CLA: Second thoughts?
Ian Goddard
conjugated linoleic acid (CLA):
http://www.sciencenews.org/20010303/bob9.asp
However, last night I ran into the following studies that raise
concerns for me. These studies found that the active CLA isomer
increased several major pro-aging markers in obese humans.
Specifically, CLA increased C-reactive protein, lipid peroxidation,
and insulin resistance. The latter marker being quite unexpected given
animal research (and one human study cited at the bottom of this post)
suggesting improved insulin sensitivity. What's up with that?
I'm not sure how to interpret this data, but given that each of the
cited pro-aging markers that CLA increased are exactly what
life-extenders should wish to decease, I'm posting this data to
encourage productive feedback and discussion.
****************************************
Circulation 2002 Oct 8;106(15):1925-9
Supplementation with conjugated linoleic acid causes isomer-dependent
oxidative stress and elevated C-reactive protein: a potential link to
fatty acid-induced insulin resistance.
"CONCLUSIONS: t10c12 CLA supplementation increases oxidative stress
and inflammatory biomarkers in obese men. The oxidative stress seems
closely related to induced insulin resistance, suggesting a link
between the fatty acid-induced lipid peroxidation seen in the present
study and insulin resistance. These unfavorable effects of t10c12 CLA
might be of clinical importance with regard to cardiovascular disease,
in consideration of the widespread use of dietary supplements
containing this fatty acid."
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12370214&dopt=Abstract
Lipids 2003 Feb;38(2):133-7: "...the trans10-cis12 CLA isomer
unexpectedly caused significant impairment of the peripheral insulin
sensitivity as well as of blood glucose and serum lipid levels. In
addition, CLA markedly elevated lipid peroxidation. "
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12733745&dopt=Abstract
The subjects in those studies had metabolic syndrome:
http://www.ext.colostate.edu/pubs/columnnn/nn971022.html
Conjugated linoleic acid induces lipid peroxidation in humans.
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10683436&dopt=Abstract
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11099394&dopt=Abstract
But these studies found that
CLA prevents diabetes in animals
http://news.uns.purdue.edu/html4ever/9805.Belury.diabetes.html
CLA may benefit human diabetics
http://hec.osu.edu/news/research/cla.htm
"The research received support from Pharmanutrients, Inc., Lake Bluff,
Ill., and Natural, Inc., Chicago. Although Belury has consulted for
both companies in the past, she was not a paid consultant during the
time of this study."
http://www.pharmanutrients.com
http://www.naturalinc.com/index_flash.html
Any thoughts?
http://IanGoddard.net/journal.htm
"To lengthen thy life, lessen thy meals." Ben Franklin
Ongoing CR monkey study update: "In the monkeys...those on
reduced feeding since the study started are dying at a rate
that is about half that of the monkeys receiving a full food
ration." Associated Press: Eating less may extend human life.
August 1, 2002 : http://www.msnbc.com/news/788746.asp?0si=-
Thomas Carter
> I've been impressed with the many potential health benefits of
> conjugated linoleic acid (CLA):
>
> http://www.sciencenews.org/20010303/bob9.asp
>
> However, last night I ran into the following studies that raise
> concerns for me. These studies found that the active CLA isomer
> increased several major pro-aging markers in obese humans.
> Specifically, CLA increased C-reactive protein, lipid peroxidation,
> and insulin resistance. The latter marker being quite unexpected given
> animal research (and one human study cited at the bottom of this post)
> suggesting improved insulin sensitivity. What's up with that?
>
> I'm not sure how to interpret this data, but given that each of the
> cited pro-aging markers that CLA increased are exactly what
> life-extenders should wish to decease, I'm posting this data to
> encourage productive feedback and discussion.
>
I stopped taking it a couple of years ago based pretty much on the
same concerns. Here is what I have saved on it. My info duplicates and
supports yours. If I were a fat diabetic I might reconsider. The
references to Tom in my records are from the old LEF forum and refer
to Paul. The reason I reinvestigated it and stopped is that he had
stopped. This is what I have on it.
Thomas
DEF: CLA: Found in red meat. Anti cancer, good for blood sugar.
Prevents muscle wasting. Antioxidant.
I have been watching this for a year or two. This paper is
definitive for me, unless some really great studies come along.
Diabetes Care 2002 Sep;25(9):1516-21 Treatment with dietary
trans10cis12 conjugated linoleic acid causes isomer-specific insulin
resistance in obese men with the metabolic syndrome. Riserus U, Arner
P, Brismar K, Vessby B. Department of Public Health and Caring
Sciences/Geriatrics, Uppsala University, Uppsala, Sweden.
ulf.r...@pubcare.uu.se OBJECTIVE: Conjugated linoleic acid (CLA) is
a group of dietary fatty acids with antiobesity and antidiabetic
effects in some animals. The trans10cis12 (t10c12) CLA isomer seems to
cause these effects, including improved insulin sensitivity. Whether
such isomer-specific effects occur in humans is unknown. The aim of
this study was to investigate whether t10c12 CLA or a commercial CLA
mixture could improve insulin sensitivity, lipid metabolism, or body
composition in obese men with signs of the metabolic syndrome.
RESEARCH DESIGN AND METHODS: In a randomized, double-blind controlled
trial, abdominally obese men (n = 60) were treated with 3.4 g/day CLA
(isomer mixture), purified t10c12 CLA, or placebo.
Euglycemic-hyperinsulinemic clamp, serum hormones, lipids, and
anthropometry were assessed before and after 12 weeks of treatment.
RESULTS: Baseline metabolic status was similar between groups.
Unexpectedly, t10c12 CLA increased insulin resistance (19%; P < 0.01)
and glycemia (4%; P < 0.001) and reduced HDL cholesterol (-4%; P <
0.01) compared with placebo, whereas body fat, sagittal abdominal
diameter, and weight decreased versus baseline, but the difference was
not significantly different from placebo. The CLA mixture did not
change glucose metabolism, body composition, or weight compared with
placebo but lowered HDL cholesterol (-2%; P < 0.05). CONCLUSIONS:
These results reveal important isomer-specific metabolic actions of
CLA in abdominally obese humans. A CLA-induced insulin resistance has
previously been described only in lipodystrophic mice. Considering the
use of CLA-supplements among obese individuals, it is important to
clarify the clinical consequences of these results, but they also
provide physiological insights into the role of specific dietary fatty
acids as modulators of insulin resistance in humans. PMID: 12196420
The Good transFat Will one family of animal fats become a medicine?
2001
Over the past 4 years, a new and surprising dietary supplement has
been edging its way onto the shelves of health-food stores. Known as
CLA, it's a mixture of trans fats, compounds usually associated with
raising the concentration of cholesterol in people's blood. The
acronym, for conjugated linoleic acid, signifies that the fats in CLA
are unusual forms of the essential nutrient linoleic acid.
The first potential health effect of CLA emerged 17 years ago, when
Michael W. Pariza of the University of Wisconsin-Madison announced
that he had isolated an unidentified agent in hamburger that reduced
the incidence of cancer in mice (SN: 12/22&29/84, p. 390). Four years
later, his team unmasked the mystery agent: one chemical form, or
isomer, of linoleic acid.
But nobody's laughing about it now. Several hundred published studies
of CLA's effects in animals and a few preliminary experiments with
people have since suggested an array of health benefits from the
unusual trans fats.
Linoleic acid is a kinked molecule built around a chain of 18 carbon
atoms. Most of the links coupling each carbon to its neighbors are
known as single bonds. Two of the links in the chain are the more
rigid double bonds.
Various chemical reactions can induce one of the double bonds to shift
so that it is separated from the other by only one single bond. The
molecule that results is called a conjugated fatty acid. Of the
different CLA isomers that can form, just two have been linked to
health effects. One's called cis-9, trans-11 (c9-t11), and the other,
trans-10, cis-12 (t10-c12). Isolating each of these isomers is
difficult and expensive. Most tests therefore use a mixture of the two
that's commercially produced from a vegetable oil.
Experiments in animals have revealed the mystery cancer fighter that
Pariza discovered in hamburger 17 years ago to be c9-t11. It continues
to be the most frequently studied of CLA's isomers.
Potential health value
His team gave 3-grams of off-the-shelf CLA supplements daily to half
of the 80 clinically obese men and women enrolled in a
weight-reduction trial. The remaining volunteers received identical
capsules filled with sunflower oil. Animal studies had shown that only
the t10-c12 alters fat accumulation, but to keep costs down the
researchers used a 50:50 supplement of it and the C9-t11. Both dieting
groups also received advice on cutting calories and upping their
exercise.
By the end of 6 months, all the participants had lost weight--on
average about 5 pounds each. However, one-third of those taking the
CLA, but only one-sixth of the others, increased muscle mass. CLA
caused the dieter's bodies to partition more of the energy from food
into lean tissue, not fat, says Pariza.
Ola Gudmundsen of Scandinavian Clinical Research AS in Kjeller,
Norway, and his colleagues reported similar data on 60 overweight or
obese volunteers in a 3-month dieting trial. Groups of 12 men and
women, 40 to 50 years old, received daily capsules containing either 9
g of olive oil or a dose of 1.7 to 6.8 g of CLA. As in Pariza's trial,
the CLA supplement was roughly a 50:50 mix of the c9-t11 and t10-c12
isomers.
Even in this short trial, people getting 3.4 g or more of CLA per day
ended up weighing 2 to 3 pounds less than the others, Gudmundsen says.
Dieters reaped no extra benefits from downing more than 3.4 g of CLA
per day, his team reports in the December 2000 Journal of Nutrition.
The group receiving the highest dose of CLA did, however, develop
slightly more lean tissue than the other groups did.
Diabetes and large doses
Larger doses of the 50:50 CLA formulation hold out tantalizing
prospects for helping people with type II diabetes, according to
another trial reported at the ACS meeting. Martha Belury of Northwest
Hospital in Seattle and her colleagues at Purdue University in West
Lafayette, Ind., tested nine people who have this adult-onset form of
diabetes. The researchers gave them daily capsules containing either 6
g of safflower oil or CLA daily for 8 weeks.
Fasting blood sugar, or glucose, was moderately improved in people
getting the CLA supplements but not in those getting the safflower
oil. Similarly, only the CLA group experienced a significant lowering
in blood concentration of triglycerides,. "We also saw this beneficial
triglyceride lowering" in a study with diabetic rats, Belury notes.
"Most exciting and definitely the most significant, statistically,"
she says, was the finding that people taking the CLA supplement had
lower blood concentrations of the hormone leptin compared with the
volunteers taking safflower oil. Other researchers have associated
elevations in blood leptin concentrations with obesity. To Belury, her
provocative leptin data "suggest CLA may act on type II diabetes via
some mechanism affecting [body-]fat accumulation."
Why did Belury consider studying CLA's effects on diabetes? Her team's
molecular studies several years ago showed that CLA shares properties
with some drugs. "We think CLA binds to a [cellular] receptor that is
similar to one that some antidiabetes drugs target," Belury explains.
Wondering whether the nutritional supplement would act similarly to
these drugs, she and her colleagues administered the fat supplements
to rats predisposed to developing diabetes. To her surprise, Belury
notes, "CLA actually delayed the onset of diabetes."
Slowing plaque buildup
In studies with rabbits, he had been looking for agents that don't
just slow a potentially deadly buildup of plaque along artery walls
but actually make these fatty deposits regress. With other chemical
agents, he says, "if you find something that gives you a few percent
regression, you do handsprings. In our studies with [a 50:50
formulation of] CLA, we saw a 30 percent reduction [in existing
plaque]--which is nothing less than phenomenal."
Figuring that such a result was too good to be true, Kritchevsky
repeated the experiments. Again, he fed the rabbits plaque-forming
diets for 3 months. He then killed one-third of the animals to measure
their plaque buildup. Over the next 3 months, the surviving animals
ate either a normal diet or one containing from 0.1 to 1 percent CLA,
by weight of food. When compared with the unsupplemented animals,
rabbits getting the 0.1 percent-CLA diets had a little less plaque.
However, those getting chow that was 1 percent CLA had 30 percent less
plaque, he reported in an April 2000 supplement of the Journal of The
American College of Nutrition.
A feed supplement
A little more than a decade ago, while looking for a low-cost feed
supplement, animal scientist Mark E. Cook and his colleagues at the
University of Wisconsin-Madison stumbled onto CLA's immune-enhancing
attributes.
. When a vaccine stimulates the animals' immune system, it triggers an
inflammatory action, which produces proteins that induce muscle
wasting. Some of these same cytokines, such as tumor necrosis factor,
cause wasting in cancer patients. "We were hoping to find something to
cut the inflammatory reaction that led to wasting," Cook says. Since
compounds fashioned from linoleic acid participate in the chain of
signals that induce wasting, he wondered whether CLA--as altered
linoleic acids--might somehow mute the vaccine's inflammatory effect.
So, he fed animals either a normal diet or one supplemented with the
50:50 CLA mix and then injected each with an immunity stimulant. "It
worked," Cook crows. "CLA totally blocked the [temporary] wasting" in
rats, mice, chicks, and pigs, without reducing their ability to fight
disease.
While that looked like a possible boon to meat producers, the earlier
findings had prompted Cook to worry whether people taking CLA
supplements might compromise their immunity.
So, he encouraged his colleagues to probe how the mixture of trans
fats perturbs an animal's immune system. In a series of patent
applications, his team reports that CLA dramatically increases several
families of infection-fighting white blood cells, including a type
known as natural killer cells. When the body isn't under assault,
however, CLA appears to dampen down the natural background level of
immune stimulation. Such a dampening, Cook notes, is usually a good
thing.
Most recently, Cook's team has shown that CLA appears to derail
allergic reactions by selectively dampening--as several drugs do--the
activity of cyclooxygenase-2 (COX-2), an enzyme that triggers many
types of inflammation. Indeed, Cook told Science News, "we're quite
excited and have just patented CLA as a COX-2 inhibitor."
Animal studies
Data from animal studies have consistently shown CLA's anticancer
promise. For example, Clement Ip of the Roswell Park Cancer Institute
in Buffalo, N.Y., recently showed that butter enriched in c9-t11 cut
the risk of mammary cancer in rats that ate it (SN: 12/11/99, p. 375).
Researchers don't know whether CLA isomers other than c9-t11 have
anticancer effects. Right now, Ip says, "we have almost no [animal]
data on the t10-c12, in terms of cancer protection."
Is it now time to begin studies to see if CLA supplements can prevent
cancer in people? "Not quite," Ip says emphatically.
References:
Belury, M.A., A. Mahon, and L. Shi. Role of conjugated linoleic acid
(CLA) in the management of type 2 diabetes: Evidence from Zucker
diabetic (fa/fa) rats and human subjects (Abstract AGFD 26). American
Chemical Society 220th National Meeting. August 20-24. Washington,
D.C.
Blankson, H. . . .and O. Gudmundsen. 2000. Conjugated linoleic acid
reduces body fat mass in overweight and obese humans. Journal of
Nutrition 130(December):2943.
Blankson, H. . . .and O. Gudmundsen. 2000. Effects of conjugated
linoleic acid (CLA) on body fat mass in overweight or obese human
volunteers: A double-blind, randomized placebo controlled
study(Abstract AGFD 23). American Chemical Society 220th National
Meeting. August 20-24. Washington, D.C.
Cook, M.E., et al. 2000. Regulation of inducible prostranoids and
leukotrienes by conjugated linoleic acid (CLA) (Abstract AGFD 10).
American Chemical Society 220th National Meeting. August 20-24.
Washington, D.C.
Hurst, W.J., et al. In press. Determination of conjugated linoleic
acid (CLA) concentrations in milk chocolate. Journal of Agricultural
and Food Chemistry.
Kritchevsky, D. 2000. Influence of conjugated linoleic acid (CLA) on
experimental atherosclerosis (Abstract AGFD 14). American Chemical
Society 220th National Meeting. August 20-24. Washington, D.C.
Kritchevsky, D., et al. 2000. Influence of conjugated linoleic acid
(CLA) on establishment and progression of atherosclerosis in rabbits.
Journal of the American College of Nutrition 19(April):472S.
Pariza, M.W. 2000. Conjugated linoleic acid: The paradox of
multifunctionality (Abstract AGFD 9). American Chemical Society 220th
National Meeting. August 20-24. Washington, D.C.
Park, Y. . . .and M.W. Pariza. 1999. Evidence that the trans-10,
cis-12 isomer of conjugated linoleic acid induces body composition
changes in mice. Lipids 34(March):235.
Further Readings:
Bee, G. 2000. Dietary conjugated linoleic acid consumption during
pregnancy and lactation influences growth and tissue composition in
weaned pigs. Journal of Nutrition 130:2981.
______. 2000. Dietary conjugated linoleic acids alter adipose tissue
and milk lipids of pregnant and lactating sows. Journal of Nutrition
130:2292.
Tom, What do you think about his study on CLA...Isn't TNFa bad as well
as increased insulin resistance? And the hepatomegaly is worrisome as
well. I am reading too much here? Thanks!
Diabetes, September 2000 Volume 49, Number 9
Conjugated Linoleic Acid Supplementation Reduces Adipose Tissue by
Apoptosis and Develops Lipodystrophy in Mice
Nobuyo Tsuboyama-Kasaoka, Mayumi Takahashi, Kentaro Tanemura, Hyoun-Ju
Kim, Tsuyoshi Tange Hitoshi Okuyama, Masaaki Kasai, Shinji Ikemoto,
Osamu Ezaki
Conjugated linoleic acid (CLA) is a naturally occurring group of
dienoic derivatives of linoleic acid found in beef and dairy products.
CLA has been reported to reduce body fat. To examine the mechanism(s)
of CLA reduction of fat mass, female C57BL/6J mice were fed standard
semipurified diets (10% fat of total energy) with or without CLA (1%
wt/wt). Terminal deoxynucleotidyl transferase-mediated dUTP-biotin
nick end-labeling (TUNEL) and DNA fragmentation analysis revealed that
fat-mass decrease by CLA was mainly due to apoptosis.
[ Apoptosis (programmed cell death) of fat cells is beneficial, since
one major problem with obesity is that once fat cells accumulate it is
hard to reduce their number. Dieting generally only reduces the size
of each making the regaining of weight very easy indeed. -- Tom ]
Tumor necrosis factor (TNF)- and uncoupling protein (UCP)-2 mRNA
levels increased 12- and 6-fold, respectively, in isolated adipocytes
from CLA-fed mice compared with control mice. Because it is known that
TNF- induces apoptosis of adipocytes and upregulates UCP2 mRNA, a
marked increase of TNF- mRNA with an increase of UCP2 in adipocytes
caused CLA-induced apoptosis. However, with a decrease of fat mass,
CLA supplementation resulted in a state resembling lipoatrophic
diabetes: ablation of brown adipose tissue, a marked reduction of
white adipose tissue, marked hepatomegaly, and marked insulin
resistance. CLA supplementation decreased blood leptin levels, but
continuous leptin infusion reversed hyperinsulinemia, indicating that
leptin depletion contributes to the development of insulin resistance.
These results demonstrate that intake of CLA reduces adipose tissue by
apoptosis and results in lipodystrophy, but hyperinsulinemia by CLA
can be normalized by leptin administration. Diabetes 49:1534–1542,
2000
[ Thanks for this abstract. It strongly suggests that while CLA may be
important for weight reduction and fighting cancer, but should not be
used by healthy thin people. I will be seriously checking this out,
with a view to ceasing my current intake of CLA. -- Tom ]
Biochem Biophys Res Commun 1998 Mar 27;244(3):678-82 Erratum in:
Biochem Biophys Res Commun 1998 Jun 29;247(3):911 Dietary conjugated
linoleic acid normalizes impaired glucose tolerance in the Zucker
diabetic fatty fa/fa rat. Houseknecht KL, Vanden Heuvel JP,
Moya-Camarena SY, Portocarrero CP, Peck LW, Nickel KP, Belury MA.
Department of Animal Sciences, Purdue University, West Lafayette,
Indiana 47907, USA. Conjugated linoleic acid (CLA) is a
naturally occurring fatty acid which has anti-carcinogenic and
anti-atherogenic properties. CLA activates PPAR alpha in liver, and
shares functional similarities to ligands of PPAR gamma, the
thiazolidinediones, which are potent insulin sensitizers. We provide
the first evidence that CLA is able to normalize impaired glucose
tolerance and improve hyperinsulinemia in the pre-diabetic ZDF rat.
Additionally, dietary CLA increased steady state levels of aP2 mRNA in
adipose tissue of fatty ZDF rats compared to controls, consistent with
activation of PPAR gamma. The insulin sensitizing effects of CLA are
due, at least in part, to activation of PPAR gamma since increasing
levels of CLA induced a dose-dependent transactivation of PPAR gamma
in CV-1 cells cotransfected with PPAR gamma and PPRE X 3-luciferase
reporter construct. CLA effects on glucose tolerance and glucose
homeostasis indicate that dietary CLA may prove to be an important
therapy for the prevention and treatment of NIDDM. PMID: 9535724
Int J Obes Relat Metab Disord 2001 Aug;25(8):1129-35 Conjugated
linoleic acid (CLA) reduced abdominal adipose tissue in obese
middle-aged men with signs of the metabolic syndrome: a randomised
controlled trial. Riserus U, Berglund L, Vessby B. Clinical Nutrition
Research Unit, Department of Public Health and Caring
Sciences/Geriatrics, Faculty of Medicine, Uppsala University, Uppsala,
Sweden. ulf.r...@geriatrik.uu.se BACKGROUND: Abdominal obesity is
strongly related to metabolic disorders. Recent research suggests that
dietary conjugated linoleic acid (CLA) reduces body fat and may
improve metabolic variables in animals. The metabolic effects of CLA
in abdominally obese humans have not yet been tested. OBJECTIVE: To
investigate the short-term effect of CLA on abdominal fat and
cardiovascular risk factors in middle-aged men with metabolic
disorders. METHODS: Twenty-five abdominally obese men (waist-to-hip
ratio (WHR), 1.05+/-0.05; body mass index (BMI), 32+/-2.7 kg/m(2)
(mean+/-s.d.)) who were between 39 and 64-y-old participated in a
double-blind randomised controlled trial for 4 weeks. Fourteen men
received 4.2 g CLA/day and 10 men received a placebo. The main
endpoints were differences between the two groups in sagittal
abdominal diameter (SAD), serum cholesterol, low-density lipoprotein,
high-density lipoprotein, triglycerides, free fatty acids, glucose and
insulin. RESULTS: At baseline, there were no significant differences
between groups in anthropometric or metabolic variables. After 4 weeks
there was a significant decrease in SAD (cm) in the CLA group compared
to placebo (P=0.04, 95% CI; -1.12, -0.02). Other measurements of
anthropometry or metabolism showed no significant differences between
the groups. CONCLUSIONS: These results indicate that CLA
supplementation for 4 weeks in obese men with the metabolic syndrome
may decrease abdominal fat, without concomitant effects on overall
obesity or other cardiovascular risk factors. Because of the limited
sample size, the effects of CLA in abdominal obesity need to be
further investigated in larger trials with longer duration.
Publication Types: Clinical Trial Randomized Controlled Trial PMID:
11477497
See
http://www.lef.org/magazine/mag2000/april00-cover.html
http://forum.lef.org/exec/readTopic.cgi?message_id=22546&view=#22546
http://www.lef.org/magazine/mag2001/oct2001_report_coq10_01.html
for the LEF discussion. It comes in three parts.
$Taking 700mg in 2000 in 2000 LE is recommending 3000 mg Stoped
taking in Mar. 2001
$To Take?
Ian Goddard
> I stopped taking it a couple of years ago based pretty much on the
>same concerns. Here is what I have saved on it. My info duplicates and
>supports yours. If I were a fat diabetic I might reconsider. The
>references to Tom in my records are from the old LEF forum and refer
>to Paul. The reason I reinvestigated it and stopped is that he had
>stopped. This is what I have on it.
>Thomas
IAN: Thanks Tom for the additional info. Seems we
all agree that the reported CLA-induced increase of
C-reactive protein, lipid peroxidation, and insulin
resistance are logical grounds for discontinuation.
I'm baffled as to why there are conflicting findings
regarding CLA's influence on insulin resistance. An
improvement of insulin efficiency seems consistent
with findings of increased lean mass. Hoping to get
an answer I contacted one of the researchers who
reported a positive effect on insulin sensitivity.
She was cited at the bottom of the initial CLA post:
http://www.google.com/groups?selm=m45mbvoupla718omnvm5msl1fqdna20g64%404ax.com
Her response avoided my question and raised what
strikes me as a straw-man argument. Here it is...
>> From: Ian Goddard
>> Sent: Wed, May 07, 2003
>> To: Martha Belury
>> Subject: CLA Research
>>
>> Hello Dr Martha Belury,
>>
>> What do you think of the findings of Riserus et al
>> that t10c12 CLA increased C-reactive protein,
>> oxidative stress, and insulin resistance?
>>
>>http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12370214&dopt=Abstract
>>
>> It seems directly opposite of so much research such
>> as yours that finds beneficial effects on insulin
>> sensitivity. But if true their study seems to
>> suggest that CLA is a health hazard.
Dr Belury's responce
> From: Martha Belury
> To: Ian Goddard
> Subject: RE: CLA Research
> Date: Thu, 8 May 2003
>
> You are incorrect. Dr. Vessby has conducted his
> research in people who have
> syndrome X, we conduct our research in people with
> type 2 diabetes. Check
> your facts then we can discuss the implications.
>
> Martha A. Belury, Ph.D., R.D.
> The Ohio State University
My responce to Belury:
From: Ian Goddard
Subject: RE: CLA Research
To: Martha Belury
Date: Thu, 8 May 2003
Thank you Dr Belury for your reply.
Given that metabolic disorder is a strong risk factor
for developing adult-onset diabetes, I'm not sure I
fully appreciate the error you suggest I've made. But
I'd be interested to know the implications of Vessby
et al as well as why we might expect CLA to have
opposite effects on diabetics and those with syndrome
X, if that's what you're implying.
Thanks once again for your attention.
"Conjugated linoleic acid induces lipid peroxidation in
humans."
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10683436&dopt=Abstract
************
No follow-up responce to date from Dr Belury.
UnclJunior
I appreciate your leg-work on this. I've stopped and re-stated taking CLA at
least three times. When Tom Matthews first raised concerns about CLA in the
LEF forum several years ago, it seemed only applicable to very thin people on
CR. Although I practice mild CR (moderate CR with mediocre compliance) I am of
average weight being once obese. Maintaining insulin sensitivity is clearly
one of the most important aims of a life-extension program and the case for CLA
is still an open question, in contradiction to LEF's biased cheerleading. A
more even handed presentation of CLA benefits (and possible risks) might lower
the sales of CLA, but would enhance their credibility. Although I still
purchase the majority of my supplements from them, I now price compare and no
longer will automatically purchase from them when their prices are slightly
higher than another reputable source.
Ian Goddard
IAN: Yeah, recently I begun taking CLA again. Previously
I took it when I was overweight and for some time during
the first 6 months of CR. My renewed interest was for its
alleged ability to improve insulin efficiency (IE) (though
my IE is impressive as it is!) and to preserve or increase
lean mass. Given the findings posted in this thread, I've
discontinued CLA. Last May I weighed 160 lbs, down from
a maximum of 220 lbs. Over the last year I've slimmed
down to 140 lbs. Starting to get a real CR look, so
I was hoping CLA might be a way to keep muscle on.
Recently I cut out in-between-meal snacking on nuts.
At first I was hit with unpleasant hunger, but like
before, it passed, although faster than before (in
less than a week). In two moths my weight dropped
from 145 to 140. I fast 12-to-15 hours between my
last meal of the day and breakfast. Recent research
that has been posted here points to benefits of
regular fasting, even without CR. So I'm getting,
I hope (and I feel), the benefits of both CR and
moderate fasting. I also seem to have more energy!