent of their kidney function (J Gerentol
31:155, 1976). This loss is believed to be secondary to overwork of
the kidneys caused by the amount of protein typically consumed on the
American diet, 12% to 15% protein (N Engl J Med 307:652, 1982). The
Zone diet recommends 30% protein, and even more protein is found in
other high-protein diets. Low protein diets (4% to 8%) are used
routinely to treat patients with liver and kidney failure....."

See http://www.drmcdougall.com/debate.html for more information.

I'd love to any references you may have on the benefits of a high fat,
high protein diet.

I agree with you that much of Bass's success at keeping the weight off
is due in large part to his life-long vigorous exercise regimen (and I
think he would be the first to agree.) That said, I think that his
diet, though not restricted in the CRAN sense of the word (he eats
about 2500 kcal per day), is important to his long-term weight loss.
For example, he doesn't keep sweets/fats in the house, he eats at the
same time, he never skips a meal, and he only puts out what he plans
to eat. He measures his weight frequently (daily, if I recall
correctly) and cuts back on his food consumption if he notices his
weight increasing.

I also agree with you that CRAN (or CRON, if you prefer) is the most
well supported intervention to increase maximum lifespan. Clarence
Bass is interesting because, even though he doesn't practice CRAN, he
does extremely well on several biomarkers of aging. His scores on the
following measures matched those of a healthy 30 year-old:

muscle and skeletal health: bone density two standard deviations above
the norm, cardiovascular health: 99th percentile on treadmill test,
"huge" coronary arteries

I don't have information for these dimensions, but I'm betting he
would score well on these measures as well:

glucose regulation immune system endocrine system oxidative stress
brain function

Will he live as long as he would've on a CRAN diet? I don't know.
The number of individuals I've met who practice CRAN is quite small;
however, here's the list:

Roy Walford [other names deleted for privacy reasons]

All are quite intelligent, knowledgeable, and well-disciplined. From
what I know of their diets, they appear to eat an adequate amount of
vitamins and nutrients. However, all of these individuals are
extremely thin--at least one has taken to sitting on an inner tube,
because so much fat was gone from his buttocks that sitting became
painful. None has much muscle mass. Walford appeared frail and weak
when I last saw him two years ago--he had difficulty getting to a
standing position from a stool. (Of course, he might have been much
worse had he not been practicing CRAN).

Will the people I know on CRAN increase their maximum lifespan more
than Bass? Perhaps. The n is much too small to make anything but
educated guesses. However, I bet that Bass would do better on most
biomarkers than any of the CRAN-following individuals at comparable
ages.

> They probably aren't going to be > body builders, though -- but
> which would you rather have, a buff body or > an extra twenty years
> of healthy life?

I don't think that it's an either/or proposition. I think that a buff
body contributes to a longer, healthier life.

> I don't imagine the low-cal lab rats that lived 20% longer were the
> studliest lab rats either...

True, the rats on CRAN were smaller. However, the descriptions I've seen all mentioned their good health (clear eyes, clean, silky fur, high activity levels, high sexual response) compared to their cohorts. The people I know on CRAN don't appear to be much healthier relative to their cohorts. (Admittedly, most began CRAN late in life, so it may only have a subtle effect).

09:24 pm - Why are we getting smarter?

A fascinating paper....

Heritability Estimates vs. Large Environmental Effects:
The IQ Paradox Resolved

Psychological Review, Vol. 108, No. 2 (April 2001)

William Dickens, Senior Fellow, Economic Studies, and
James R. Flynn, University of Otago

(Note: this is a synopsis of an article in Psychological
Review, vol. 108, no. 2, April 2001.)

Darwin's Origin of Species sparked the modern debate about
genes versus environment in explaining differences between
human individuals and groups. Ever since, the pendulum of
scientific opinion has swung back and forth with consensus
always out of reach. For the last 15 years, psychologists
have been plagued by a paradox that suggests that
environment is both feeble and overwhelmingly potent.

The paradox emerged from a debate about race. US whites
outscore US blacks on IQ tests by 15 points. Does that gap
have environmental causes or is it partially due to genes?
In 1973, Arthur Jensen constructed a model that applied
kinship data to group differences in IQ. Evidence from
kinship studies showed identical twins separated at birth
and raised in different homes grow up with very similar
IQs. The fact that they have identical genes provides an
obvious explanation. Jensen argued that fully 75 percent
of IQ variance between individuals was due to genetic
differences (a value which sits in the middle of the range
recently endorsed by a select committee of the American
Psychological Association for adult IQ). Jensen's model
showed that a purely environmental explanation of the
black/white IQ gap meant that the environment of the
average US black must be as unfavorable for the
development of IQ as the lowest one percent of white
environments measured in terms of their effects on
IQ. That simply did not seem possible.

Jensen's model seemed to preclude a purely environmental
explanation for any large IQ gap between groups. Then, in
1987, Flynn showed that in nation after nation, the
current generation outscores the last generation by some 9
to 20 IQ points. The gains are greatest on those tests
often called the best measures of intelligence. Their size
and speed dictate an environmental explanation. Flynn
applied Jensen's model. An environmental explanation meant
putting the current generation within the top one-tenth of
one percent of the last generation in terms of
environmental quality. What was known to be true was shown
to be impossible.

How could solid evidence show both that environment was so
feeble (kinship studies) and yet so potent (IQ gains over
time)?

Dickens has proposed a model that we believe solves the
paradox. It assumes that people who have an advantage for
a particular trait will become matched with superior
environments for that trait; and that genes can derive a
great advantage from this because genetic differences are
persistent. A genetic advantage remains with you
throughout life, while environmental differences tend to
come and go, unless sustained by the steady pressure of
genes.

Take those born with genes that make them a bit taller and
quicker than average. When they start school, they are
likely to be a bit better at basketball. The advantage may
be modest but then reciprocal causation between the talent
advantage and environment kicks in. Because you are better
at basketball, you are likely to enjoy it more and play it
more than someone who is bit slow or short or
overweight. That makes you better still. Your genetic
advantage is upgrading your environment, the amount of
time you play and practice, and your enhanced environment
in turn upgrades your skill. You are more likely to be
picked for your school team and to get professional
coaching.

Thanks to genes capitalizing on the powerful multiplying
effects of the feedback between talent and environment, a
modest genetic advantage has turned into a huge
performance advantage. Just as small genetic differences
match people with very different environments, so
identical genes tend to produce very similar
environments-even when children are raised in separate
homes.

In other words, kinship studies of basketball, no matter
whether they involved people with identical genes or
different genes, would underestimate the potency of
environmental factors. Playing, practicing, being on a
team, coaching, all of these would be credited to
genes-simply because differences in them tend to accompany
genetic differences between individuals. Genes might seem
to account for as much as 75 percent of variance across
individuals in basketball performance. If someone showed
that the present generation was far more skilled at
basketball than the last (as indeed they are), Jensen's
math would prove that it was impossible. It would show
that those aspects of environment that are not correlated
with genes (which is all that environment gets credit for
in kinship studies) were very feeble. So feeble that the
present generation would have to be within the top one
percent of the last in terms of quality of environment for
basketball.

The cognitive ability differences measured by IQ tests may
have the same dynamics. People whose genes send them into
life with a small advantage for these abilities start with
a modest performance advantage. Then genes begin to drive
the powerful engine of reciprocal causation between
ability and environment. You begin by being a bit better
at school and are encouraged by this, while others who are
a bit 'slow' get discouraged. You study more, which
upgrades your cognitive performance, earn praise for your
grades, start haunting the library, get into a top
stream. Another child finds that sport is his or her
strong suit, does the minimum, does not read for pleasure,
and gets into a lower stream. Both of you may go to the
same school but the environments you make for yourselves
within that school will be radically different. The modest
initial cognitive advantage conferred by genes becomes
enormously multiplied.

Once again, just as different genes are matched with very
different environments, so identical genes will be matched
with very similar environments. You and your separated
identical twin will get very similar scores on IQ tests at
adulthood. Using Jensen's model, genes will get credit for
all of the potent environmental influences you both
share. And environment will appear so feeble that it could
not possibly account for the huge IQ advantage your
children enjoy over yourself. Our model shows why this is
a mistake. It shows that kinship studies hide or 'mask'
the potency of environmental influences on IQ. Therefore,
they do not really demonstrate the impossibility of an
environmental explanation of massive gains over time.

The model's next task it to suggest just how environment
performs its demanding role. Social forces affecting the
whole of society can provide something that an
individual's life experiences normally do not. They
provide environmental influences that are just as
persistent over time as the individual's genetic
endowment, and that are not at the mercy of genes. After
all, the present generation has no advantage in genetic
quality over the last, indeed, it is often argued that the
reverse is true due to the lower fertility of the more
highly educated. So between generations, the mask slips
and environmental forces stand out in bold
relief. Relatively small environmental differences between
generations gain enormous potency just as small genetic
differences between individuals did: They seize control of
the powerful reciprocal causation that exists between
cognitive ability and environment.

No one knows for certain what environmental trends caused
massive IQ gains but we can suggest a scenario consistent
with their history. There is indirect evidence that
massive gains in the cognitive abilities IQ tests measure
began in Britain as far back as those born in 1872. They
probably began with the industrial revolution and were
there waiting for IQ tests to be invented to measure
them. The industrial revolution upgraded years and quality
of schooling, nutrition, disease control, all things that
could have had a profound influence in raising IQ, at
least up to about 1950.

After 1950, in nations like the US and Britain, IQ gains
show a new and peculiar pattern. The are missing or small
on the kind of IQ tests closest to school-taught material
like reading and arithmetic. They are huge on tests that
emphasize on-the-spot problem-solving, like seeing what
verbal abstractions have in common, or finding the missing
piece of a Matrices pattern, or making a pattern out of
blocks, or arranging pictures to tell a story.

Perhaps the industrial revolution stopped demanding
progress in the basics and started demanding that people
take abstract problem-solving more seriously. Post-World
War Two affluence may be the key. It brought a dilution of
the pragmatic depression psychology, smaller families in
which children's whys were taken more seriously, work
roles in which people were expected to take more
initiative, more energy for making leisure more
cognitively demanding, whether devoted to chess or bridge
or video games or simply to conversation in which people
were expected to take ideas and logic seriously.

We call these products of the industrial revolution that
may have set massive IQ gains rolling 'triggers'. The
model itself does not specify ultimate causes and we
suggest those listed very tentatively. What the model does
do is demonstrate the potency triggers would gain from
seizing control of reciprocal causation between cognitive
ability and environment. The most dramatic tool at their
disposal is the 'social multiplier'. This posits that when
something raises the average performance of society, that
rise becomes a powerful cause in its own right, and raises
the average performance further, and raises it further,
until the original rise is greatly multiplied.

The most potent facet of our environment is other
people. When something, perhaps the popularity basketball
got from television, triggered greater participation in
basketball, the average performance rose as individuals
played more and got better. Initially, a few people learn
to shoot with either hand, then others imitate them. The
rise in average performance feeds back into a new
challenge for each individual. Those who want to excel
have to learn to pass with either hand and this spreads
and raises the average performance once again. In other
words, every rise in individual performance raises the
group average, which forces everyone to raise their
individual performance a notch higher, which raises the
group average a notch higher, and so on. Even a modest
environmental trigger of enhanced performance can become
potent by seizing control of the social multiplier-and
cause huge performance gains in a relatively short time.

The same kind of reciprocal causation explains IQ
gains. Environmental triggers raise the cognitive demands
of work, family interaction, leisure, and everyday
conversation. Those who respond by upgrading their
cognitive performance raise the average cognitive
performance. Then the rising average affects your
employer, family, and friends and they demand or expect
more, and you (and many others) rise to meet their
expectations, so the average cognitive performance jumps
once again, and so on, and so on. The model quantifies
this process and shows that quite plausible initial
environmental changes would be enough to explain huge IQ
gains-gains of 20 points over a single generation.

The model has a third task. It offers an explanation for a
whole range of other phenomena that have proved
baffling. Why people's genes seem to count more for IQ as
they age. Why enrichment programs boost IQ a lot at the
start, then little more, and then see their effects fade
away after children leave the program. Why cross-racial
adoptions do not raise the IQs of black adoptees to the
white average. Why certain methodologies produce nonsense
results, such as showing that group IQ differences known
to be environmental in origin have a genetic component.
And to return to the race and IQ debate, it shows that
environment could explain racial IQ differences just as it
explains IQ differences between generations.

Finally, the model has an overriding purpose. In
principle, it applies to the dynamics of any human ability
where there is positive feedback between that ability and
environment. We hope it will reconcile social scientists
who have divided themselves, sometimes with bitterness,
between hereditarians who think genes dominant and
environmentalists who think culture dominant. They are
both right: It all depends on whether genetic differences
or environmental factors seize control of potent processes
like the social multiplier. We hope that our model will
allow them all, from the psychologists inspired by Sir
Cyril Burt to the anthropologists inspired by Franz Boas,
to find common ground, and work together to advance our
understanding of human intelligence and other important
traits.

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