CR Society Archives

[CRCOMMUNITY] Re: Cadmium in paint

Alida T — Thu, 17 May 2012 16:53:51 -0400

Kathy,
Personally, I wouldn't worry much if you are careful handling paint.
Limited skin exposure is much different that breathing dust. It sounds you
are prudent in handling paint (and pastels) and that you do not get much
exposure to cadmium.
Below is an article about cadmium in flax seed from 2007 crcomm archives.
Perhaps that can be as much or more a concern than paint depending on your
diet. (I limited flax to no more than 1-2T a day after reading it, but I
think there are a few cadmium free flax seed sources that you can google.)
Who know how much good or bad is hiding in everyday pollutants and foods.
(For instance the selenium content of brazil nuts varies.)
I happen to be an art teacher. There are warnings on the ceramic clay we
use... to be sure not to breathe the dust as it contains silica. I still
have the kids sand their pottery before polishing it, though i don't let
them clap their hands together to make a cloud of dust. I figure our
limited exposure is much less than someone working in an
industrial situation of constant exposure.... similarly, a cigarette or two
won't kill you, not even one or two a month, but one should abstain from
smoking (I never smoke). I am thankful I live in an area without a lot of
smog, etc. I often wonder how one can jog on city streets. I have places
to walk with fresh air. I'm also thankful that I can afford a healthy diet
and supplements and hope it all balances out in the end. Alida

Is cadmium in flaxseeds a risk, generally? The below paper is pdf-availed.
"cadmium exposure through the diet was six-fold higher than allowed for
humans by World Health Organization"? In pregnancy, flaxseed abstention
may
be prescribed.

Khan G, Penttinen P, Cabanes A, Foxworth A, Chezek A, Mastropole K, Yu B,
Smeds A, Halttunen T, Good C, Makela S, Hilakivi-Clarke L.
Maternal flaxseed diet during pregnancy or lactation increases female rat
offspring's susceptibility to carcinogen-induced mammary tumorigenesis.
Reprod Toxicol. 2007 Feb 22; [Epub ahead of print]
PMID: 17398067
Flaxseed contains several dietary components that have been linked to low
breast cancer risk; i.e., n-3 polyunsaturated fatty acids (PUFAs), lignans
and fiber, but it also contains detectable levels of cadmium, a heavy metal
that activates the estrogen receptor (ER).
Since estrogenic exposures early in life modify susceptibility to develop
breast cancer, we wondered whether maternal dietary intake of 5% or 10%
flaxseed during pregnancy or lactation (between postpartum days 5 and 25)
might affect 7,12-dimethylbenz[a]anthracene (DMBA)-induced mammary
tumorigenesis in the rat offspring.
Our data indicated that both in utero and postnatal 5% and 10% flaxseed
exposures shortened mammary tumor latency, and 10% flaxseed exposure
increased tumor multiplicity, compared to the controls. Further, when
assessed in 8-week-old rats, in utero 10% flaxseed exposure increased
lobular ER-alpha protein levels, and both in utero and postnatal flaxseed
exposures dose-dependently reduced ER-beta protein levels in the terminal
end buds (TEBs) lobules and ducts. Exposures to flaxseed did not alter the
number of TEBs or affect cell proliferation within the epithelial
structures. In a separate group of immature rats that were fed 5% defatted
flaxseed diet (flaxseed source different than in the diets fed to pregnant
or lactating rats) for 7 days, cadmium exposure through the diet was
six-fold higher than allowed for humans by World Health Organization, and
cadmium significantly accumulated in the liver and kidneys of the rats.
It remains to be determined whether the increased mammary cancer in rats
exposed to flaxseed through a maternal diet in utero or lactation was caused
by cadmium present in flaxseed, and whether the reduced mammary ER-beta
content was causally linked to increased mammary cancer risk among the
offspring.
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[CRCOMMUNITY] 7-Keto?

deb belcore — Thu, 17 May 2012 16:49:50 -0400

Apparently, Dr. Oz mentioning this product as effective for belly fat loss on a recent episode has caused a sales explosion. It is a metabolite of DHEA, but that is all I know about it. Anyone ever heard of it or tried it?
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[CRSOCIETY] Pathway of dietary fats & sugars to liver

Watson, Alastair — Thu, 17 May 2012 14:29:55 -0400

Just an anatomical note to clarify what may be providing some ambiguity.

Dietary fats are usually absorbed from the intestines into the abdominal lymphatic vessels, which eventually drain their lymph into one of the large veins near the heart, and so these returning body fluids (dietary fats) re-enter the blood circulatory system by which they will eventually reach the liver (via the hepatic artery).

Dietary carbohydrates (including "sugars"), proteins/amino-acids and other nutrients are absorbed from the stomach and intestines into small veins, which specifically enter the liver via the hepatic portal vein (there is no portal artery here). Thus any fructose (be it in HFCS additive, or directly derived from foods like fruits etc.) is directly delivered to the liver on the blood's first pass. Previous posts have outlined the dangers of dietary "high" doses of fructose being delivered to the liver, which is its primary organ for its metabolism ... and consequent cascading affects on insulin (resistance), fat metabolism, and so on.

{Sourced from primary Gastro-Intestinal/CardioVascular Anatomy and Physiology: a full reading of Guyton or others will reveal these fundamental details.}

Alastair
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[CRSOCIETY] Array-based expression analysis of mouse liver genes: effect of age and of the longevity mutant Prop1df

Al Pater — Thu, 17 May 2012 14:18:19 -0400

The below paper is pdf-availed.

Array-based expression analysis of mouse liver genes: effect of age and of
the longevity mutant Prop1df.
Dozmorov I, Bartke A, Miller RA.
J Gerontol A Biol Sci Med Sci. 2001 Feb;56(2):B72-80.
PMID: 11213270

Abstract

Ames dwarf mice, homozygous for the df allele at the Prop1 locus, live 40%
to 70% longer than nonmutant siblings and represent the first single-gene
mutant that extends life span in a mammal.

To gain insight into the basis for the longevity of the Ames dwarf mouse,

we measured liver mRNA levels for 265 genes in a group of 11 df/df mice,
(three to four mice per age group), at ages 5, 13, and 22 months, and in 13
age- and sex-matched control mice.

The analysis showed seven genes where the effects of age reach p < .01 in
normal mice and six others with possible age effects in dwarf mice, but none
of these met Bonferroni-adjusted significance thresholds. Thirteen genes
showed possible effects of the df/df genotype at p < .01. One of these,
insulin-like growth factor 1 (IGF-1), was statistically significant even
after adjustment for multiple comparisons; and genes for two IGF-binding
proteins, a cyclin, a heat shock protein, p38 mitogen-activated protein
kinase, and an inducible cytochrome P450 were among those implicated by the
survey. In young control mice, half of the expressed genes showed SDs that
were more than 58% of the mean, and a simulation study showed that genes
with this degree of interanimal variation would often produce false-positive
findings when conclusions were based on ratio calculations alone (i.e.,
without formal significance testing). Many genes in our data set showed
apparent young-to-old or normal-to-dwarf ratios above 2, but the large
majority of these proved to be genes where high interanimal variation could
create high ratios by chance alone, and only a few of the genes with large
ratios achieved p < .05. The proportion of genes showing relatively large
changes between 5 and 13 months, or from 13 to 22 months of age, was not
diminished by the df/df genotype, providing no support for the idea that the
dwarf mutation leads to global delay or deceleration of the pace of
age-dependent changes in gene expression.

These survey data provide the foundation for replication studies that should
provide convincing proof for age- and genotype-specific effects on gene
expression and thus reveal key similarities among the growing number of
mouse models of decelerated aging.

-- Al Pater, alpater@SHAW.ca

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[CRSOCIETY] Re: Increasing requests for vitamin D measurement: costly, confusing, and without credibility

Al Pater — Thu, 17 May 2012 13:57:39 -0400

The below paper was originally described in full, but, for this context, may
be worth presenting for direct comparison regarding the comments next below
on the paper.

Comments on:

Lancet. 2012 Jan 14;379(9811):95-6.
Increasing requests for vitamin D measurement: costly, confusing, and
without credibility.
Sattar N, Welsh P, Panarelli M, Forouhi NG.
PMID:22243814
http://arc.crsociety.org/read.php?2,208721,208721#msg-208721

The below paper is pdf-availed.

Increasing requests for vitamin D measurement: costly, confusing, and
without credibility
The Lancet Volume 379, Issue 9811, 14-20 January 2012, Pages 95-96
Naveed Sattar, Paul Welsh, Maurizio Panarelli, Nita G Forouhi

�Sunbathing boosts men's sex drives� proclaimed newspaper reports. [1] and
[2] This headline was extrapolated from a cross-sectional study showing that
serum 25-hydroxyvitamin D (25OHD) concentrations -- a biochemical measure of
vitamin D status -- correlate to circulating testosterone concentrations in
men referred for angiography, but neither sun exposure nor sex drive was
directly assessed.3 This anecdote epitomises what has become a bandwagon of
vitamin-D-related epidemiological research fuelling easily accessible
headlines in lay media. Such frequent and prominent headlines have cast
vitamin D in the role of a putative miracle cure that can prevent and treat
a burgeoning list of chronic disorders such as cardiovascular disease,
diabetes, and cancer.

This media coverage has caused a massive rise in demand for measurement of
blood concentrations of 25OHD from the public and physicians. Glasgow Royal
Infirmary -- the main provider of 25OHD tests in Scotland -- has seen a rise
in vitamin D test requests from 18,682 in 2008, to 37,830 in 2010, which has
resulted in a longstanding backlog of 2000 tests. Similarly, a hospital in
London, UK, had a sixfold increase in 25OHD test requests over 4 years,
rising from 7537 tests in 2007, to nearly 46,000 in 2010 (personal
communication). Similar trends have been noted in other countries -- eg,
Canada and the USA. [4] and [5] To match demand, manufacturers (eg, Abbott,
Roche, and Siemens) are developing immunoassays (similar to liquid
chromatography tandem mass spectrometry gold standard) for clinical use, and
promoting them widely in North America, Europe, and elsewhere. A 25OHD test
costs the UK National Health Service around pounds20. The economic burden of
widespread routine vitamin D testing in the UK and elsewhere is therefore
substantial.

But is this skyrocketing of 25OHD test requests and related costs justified?
The prevalence of apparent vitamin D inadequacy is high in the UK. [6] and
[7] For example, roughly 50% of 45-year-old UK adults (1958 British birth
cohort) were vitamin D insufficient during winter months, with the greatest
inadequacy recorded in Scotland (average concentration 35 nmol/L).7 A
patient in the UK attending a general practitioner in winter is therefore
likely to be vitamin D insufficient (serum concentrations <50 nmol/L) or
deficient (serum concentrations <25 nmol/L). But how should general
practitioners interpret such test results? The key question is: does knowing
the result usefully improve clinical practice and patient wellbeing?

To address this issue, whether vitamin D inadequacy has a predisposing
relation with health consequences that could be avoided by intervention (eg,
supplementation, diet, or sun exposure) needs to be established. Most
evidence promoting a role for vitamin D in chronic disease has been
extrapolated from epidemiological studies, but these results are often
limited by factors such as potential reverse causality and residual
confounding -- particularly relevant limitations for vitamin D as a
biomarker of health (table). Therefore, any conclusions about causality
extrapolated from observational data are premature.10

Table. Potential limitations in making causal inferences from observational
epidemiology for vitamin D
----------------------------------------------------------
Limitation Why important for vitamin D? Examples
----------------------------------------------------------
Confounding and residual confounding Many risk factors are related to both
low 25OHD and poor health outcomes; statistical models might be incomplete
if such factors are not measured, or measured imprecisely Little physical
activity (outdoor activity often related to sunlight exposure); low
socioeconomic status; obesity; smoking; season
----------------------------------------------------------
Reverse causality Sunlight exposure is a major determinant of
circulating-25OHD concentrations; pain or illness can limit sunlight
exposure through inactivity, and thus disease could cause inadequacy rather
than the reverse Clinical diagnosis of many disorders (eg, multiple
sclerosis) can be preceded by a period of preclinical disease when little
time is spent outdoors; acute infl ammation can drive down circulating 25OHD
concentrations so that in acute illnesses or many hospitalised patients, low
measurements are secondary to an acute-phase response
----------------------------------------------------------
Publication and citation bias Null or negative findings are less likely to
be published, especially when overwhelming perception is of a positive
association; thus, investigators are less likely to pursue publication or
persist after manuscript rejection than if results were positive; null
findings that are published are not frequently cited and result in little
media interest, and therefore perception of the weight of evidence can be
heavily skewed Marniemi and colleagues� 2005 report8 of no association of
25OHD with 130 cases of myocardial infarction in elderly people has been
cited 33* times in Web of Science; by contrast, Wang and co-workers� 2008
article9 reporting 25OHD inadequacy associated with 120 cases of
cardiovascular disease in Framingham off spring has been cited 409* times
----------------------------------------------------------
25OHD=serum 25-hydroxyvitamin D. *As of Nov 28, 2011.

The only reliable tests of causality are randomised trials. The
effectiveness of vitamin D supplementation in rickets and osteomalacia has
been proven. Vitamin D supplementation in appropriate doses with concomitant
calcium supplements might reduce the risk of fractures in elderly people at
risk of osteoporosis.11 However, the need to measure circulating vitamin D
in people with osteoporosis (diagnosed on the basis of dual energy x-ray
imaging scans) is questionable because treatment is likely to include
vitamin D supplements irrespective of the result. Meanwhile, convincing
evidence that vitamin D supplements reduce the risk of cardiovascular
disease or diabetes, or lower glucose concentrations in patients with
diabetes, does not exist.12 Proponents argue that longer trials with higher
doses of vitamin D than have been tested heretofore are needed, and we
agree. However, until the investigators of such trials report their results,
we must remain cautious about the recommendation of widespread
supplementation for chronic disease prevention. The reports13 of increased
rates of infantile hypercalcaemia in the UK in the 1950s after
overenthusiastic food fortification with vitamin D show the importance of
caution -- a point re-emphasised in 2011.14

In short, widespread testing of asymptomatic people's vitamin D status is
unhelpful. Economic constrictions are a concern for health-care providers
worldwide. Until the results of large randomised trials are reported, we
urge all clinicians to stop and think critically before measuring 25OHD,
particularly in conditions not linked to bone disease. Such practice will
avoid many unnecessary tests, reduce laboratory backlog, and save a lot of
health-service time and money without affecting patients' health.

Comment in
Lancet. 2012 May 5;379(9827):1699; author reply 1700-1.
Lancet. 2012 May 5;379(9827):1699; author reply 1700-1.
Lancet. 2012 May 5;379(9827):1699-700; author reply 1700-1.
Lancet. 2012 May 5;379(9827):1700; author reply 1700-1.

Vitamin D testing.
Grey A, Bolland M, Davidson J.
Lancet. 2012 May 5;379(9827):1699; author reply 1700-1. No abstract
available.
PMID:22559889

Naveed Sattar and colleagues (Jan 14, p 95)1 appeal to clinicians to adopt
an evidence-based approach to vitamin D testing to conserve financial and
laboratory resources. In Auckland, New Zealand, annual requests for vitamin
D measurement quadrupled between 2000 (8500) and 2010 (32?800).2 In 2010,
61% of test requests were generated by 9% of requesting practitioners.2 Only
15% of tests identified a serum 25-hydroxyvitamin D concentration less than
25 nmol/L.3

The progressive increase in test requests continued despite the addition to
the laboratory report form of information on the cost of the assay and
advice on a rational approach to testing. In 2011, in the face of a total
annual laboratory cost of about NZ$1 million for vitamin D testing alone, a
decision was made to restrict direct access to the test to a limited range
of clinicians or for the investigation of metabolic bone disease or
hypocalcaemia. The restriction was applied in October, 2011, resulting in a
rapid and substantial reduction in tests done (table).

Table. Vitamin D tests done in Auckland, New Zealand in 2011, by month
-------------------------
Month Number of tests done
-------------------------
July 2670
August 2200
September 2363
October 884
November 563
December 592
-------------------------
Restrictions on testing were implemented in October.

Evidence-based appeals, although laudable, might be insufficient to change
expensive and unnecessary laboratory test-requesting practices.

Vitamin D testing.
Caillet P, Schott AM.
Lancet. 2012 May 5;379(9827):1699; author reply 1700-1. No abstract
available.
PMID:22559887

Naveed Sattar and colleagues1 urge clinicians to stop and think critically
before measuring 25-hydroxyvitamin D concentrations, mainly because of the
lack of evidence from randomised clinical trials. There is another reason to
do so: measurement of concentrations of circulating 25-hydroxyvitamin D
routinely and accurately is still a challenge.

Numerous commercial assays are available, and important inconsistencies in
performance have been reported owing to several different causes (eg,
occasional changes of antibody, or the reformulation of reagents).2
Inconsistencies were so important that, after assessment of long-term data
from the US National Health and Nutrition Examination Survey (NHANES), and
the observation of normative data shifts between surveys, the NHANES
laboratory developed and validated an in-house liquid chromatography-tandem
mass spectrometry (LC-MS/MS) method to replace the commercial immunoassay
that was found to have given inconsistent results.3

In routine clinical care, where multiple laboratories are involved, these
inconsistencies are expected to be even more important and to lead
clinicians to irrelevant decisions. Snellman and colleagues4 measured serum
samples from 204 patients in three different laboratories by use of
different methods. The proportion of patients identified as vitamin D
insufficient (<50 nmol/L) varied from 8% to 43%. An external proficiency
programme (Vitamin D External Quality Assessment Scheme [DEQAS]5) has been
developed internationally.

Until a better standardisation is achieved in routine practice, we urge
clinicians not only to stop and think critically before ordering a
25-hydroxyvitamin D test, but also to give special attention to the choice
of a DEQAS-accredited laboratory that uses the most accurate method
(LC-MS/MS) when possible.

Vitamin D testing.
Pattman S, Quinton R, Pearce S, Datta H.
Lancet. 2012 May 5;379(9827):1699-700; author reply 1700-1. No abstract
available.
PMID:22559888

Naveed Sattar and colleagues1 highlight the rising number of requests for
serum 25-hydroxyvitamin D measurement, but provide no evidence to support
their contention that much of the volume of requests arises from
asymptomatic patients and that the assays are therefore unhelpful.

We too noted a similar local increase (about 400%) in requests from primary
care between the last quarter of 2009 and the same period in 2010. But the
clinical reasons for request given, including fatigue, myopathy, low-trauma
fractures, and raised alkaline phosphatase concentration, are generally
appropriate. Indeed it would be unwise, and expensive, to diagnose and treat
empirically disorders such as fibromyalgia, polymyalgia rheumatica, or
chronic fatigue syndrome without knowledge of a patient's vitamin D status.

Sattar and colleagues also question the need to measure 25-hydroxyvitamin D
in patients with osteoporosis, contending that medication with tablets
containing calcium and vitamin D will cover all eventualities. However, the
UK's National Institute for Health and Clinical Excellence sensibly
recommends vitamin D supplementation only for patients who are not already
vitamin D replete.2 Further, dual-energy X-ray absorptiometry cannot
distinguish low bone density resulting from osteoporosis from that of
osteomalacia, so failure to request 25-hydroxyvitamin D measurement will
necessarily lead to inappropriate treatments. Recent guidance highlights the
inadequacy of commonly used calcium and vitamin D products that contain just
400 IU of the vitamin for treating patients with profoundly low
concentrations of 25-hydroxyvitamin D in serum. Such patients require higher
pharmacological doses. [3] and [4]

Although the current situation is far from ideal, we feel that Sattar and
colleagues overlook several situations in which quantification of
25-hydroxyvitamin D is important, and cast unwarranted aspersions on the
ability of primary-care physicians to make clinically based requests in this
area.

Vitamin D testing.
Peiris AN, Bailey BA, Grant WB, Mascitelli L.
Lancet. 2012 May 5;379(9827):1700; author reply 1700-1. No abstract
available.
PMID:22559891

Naveed Sattar and colleagues1 highlight increasing requests for vitamin D
measurement and the associated costs. The need to contain health-care costs
is universal, especially in western countries where they are increasing at
an unsustainable rate. We agree that vitamin D deficiency is prolific
worldwide. However, we have major areas of disagreement regarding testing
and monitoring of vitamin D.

There are many correlates with serum 25-hydroxyvitamin D concentrations, but
studies that used common laboratory tests and included latitude and
seasonality were unable to predict vitamin D deficiency, suggesting that
there is no substitute for 25-hydroxyvitamin D testing.2 We too have noticed
a marked increase in testing for vitamin D status in recent years. However,
in a study of six Veterans Medical Centers in the southeastern USA, the
lowest overall medical costs were in the medical centres that did follow-up
vitamin D testing.3 In particular, across all sites, vitamin D deficiency
combined with lack of monitoring predicted increased inpatient health-care
costs.3

One option to reduce the costs of vitamin D testing would be to supplement
the general population with 1000-2000 IU vitamin D3, as recommended by the
Endocrine Society.4 Indeed, such an approach has been postulated to result
in a substantial reduction in global health-care costs.5 The greatest
benefits accrue to those with serum 25-hydroxyvitamin D concentrations below
50 nmol/L; optimum concentrations should be at least 75-100 nmol/L. [4] and
[5]

WBG receives funding from the UV Foundation (McLean, VA, USA), Bio-Tech
Pharmacal (Fayetteville, AR, USA), the Vitamin D Council (San Luis Obispo,
CA, USA), and the Vitamin D Society (Canada). The other authors declare that
they have no conflicts of interest.

Vitamin D testing - Authors' reply
Naveed Sattar, Paul Welsh, Maurizio Panarelli, Nita G Forouhi
Lancet. 2012 May 5;379(9827):1699; author reply 1700-1. No abstract
available.

Naveed Sattar, Paul Welsh, Maurizio Panarelli, Nita G Forouhi

We welcome further debate on the issue of vitamin D testing, and, given the
range of responses received, there is clearly a need for it. Andrew Grey and
colleagues provide interesting data to suggest that vitamin D requests are
dominated by a relatively small proportion of clinicians. Our hospital
biochemistry department in Glasgow, UK, recently applied selected
restrictions on requests for 25-hydroxyvitamin D testing and is seeing
similar efficiencies. Thus we agree that, if the evidence base is ignored,
direct measures to limit health-care expenditure on inappropriate vitamin D
tests are warranted.

We agree with Pascal Caillet and Anne-Marie Schott that non-standardised
assays are a barrier to the incorporation of accurate and reliable
25-hydroxyvitamin D testing and that misclassification remains a challenge.
That noted, whether even robust measurement of the 25-hydroxyvitamin D
metabolite in serum accurately reflects whole-body vitamin D status in all
individuals remains uncertain.

Stewart Pattman and colleagues suggest that fibromyalgia and chronic fatigue
are appropriate conditions to request vitamin D measures. We cannot identify
convincing evidence to support this assertion, and there is no evidence from
large placebo-controlled randomised trials:1 replete vitamin D status does
not exclude these disorders, and there is no robust evidence that vitamin D
supplementation improves symptoms. Further, people with fatigue and pain
will probably spend less time outdoors, which leads to lower
25-hydroxyvitamin D (ie, reverse causality).

We agree that diagnosis of osteomalacia requires biochemical testing that
could include 25-hydroxyvitamin D. We do not, however, believe that an
increasing incidence of osteomalacia accounts for the increasing vitamin D
requests. The National Institute for Health and Clinical Excellence
guidelines for the secondary prevention of osteoporotic fragility fractures
in postmenopausal women state that �vitamin D supplementation should be
provided unless clinicians are confident that women who receive treatment
for osteoporosis�are vitamin D replete�.2 Given that a significant majority
of elderly women, particularly in northern latitudes, and particularly
through the winter months, are likely to have insufficient 25-hydroxyvitamin
D, the benefit of widespread testing is unclear, especially if supplements
are to be prescribed irrespective of the result.

Our comments were intended as general guidance and clinical decisions are
best made on a case-specific basis with specialist input as appropriate.
Furthermore, we respectfully suggest that asking clinicians to think through
critically whether vitamin D testing is appropriate, particularly among
asymptomatic people and particularly in conditions not linked to bone
disease, is not to cast �unwarranted aspersions�.

Alan Peiris and colleagues suggest that latitude and seasonality cannot
predict vitamin D deficiency, citing data from an observational study of
individuals who attended a vitamin D seminar and took supplements. Latitude
and season are not investigated in that paper.3 Peiris and colleagues
suggest that widespread supplementation programmes could proceed without
further evidence or trials of efficacy or safety. The Institute of Medicine
does not seem to concur with this view.4 We therefore reiterate the need to
resist making causal inferences on the basis of observational evidence,
which Peiris and colleagues seem to advocate.5

-- Al Pater, alpater@SHAW.ca

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[CRSOCIETY] Re: Fwd: Am I hypertensive? Reduce or eliminate Lasix?

Saul Lubkin — Thu, 17 May 2012 12:59:31 -0400

On Thu, May 17, 2012 at 11:27 AM, jwwright wrote:

>
> ----- Original Message ----- From: "Saul Lubkin"
> To: "The CR Society Main Discussion List" > org >
> Cc: "Luigi Fontana" ; "Paul McGlothin" <
> paul.mcglothin@gmail.com>
> Sent: Thursday, May 17, 2012 7:57 AM
> Subject: [CR] Fwd: Am I hypertensive? Reduce or eliminate Lasix?
>
>
>
> Dear ALL,
>>
>> I'd like to share an email message that I just
>> sent to my nephrologist, who has been monitoring my BP for the last
>> several
>> years.
>>
>> It's a bit (almost) shocking to me -- I should note that, when Luigi
>> tested me at WUSTL, he diagnosed "marginal hypertension -- but I was
>> taking
>> Benicar, 40 mg twice per day, at the time
>> [which is twice the recommended maximum daily allowance]
>>
>>
>> ---------- Forwarded message ----------
>> From: Saul Lubkin
>> Date: Thu, May 17, 2012 at 9:51 AM
>> Subject: RE: Am I hypertensive? Reduce or eliminate Lasix?
>> To: Jeremy Taylor
>> >
>>
>>
>> Hello again, Dr. Taylor!
>>
>> With 40mg of Lasix, twice per day (and no Benicar), BP continues to be
>> very
>> low -- typically systolic is in the 90's.
>>
>> My growing suspicion:
>>
>> I am not hypertensive.
>>
>> I (had been) taking Benicar, 40mg, twice per day (which is double the
>> maximum recommended amount); perhaps I have a bad reaction (maybe allergy)
>> to Benicar?
>>
>> Or, perhaps I have suffered from extreme doctor's office syndrome for
>> years? (I doubt that this could be a MAJOR factor -- a contributing
>> factor, probably).
>>
>> Other possibility: My diet has changed somewhat recently: I am now
>> restricting protein more avidly than before. (Typical day: Protein
>> deduced from about 3/4 cup of white beans, or else from 1.5 ounces of
>> sashimi [1 oz salmon, 1/2 oz yellowtail. Plus, lots of raw low cal
>> veggies).
>>
>> My question: Should I reduce Lasix to 20mg, twice per day, or drop it
>> entirely?
>>
>> :-)
>>
>> -- Saul
>>
>
>
> Thanks, Saul,
> The part I love about your post is that I have HTN, and your are
> significantly lower in weight.
> As I have said before, I ran a test in myself losing 60 # and my BP never
> went down to the point I could drop the verapamil.
> I think you do have "true" HTN, which is idiopathic, but recognize we can
> think it's caused by an adrenal adenoma.
> Not to worry, because it's far to hard to treat anyway.
>
> Take whatever works.
> There are many medications and literally, we/they cut and try.
>
> I've a friend who runs, can't be more that 125# soaking wet, and developed
> HTN during training. At 35 yo.
> Uses diovan.
> I use verapamil because it's the only thing that works for me.
>
> Yes, the diastolic seems the be the biggest problem.
> I've never found any logic that tells me why, except excess fatty foods
> raises it.
>
> IMO, it's a good thing to wean off any HTN drug while you add or change
> meds.
> FWIW, I think a higher diastolic raising BP but keeping pulse pressure
> lower is better.
> (pulse pressure is the difference between Sys and Dia.)
>
> Would try reducing it first and if remains low then stopping completely. I suspect your dietary changes have something to do with this.
>
>
> Jeremy Taylor MD
> University of Rochester
> Division of Nephrology
> Clinical Director
> 601 Elmwood Ave
> Rochester NY, 14642
>
> So, today I switch to 20mg Lasix, twice per day; and, if all continues
> well (systolic in numbers like 90), will drop this last remaining
> hypertensive.
>

Intersting opinion by Dr. Taylor: Maybe lower protein (just 1.5 oz
sashime, or 1/2-3/4 cup white beans, daily, plus raw veggies) did the tirck.

Fascinating.

-- Saul

> Regards
>
> Hi JW!
>

No, what you are describing doesn't fit me at all. Diastolic has always
been fine, and also heartrate; systolic was the problem.

My highly educated, CR-friendly nephrologist just responded:

>
>
>
>
>
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[CRSOCIETY] Re: Protein and Cortisol levels?

Richard Schulman — Thu, 17 May 2012 12:18:19 -0400

Tanya Daykin writes:

>Hi All :) My apologies for making a personal request :)
>Just got back my blood results investigating my peripheral�oedema and the endo's opinion is that low protein is the cause [Total Protein 49g/l (ref 68-85)

Your protein is pretty far out of the reference range. I'd suggest you
signifcantly up your daily protein intake and retest in a few weeks.

I assume you're using software and a gram-weight scale to monitor your
daily food intake. If not, please do.

I can't answer your questions about the other out-of-range results,
but some, perhaps most, of these adverse results might disappear once
you get back consistently within the lower end of the protein
reference range.

>Finally, while I am annoying you all, has anyone tried protein and vegie alternation? It was just a thought that�occurred�to me as I truly don't think I can eat any more than I do already. If anyone has/is having their Protein on alternate days to their vegies I would love to hear how that is working for you before I commit (obviously I suspect protein�absorption over not ramming enough down my throat) :)

Having protein on alternate days sounds like a really bad idea to me,
*especially* for you, given your test results. The amino acids in
protein get recycled pretty quickly rather than stored. You need them
for tissue maintenance. Human alternate day fasting hasn't a
well-researched track record behind it to date, and as far as I know,
there's zero research on alternate day protein denial. Why go there?

RS

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[CRCOMMUNITY] Anti-proliferative activity and chemoprotective effects towards DNA oxidative damage of fresh and cooked Brassicaceae

Al Pater — Thu, 17 May 2012 11:27:10 -0400

The below paper is pdf-availed.

http://ehjcimaging.oxfordjournals.org/content/9/2/261/T1.expansion.html

http://ehjcimaging.oxfordjournals.org/content/9/2/261.full

Anti-proliferative activity and chemoprotective effects towards DNA
oxidative damage of fresh and cooked Brassicaceae.
Ferrarini L, Pellegrini N, Mazzeo T, Miglio C, Galati S, Milano F, Rossi C,
Buschini A.
Br J Nutr. 2011 Nov 17:1-9. [Epub ahead of print]
PMID:22088277

Abstract

Epidemiological evidence shows that regular consumption of Brassicaceae is
associated with a reduced risk of cancer and heart disease. Cruciferous
species are usually processed before eating and the real impact of cooking
practices on their bioactive properties is not fully understood.

We have evaluated the effect of common cooking practices (boiling,
microwaving, and steaming) on the biological activities of broccoli,
cauliflower and Brussels sprouts.

Anti-proliferative and chemoprotective effects towards DNA oxidative damage
of fresh and cooked vegetable extracts were evaluated by
3-(4,5-dimethylthiazol-2-yl)-5-(3-carboxymethoxyphenyl)-2-(4-sulfophenyl)-2H-tetrazolium
and Comet assays on HT-29 human colon carcinoma cells.

The fresh vegetable extracts showed the highest anti-proliferative and
antioxidant activities on HT-29 cells (broccoli>cauliflower = Brussels
sprouts). No genotoxic activity was detected in any of the samples tested.
The cooking methods that were applied influenced the anti-proliferative
activity of Brassica extracts but did not alter considerably the antioxidant
activity presented by the raw vegetables. Raw, microwaved, boiled (except
broccoli) and steamed vegetable extracts, at different concentrations,
presented a protective antioxidative action comparable with vitamin C (1
mm).

These data provide new insight into the influence of domestic treatment on
the quality of food, which could support the recent epidemiological studies
suggesting that consumption of cruciferous vegetables, mainly cooked, may be
related to a reduced risk of developing cancer.

Key Words: Brassica vegetables; Cooking methods; Chemoprevention; Comet
assay

Abbreviations: DMEM, Dulbecco's modified Eagle's medium; g eq ww/ml,
equivalent of wet weight g/ml; LED, lowest effective dose; MTS,
3-(4,5-dimethylthiazol-2-yl)-5-(3-carboxymethoxyphenyl)-2-(4-sulfophenyl)-2H-tetrazolium;
TI, tail intensity

Epidemiological studies have shown that regular consumption of Brassica
vegetables is associated with a reduced risk of some chronic diseases; in
particular, gastric or lung cancers and CVD(1,2). Brassica vegetables
contain a wide range of natural chemopreventive agents, such as folate,
fibre, vitamin C, tocopherols, polyphenols, carotenoids and
chlorophylls(3-6). Furthermore, cruciferous vegetables are a rich source of
glucosinolates, sulphur-containing compounds, whose hydrolysis results in
the formation of biologically active compounds, including indoles and
isothiocyanates(7-9). All these molecules can retard the development and
progression of precancerous cells into malignant cells(10) acting through
different mechanisms and in different compartments, but they are thought to
be mainly free radical scavengers(11).

It is known that cooking induces significant changes in chemical
composition, influencing the concentration and availability of bioactive
compounds in vegetables. Both positive and negative effects have been
reported depending upon the differences in process conditions and
morphological and nutritional characteristics of the vegetable
species(6,12-16). The cooking of vegetables can decrease water-soluble and
heat-sensitive nutrients, such as vitamin C, but also can lead to disruption
of the food matrix and dissociation of some compounds from the plant matrix
components. This determines the release of plant components, which, in turn,
can improve their digestion and absorption, increasing their
bioavailability(17-19).

Although some of the vegetables consumed in the human diet are processed to
be eaten, there are few works that correlate their biological activity on
human cell lines in vitro to cooking treatments. Recently, the effect of
grilling and boiling processes on eggplant showed a positive effect on
antioxidant concentrations and chemopreventive activities of the human
polymorphonuclear neutrophils(20).

There is an increasing attention in the evaluation of the antiproliferative
effects induced by vegetable extracts on human cancer cell lines, performed
mainly by cytotoxicity tests such as
3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) and
3-(4,5-dimethylthiazol-2-yl)-5-(3-carboxymethoxyphenyl)-2-(4-sulfophenyl)-2H-tetrazolium
(MTS) assays(21,22). Furthermore, an interesting method for studying the
effects of foods on the risk of cancer is the Comet assay, a single-cell gel
electrophoresis technique for measuring DNA breakage in individual
cells(23). The comet assay is performed mainly to evaluate the effects of
antioxidants in vitro(24,25) or in intervention studies(26).

The goal of the present study was to evaluate the effect of common cooking
practices (i.e. boiling, microwaving and steaming) on the biological
activities of broccoli, cauliflower and Brussels sprouts. The
anti-proliferative activity and chemoprotective effect towards DNA oxidative
damage of fresh and cooked vegetable extracts were evaluated by MTS and
Comet assays.

Experimental methods

Chemicals

Preparation of vegetables

...

Preparation of vegetables

Freshly harvested broccoli (Brassica oleracea L. cv. Italica), Brussels
sprouts (B. oleracea L. cv. gemmifera) and white cauliflower (B. oleracea L.
cv. botrytis cauliflora) of a single batch were analysed. Fresh Brussels
sprouts were purchased from a local market on the day of processing after
road transport under refrigerated conditions within 24 h of harvest and
stored at 7�C for up to 1 d before they were taken. Fresh broccoli and
cauliflower were obtained by a local purchaser and analysed within 3 d of
harvest. The samples were stored at 4�C before analysis.

Fresh broccoli and cauliflower were cleaned by removing of inedible parts
and then chopped into homogeneous pieces, leaving a stem of 2�5 cm. Brussels
sprouts were deprived of the external leaves.

To obtain more homogeneous samples, each vegetable was prepared in batches
of 500 g. Each batch was then divided into five equal portions. One portion
was retained raw; the others were cooked in four different methods in
triplicate, as given below.

Cooking treatments

Cooking conditions were optimised by preliminary experiments carried out for
each vegetable. For all cooking treatments, the minimum cooking time to
reach tenderness for adequate palatability and taste, according to Italian
eating habits, were used.

Boiling

Brassica vegetables were added to boiling tap water in a covered stainless
steel pot (1:5, food/water) and cooked on a moderate flame. Cooking time was
8, 10 and 10 min for broccoli, Brussels sprouts and cauliflower,
respectively. For each cooking trial, ten samples were boiled. Then, the
samples were drained off for 30 s.

Steaming

Two types of steaming equipment were employed: an air/steam impingement oven
and a domestic cooker equipped with a mesh basket. Air/steam oven treatments
were carried out in a Combi-Steal SL oven (V-Zug, Zurich, Switzerland). Nine
specimens of vegetables were placed in the oven equilibrated to room
temperature before each cooking trial. Eight samples were arranged in a
circle, and one put at the centre to ensure uniform heating conditions in
all samples for each cooking trial. Cooking time was 13, 17 and 13 min for
broccoli, Brussels sprouts and cauliflower, respectively. The samples were
put into the oven when a temperature of 100�C was reached (displayed by the
apparatus).

A single layer of nine specimens of Brassica vegetables was steamed in a
domestic closed vessel using a stainless steel steam basket suspended above
a small amount of boiling water. Cooking time was 15, 18 and 11 min for
broccoli, Brussels sprouts and cauliflower, respectively.

Microwaving

Microwave treatments were carried out in a domestic microwave oven (Samsung
Electronics Company Limited, Paldal-Gu Suwon Kyungki-Do, Korea) without
water. Ten specimens of vegetables were exposed at a frequency of 2450 Hz at
low power (300 W) on the rotatory turntable plate of the oven. Cooking time
was 30, 18 and 30 min for broccoli, Brussels sprouts and cauliflower,
respectively.

After all cooking experiments, the samples were cooled rapidly on ice and
then freeze-dried utilising a Brizzio-Basi instrument (Milan, Italy). The
dried sample material was finely ground, kept in sealed bags, and stored
at - 20�C until the analysis.

...

Cell lines

The colon is the major cancer site thought to be protected by vegetables, so
for in vitro studies we employed a cell line, HT-29, used widely as a model
for colon cancer.

The human colon adenocarcinoma cell line HT-29 ...

...

Genotoxicity studies

DNA damage was measured using single-cell gel electrophoresis (Comet assay).
The alkaline version (pH >13) of the assay was performed to detect
single-strand breaks and alkali-labile sites, such as apyrimidinic and
apurinic sites that are formed when bases are lost and oxidised.

...

Antioxidant activity

The Comet assay was used to study the antioxidant effect of the test
extracts. In that case, the amount of DNA damage caused by an oxidative
damage-inducing agent on the cells pre-treated with the vegetable extracts
was evaluated.

...

Results

Anti-proliferative activity

Anti-proliferative activity was detected by the MTS assay, a colorimetric
method for determining the number of viable cells in proliferation (Fig. 2).
In the range of the doses used (10- 3/101g eq ww/ml), the raw vegetable
extracts that were analysed showed high anti-proliferative/toxic activity on
the HT-29 colon carcinoma cells. The lowest effective dose (LED, P < 0�001)
was 0�25 g eq ww/ml for broccoli and 0�50 g eq ww/ml for cauliflower and
Brussels sprouts.

The strong anti-proliferative activity detected with the raw broccoli
extract was maintained with the microwave cooking method (LED: 0�25 g eq
ww/ml, P < 0�001), while the boiled and steamed broccoli extracts showed no
cytotoxic activity up to 4�00 g eq ww/ml.

All the cooking methods, except basket steaming up to 4�00 g eq ww/ml,
partially maintained the anti-proliferative activity detected in the raw
cauliflower extract: microwaving LED: 1�00 g eq ww/ml (P < 0�01); boiling
LED: 2�00 g eq ww/ml (P < 0�01); oven steaming LED: 1�00 g eq ww/ml (P <
0�05).

In the case of Brussels sprouts, all the cooking methods applied decreased
the anti-proliferative activity of the raw extract and no cytotoxic activity
was traceable up to 4 g eq ww/ml.

Genotoxicity

On the basis of MTS values of raw and cooked vegetables we determined the
sub-toxic concentrations to adopt for the DNA migration analysis (alkaline
Comet assay) on HT-29 cells. To better compare the results between the
extracts from fresh and cooked vegetables, which presented different
antiproliferative activity, we analysed the genotoxicity induced by the
highest non-toxic concentration identified with the raw extracts for all
samples (i.e. broccoli: 0�01 g eq ww/ml; cauliflower and Brussels sprouts:
0�10 g eq ww/ml) and a concentration ten times higher only for cooked
samples (broccoli: 0�10 g eq ww/ml; cauliflower and Brussels sprouts: 1�00 g
eq ww/ml).

None of the vegetable extracts was able to induce DNA damage at the
concentrations tested (Table 1).

Table 1. Genotoxicity evaluated by the Comet assay on HT-29 cells treated
(24 h) with raw and cooked vegetable extracts at different concentrations*
(Mean values and standard deviations)
----------------------------------
- - - ===TI (%)
Vegetable extract Cooking method Extract concentration (g eq ww/ml)===Mean
SD
----------------------------------
Untreated cells � � 0�31 0�20
H2O2 (100 mM) � � 6�45 2�89
Vitamin C (1mM) � � 0�30 0�12
----------------------------------
Broccoli
----------------------------------
Raw 0�01 0�22 0�12
Microwaved
0�01 0�37 0�30
0�10 0�31 0�22
Boiled 0�01
0�27 0�08
0�10 0�18 0�02
Basket steamed
0�01 0�22 0�03
0�10 0�35 0�21
Oven steamed
0�01 0�12 0�04
0�10 0�34 0�24
----------------------------------
Cauliflower
----------------------------------
Raw 0�10 0�49 0�24
Microwaved
0�10 0�50 0�18
1�00 0�33 0�17
Boiled
0�10 0�58 0�08
1�00 0�36 0�15
Basket steamed
0�10 0�35 0�10
1�00 0�30 0�15
Oven steamed
0�10 0�38 0�05
1�00 0�25 0�08
----------------------------------
Brussels sprouts
----------------------------------
Raw 0�10 0�27 0�20
Microwaved
0�10 0�43 0�35
1�00 0�40 0�01
Boiled
0�10 0�46 0�20
1�00 0�19 0�11
Basket steamed
0�10 0�36 0�24
1�00 0�26 0�09
Oven steamed
0�10 0�25 0�14
1�00 0�40 0�07
----------------------------------
TI, tail intensity; g eq ww/ml, equivalent of wet weight g/ml.
* Negative controls: HT-29 untreated and vitamin C treated (1 mm);
positive control: H2O2 (100 �m).

Antioxidant activity

The cells were treated for 24 h with vegetable extracts, after discharging
the medium plus the exhausted extract; they were subjected to 5 min shock
with H2O2 (one of the most common oxidative damage-inducing agents). The
ability to reduce the DNA damage induced by H2O2 treatment in HT-29 cells
was chosen as an indicator of the chemopreventive capability of the
vegetable extracts. Among the antioxidants, ascorbic acid (vitamin C) plays
a central role as it contributes to the regeneration of vitamin E and
constitutes a strong line of defence in retarding free radical-induced
cellular damage(30). The antioxidant activity of ascorbic acid (1 mm) was
determined. Vitamin C pre-treatment produced a significantly strong decrease
(approximately 50 %) of DNA damage induced by H2O2 at 100 �m (P < 0�05). All
the raw vegetable extracts had significant antioxidant activity (P < 0�05)
comparable with vitamin C, in particular the raw broccoli extract showed its
defensive capability at a ten-fold lower concentration than the other two
raw vegetable extracts (Fig. 3).

Cooking broccoli with microwaving and steaming methods determined a slight
lowering of the antioxidative properties shown by the raw vegetable. In
fact, the same significant DNA migration reduction (P < 0�05) induced by the
raw extract was detected for cooked vegetables extracts at a concentration
that was ten-fold higher. Otherwise, no antioxidant activity was detected in
the boiled broccoli at the extract concentrations tested (Fig. 3), in
agreement with literature data(31).

A significant antioxidant activity (P < 0�05) was detected in the
cauliflower extracts, independently from the cooking method performed (Fig.
3). In particular, the microwaved vegetable extract seems more effective
than the raw extract and vitamin C.

The microwaved Brussels sprouts extract showed an antioxidant activity
comparable with the raw extract and vitamin C, whereas the extracts of
boiled and steamed Brussels sprouts showed the same protective activity at
ten-fold higher concentrations (Fig. 3).

Discussion

In this study, the effect of cooking practices on the anti-proliferative
and/or antioxidant properties of three fresh Brassica species (broccoli,
cauliflower and Brussels sprouts) was evaluated by MTS and Comet assays.
Data demonstrated a significant dose-dependent anti-proliferative effect
when the human colon cancer cells (HT-29) were treated with uncooked
vegetable extracts. The highest anti-proliferative activity was found with
the broccoli extract with the LED twofold lower than the Brussels sprouts
and cauliflowers extracts. This anti-proliferative rank order could be
linked to the higher content of bioactive compounds, mainly glucosinolates,
present in broccoli than in the other Brassica vegetables analysed (Fig.
1)(27), even though a difference in single compounds present cannot be ruled
out. It is known that some chemopreventive vegetable components could induce
cell cycle arrest in HT-29 cells; in particular the hydrolysis of
glucosinolates by myrosinase could induce the formation of chemopreventive
molecules such as isothiocyanates(32,33). Even though we did not measure the
myrosinase activity in the extracts, during their preparation the Stomaker
treatment could have mimicked the mastication process, determining the
activation of myrosinase and, hence, the formation of hydrolysis products,
as during the Brassica processing before cooking (i.e. chopping, treading,
etc.)(34). Among the vegetables analysed, broccoli has the highest
concentration of the glucosinolate glucoraphanin, which could be hydrolysed
by myrosinase in the reactive isothiocyanate sulforaphane with
chemopreventive properties. Sulforaphane exerts its anti-proliferative
effect by arresting the cell cycle; this arrest has been documented in the
colon, prostate, breast, bladder and T cells(33).

The release of active molecules from the Brassicaceae tissues, following the
glucosinolate hydrolysis by myrosinase, is strongly influenced by the
cooking practice adopted(34). The lowering or disappearance of the Brassica
anti-proliferative effects detected after cooking practices, particularly
boiling and steaming, could be ascribed to an alteration of the
glucosinolate-myrosinase system(35). Conversely, the higher retention of the
anti-proliferative effect of microwaved Brassica samples with respect to
other cooking practices could be linked to a reduced inactivation of
myrosinase due to the mild cooking conditions applied (i.e. low energy
inputs with consequent low temperature cooking), as demonstrated by Verkerk
& Dekker(36).

Many in vitro and in vivo studies demonstrated that some molecules (i.e.
polyphenols, catechins, etc.) present in food are anti-carcinogenic by
inducing apoptosis and inhibiting cell growth(10,22). Probable mechanisms of
action include antioxidant and free-radical scavenging activity. On the
other hand, vegetables, including Brassica, present a variable chemical
complex mixture and could also contain compounds with genotoxic
activity(37,38). The vegetable extracts, evaluated in this research, were
analysed both for their genotoxic or anti-genotoxic (antioxidant) activities
by the Comet assay. DNA migration analysis of HT-29 cells treated (24 h)
with vegetable extracts alone, at sub-toxic concentrations determined on MTS
values, did not show any induced DNA damage, whereas HT-29 cells pre-treated
for 24 h with raw and cooked Brassica and treated with H2O2 (100 �m, 5 min
at 0�C) showed different sensitivity to DNA oxidative damage, as revealed by
the alkaline Comet assay.

The chemopreventive action that was detected was determined by an endogenous
response, due to the fact that the vegetable extract was removed before H2O2
treatment. In particular, raw, microwaved, boiled (except broccoli) and
steamed vegetable extracts, presented a protective antioxidative action
comparable with vitamin C (1 mm), as demonstrated by the reduced DNA
migration. It is noteworthy that only the cooked cauliflower extracts showed
an antioxidant activity comparable to the raw extract (0�10 g eq ww/ml) with
the same TI (%) variation coefficient.

Among the different cooking practices, the boiling treatment seems to
determine a different antioxidant status depending on the kind of Brassica
analysed; although the highest loss of activity was found with broccoli,
their cooked extracts remained the more active. The steaming and microwaving
practices showed a general good retention of the antioxidant activity. Based
on the present results, the antioxidant activity of raw extracts could be
probably ascribed to the glucosinolate hydrolysis products. On the contrary,
the antioxidant activity of cooked Brassica vegetables could be due to the
formation of new compounds following the cooking, for instance, polyphenols
with a different oxidation state that could exhibit their antioxidant
activity not being masked by the glucosinolates hydrolysis products.
However, these hypotheses should be confirmed by the identification and
quantification of phytochemical compounds present in the aqueous extracts as
no clear relationships were found when data on biological activities were
compared with the concentration of chemical compounds present in the
vegetables, before the extraction process.

At a first glance, the comparative analysis of the raw extract toxicological
data (anti-proliferative and antioxidant activities) seems to suggest that
high anti-proliferative activity could be concomitant with high antioxidant
activity, suggesting that the chemopreventive action could be related to the
control of the redox cellular status. This correlation disappears when data
of cooked vegetable extracts are observed; generally, the loss of
anti-proliferative activity seems independent of the antioxidant activity,
suggesting a more complex design involving several pathways differently
regulated by the complex mixtures present in the extracts. These results are
in agreement with Boivin et al.(39), who found that the anti-proliferative
effect of Brassica vegetables, among others, largely independent of their
antioxidant properties evaluated in in vitro experiments.

In conclusion, the analyses of the present data on the human colon carcinoma
cell line HT-29 indicate that Brassica extracts could positively alter
cellular endogenous chemoprotective status.

The lack of a chemical characterisation of the water extracts prevents us
from a clear correlation among the biological activities tested and the
specific compounds. Nevertheless, the increased ability of cells, treated
with the Brassica samples, to contrast the reactive oxygen species damaging
activity seems to be related to the complex mixture of the protective
substances present in the vegetables more than to a single class of
molecules.

The cooking methods applied influence the anti-proliferative activity of the
Brassica extracts but do not alter considerably the high antioxidant
activity presented by the raw vegetables. These data provide a new insight
into the influence of domestic treatment on the quality of food, which could
support the recent epidemiological studies suggesting that the consumption
of cruciferous vegetables, mainly cooked food, may be related to a reduced
risk of developing cancer.

-- Al Pater, alpater@SHAW.ca

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[CRSOCIETY] Re: Fwd: Am I hypertensive? Reduce or eliminate Lasix?

jwwright — Thu, 17 May 2012 11:27:02 -0400

----- Original Message -----
From: "Saul Lubkin"
To: "The CR Society Main Discussion List"

Cc: "Luigi Fontana" ; "Paul
McGlothin"
Sent: Thursday, May 17, 2012 7:57 AM
Subject: [CR] Fwd: Am I hypertensive? Reduce or
eliminate Lasix?

> Dear ALL,
>
> I'd like to share an email message that I just
> sent to my nephrologist, who has been monitoring
> my BP for the last several
> years.
>
> It's a bit (almost) shocking to me -- I should
> note that, when Luigi
> tested me at WUSTL, he diagnosed "marginal
> hypertension -- but I was taking
> Benicar, 40 mg twice per day, at the time
> [which is twice the recommended maximum daily
> allowance]
>
>
> ---------- Forwarded message ----------
> From: Saul Lubkin
> Date: Thu, May 17, 2012 at 9:51 AM
> Subject: RE: Am I hypertensive? Reduce or
> eliminate Lasix?
> To: Jeremy Taylor
>
>
>
> Hello again, Dr. Taylor!
>
> With 40mg of Lasix, twice per day (and no
> Benicar), BP continues to be very
> low -- typically systolic is in the 90's.
>
> My growing suspicion:
>
> I am not hypertensive.
>
> I (had been) taking Benicar, 40mg, twice per day
> (which is double the
> maximum recommended amount); perhaps I have a bad
> reaction (maybe allergy)
> to Benicar?
>
> Or, perhaps I have suffered from extreme doctor's
> office syndrome for
> years? (I doubt that this could be a MAJOR
> factor -- a contributing
> factor, probably).
>
> Other possibility: My diet has changed somewhat
> recently: I am now
> restricting protein more avidly than before.
> (Typical day: Protein
> deduced from about 3/4 cup of white beans, or else
> from 1.5 ounces of
> sashimi [1 oz salmon, 1/2 oz yellowtail. Plus,
> lots of raw low cal
> veggies).
>
> My question: Should I reduce Lasix to 20mg, twice
> per day, or drop it
> entirely?
>
> :-)
>
> -- Saul

Thanks, Saul,
The part I love about your post is that I have HTN,
and your are significantly lower in weight.
As I have said before, I ran a test in myself losing
60 # and my BP never went down to the point I could
drop the verapamil.
I think you do have "true" HTN, which is idiopathic,
but recognize we can think it's caused by an adrenal
adenoma.
Not to worry, because it's far to hard to treat
anyway.

Take whatever works.
There are many medications and literally, we/they
cut and try.

I've a friend who runs, can't be more that 125#
soaking wet, and developed HTN during training. At
35 yo.
Uses diovan.
I use verapamil because it's the only thing that
works for me.

Yes, the diastolic seems the be the biggest problem.
I've never found any logic that tells me why, except
excess fatty foods raises it.

IMO, it's a good thing to wean off any HTN drug
while you add or change meds.
FWIW, I think a higher diastolic raising BP but
keeping pulse pressure lower is better.
(pulse pressure is the difference between Sys and
Dia.)

Regards

.

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[CRSOCIETY] Fwd: Am I hypertensive? Reduce or eliminate Lasix?

Saul Lubkin — Thu, 17 May 2012 09:57:35 -0400

Dear ALL,

I'd like to share an email message that I just
sent to my nephrologist, who has been monitoring my BP for the last several
years.

It's a bit (almost) shocking to me -- I should note that, when Luigi
tested me at WUSTL, he diagnosed "marginal hypertension -- but I was taking
Benicar, 40 mg twice per day, at the time
[which is twice the recommended maximum daily allowance]

---------- Forwarded message ----------
From: Saul Lubkin
Date: Thu, May 17, 2012 at 9:51 AM
Subject: RE: Am I hypertensive? Reduce or eliminate Lasix?
To: Jeremy Taylor

Hello again, Dr. Taylor!

With 40mg of Lasix, twice per day (and no Benicar), BP continues to be very
low -- typically systolic is in the 90's.

My growing suspicion:

I am not hypertensive.

I (had been) taking Benicar, 40mg, twice per day (which is double the
maximum recommended amount); perhaps I have a bad reaction (maybe allergy)
to Benicar?

Or, perhaps I have suffered from extreme doctor's office syndrome for
years? (I doubt that this could be a MAJOR factor -- a contributing
factor, probably).

Other possibility: My diet has changed somewhat recently: I am now
restricting protein more avidly than before. (Typical day: Protein
deduced from about 3/4 cup of white beans, or else from 1.5 ounces of
sashimi [1 oz salmon, 1/2 oz yellowtail. Plus, lots of raw low cal
veggies).

My question: Should I reduce Lasix to 20mg, twice per day, or drop it
entirely?

:-)

-- Saul
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[CRSOCIETY] Re: Headline: Sugar Can Make You Dumb

jwwright — Thu, 17 May 2012 10:34:49 -0400

I try to write to eliminate ambiguity, and even if
the term is used as you suggest it should be made
clear in a technical report.
The word sugar for sure is on a bag in the store and
is not anything but sucrose, even if it comes from
beets.
In the case of HFCS, they recently wanted the gov't
to approve the term to apply to HFCS which would
completely hide what they actually put in the foods.

I think Lustig has a point although I think it
doesn't apply to me because I KNOW HFCS holds more
water in my body and corn syrup(also available in
the dextrose(glucose) form) does the same (in ME).
That raises my blood pressure (BP).
I measure my BP several times per day for
years(1990). If everyone did that, we'd know a lot
more about BP and foods.

Consumers had an effect on MSG, which also held
water and raised BP.
I could tell that immediately, and leave the
restaurant that used that, even though articles were
saying that was BS.
The articles could not include patient experience.

That's why I try to use and expect to hear/read
precise terms in technical reports.
Notice that if we get the full text, things clear up
a little.

That doesn't stop experts from using the term
sugars, I understand that, but I become suspicious
every time they do.
They often use it to cover up something.

And the media further denigrates the info by
changing the title, meanings.

Beth sent me the URL to Lustig's lecture, and I
watched that twice and he has some points, and I
think I heard that it's not only HFCS, but added
SUGAR in foods. I think he as the added SUGAR in
foods in foods is a worse problem.
But I also notice some sweetened items are using
maltose and other sweet carbs to IMPROVE flavor.

And since I know that ALL carbs change into glucose
in the body, in fact, the body can change protein
and fatty acids as well into glucose.
As Lustig puts it, "Glucose is the energy of life".

It seems to me that good health boils down to eating
less food and minimizing excess glucose in the blood
and maybe elsewhere, like blood lipids,
interstitium, and lymph system.

I think in court, Lustig would lose his argument
about HFCS causing anything, even though I agree the
HFCS added to soft drinks is too easy to get excess
calories. In fact, the makers can argue their
product is the same as sucrose, aided by Lustig's
own lecture which says sucrose is 50% glucose.

BTW, my wife's comment was:
"Why are people living longer?"

Regards

----- Original Message -----
From: "Taurus"
To: "The CR Society Main Discussion List"

Sent: Wednesday, May 16, 2012 7:51 PM
Subject: Re: [CR] Headline: Sugar Can Make You Dumb

> jwwright
>> sugar is sucrose, breaks down into glucose and
>> fructose.
>> confusion in terms as always.
>
> Indeed; just to be clear here, those are all
> sugars.
> - Taurus
>

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[CRSOCIETY] Re: Longevity of Tour de France cyclists

Rodney Nicholson — Wed, 16 May 2012 23:38:40 -0400

Of course if someone is in generally poor health they are very unlikely to qualify for the Tour de France.
�
So�effectively this study�automatically selected�people�in excellent health by choosing to study Tour de France calibre cyclists.� People in excellent health might be expected to live longer than average.
�
Nevertheless, the fact that they do not die sooner than the rest of the population certainly suggests that huge amounts of endurance exercise in early adulthood is not harmful.� Which is good to know.
�
Rodney.

>________________________________
> From: Richard Schulman
>To: The CR Society Main Discussion List
>Sent: Wednesday, May 16, 2012 8:39:50 AM
>Subject: [CR] Longevity of Tour de France cyclists
>
>[While moderate exercise is undoubtedly good advice for most, and is
>probably most consistent with keeping calorie intake to minimum
>requirements, it doesn't seem to be the case that properly trained
>intense exercisers die earlier than the populations they spring from]:
>"Int J Sports Med. 2011 Aug;32(8):644-7. Epub 2011 May 26.
>Increased average longevity among the "Tour de France" cyclists.
>Sanchis-Gomar F, Olaso-Gonzalez G, Corella D, Gomez-Cabrera MC, Vina
>J.
>
>"Department of Physiology, Faculty of Medicine, University of
>Valencia, Spain.
>
>"Abstract
>
>"It is widely held among the general population and even among health
>professionals that moderate exercise is a healthy practice but long
>term high intensity exercise is not. The specific amount of physical
>activity necessary for good health remains unclear. To date, longevity
>studies of elite athletes have been relatively sparse and the results
>are somewhat conflicting. The Tour de France is among the most
>gruelling sport events in the world, during which highly trained
>professional cyclists undertake high intensity exercise for a full 3
>weeks. Consequently we set out to determine the longevity of the
>participants in the Tour de France, compared with that of the general
>population. We studied the longevity of 834 cyclists from France
>(nF5), Italy (n6) and Belgium (n3) who rode the Tour de France
>between the years 1930 and 1964. Dates of birth and death of the
>cyclists were obtained on December 31 (st) 2007. We calculated the
>percentage of survivors for each age and compared them with the values
>for the pooled general population of France, Italy and Belgium for the
>appropriate age cohorts. We found a very significant increase in
>average longevity (17%) of the cyclists when compared with the general
>population. The age at which 50% of the general population died was
>73.5 vs. 81.5 years in Tour de France participants. Our major finding
>is that repeated very intense exercise prolongs life span in well
>trained practitioners. Our findings underpin the importance of
>exercising without the fear that becoming exhausted might be bad for
>one's health. PMID: 21618162"
>
>RS
>
>_______________________________________________
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>
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>
>
>
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[CRCOMMUNITY] Offlist -- Re: All-cause mortality by diet pattern in German elderly

Wed, 16 May 2012 12:37:19 -0400

Hello Al & CR Community,

I love this message that you have posted (below)! Wonderful!!!

It is the first time that I have seen (dietary eating pattern)

statistical analysis related to (all-cause mortality) that

makes sense and gets statistically significant results that

can be clearly interpreted without controversy.

"REDUCED RANK REGRESSION" (RRR) is a powerful multivariate

statistical approach that will surely find further use in

"epidemiological identification" of "statistically significant

factors" (linear combinations of measurable variables) affecting

"all-cause mortality," after adjusting for the effects of confounding.

RRR is already used in economics and time series analysis, where

the complexity is so great that only the most powerful statistical

methods will work -- after proper statistical adjustment for

external variables to eliminate confounding.

It is a great research paper that you have uncovered here.

I was very, Very, VERY impressed. Thank you!

-- Warren

PS: This multivariate "REDUCED RANK REGRESSION" (RRR)is more

powerful than the classical multivariate approaches of

"principal component analysis" (PCA) and "factor analysis" (FA) ---

since it can produce statistically significant results that

neither of the two can replicate. This did surprise me quite

a bit, when I read the research monograph. The authors did

indeed try the PCA/FA approach on their data --- and showed

that RRR gave superior results.

I also note that I could find no specific entry about RRR

in Wikipedia. This too was a surprise to me --- RRR, a

multivariate statistical research method beating out PCA/FA,

and missing from Wikipedia.

PPS: Oh, a second comment. Note that

--- the dietary pattern showing high mortality consisted

entirely of "zero-fiber" foods (not a single food had either

soluble or insoluble fiber; all were /*ZERO*/ fiber),

--- while the dietary patter of low mortality consisted

of "high-fiber" foods (All of them were full of both

soluble and insoluble fiber).

Also of note --- the RRR multivariate statistical method

teased out only these /*TWO*/ specific dietary patterns that

had a statistically significant relationship to all-cause

mortality.

It is a great research paper that you posted here!

The clarity of explanation (to members of the statistical

community, of the RRR method) is appealing to. '

I thank you, Dr. Al Pater, for posting your message below.

It was good, Good, GOOD, /*GOOD*/!

================ ==============

-----Original Message-----
From: crcomm-bounces@lists.calorierestriction.org
[mailto:crcomm-bounces@lists.calorierestriction.org] On Behalf Of Al Pater
Sent: Tuesday, May 15, 2012 6:34 PM
To: CR Society Community
Subject: [CRCOMMUNITY] All-cause mortality by diet pattern in German elderly

Comparison of two statistical approaches to predict all-cause mortality by
dietary patterns in German elderly subjects.

Hoffmann K, Boeing H, Boffetta P, Nagel G, Orfanos P, Ferrari P, Bamia C.

Br J Nutr. 2005 May;93(5):709-16.

PMID:15975171

http://journals.cambridge.org/action/displayFulltext?type=6
BJN&volumeId=93&issueId=05&aid=919128&bodyId=&membershipNumber=&societyETOCS
ession=&fulltextType=RA&fileId=S000711450500111X>
&fid=919132&jid=BJN&volumeId=93&issueId=05&aid=919128&bodyId=&membershipNumb
er=&societyETOCSession=&fulltextType=RA&fileId=S000711450500111X

http://journals.cambridge.org/download.php?file=%2FBJN%2FBJN93_05%2FS0007114
50500111Xa.pdf
450500111Xa.pdf&code=1795e25db6c729f2db323feb4fadd1e3>
&code=1795e25db6c729f2db323feb4fadd1e3

Abstract

Dietary patterns are comprehensive variables of dietary intake appropriate
to model the complex exposure in nutritional research. The objectives of
this study were to identify dietary patterns by applying two statistical
methods, principal component analysis (PCA) and reduced rank regression
(RRR), and to assess their ability to predict all-cause mortality. Motivated
by previous studies we chose percentages of energy from different
macronutrients as response variables in the RRR analysis. We used data from

9356 German elderly subject enrolled in the European Prospective
Investigation into Cancer and Nutrition study. The first RRR pattern,
subjects which explained 30.8 % of variation in energy sources and
especially much variation in intake of saturated fat, monounsaturated fat
and carbohydrates was a significant predictor of all-cause mortality. The
pattern score had high positive loadings in all types of meat, butter,
sauces and eggs, and was inversely associated with bread and fruits. After
adjustment for other known risk factors, the relative risks from the lowest
to highest quintiles of the first RRR pattern score were 1.0, 1.01, 0.96,
1.32, 1.61 (P for trend: 0.0004). In contrast, the first two PCA patterns
explaining 19.7 % of food intake variation but only 7.0 % of variation in
energy sources were not related to mortality. These results suggest that
variation in macronutrients is meaningful for mortality and that the RRR
method is more appropriate than the classic PCA method to identify dietary
patterns relevant to mortality.

...

"a diet rich in [total, saturated, monounsaturated and polyunsaturated] fat
and poor in carbohydrates [as in bread and fruits] decreases life
expectancy. [Mean age (years), 62-63]"

van Dam RM.

New approaches to the study of dietary patterns.

Br J Nutr. 2005 May;93(5):573-4. No abstract available.

PMID: 15975154

http://journals.cambridge.org/action/displayFulltext?type=6
BJN&volumeId=93&issueId=05&aid=918856&bodyId=&membershipNumber=&societyETOCS
ession=&fulltextType=AC&fileId=S0007114505000942>
&fid=918860&jid=BJN&volumeId=93&issueId=05&aid=918856&bodyId=&membershipNumb
er=&societyETOCSession=&fulltextType=AC&fileId=S0007114505000942

http://journals.cambridge.org/download.php?file=%2FBJN%2FBJN93_05%2FS0007114
505000942a.pdf
4505000942a.pdf&code=36e4a6f74485dd2d5eecd461067b11c3>
&code=36e4a6f74485dd2d5eecd461067b11c3

-- Al Pater, alpater@SHAW.ca

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[CRSOCIETY] Re: Headline: Sugar Can Make You Dumb

Al Pater — Wed, 16 May 2012 22:08:10 -0400

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[CRCOMMUNITY] Coffee drinking linked to longer life

Al Pater — Wed, 16 May 2012 22:15:19 -0400

The below messages-referred-to papers described are pdf-availed.

http://edition.cnn.com/2012/05/16/health/coffee-drinking-longer-life/index.html?hpt=he_c2

Coffee drinking linked to longer life
By Amanda Gardner, Health.com
May 16, 2012 -- Updated 2118 GMT (0518 HKT)

Coffee contains some 1,000 compounds, many of which are health-promoting
antioxidants.

STORY HIGHLIGHTS

Daily cup may lower risk of dying from chronic diseases such as diabetes

NIH followed 400,000 men and women for 13 years, during which 13% died

In the study, both regular and decaf were associated with a lower risk of
dying

(Health.com) -- Drinking a daily cup of coffee -- or even several cups --
isn't likely to harm your health, and it may even lower your risk of dying
from chronic diseases such as diabetes and heart disease, a new study in the
New England Journal of Medicine suggests.

The relationship between coffee drinking and health has been a hot topic in
recent years, but research has produced mixed results.

Some studies have linked coffee consumption to better health and a lower
risk of premature death, while others suggest that coffee -- or rather
caffeine -- might contribute to heart disease through negative effects on
blood pressure, cholesterol, and heart rate.

The new study is by far the largest of its kind to date. As part of a joint
project with the AARP, researchers from the National Institutes of Health
followed more than 400,000 healthy men and women between the ages of 50 and
71 for up to 13 years, during which 13% of the participants died.

Health.com: Big perks -- coffee's health benefits

Overall, coffee drinkers were less likely than their peers to die during the
study, and the more coffee they drank, the lower their mortality risk tended
to be. Compared with people who drank no coffee at all, men and women who
drank six or more cups per day were 10% and 15% less likely, respectively,
to die during the study.

This pattern held when the researchers broke out the data by specific causes
of death, including heart disease, lung disease, pneumonia,stroke, diabetes,
infections, and even injuries and accidents. Cancer was the only major cause
of death not associated with coffee consumption.

"There has been some concern that coffee might increase the risk of death,
and this provides some reassurance against that worry," says Neal D.
Freedman, Ph.D., the lead author of the study and an investigator with the
division of cancer epidemiology and genetics at the National Cancer
Institute, in Rockville, Maryland.

Even moderate coffee consumption was linked to better survival odds.
Drinking a single cup per day -- which was much more common than a
six-cup-a-day habit -- was associated with a 6% lower risk of dying among
men and a 5% lower risk among women.

Although these reductions in risk might seem modest, they could have
potentially dramatic implications for public health if spread out over the
tens of millions of coffee drinkers in the United States, says Susan Fisher,
Ph.D., chair of community and preventive medicine at the University of
Rochester Medical Center, in Rochester, New York.

"Even a small decrease, when you're talking about a [behavior] that is so
ubiquitous across the human population, could mean many, many lives saved,"
Fisher says.

The findings, however, stop short of saying that coffee drinking directly
lowers the risk of chronic disease. Like much of the previous research on
coffee, the study was based on survey data -- in this case, a single
questionnaire distributed in the mid-1990s -- that may provide an incomplete
picture of the participants' overall health and lifestyle.

Although the researchers took into account a wide range of extenuating
factors, including diet and exercise regimens, smoking, alcohol consumption,
body mass index, and marital status, it's possible that people who drink
coffee differ from the rest of the population in as-yet unidentified ways
that make them less vulnerable to disease and early death.

The explanation for the study findings "might not specifically be the
coffee," Fisher says. "It might be some characteristic of the coffee
drinker."

Still, it's plausible that coffee drinking actually improves health. Coffee
contains some 1,000 compounds, many of which are health-promoting
antioxidants, Freedman says.

"There's some data showing that some of these components may prevent insulin
resistance and have a role in diabetes," he says.

In the study, both regular and decaf were associated with a lower risk of
dying, which suggests that these and other substances in coffee might be
more important than caffeine. But even decaf contains trace amounts of
caffeine, so the authors can't entirely rule out the possibility that
caffeine has an effect on health, Freedman says.

http://www.cbc.ca/news/health/story/2011/03/10/coffee-stroke.html

Coffee tied to lower stroke risk in women
The Associated Press
Posted: Mar 10, 2011 6:41 PM ET Last

Moayyad, director of coffee purchasing for Peet's Coffee, smells coffee
during a blind taste test in 2007. The beverage may help lower the risk of
stroke in women compared with not drinking any. (Kimberly White/Reuters)

(Note:CBC does not endorse and is not responsible for the content of
external links.)

Women who enjoy a daily dose of coffee may like this perk: It might lower
their risk of stroke.

Women in a Swedish study who drank at least a cup of coffee everyday had a
0.22 to 0.25 times lower risk of stroke, compared to those who drank less
coffee or none at all.

"Coffee drinkers should rejoice," said Dr. Sharonne Hayes, a cardiologist at
Mayo Clinic in Rochester, Minn. "Coffee is often made out to be potentially
bad for your heart. There really hasn't been any study that convincingly
said coffee is bad."

"If you are drinking coffee now, you may be doing some good and you are
likely not doing harm," she added.

But Hayes and other doctors say the study shouldn't send non-coffee drinkers
running to their local coffee shop. The study doesn't prove that coffee
lowers stroke risk, only that coffee drinkers tend to have a lower stroke
risk.

"These sorts of epidemiological studies are compelling but they don't prove
cause," said Dr. David S. Seres, director of medical nutrition at Columbia
University's College of Physicians and Surgeons in New York.

The findings were published online Thursday in the American Heart
Association journal Stroke.

Scientists have been studying coffee for years, trying to determine its
risks and benefits. The Swedish researchers led by Susanna Larsson at the
Karolinska Institute in Stockholm said previous studies on coffee
consumption and strokes have had conflicting findings.

"There hasn't been a consistent message come out," of coffee studies, said
Dr. Cathy Sila, a stroke neurologist at University Hospitals Case Medical
Center in Cleveland.

For the observational study, researchers followed 34,670 Swedish women, ages
49 to 83, for about 10 years. The women were asked how much coffee they
drank at the start of the study. The researchers checked hospital records to
find out how many of the women later had strokes.

There were 1,680 strokes, including those who drank less than a cup or none.

Cup a day enough

Researchers adjusted for differences between the groups that affect stroke
risk, such as smoking, weight, high blood pressure and diabetes, and still
saw a lower stroke risk among coffee drinkers. Larsson said the benefit was
seen whether the women drank a cup or several daily.

"You don't need to drink so much. One or two cups a day is enough," she
said.

Larsson, who in another study found a link between coffee drinking in
Finnish men who smoked and decreased stroke risk, said more research needs
to be done to figure out why coffee may be cutting stroke risk. It could be
reducing inflammation and improving insulin sensitivity, she said, or it
could be the antioxidants in coffee.

Since study participants were asked about their past coffee consumption and
then followed over time, there is no way to know if they changed their
behaviour.

Women in the study were not asked whether they drank decaf coffee, but most
Swedes drink caffeinated coffee, the researchers said.

Larsson and others point out that those who want to reduce their chances of
a stroke should focus on the proven ways to lower risk:

Don't smoke.

Keep blood pressure in check.

Maintain a healthy weight.

Last year, British researchers also reported a link between any coffee
drinking and reduced risk of stroke in a general population.

Association of Coffee Drinking with Total and Cause-Specific Mortality
N.D. Freedman, Y. Park, C.C. Abnet, A.R. Hollenbeck, and R. Sinha
N Engl J Med 2012; 366:1891-1904May 17, 2012

Journal pre-amble: In this study involving long-term follow-up of more than
400,000 adults, coffee consumption was inversely associated with total
mortality and mortality due to heart disease, respiratory disease, stroke,
injuries and accidents, diabetes, and infections, but not cancer.

Abstract

Background

Coffee is one of the most widely consumed beverages, but the association
between coffee consumption and the risk of death remains unclear.

Methods

We examined the association of coffee drinking with subsequent total and
cause-specific mortality among 229,119 men and 173,141 women in the National
Institutes of Health�AARP Diet and Health Study who were 50 to 71 years of
age at baseline. Participants with cancer, heart disease, and stroke were
excluded. Coffee consumption was assessed once at baseline.

Results

During 5,148,760 person-years of follow-up between 1995 and 2008, a total of
33,731 men and 18,784 women died. In age-adjusted models, the risk of death
was increased among coffee drinkers. However, coffee drinkers were also more
likely to smoke, and, after adjustment for tobacco-smoking status and other
potential confounders, there was a significant inverse association between
coffee consumption and mortality. Adjusted hazard ratios for death among men
who drank coffee as compared with those who did not were as follows: 0.99
(95% confidence interval [CI], 0.95 to 1.04) for drinking less than 1 cup
per day, 0.94 (95% CI, 0.90 to 0.99) for 1 cup, 0.90 (95% CI, 0.86 to 0.93)
for 2 or 3 cups, 0.88 (95% CI, 0.84 to 0.93) for 4 or 5 cups, and 0.90 (95%
CI, 0.85 to 0.96) for 6 or more cups of coffee per day (P<0.001 for trend);
the respective hazard ratios among women were 1.01 (95% CI, 0.96 to 1.07),
0.95 (95% CI, 0.90 to 1.01), 0.87 (95% CI, 0.83 to 0.92), 0.84 (95% CI, 0.79
to 0.90), and 0.85 (95% CI, 0.78 to 0.93) (P<0.001 for trend). Inverse
associations were observed for deaths due to heart disease, respiratory
disease, stroke, injuries and accidents, diabetes, and infections, but not
for deaths due to cancer. Results were similar in subgroups, including
persons who had never smoked and persons who reported very good to excellent
health at baseline.

Conclusions

In this large prospective study, coffee consumption was inversely associated
with total and cause-specific mortality. Whether this was a causal or
associational finding cannot be determined from our data.

-- Al Pater, alpater@SHAW.ca

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[CRSOCIETY] Re: Headline: Sugar Can Make You Dumb

Taurus — Wed, 16 May 2012 21:51:37 -0400

jwwright
> sugar is sucrose, breaks down into glucose and
> fructose.
> confusion in terms as always.

Indeed; just to be clear here, those are all sugars.
- Taurus

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[CRSOCIETY] Re: Headline: Sugar Can Make You Dumb

Michael Rae — Wed, 16 May 2012 20:45:43 -0400

All:

James Cain wrote:
> As usual, the media reporting of science is simplified and usually somewhat
> misleading or misrepresented. The actual article seems more focused on
> omega-3 deficiency as the cause of poor learning, rather than the
> sugar/fructose per se.

It's both, really. What's far more egregious is that all the press is
reporting the story as being on HFCS, when in fact as Jack has noted
they used pure fructose.

In addition, the fructose was not in the chow, but put into the drinking
water as a 15% fructose solution, to which the animals had AL intake,
meaning that there was no control on total carb or Caloric intake. They
do indicate that "Animals showed a preference towards fructose drinking
in comparison to the food intake; however, total caloric intake (F3,20 =
1.832, P > 0.05) was similar in all the groups," but the Table seems to
indicate a one-time measurement, which Steven Spindler has shown
decisively is inadequate. And, if the animals really DID balance out
their energy intake, they would have to have been eating less of theeir
chow, which (a) the authors didn't measure, and (b) would leave them
deficinet in micronutrients -- including eating less of the n3 in
supplemented and deficient chow.

This is a long-standing, oft-used, and very sloppy methodology that
generates meaningless, tho' sometimes oft-cited, results; I'm annoyed
that it's reared its ugly head again.

Another misreport: the n-3 fatty acids were not straight DHA, but "0.5%
of flaxseed oil and 1.2% of docosahexaenoic acid capsule oil".

As you say, it dos seem that the article is more "focused on omega-3
deficiency as the cause of poor learning"; it's not clear how sensible
this is in light of the results, tho' again, the methodology makes
drawing any conclusions shaky anyway.

Pleased to see you on CR Society, James.

-Michael

> J Physiol. 2012 Apr 2. [Epub ahead of print]
> "Metabolic syndrome" in the brain: Deficiency in omega-3-fatty acid
> exacerbates dysfunctions in insulin receptor signaling and cognition.
> Agrawal R, Gomez-Pinilla F.
> PMID: 22473784
http://jp.physoc.org/content/590/10/2485.full

--
SENS: The biotechnologies of rejuvenation. See the outline <
http://tinyurl.com/SENS-outline>; learn the detailed science! <
http://tinyurl.com/End-Aging>

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[CRCOMMUNITY] New data on the health of these United States

Al Pater — Wed, 16 May 2012 20:04:12 -0400

New data on the health of these United States

http://thechart.blogs.cnn.com/2012/05/16/new-data-on-the-health-of-these-united-states/?hpt=he_c2

-- Al Pater, alpater@SHAW.ca

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[CRSOCIETY] Re: Headline: Sugar Can Make You Dumb

jwwright — Wed, 16 May 2012 19:01:34 -0400

sugar is sucrose, breaks down into glucose and
fructose.
confusion in terms as always.
In plants, fructose may be present as the
monosaccharide and/or as a component of sucrose.
http://en.wikipedia.org/wiki/Fructose_intoxication

He increased the fructose.
Needs to do the same with sugar.

Regards

----- Original Message -----
From: "Taurus"
To: "The CR Society Main Discussion List"

Sent: Wednesday, May 16, 2012 3:56 PM
Subject: Re: [CR] Headline: Sugar Can Make You Dumb

> jwwright wrote
>> IMO, he suggests the action is from fructose not
>> sugar.
>
> Fructose is sugar.
> - Taurus
>
>

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[CRSOCIETY] Re: Headline: Sugar Can Make You Dumb

Taurus — Wed, 16 May 2012 17:56:12 -0400

jwwright wrote
> IMO, he suggests the action is from fructose not
> sugar.

Fructose is sugar.
- Taurus

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[CRSOCIETY] Re: Headline: Sugar Can Make You Dumb The DHA-deprivedanimalswere slower

Elizabeth Kirby — Wed, 16 May 2012 16:52:47 -0400

On Wed, May 16, 2012 at 2:06 PM, jwwright wrote:
>
>
> You jumped a few steps there.
> Digestion, absorption of glucose, fructose, galactose into portal artery.
> You'll need to give me a cite on that one, please.
>

http://youtu.be/dBnniua6-oM

It's long, but detailed.

>
> Whether they enter blood or lymph, the ones we measure are in blood.
> Since they come from dietary fats
>

Also from carbs.

>
>

> This the right Lustig?
>
>

>
> Pediatrics. 2012 Mar;129(3):557-70. Epub 2012 Feb 20.
> Toward a unifying hypothesis of metabolic syndrome. PMID:22351884
>

Yes -- thanks for the reference.

Beth
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[CRSOCIETY] Re: Headline: Sugar Can Make You Dumb

jwwright — Wed, 16 May 2012 17:37:50 -0400

----- Original Message -----
From: "Al Pater"
To: "The CR Society Main Discussion List"

Sent: Wednesday, May 16, 2012 2:02 PM
Subject: Re: [CR] Headline: Sugar Can Make You Dumb

>> J Physiol. 2012 Apr 2. [Epub ahead of print]
>> "Metabolic syndrome" in the brain: Deficiency in
>> omega-3-fatty acid
>> exacerbates dysfunctions in insulin receptor
>> signaling and cognition.
>> Agrawal R, Gomez-Pinilla F.
>> PMID: 22473784
>
> ... as shown more clearly in the free full-texts.
>
> http://jp.physoc.org/content/590/10/2485.full
> http://jp.physoc.org/content/590/10/2485.full.pdf+html
>
> -- Al Pater, alpater@SHAW.ca
TVM, Alan,
What a difference a title makes.

"Therefore the present study was planned to study
the potential of an n-3 fatty acid (docosahexaenoic
acid;DHA) enriched diet to counteract insulin
resistance in brain."

"After acclimatization for 1 week on standard rat
chow, rats were trained on the Barnes maze test for
5 days to learn the task, and then randomly assigned
to an omega-3 fatty acid diet (n-3 diet) or omega-3
fatty acid deficient diet (n-3 def) diet with or
without fructose solution (15%) as drinking water
for 6 weeks."
{The best outcome was the DHA diet w/o Fru.

{The second best was the non DHA diet w/o Fru.

IMO, he suggests the action is from fructose not
sugar.

Regards

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[CRSOCIETY] Re: Headline: Sugar Can Make You Dumb The DHA-deprivedanimalswere slower

jwwright — Wed, 16 May 2012 17:06:51 -0400

You'll need to give me a cite on that one, please.

----- Original Message -----
From: "Elizabeth Kirby"
To: "The CR Society Main Discussion List"

Sent: Wednesday, May 16, 2012 12:42 PM
Subject: Re: [CR] Headline: Sugar Can Make You Dumb
The DHA-deprivedanimalswere slower

> Lustig has also been saying that fructose can be
> metabolized in the liver
> into fat (depending to some extent on the amount
> that arrives at a given
> time).
>
> Thus, a high fructose diet (e.g. one that contains
> a lot of sugar and/or
> HCFS) is a high fat diet. Perhaps even more to
> the point, the resulting
> fat is dumped into the bloodstream.
>
> I read recently that fat in the diet is dropped
> into the lymphatic system
> (not the portal vein), so it has minimal effect on
> the TG levels in the
> blood.
>
> Beth

Beth,
You jumped a few steps there.
Digestion, absorption of glucose, fructose,
galactose into portal artery.
You'll need to give me a cite on that one, please.

Yes, long chain FA's are absorbed directly into
lymph, per Guyton.
Fructose is absorbed into the portal artery(already
cited) into the liver.
Excess fructose may "play havoc", I don't doubt it,
probably the cause of obesity and Metabolic
syndrome increases, and I add, in some people.

There are increases in triglycerides in some
people - that's a glycerol + 3 fatty acids.
Where is that done?
Guyton says intestine. "Digestion of Fats", pg
835-836.

Whether they enter blood or lymph, the ones we
measure are in blood.
Since they come from dietary fats

What I don't see so far, is the mechanism, that
shows how HFCS (I hate it) causes anything.
What enters the blood is glucose, fructose,
galactose which are processed into mostly glucose
out of liver.
I have to wonder if and why the liver would capture
ALL the glucose and ALL the fructose, so it could be
that an excess of fructose is not handled first
pass. My take.

This the right Lustig?
"In contrast to the systemic metabolism of glucose,
the liver is the primary metabolic clearinghouse for
4 specific foodstuffs that have been associated with
the development of MetS: trans-fats, branched-chain
amino acids, ethanol, and fructose. These 4
substrates (1) are not insulin regulated and (2)
deliver metabolic intermediates to hepatic
mitochondria without an appropriate "pop-off"
mechanism for excess substrate, enhancing
lipogenesis and ectopic adipose storage. Excessive
fatty acid derivatives interfere with hepatic
insulin signal transduction. Reactive oxygen species
accumulate, which cannot be quenched by adjacent
peroxisomes; these reactive oxygen species reach the
endoplasmic reticulum, leading to a compensatory
process termed the "unfolded protein response,"
driving further insulin resistance and eventually
insulin deficiency. "

Pediatrics. 2012 Mar;129(3):557-70. Epub 2012 Feb
20.
Toward a unifying hypothesis of metabolic syndrome.
PMID:22351884

And,
Yes I believe fructose is metabolized into fat in
the presence of adequate glucose, so it would appear
HFCS is a good way to increase body fat.
http://en.wikipedia.org/wiki/Fructose
fructose is metabolized primarily in the liver.[60]
EDITORIAL
Bray, George A. (2007). How bad is fructose?.
American Journal of Clinical Nutrition

http://www.ajcn.org/content/86/4/895.full

"Fructose differs in several ways from glucose, the
other half of the sucrose (sugar) molecule (4).
Fructose is absorbed from the gastrointestinal tract
by a different mechanism than that for glucose.
Glucose stimulates insulin release from the isolated
pancreas, but fructose does not. Most cells have
only low amounts of the glut-5 transporter, which
transports fructose into cells. Fructose cannot
enter most cells, because they lack glut-5, whereas
glucose is transported into cells by glut-4, an
insulin-dependent transport system. Finally, once
inside the liver cell, fructose can enter the
pathways that provide glycerol, the backbone for
triacylglycerol. The growing dietary amount of
fructose that is derived from sucrose or HFCS has
raised questions about how children and adults
respond to fructose alone or when it is accompanied
by glucose. In one study, the consumption of
high-fructose meals reduced 24-h plasma insulin and
leptin concentrations and increased postprandial
fasting triacylglycerols in women, but it did not
suppress circulating ghrelin, a major
appetite-stimulating hormone (4). "

"Fructose is metabolized, primarily in the liver, by
phosphorylation on the 1-position, a process that
bypasses the rate-limiting phosphofructokinase step
(4). Hepatic metabolism of fructose thus favors
lipogenesis, and it is not surprising that several
studies have found changes in circulating lipids
when subjects eat high-fructose diets (4)."
{and more}

Regards

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[CRSOCIETY] Re: Headline: Sugar Can Make You Dumb

Al Pater — Wed, 16 May 2012 16:02:24 -0400

From: "James Cain"

> As usual, the media reporting of science is simplified and usually
> somewhat
> misleading or misrepresented. The actual article seems more focused on
> omega-3 deficiency as the cause of poor learning, rather than the
> sugar/fructose per se.
>
> -------------------
> J Physiol. 2012 Apr 2. [Epub ahead of print]
> "Metabolic syndrome" in the brain: Deficiency in omega-3-fatty acid
> exacerbates dysfunctions in insulin receptor signaling and cognition.
> Agrawal R, Gomez-Pinilla F.
> PMID: 22473784

... as shown more clearly in the free full-texts.

http://jp.physoc.org/content/590/10/2485.full
http://jp.physoc.org/content/590/10/2485.full.pdf+html

-- Al Pater, alpater@SHAW.ca

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[CRSOCIETY] Re: Longevity of Tour de France cyclists

Al Pater — Wed, 16 May 2012 15:30:00 -0400

From: "Richard Schulman"

> [While moderate exercise is undoubtedly good advice for most, and is
> probably most consistent with keeping calorie intake to minimum
> requirements, it doesn't seem to be the case that properly trained
> intense exercisers die earlier than the populations they spring from]:

> "Increased average longevity among the "Tour de France" cyclists.
Sanchis-Gomar F, Olaso-Gonzalez G, Corella D, Gomez-Cabrera MC, Vina J.
Int J Sports Med. 2011 Aug;32(8):644-7. Epub 2011 May 26.
PMID:21618162

This is hardly a proper prospective trial, being retrospective. To do a
semi-decent study with these goals of being a good prospective study, you
need to know their baseline longevity-associated characteristics and those
of the "controls". Healthy people more often participate in good
health-requiring activities.

-- Al Pater, alpater@SHAW.ca

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[CRSOCIETY] Re: Headline: Sugar Can Make You Dumb The DHA-deprived animalswere slower

Elizabeth Kirby — Wed, 16 May 2012 14:42:02 -0400

Lustig has also been saying that fructose can be metabolized in the liver
into fat (depending to some extent on the amount that arrives at a given
time).

Thus, a high fructose diet (e.g. one that contains a lot of sugar and/or
HCFS) is a high fat diet. Perhaps even more to the point, the resulting
fat is dumped into the bloodstream.

I read recently that fat in the diet is dropped into the lymphatic system
(not the portal vein), so it has minimal effect on the TG levels in the
blood.

Beth

>
> Also true, but as Lustig has been very loudly highlighting, it's exactly
> what happens in the liver that makes excess fructose (including sucrose as
> a fructose-containing disaccharide, and HFCS as a fructose-containing blend
> of sugar monomers) play metabolic havoc.
>
>
>
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[CRCOMMUNITY] Body composition & healthy aging

Al Pater — Wed, 16 May 2012 14:10:11 -0400

The below paper is pdf-availed.

"Using BMI or percentage of fat to evaluate changes in body composition of
older men
masks the loss of fat-free mass associated with ageing of healthy men."

Br J Nutr. 2011 Aug 3:1-7. [Epub ahead of print]
Longitudinal changes in body composition associated with healthy ageing:
men, aged 20-96 years.
Jackson AS, Janssen I, Sui X, Church TS, Blair SN.
PMID:21810289

Abstract

Obesity and sarcopenia are health problems associated with ageing.

The present study modelled the longitudinal changes in body composition of
healthy men, aged from 20 to 96 years, and evaluated the fidelity of BMI to
identify age-dependent changes in fat mass and fat-free mass.

The data from 7265 men with multiple body composition determinations (total
observations 38 328) were used to model the age-related changes in body
mass, fat mass, fat-free mass, BMI and percentage of body fat. Changes in
fat mass and fat-free mass were used to evaluate the fidelity of BMI and to
detect body composition changes with ageing.

Linear mixed regression models showed that all trajectories of body
composition with healthy ageing were quadratic. Fat mass, BMI and percentage
of body fat increased from age 20 years and levelled off at approximately 80
years. Fat-free mass increased slightly from age 20 to 47 years and then
declined at a non-linear rate with ageing. Levels of aerobic exercise had a
positive influence on fat mass and a slight negative effect on fat-free
mass. BMI and percentage of body fat were sensitive in detecting the
increase in fat mass that occurred with healthy ageing, but failed to
identify the loss of fat-free mass that started at age 47 years.

Key Words:

Longitudinal changes; Ageing; BMI; Fat-free mass; Fat mass; Sarcopaenia

Abbreviations: ACLS, Aerobics Center Longitudinal Study; DXA, dual-energy
X-ray absorptiometry; LMM, linear mixed models; PAI, physical activity index

BMI, the ratio of weight to height, is often used to evaluate body
composition and define obesity(1-4). Cross-sectional data from the National
Health and Nutrition Examination Survey suggest two body composition trends.
First, a secular trend, the prevalence of obesity among American adults has
systematically increased over the past 30 years(1,2,4-9). Second, the
prevalence of obesity increases with ageing(9,10). The major source of BMI
variation is body mass, which consists of fat mass and fat-free mass
components. A limitation of using BMI to evaluate body composition is that
changes can be due to either fat mass or fat-free mass.

The present focus of body composition research is on the �obesity epidemic�(1-4).
BMI is associated with the risk of all-cause mortality(11-14) that is
attenuated in the elderly. There is a growing concern about the health risks
associated with the loss of fat-free mass with ageing. Longitudinal research
findings document that a stable body mass of older individuals often masks
body composition changes that occur in fat mass and fat-free mass
components(15-18). Investigators have reported(15-17,19-21) a longitudinal
loss of fat-free mass with ageing of older men. Sarcopenia, the loss of
skeletal muscle mass, strength and function, is a growing health risk of
older individuals(22,23), which has been linked to functional impairment and
physical disability(24,25). Muscle mass makes up the majority of fat-free
mass, suggesting an association between the loss in fat-free mass and
sarcopenia risk.

The samples used to define the longitudinal changes in fat-free mass are
restricted to older individuals, thereby limiting the generalisability of
longitudinal findings(15-17,19-21). The Aerobics Center Longitudinal Study
(ACLS) cohort provides a unique opportunity to model longitudinal changes in
body composition associated with healthy ageing across the adult age range.
The ACLS is an open cohort study with individuals of all ages who have
multiple follow-up body composition measurements. The cohort examined
consisted of healthy men who completed a maximal exercise test and had their
body composition measured. The goal of the present study was to model the
longitudinal changes in body composition associated with healthy men aged
20-96 years. The study had four major objectives: (1) define the
longitudinal changes in body mass and the body composition components of fat
mass and fat-free mass; (2) model the longitudinal changes in BMI and
percentage of fat with ageing; (3) define the independent role of aerobic
exercise on body composition; (4) define the fidelity of BMI and percentage
of fat for evaluating the changes in fat mass and fat-free mass associated
with ageing.

Methods

Study population

Body composition and activity methodsStatistical
analysesResultsDiscussionAcknowledgementsReferencesStudy population
The present analysis included 8099 men who received at least three
comprehensive medical examinations at the Cooper Clinic in Dallas, TX, USA
between 1971 and 2006. The men selected for the study completed from three
to thirty-three tests (mean 5�6 tests) for a total of 45 643 observations. A
preliminary examination of the data revealed that the activity data before
1975 were incomplete. The 6653 tests completed from 1971 to 1974 were
excluded. An additional 695 tests were excluded because the patient did not
reach 85 % of his age-predicted maximal heart rate during the exercise test.
An additional thirty-three tests were excluded due to outliers and erroneous
data. The final study sample included 7265 men with a total of 38 328
observations, an average of 5�3 tests per individual from 1975 to 2006.

The men were clinically healthy members of the ACLS. Participants came to
the clinic for periodic preventive health examinations and for counselling
regarding diet, exercise, weight control and other lifestyle factors
associated with the increased risk of chronic disease. Participants were
volunteers, not paid and not recruited to the study. Many were sent by their
employers for the examination, some were referred by their physicians and
others were self-referred. Participants were predominantly white, well
educated, and belonged to middle and upper socio-economic strata; all had
access to health care. Because we excluded individuals with major chronic
diseases (heart attack, stroke and cancer), those who failed to achieve at
least 85 % of their estimated maximal heart rate on the treadmill test, and
those with abnormal exercise tests, the study population was healthier than
the general population. ...

...

Results

Methods

Study population

Body composition and activity methodsStatistical
analysesDiscussionAcknowledgementsReferencesTable 1 gives the descriptive
statistics for all observations and categorised by age group. The men ranged
in age from 20 to 96 years. Height decreased across the age groups. Body
mass, BMI and fat-free mass were lower for men =/> 60 years. Percentage of
fat and fat mass increased across the age groups. Fat-free mass increased up
to age 50 years and then decreased. The proportion of overweight or obese
(BMI =/> 25 kg/m2) men varied from a high of 57 % for men aged 50-59 years
and a low of 37 % for men aged =/> 70 years. Trends in PAI by age group did
not appear to be evident. The percentage of active men (PAI =/> 3) ranged
from 27�4 % for men aged less than 40 years to 29�3 % for men aged 60-69
years. Nearly 28 % of men aged =/> 70 years reported they walked or jogged
=/> 10 miles/week.

Table 1. Descriptive statistics for all observations and by age group
(Mean values and standard deviations)
---------------------------------------------------
===Observations by age group===All observations
===<40 years 40�49 years 50�59 years 60�69 years =/>70 years==Variables===Mean SD Mean SD Mean SD Mean SD Mean SD===Mean SD
---------------------------------------------------
Sample size (n) 7006 14 554 12 259 3976 533 38 328
Age (years) 35�0 3�7 44�7 2�8 54�0 2�8 63�2 2�6 73�0 3�4 48�2 9�4
Height (cm) 179�9 6�6 179�4 6�5 178�8 6�2 177�8 6�3 175�8 6�2 179�1 6�4
Body mass (kg) 82�2 12�1 83�1 11�7 83�0 11�0 80�6 10�2 76�7 10�1 82�6 11�4
BMI (kg/m2) 25�4 3�2 25�8 3�1 26�0 3�0 25�5 2�8 24�8 2�9 25�7 3�0
Percentage of fat 18�1 6�0 20�2 5�6 21�7 5�2 22�0 5�1 22�1 5�2 20�5 5�6
Fat mass (kg) 15�3 6�9 17�1 6�6 18�3 6�3 18�0 5�8 17�3 5�9 17�3 6�6
Fat-free mass (kg) 66�9 7�8 66�0 7�2 64�7 6�8 62�6 6�3 59�4 6�0 65�3 7�2
BMI =/>25 kg/m2 (%) 48�8 55�3 59�1 53�5 39�4 54�9
PAI 0 (%) 20�6 19�0 17�9 17�5 23�1 18�9
PAI 1 (%) 20�7 22�2 23�1 25�9 26�3 22�6
PAI 2 (%) 31�2 29�5 29�9 27�2 22�9 29�6
PAI 3 (%) 17�6 19�3 20�3 20�9 20�4 19�5
PAI 4 (%) 9�70 10�0 8�8 8�5 7�3 9�4
---------------------------------------------------
PAI, physical activity index.

Table 2 gives the longitudinal ageing models of the body composition
variables. Provided are the maximum-likelihood estimates of the LMM
regression weights (�) and the 95 % CI of each weight. The quadratic model
provided a more accurate fit (P < 0�0001) than a linear model for all body
composition variables. Figs. 1 and 2 illustrate the ageing trajectories for
the body composition components defined by these models. Table 3 provides
the estimated body composition at age 20 years and the estimated decade
change for each body composition variable. Fig. 1 shows that body mass
increased with ageing and levelled off at age 69 years and decreased at a
non-linear rate with ageing. Table 3 shows that the loss of body mass was
0�80 and 1�97 kg in the seventh and eighth decades, respectively. Fat mass
increased with ageing, levelled off and then decreased slightly (0�25 kg,
approximately 0�6 pounds) in the eighth decade. Fat-free mass increased
slightly from age 20 to 47 years and then decreased. Table 3 shows that
fat-free mass decreased to 0�42 kg in the fifth decade that progressively
increased to 1�96 kg in the eighth decade. Percentage of fat and BMI
increased at non-linear rates and levelled off at age 88 years for
percentage of fat and 77 years for BMI. Percentage of fat increased in each
age decade while BMI increased with age until the eighth decade where it
decreased slightly, - 0�13 kg/m2.

Table 2. Maximum-likelihood regression estimates defining the longitudinal
body composition quadratic ageing trajectories of men
(Regression estimates and 95 % confidence intervals)
---------------------------------------------------
- ===Constant Age Age2
Variables b 95% CI b 95% CI b 95% CI
---------------------------------------------------
Body mass (kg) 59�1131* 58�0159, 60�2104 0�7973* 0�75432,
0�84037 -0�0058* -0�0063, -0�0054
Fat mass (kg) -0�3566 -1�3569, 0�6438 0�5417* 0�5015,
0�5819 -0�0033* -0�0037, -0�0029
Fat-free mass (kg) 60�3428* 59�5200, 61�1656 0�2384* 0�2058,
0�2711 -0�0026* -0�0029, �0�0023
BMI (kg/m2) 19�3111* 18�9670, 19�6553 0�2009* 0�1873,
0�2145 -0�0013* -0�0014, -0�0011
Percentage of fat 5�1705* 4�1833, 6�1577 0�4527* 0�4127,
0�4926 -0�0026* -0�0030, -0�0022
---------------------------------------------------
* Coefficients were significantly different (P < 0�001).

Table 3. Linear mixed model (LMM) change in body composition from age 20
years for each age decade of men
---------------------------------------------------
Age decade (years) Body mass (kg) Fat mass (kg) Fat-free mass (kg) BMI
(kg/m2) Percentage of fat
---------------------------------------------------
Age 20* 72�72 9�14 64�09 22�83 13�20
20�29 5�05 3�75 1�11 1�38 3�25
30�39 3�88 3�08 0�60 1�13 2�74
40�49 2�71 2�42 0�09 0�87 2�23
50�59 1�54 1�75 -0�42 0�62 1�72
60�69 0�37 1�08 -0�94 0�37 1�21
70�79 -0�80 0�42 -1�45 0�12 0�70
80�89 -1�97 -0�25 -1�96 -0�13 0�19
---------------------------------------------------
* LMM estimated value at age 20 years.

Table 4 provides the maximum-likelihood estimates (�, 95 % CI) of the ageing
and physical activity models. A log-likelihood ratio test confirmed that
adding activity to the quadratic age models improved the fit (P < 0�0001)
for all body composition components, but the effect for body and fat mass
differed from that for fat-free mass. After controlling for age, each PAI
regression coefficient for body mass and fat mass was statistically
significant. Each PAI increase in physical activity was associated with a
greater weight loss. The largest coefficients were for PAI levels 3 and 4.
Body mass and fat mass regression weights for the PAI level 4 were
identical, - 2�30, demonstrating that after controlling for age, men who
walked or jogged =/> 20 miles/week were approximately 5 pounds (2�3 kg)
lighter than those who were inactive (PAI = 0). The body and fat mass of
those active at the PAI 3 level was approximately 1�3 kg (approximately 2�9
pounds) lower than that of inactive men. The coefficients for PAI levels 1
and 2 were significant, but low, ranging from - 0�52 to - 0�69 kg. There was
a significant PAI effect (P < 0�001) for fat-free mass that was traced to
the PAI levels 3 and 4. After controlling for age, the most active men (PAI
=/> 3) had less fat-free mass than inactive men, but the effect was small.
The fat-free mass of those active at the PAI levels 3 and 4 was 0�16 kg
(approximately 0�35 pounds) and 0�26 kg (approximately 0�57 pounds),
respectively, lower than those less active (PAI
Table 4. Maximum-likelihood regression estimates for age and the level of
aerobic exercise of men
(Regression estimates and 95 % confidence intervals)
---------------------------------------------------
- ===Body mass Fat mass Fat-free mass
Variables===b 95% CI P b 95% CI P b 95% CI P
---------------------------------------------------
Constant 59�3014 58�2146, 60�3883 <0�0001 -0�0071 -1�0624, 0�9204 0�888
60�3089 59�485, 61�1321 <0�0001
Age 0�8245 0�7818, 0�8671 <0�0001 0�5670 0�5271, 0�6069 <0�0001 0�2414
0�2087, 0�2741 <0�0001
Age2 -0�0062 -0�0066, -0�0057 <0�0001 -0�0036 -0�0040, -0�0032
<0�0001 -0�0026 -0�0029, -0�0023 <0�0001
PAI 1 -0�5183 -0�6351, -0�4014 <0�0001 -0�5567 -0�6687, -0�4447 <0�0001
0�0055 -0�0843, 0�0953 0�905
PAI 2 -0�5657 -0�6787, -0�4529 <0�0001 -0�6940 -0�8021, -0�5858 <0�0001
0�0518 -0�0351, 0�1388 0�243
PAI 3 -1�3230 -1�4539, -1�1921 <0�0001 -1�3023 -1�4273, -1�1773
<0�0001 -0�15984 -0�2606, -0�0591 <0�0001
PAI 4 -2�3048 -2�4770, -2�1326 <0�0001 -2�3005 -2�4643, -2�1367
<0�0001 -0�2636 -0�3960, -0�1312 <0�0001
PAI, physical activity index.

Discussion

These longitudinal results confirmed that changes in body composition
associated with healthy ageing were quadratic, but the trajectories of
change differed. Fat mass increased with ageing and levelled off at
approximately 70 years. Fat-free mass increased slightly between age 20 and
47 years, and then steadily decreased at a non-linear rate with ageing. The
modelled loss in fat-free mass between 50 and 89 years was 4 kg (10�5
pounds), and approximately 40 % of the loss was in the eighth decade. The
ageing trajectory for body mass increased from age 20 to 60 years, levelled
off and then decreased with ageing. The increase in body mass was primarily
due to the increase in fat mass and the decline after age 70 years was due
to the loss of fat-free mass. The ageing trajectories for BMI and percentage
of fat were similar; they increased to about age 70 years and levelled off.
Neither BMI nor percentage of fat identified the decline in fat-free mass
with ageing. After about age 60 years, changes in percentage of fat became
more of a function of the loss of fat-free mass than the increase in fat
mass. In the eighth decade, percentage of fat increased by approximately 0�2
% and fat mass decreased by 0�25 kg. The increase in percentage of fat was
due to the 1�96 kg (4�3 pounds) decrease in fat-free mass.

A major strength of these ACLS results is the modelled ageing trajectories
which were defined with data across the adult lifespan. Other
investigators(15,16,19,20,35) using longitudinal data with restricted age
ranges have reported fat-free mass decreases with ageing. Investigators of
the Fels Longitudinal Study have reported that fat-free mass declined at a
linear rate of 0�07 kg/year for men aged 40-66 years(20). The ACLS fat-free
mass quadratic model estimated a similar rate of decline of 0�06 kg/year to
the Fels data. Hughes et al.(16) reported that men lost an average of 1�1 kg
of fat-free mass between the age of 61 and 71 years. The ACLS modelled
fat-free mass loss between these ages was estimated to be 1�4 kg. Ding et
al.(19) studied men aged 70-79 years and reported that fat-free mass
measured with dual-energy X-ray absorptiometry (DXA) declined at a quadratic
rate over the 6 years of serial testing. Similar to these ACLS findings,
Fleg et al.(35) reported that fat-free mass remained stable at a young age,
but started an accelerated decline at about age 50 years and that the
age-related change in body composition was due to the rapid loss of fat-free
mass with ageing. Interestingly, although the ACLS men examined in the
present study were quite healthy relative to the cohorts examined in the
previous literature(15,16,19,20,35), the rate and patterns of fat-free mass
loss were quite comparable, supporting the fidelity and generalisability of
the fat-free mass model.

Cross-sectional and longitudinal results(15,36) suggest that the age-related
decline in fat-free mass was largely a function of the loss of appendicular
muscle mass. Gallagher et al.(15) examined appendicular muscle mass loss of
men after age 60 years using regional body composition estimates obtained
with DXA. They reported that the 5-year decline in total DXA fat-free mass
was 1�4 kg. The DXA regional measures defined the loss of total appendicular
muscle mass at 0�8 kg, of which 0�7 kg was the loss of leg muscle mass.
Janssen et al.(36) reported a cross-sectional quadratic ageing decline in
skeletal muscle mass measured by MRI. The reported decline in the lower body
muscle mass of 0�063 kg/year was over two times greater than the upper body
loss of 0�029 kg/year.

These ACLS results showed that aerobic exercise was associated with a lower
fat-free mass than that of inactive men, but the effect was small and
consistent with longitudinal and cross-sectional data(17,37). There is
evidence that physical activity attenuates weight loss in older individuals.
Stephen & Janssen(38) reported that the weight of older individuals who were
active at their initial visit was lower than those who were inactive, but
over the 8 years of follow-up, the active individuals lost 2�4 kg less
weight than those who were inactive. The age-related weight-loss trajectory
of those who did not survive to the 9th year of follow-up was steeper than
the survivors. Dziura et al.(39) reported that the loss of weight in older
individuals (>65 years) increased with ageing, but increases in exercise
frequency attenuated the rate of decline. The weight-loss trajectory of
those who did not survive the 12 years of follow-up was steeper than the
survivors. Flicker et al.(40) reported that in 10 years of follow-up, older
men ( =/> 70 years) who were sedentary had a 28 % higher risk of all-cause
mortality than men who reported they walked or jogged.

These ACLS findings show that aerobic exercise does not prevent the loss of
fat-free mass. Fleg et al.(35) suggest that strength training is needed to
preserve the fat-free mass of older individuals. In a review of eighteen
studies, Doherty(22) reported that the median knee extensor strength of men
aged =/> 70 years was 67�5 % of a young adult referent group and resistance
training was effective in increasing the strength of older people.
Doherty(22) reported that the one-repetition maximum strength gains produced
with resistance training ranged from 26 to 152 % (median 39 %) for thirteen
studies of men and women, aged 60 years and older. These results suggest
that while aerobic exercise does not influence the loss of fat-free mass
associated with ageing, resistance training may.

The physiological basis for using BMI to evaluate body composition is based
on moderate correlations (r approximately 0�60) between BMI and percentage
of body fat(41). The wide use of BMI to evaluate body composition is
probably due to the availability of body mass and height data in a variety
of research settings. While BMI has been shown to predict the risk of
all-cause mortality in the general population(11-14), its fidelity with
older populations is dubious. There is evidence that BMI does not predict
mortality risk within individuals aged =/> 70 years unless they were also
obese at age 50 years or younger(40,42,43). An earlier report(44) from the
ACLS showed that BMI and body composition were associated with higher
mortality risk in women and men aged =/> 60 years. However, in this report,
the associations with BMI and body composition were eliminated after
adjusting for cardiorespiratory fitness. The present findings from the ACLS
demonstrated that the stability of BMI and percentage of fat of healthy
older men masked changes in body composition, largely due to the non-linear
decline in fat-free mass with ageing. These results are consistent with
research showing that the stable body mass of older individuals of a
restricted age range masked changes in fat mass and fat-free mass
components(15-18).

An important finding of the present study is that the modelled ageing change
in fat-free mass was not detected by modelled changes in BMI and percentage
of body fat. What is unanswered is the association between the loss of
fat-free mass and the risk of sarcopenia. The diagnostic criteria for
age-related sarcopenia include both low muscle mass and low muscle function
involving both strength and performance(45). While muscle makes up the
majority of the fat-free mass body compartment of these ACLS data, it also
includes organs and bone. Most of the loss in fat-free mass with ageing is
due to skeletal muscle, but would also include contributions from organs and
bone. Sarcopenia is a growing health risk associated with functional
impairment and physical disability in ageing populations(22-25). These ACLS
results suggest that age-related changes in fat-free mass may be a valid
screening tool to identify individuals at risk of sarcopenia, but awaits
validation research.

The major strength of the present study was the use of a very large sample
of healthy men ranging in age from 20 to 96 years with multiple body
composition measures over time. The multiple data points allowed us to
define longitudinal changes in body composition representative of healthy
ageing across the adult age range of men. The LMM is an ideal statistical
method to model longitudinal data where subjects have a different number of
tests at different times because it accommodates unbalanced and unequally
spaced observations over time(33,34).

A limitation of the study was that percentage of fat was measured by two
different methods. Post hoc analysis showed that there was a significant
intercept difference (P < 0�001) between the underwater weighing and
skinfold methods. The underwater weighing measure was systematically lower
than the skinfold estimate, but the effect was small, - 0�13 % fat (95 %
CI - 0�20, - 0�06). An examination of the skinfold and underwater residuals
(measured - estimated percentage of fat) showed that the distributions of
the skinfold and underwater weighing residuals were similar and normally
distributed. The means and standard deviations of the residuals were - 0�029
(sd 2�839) and 0�034 (sd2�610) for the underwater weighing and skinfold
methods. An examination of the bivariate distribution (data not shown)
showed that the residuals for both methods were evenly distributed across
age, supporting the validity of the underwater and skinfold methods.

The findings of the present study can only be generalised to the LMM fixed
effects of ageing and self-report physical activity for a sample
representative of healthy ageing. The models accurately define the ageing
changes in body composition for a population of men, but lack accuracy in
defining the changes in individuals. There are variables other than ageing
and activity that influence weight change over time (e.g. variation in
diet). Intra-class analyses(33) of the body mass LMM variance components
found that 94 % of the body mass variance was not explained by ageing and
self-report aerobic exercise, but by other sources of variability within men
over time.

In summary, the relationship between ageing and body composition of healthy
men is quadratic. The increase in body mass from age 20 to approximately 70
years is primarily due to increases in fat mass and the decrease after age
70 years is associated with the loss of fat-free mass. Aerobic exercise has
a positive influence on lowering fat mass, but does not prevent the loss of
fat free mass with ageing. Neither BMI nor percentage of fat was sensitive
in detecting the age-related loss of fat-free mass. Using BMI or percentage
of fat to evaluate changes in body composition of older men masks the loss
of fat-free mass associated with ageing of healthy men.

-- Al Pater, alpater@SHAW.ca

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[CRSOCIETY] Re: Headline: Sugar Can Make You Dumb The DHA-deprived animalswere slower

Michael Rae — Wed, 16 May 2012 14:01:31 -0400

All:

jwwright wrote:
> "Michael Rae"
>> jwwright wrote:
>>> page 856, 9th ed, Guyton's Medical Physiology,
>>> Indicates 80 % of carbohydrate digestion is glucose.
>>>
>>> I think that's different from the already digested HFCS, which can vary
>>> but is about 55% fructose.
>>
>> That *seems* to be gibberish. What exactly are you saying (or,
>> perhaps: what exactly does Guyton say)?

> 1) I'm saying sugar (sucrose) is NOT glucose and fructose until after
> digestion.

Of course.

> 2) HFCS is already digested to those, perhaps useful to those with
> impaired digestion.

I doubt that any but a tiny fraction of the population would have any
difficulty hydrolyzing sucrose.

> 3) Guyton doesn't comment on the HFCS process as near as I can find, it
> covers carbohydrate metabolism.
>
> "In general, the starches are almost totally
> converted into maltose and other very small glucose
> polymers before they have passed beyond the duodenum
> or upper jejunum." pg 834.
> "Thus the final products of carbohydrate digestion
> are all monosaccharides, and they are absorbed into
> the portal blood."

Right. But what you said was, "Guyton ... Indicates 80 % of
*carbohydrate* digestion is glucose". STARCHES are polymers entirely
composed of glucose, so of course it's broken down into maltose and
other glucose polymers and ultimately monosaccharide (glucose); but
sucrose is glucose bound to fructose, and so certainly isn't digested
into glucose!
>
> Glucose, Fructose and galactose entering the blood go thru the liver and:
> "In liver cells, appropriate enzymes are available to promote
> interconversions among the monosaccharides, as shown in figure 67-2.

Also true, but as Lustig has been very loudly highlighting, it's exactly
what happens in the liver that makes excess fructose (including sucrose
as a fructose-containing disaccharide, and HFCS as a fructose-containing
blend of sugar monomers) play metabolic havoc.

-Michael

--
SENS: The biotechnologies of rejuvenation. See the outline <
http://tinyurl.com/SENS-outline>; learn the detailed science! <
http://tinyurl.com/End-Aging>

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[CRSOCIETY] Re: Headline: Sugar Can Make You Dumb The DHA-deprived animalswere slower

jwwright — Wed, 16 May 2012 13:36:45 -0400

----- Original Message -----
From: "Michael Rae"
To: "The CR Society Main Discussion List"

Sent: Wednesday, May 16, 2012 9:59 AM
Subject: Re: [CR] Headline: Sugar Can Make You Dumb
The DHA-deprived animalswere slower

> All:
>
> jwwright wrote:
>> page 856, 9th ed, Guyton's Medical Physiology,
>> Indicates 80 % of carbohydrate digestion is
>> glucose.
>>
>> I think that's different from the already
>> digested HFCS, which can vary
>> but is about 55% fructose.
>
> That *seems* to be gibberish. What exactly are you
> saying (or, perhaps: what exactly does Guyton
> say)?
>
> -Michael
>

1) I'm saying sugar (sucrose) is NOT glucose and
fructose until after digestion.
2) HFCS is already digested to those, perhaps useful
to those with impaired digestion.
3) Guyton doesn't comment on the HFCS process as
near as I can find, it covers carbohydrate
metabolism.

"In general, the starches are almost totally
converted into maltose and other very small glucose
polymers before they have passed beyond the duodenum
or upper jejunum." pg 834.
"Thus the final products of carbohydrate digestion
are all monosaccharides, and they are absorbed into
the portal blood."

Glucose, Fructose and galactose entering the blood
go thru the liver and:
"In liver cells, appropriate enzymes are available
to promote interconversions among the
monosaccharides, as shown in figure 67-2.
Furthermore, the dynamics of the reactions are such
that when the liver releases the monosaccharides
back into the blood, the final product is almost
entirely glucose.
The reason for this is the liver cells contain large
amounts of glucose phosphatase. Therefore,
glucose-6-phosphate can be degraded back to glucose
and phosphate and the glucose can be transported
through the liver membrane back into the blood."
"Once again it should be emphasized that usually
more than 95 % of all monosaccharides that circulate
in the blood are the final conversion product,
glucose."

Additionally, glucose is aided by protein carrier
molecules which take it across cell membranes and
released. pg 856,
"Central Role of Glucose in Carbohydrate
Metabolism."

http://www.sugar-and-sweetener-guide.com/hfcs-55.html
"HFCS-55 is a form of high fructose corn syrup that
contains 55% fructose. It is produced from corn
starch. It is the most commonly used of the three
formulations. It is added to most sodas instead of
sugar in the United States. It is about 25% sweeter
than sugar, which means that less of it is needed."

A typical breakdown would be:

Sugar Percentage
Fructose 55%
Glucose 41%
Maltose 4%

http://www.princeton.edu/main/news/archive/S26/91/22K07/
A sweet problem: Princeton researchers find that
high-fructose corn syrup prompts considerably more
weight gain
So it's a question of digestion AND absorption,
where and when, and how much.

Regards

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[CRSOCIETY] Re: Headline: Sugar Can Make You Dumb The DHA-deprived animals were slower

Michael Rae — Wed, 16 May 2012 11:59:33 -0400

All:

jwwright wrote:
> page 856, 9th ed, Guyton's Medical Physiology,
> Indicates 80 % of carbohydrate digestion is glucose.
>
> I think that's different from the already digested HFCS, which can vary
> but is about 55% fructose.

That *seems* to be gibberish. What exactly are you saying (or, perhaps:
what exactly does Guyton say)?

-Michael

--
SENS: The biotechnologies of rejuvenation. See the outline <
http://tinyurl.com/SENS-outline>; learn the detailed science! <
http://tinyurl.com/End-Aging>

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