what experts say about aspartame and Abby Cormack, New Zealand: Betty
Martini 2007.08.13: Murray 2007.11.22
http://rmforall.blogspot.com/2007_11_01_archive.htm
Thursday, November 22, 2007
http://groups.yahoo.com/group/aspartameNM/message/1493

www.radionz.co.nz/news/latest/200711211852/committee_hears_artificial_sweeteners
_potential_health_risk
Committee hears artificial sweetener's potential health risk
Posted at 6:52 pm on 21 Nov 2007

A woman who believes eating sugar-free gum made her ill has asked the
Health Select Committee to warn the public about potential health
effects of the gum's artificial sweetener, aspartame.

Abby Cormack suffered from a range of health complaints, including
severe cramps, incontinence and depression, until she stopped
consuming aspartame.

Miss Cormack told the committee that since publicising her situation,
several other people have contacted her with similar problems.

She says there needs to be better labeling, so people can make an
informed choice. Miss Cormac wants to see a warning about possible
adverse health effects, and information about the amount of aspartame
in products.

She says doctors also need to be better informed about the potential
health impacts of aspartame.

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http://www.stuff.co.nz/stuff/4283400a20475.html
Sweetener can make some sick say officials
By RUTH HILL - The Dominion Post | Thursday, 22 November 2007

by PHIL REID/Dominion Post

HABIT: Abby Cormack who believes chewing four packs of gum a day
resulted in her health problems. Ms Cormack has asked Parliament's
health committee to ban aspartame, the artifical sweetener in gum.
[ photo ]

The artificial sweetener aspartame could cause allergic reactions in
some people, Food Safety Authority officials have admitted to MPs.

Wellingtonian Abby Cormack, who blames the serious health problems she
suffered on her habit of eating four packs a day of sugar-free chewing
gum, asked Parliament's health select committee yesterday to recommend
banning aspartame.

"I don't believe this should be in the food chains," she told MPs.

The previously fit and healthy 25-year-old said she suffered
debilitating physical and psychological symptoms for more than four
months this year.

She was tested for diabetes, lupus, multiple sclerosis, electrolyte
imbalances and mineral deficiencies before chancing on the link with
aspartame on the Internet.

"Within 48 hours of removing aspartame from my diet, my excruciating
limb discomfort starting subsiding," she told the committee.

"One change to my lifestyle, and within the following two weeks, every
single one of both my physical and psychological symptoms
disappeared."

There needed to be more education for doctors on the subject to avoid
more misdiagnoses.

"Many people don't know what they are suffering from."

Ten other people gave written testimony to the committee about the
effects of aspartame on their health.

Woodrow Monte, formerly director of the nutrition laboratory at
Arizona State University, told MPs aspartame was "a proven grade one
carcinogen" and there was no safe level of it.

It broke down into methanol, which was metabolised by the body into
formaldehyde, he said.

"Why are we allowing multinational companies to give this poison to
our children?"

The Food Safety Authority's principal adviser on toxicology, John
Reeve, agreed it was not possible to rule out aspartame as the cause
of Ms Cormack's symptoms.

"Some people could be more sensitive than we would otherwise expect."

It was equally possible, however, that she reacted to other substances
she had removed from her diet, such as caffeine, which had a proven
effect on the nervous system.

While aspartame was metabolised into methanol, formaldehyde and formic
acid, it also occurred naturally in many other foods, including fruit
and vegetables, he said.

Consumption many times higher than the authority's standard daily
maximum of 40 milligrams of aspartame per kilogram of body weight was
likely to be well within safety limits.

Health Ministry spokesman Chris Laurenson said international research
showed aspartame was a safe and useful product for those wanting to
cut down on sugar.

While the ministry was "not unmoved" by Ms Cormack's description of
her ordeal, it could not rely on anecdotal evidence.

There was no scientific evidence to back the claim that aspartame was
a carcinogen or neurotoxin.

http://www.wnho.net/experts_on_aspartame_and_abby_cormack.htm
what experts say about aspartame and Abby Cormack, New Zealand
Posted: 13 August 2007

http://www.mpwhi.com.abby_cormack_story.htm

THE ABBY CORMACK ASPARTAME STORY
By Abby Cormack  Posted: 13 August 2007 [ photo ]

Would you believe Sugar Free chewing gum could destroy you? That it
could bring anxiety, insomnia, depression, mind-fog, abdominal pain,
unbearable leg and arm cramps, blurred vision, endless trips to the
doctors, hysteria, suicidal thoughts and paranoia?

As the weird and horrifying symptoms progressed I sought the help of
several doctors, a psychiatrist and made two visits to the Emergency
ward. I was prescribed Valium, anti inflammatory, and excessive
amounts of pain killers. This gave me no relief. Multiple tests were
done for Electrolyte imbalances, mineral deficiencies, Multiple
Sclerosis, Diabetes, Lupus, all clear. These conditions all mimic the
symptoms of Aspartame poisoning.

Here I was an athletic, health-conscious young woman with every reason
to enjoy my youth and life, but this was rapidly being destroyed and
the doctors couldn't help me.

I was being poisoned by the 4 packets of sugar free chewing gum I
consumed each day. I had no idea that the sweetener used is a
neurotoxic chemical that's raining devastation on consumers worldwide.
The poison is aspartame; and the American FDA once published a list of
92 symptoms from 10,000 volunteered consumer complaints by victims
like myself.

Every one of my symptoms is on that list. It's addictive, carcinogenic
and deadly; decomposing into formaldehyde and a whole catalogue of
other deadlies as we digest it:
diketopiperazine, the brain tumor agent,
methyl alcohol: bringer of blindness,
aspartic acid destroyer of the nervous system.
It makes the neurons fire incessantly until they die.
Aspartame destroys the brain, your eyesight,
your intelligence... gradually and unsuspectedly.

So why is it on the market?  America's Secretary of Defense, Don
Rumsfeld, the genius behind the Iraq war. He was the head of a company
with a product he couldn't sell, ruling G. D. Searle, maker of
aspartame. But the Food & Drug Administration (FDA) wouldn't approve
it since it murdered the rats with brain tumors and a host of other
diseases. Don got a government job... and the next day a replacement
FDA Commissioner was appointed who approved aspartame over the
objections of his own scientists; several resigned in protest. Never
underestimate the damage a man without a conscience can do to the
world.

The product was a goldmine! It's in thousands of foods and drinks, and
little packs of aspartame/NutraSweet/Equal/E951 sit on millions of
restaurant tables worldwide. Aspartame had muscle, being backed up at
the very top levels of American politics, and soon the FDA became the
Washington Branch Office for the drug and chemical companies. In fact,
today FDA gets most of its cash from the companies it regulates.

I finally researched my symptoms on the internet, to learn about
phenylalanine (half of aspartame). And came upon the encyclopedic
http://www.dorway.com . There are thousands of other aspartame
websites and tens of thousands of case histories like mine or worse. I
kicked the habit May 23 and after 6 weeks of detoxing I am feeling
like a new person.

Abby Cormack

Dr. Ralph G. Walton:

Tragically, Abby's experience with aspartame is far from unique. In
1985 I first encountered a clinical situation in which aspartame
clearly triggered a manic episode in one of my patients.

I initially made an incorrect diagnosis of bipolar disorder and
actually started a treatment regimen of lithium carbonate. The overall
picture however was not totally consistent with bipolar illness,
especially as a grand mal seizure accompanied the "manic" episode.

Some detective work as to what was different in my patient's life
resulted in the conclusion that the only significant change was the
sudden introduction of a large amount of Crystal Lite (aspartame) into
her diet.

The total elimination of all aspartame resulted in fairly rapid
resolution of her symptoms. The lithium was discontinued and she has
remained symptom, and aspartame, free.

I believe it is essential for all physicians to include a dietary
history when assessing patients. Whenever aspartame is found to be
included in the diet, I would encourage all health care professionals
to educate their patients about the hazards and encourage complete
abstinence from this artificial sweetener.

In my own practice, I have found that many patients improve
substantially with just this simple change.

In particular, patients with underlying mood disorders appear to be
particularly sensitive to the adverse consequences of this extremely
hazardous substance.

Attorney James Turner, Atty, who with Dr. John Olney tried to prevent
approval of aspartame:

"Aspartame/NutraSweet cripples the lives of thousands of people. When
I tried to persuade the president of the Searle Drug company,
manufacturers of that chemical sweetener, to do the tests that would
find any dangers it posed before It was marketed he blew me off.

His name was Donald Rumsfeld (Iraq war architect). In exchanges about
aspartame safety with him and his company I learned how little he
values human life."

http://www.soungandfury.tv/Paes/Rumsfeld.html
Turner talks about Don Rumsfeld

http://groups.yahoo.com/group/aspartameNM/message/1483
Donald Rumsfeld CEO 1977-85 G.D. Searle & Co., got new President
Reagan
to prohibit FDA opposition to aspartame 1981.01.25, history by lawyer
James S. Turner: Murray 2007.10.29

Dr. H. J. Roberts, M.D., FACP, FCCP  author of 1,000 page medical text
-- Aspartame Disease: An Ignored Epidemic:

I have reviewed the recent experience of Abby Cormack while chewing
four (4) packs of aspartame gum daily, based on her "medical timeline
2007" -- coupled with the details of her testing and doctoring by
interested and competent professionals, and the dramatic improvement
of her psychological and most other symptoms following the avoidance
of aspartame products.

Her problem appears to be largely due to aspartame disease, as I have
detailed in many publications. I have reported severe depression,
anxiety, insomnia, cramps, speech disturbance, confusion, blurred
vision, eruptions, and neuropathic symptoms in numerous aspartame
reactors consuming both gum and other products containing this
chemical.

Fortunately, her mother suspected the cause which had escaped the
attention of several doctors.

I have admired the great emphasis by persons in New Zealand and its
government on avoiding exposure to a variety of toxic substances.

The serious documented affliction of this young woman due to consuming
aspartame is probably replicated by many other consumers in the
country, and warrants the profound attention of its regulatory
agencies.

http://www.dorway.com/tldaddic.html 5-page review
Roberts HJ Aspartame (NutraSweet) addiction.
Townsend Letter 2000 Jan; HJRobertsMD@aol.com
http://www.sunsentpress.com/ sunsentpress@aol.com
Sunshine Sentinel Press P.O.Box 17799 West Palm Beach, FL 33416
800-814-9800 561-588-7628 561-547-8008 fax

http://groups.yahoo.com/group/aspartameNM/message/669
1038-page medical text "Aspartame Disease: An Ignored Epidemic"
published May 30 2001 $ 60.00 postpaid data from 1200 cases
available at http://www.amazon.com
over 600 references from standard medical research

Dr. Woodrow Monte Ph.D., University of Arizona professor of Food
Science, early investigator of aspartame, now residing in New Zealand:

"Curiosity about the safety of Aspartame need go no further than the
indisputable fact that each molecule of the sweetener turns into a
molecule of formaldehyde when metabolized in the human body. Enough
said!"

http://www.dorway.com/monte84.html
Read Dr. Monte's journal article:
Aspartame, Methanol and the Public Health:

Trocho Study: http://www.wnho.net/formaldehyde_from_aspartame.pdf
Formaldehyde derived from dietary aspartame
binds to tissue components in vivo.
Life Sci June 26 1998; 63(5): 337-49.
Departament de Bioquimica i Biologia Molecular,
Facultat de Biologia, Universitat de Barcelona, Spain.
http://www.bq.ub.es/cindex.html Lanies de Recerca: Toxicitat de
l'aspartame http://www.bq.ub.es/grupno/grup-no.html
Sra. Carme Trocho,
Sra. Rosario Pardo,
Dra. Immaculada Rafecas,
Sr. Jordi Virgili,
Dr. Xavier Remesar,
Dr. Jose Antonio Fernandez-Lopez,
Dr. Maria Alemany [male]
Fac. Biologia Tel.: (93)4021521, FAX: (93)4021559
Sra. Carme Trocho "Trok-ho" Fac. Biologia Tel.: (93)4021544,
FAX: (93)4021559 alemany@porthos.bio.ub.es ; bioq@sun.bq.ub.es

Ralph G. Walton, M.D. Medical Director, Safe Harbor Behavioral Health,
Professor of Clinical Psychiatry, Northeastern Ohio Universities
College of Medicine:

Although undoubtedly well intentioned, any attempt to replace sugared
beverages with aspartame containing diet products will, in my opinion,
have a devastating impact on the health of our children and
adolescents.

The alarming increase in obesity, type II diabetes, and a wide variety
of behavioral difficulties in our children is obviously attributable
to multiple factors, but I am convinced that one powerful force in
accentuating these problems is the ever increasing use of aspartame.

Aspartame is a multipotential toxin and carcinogen. The dipeptide
component of the molecule can alter brain chemistry, significantly
changing the ratio of catecholamines to indolamines, with resultant
lowering of seizure threshold, production of carbohydrate craving and
in vulnerable individuals leading to panic, depressive and cognitive
symptoms.

The methyl ester component of aspartame is metabolized to methanol,
which in turn is broken down into formic acid and formaldehyde.
Methanol can lead to serious eye problems, formic acid and
formaldehyde are potent carcinogens.

The diet food industry and the F.D.A. are fond of saying that
aspartame is "the most studied product in history" with an outstanding
safety record. In fact however virtually all of the studies in the
medical literature attesting to its safety were funded by the
industry, whereas independently funded studies, now numbering close to
100, identify one or more problems.

It would be especially tragic if an attempt to improve the health of
our children led to even greater exposure to this highly toxic
product.

Thank you for your attention to this urgent public health issue.

http://www.mindfully.org/Health/Aspartame-Adverse-Reactions-1993
See Dr. Waltons study: "Adverse Reactions to Aspartame: Double-Blind
Challenge in Patients from a Vulnerable Population:

Read Dr. Walton's research on Scientific Peer Reviewed Studies and
Funding:  http://www.dorway.com/doctors.html#walton

DR. MORANDO SOFFRITTI, lead researcher on two groundbreaking long-term
aspartame studies.  He was recently honored at New York's Mt Sinai
School of Medicine with the Irving J. Selikoff Award For his
outstanding contributions to the identification of environmental and
industrial carcinogens and his promotion of independent scientific
research.

Reviewing his two impeccable aspartame studies Dr. Soffritti explains:

The first ERF study (2005) was conducted on 1800 Sprague-Dawley rats
(100-150/per sex/per group).

In order to simulate daily human intake, aspartame was added to the
standard rat diet in quantities of 5000, 2500, 100, 500, 20, 4, and 0
mg/Kg of body weight.

Treatment of the animals began at 8 weeks of age and continued until
spontaneous death.

The results show that APM causes a statistically significant, dose-
related increase of lymphomas/leukemias and malignant tumors of the
renal pelvis in females and malignant tumors of peripheral nerves in
males.

These results demonstrate for the first time that APM is a
carcinogenic agent, capable of inducing malignancies at various dose
levels, including those lower than the current acceptable daily intake
(ADI) for humans (50 mg/kg of body weight in the US, 40 mg/kg of body
weight in the EU).

The second ERF study (2007) was conducted on 400 Sprague-Dawley rats
(70-95/per sex/per group).

In order to simulate daily human intake, aspartame was added to the
standard rat diet in quantities of 100, 20, and 0 mg/Kg of body
weight.

Treatment of the animals began on the 12th day of fetal life until
natural death.

The results of the second study show an increased incidence of
lymphomas/leukemias in female rats with respect to the first study.

Moreover, the study shows that when lifespan exposure to APM begins
during fetal life, the age at which lymphomas/leukemias develop in
females is anticipated.

For the first time, a statistically significant increase in mammary
cancers in females was also observed in the second study.

The results of this transplacental carcinogenicity bioassay not only
confirm, but also reinforce the first experimental demonstration of
APM's multipotential carcinogenicity.

www.ehponline.org/members/2007/10271/10271.pdf free full text 24 pages
National Institutes of Health
U.S. Department of Health and Human Services
ENVIRONMENTAL HEALTH PERSPECTIVES
Lifespan Exposure to Low Doses of Aspartame Beginning During Prenatal
Life Increases Cancer Effects in Rats
doi:10.1289/ehp.10271 (available at http://dx.doi.org/)
Online 13 June 2007
Morando Soffritti 1,
Fiorella Belpoggi 1,
Eva Tibaldi 1,
Davide Degli Esposti 1,
Michela Lauriola 1
1 Cesare Maltoni Cancer Research Center, European Ramazzini Foundation
of Oncology and Environmental Sciences, Bologna Italy
Address of the institution: Cesare Maltoni Cancer Research Center,
European Ramazzini Foundation of Oncology and Environmental Sciences
Castello di Bentivoglio, Via Saliceto, 3, 40010 Bentivoglio, Bologna,
Italy +39 051 6640460 fax +39 051 6640223
crcfr@ramazzini.it,  www.ramazzini.it
Address correspondence to: M. Soffritti
Acknowledgements:
This research was supported entirely by the European Ramazzini
Foundation Environmental Sciences.
The authors declare that they have no competing financial interests.
http://groups.yahoo.com/group/aspartameNM/message/1441

http://www.ramazzini.it/fondazione/docs/NYAS_Aspartame_Ramazzini.pdf
Results of Long-Term Carcinogenicity Bioassay on Sprague-Dawley Rats
Exposed to Aspartame Administered in Feed
Ann. N.Y. Acad. Sci. 2006 Sep; 1076: 559-577.
Fiorella Belpoggi,
Morando Soffritti,
Michela Padovani,
Davide Degli Esposti,
Michelina Lauriola, and
Franco Minardi.
The end judges everything -- HERODOTUS (480-425 B.C.) The History
Cesare Maltoni Cancer Research Center,
European Foundation of Oncology and Environmental Sciences
'B. Ramazzini', 40010 Bentivoglio, Bologna, Italy
http://groups.yahoo.com/group/aspartameNM/message/1382
[ and, previously ]
First experimental demonstration of the multipotential
carcinogenic effects of aspartame administered in the feed to Sprague-
Dawley rats.
Environ. Health Perspect. 2006 Mar; 114: 379-385. PMID: 16507461
Soffritti M, Belpoggi F, Degli Esposti D, Lambertini L, Tibaldi E,
Rigano A.
Environmental Health Perspectives Volume 113, Number 11
November 2005 Current print issue
The full version of this article is available for free in PDF format.
http://ehp.niehs.nih.gov/members/2005/8711/8711.pdf 35 pages
First Experimental Demonstration of the
Multipotential Carcinogenic Effects of Aspartame
Administered in the Feed to Sprague-Dawley Rats.
Morando Soffritti, Fiorella Belpoggi, Davide Degli Esposti,
Luca Lambertini, Eva Tibaldi, and Anna Rigano.
doi:10.1289/ehp.8711 (available at http://dx.doi.org/)
Online 17 November 2005
The National Institute of Environmental Health Sciences
National Institutes of Health
U.S. Department of Health and Human Services
http://www.ehponline.org/
Cesare Maltoni Cancer Research Center,
European Ramazzini Foundation of Oncology and
Environmental Sciences
Sofritti, M. et al. 2005.
Aspartame induces lymphomas and leukaemias in rats.
Eur. J. Oncol. 2005; 10: 107-116.
http://groups.yahoo.com/group/aspartameNM/message/1250

Russell Blaylock, M.D. Neurosurgeon: Author: Excitotoxins: The Taste
That Kills. Lecture: The Truth About Aspartame
http://www.atavistik.com  Damian Blaylock atavistik@gmail.com

Commenting on the Ramazzini studies, above, Dr Blaylock states:

My review of the first Ramazzini Study concluded that the study was
one of the best designed, comprehensive and conclusive studies done to
date on the multipotential carcinogenic danger of aspartame.

This second study is even more conclusive, in that it shows a dose-
dependent statistically significant increase in lymphomas/leukemia in
both male and female rats exposed to aspartame.

These two cancers are the fastest growing cancers in people under age
30.

Also, of major concern is their finding of statistically significant
increases in breast cancer in animals exposed to aspartame.

With newer studies clearly indicating that toxic exposures during
fetal development can dramatically increase the cancer risk of the
offspring, this study takes on a very important meaning to all
pregnant women consuming aspartame products.

Likewise, small children are at considerable risk of the later
development of these highly fatal cancers.

It should be appreciated that the doses used in these study fall
within the range of doses seen in everyday users of aspartame.

This study, along with the first study, should convince any reasonable
scientific mind, as well as the public, that this product should be
removed from the market.

Russell L. Blaylock, MD 601-982-1175 Madison, Mississippi
"Excitotoxins: The Taste that Kills", 1977, 298 p., 493 references.
"Health and Nutrition Secrets that can save your life", 2002, 459 p.,
558 + 30 references, $ 30 http://www.russellblaylockmd.com/

Dr. Betty Martini
Founder, Mission Possible World Health International
9270 River Club Parkway
Duluth, Georgia 30097
770-242-2599
E-Mail: BettyM19@mindspring.com
http://www.wpwhi.com
http://www.whno.net
http://www.dorway.com

http://www.HolisticMed.com/aspartame mgold@holisticmed.com
Aspartame Toxicity Information Center Mark D. Gold
12 East Side Drive #2-18 Concord, NH 03301 603-225-2100
http://www.holisticmed.com/aspartame/abuse/methanol.html
"Scientific Abuse in Aspartame Research"
[ Gold points out that industry methanol assays were too insensitive
to
properly measure blood methanol levels.

http://groups.yahoo.com/group/aspartameNM/message/1045
http://www.holisticmed.com/aspartame/scf2002-response.htm
Mark Gold exhaustively critiques European Commission Scientific
Committee on Food re aspartame ( 2002.12.04 ):
59 pages, 230 references
//////////////////////////////////////////////////////////

Aspartame and Psychiatric Disorders, Ralph G. Walton, M.D.: Murray
2007.09.20
http://rmforall.blogspot.com/ Wednesday, September 19, 2007
[ You are invited to give civil, relevant comments. ]
http://groups.yahoo.com/group/aspartameNM/message/1474

From: Betty Martini 2007.09.19 7:11 pm [ Kauai time ]

Aspartame and Psychiatric Disorders, Ralph G. Walton, MD, Sept. 2007
To: Bettym19@mindspring.com

Although psychiatry is far from an exact science, over the past half
century there has been an explosive growth in our understanding of the
human brain and consequently in our ability to diagnose and treat
mental
disorders. We have also become much more sophisticated about the
impact
of a variety of toxins on psychological processes. I am convinced that
one such toxin is aspartame.

Two years after aspartame was introduced onto the market [ 1981 ], I
first became aware of the negative impact of this artificial sweetener
on the central nervous system. I had been treating a then 54 year old
woman with imipramine, a tricyclic antidepressant, because of
recurrent
major depressive episodes. Previous psychoanalytically based therapy
had proven ineffective, but she responded dramatically to 150 mg of
imipramine per day. She had done well for 11 years on this medication,
but was then suddenly hospitalized with a grand-mal seizure and
subsequent manic episode.

One could postulate that she was bipolar, and the antidepressant had
triggered the mania -- but she had been on the same medication for a
total of 11 years, and for the previous 5 years at the same 150 mg per
day dose. Neither the seizure nor her mania was consistent with what
we
know about the clinical course of bipolar disorder or epilepsy.
Careful
history revealed that the only change in her life was a recent
decision
to switch from the sugar which she had always used to sweeten her iced
tea to a newly marketed product with aspartame.

Since aspartame can alter the balance of certain neurotransmitters
which
we believe are involved in mood disorders and can, in my opinion,
alter
the seizure threshold, I advised my patient to avoid all aspartame
products. She did so, and had no further seizures, no further manic or
depressive episodes. I discontinued the lithium carbonate which I had
started when I mistakenly concluded that she had a bipolar disorder,
reinstated her imipramine and she has continued to do well.

After this case report was published in the medical literature, many
patients with unexplained seizures or treatment resistant psychiatric
problems were referred to me. I became increasingly convinced that
aspartame could both trigger seizure activity and mimic or exacerbate
a
variety of psychiatric disorders. I presented a paper based on those
patients at a 1987 MIT sponsored conference on
Dietary Phenylalanine and Brain Function.

Industry sponsored criticism was made that my conclusions regarding
aspartame's toxicity could not be accepted as valid because my case
reports were "merely anecdotal" and not based on double blind
research.

Unfortunately case reports do not currently have the respect in the
mainstream medical literature which they deserve (historically, much
of
medical progress has been based on careful observation of individual
patients).

Nevertheless, I was so convinced of aspartame's toxicity, and the need
to have its hazards more widely appreciated in the medical community,
that I did undertake a double blind study. That study, "Adverse
Reactions to Aspartame: Double-Blind Challenge in Patients from a
Vulnerable Population," was published in Biological Psychiatry in
1993.

It demonstrated that individuals with mood disorders are particularly
sensitive to aspartame and experienced an accentuation of depression
and
multiple physical symptoms. I had expected that the difficulties
experienced by patients receiving aspartame would be fairly subtle
(the
dose of 30 mg/kg/day was well below the level of 50 mg/kg/day which
the
FDA considered "safe"). I was not prepared for the severity of the
reactions, and for obvious ethical reasons cannot perform any further
human studies with aspartame.

Over the ensuing years I have continued to see the multiple neurologic
and psychiatric consequences of aspartame use.

It can lower the seizure threshold and lead to an incorrect diagnosis
of
epilepsy, with subsequent inappropriate prescription of
anticonvulsants.

It can mimic or exacerbate symptoms of MS.

It can paradoxically produce carbohydrate craving and weight gain.

The world-wide epidemic of obesity and type 2 diabetes obviously has
multiple causes, but I am convinced aspartame is a major factor.

The explosive increase in our knowledge base in the neurosciences I
referred to earlier is a topic beyond the scope of this brief report,
but to drastically oversimplify, we know that in a variety of
psychiatric disorders there is a disturbance in the balance of certain
neurotransmitters.

Specifically, serotonin, norepinephrine, dopamine and acetylcholine
are
all major players.

Aspartame can affect the levels & balance of all these transmitters.
It
impairs the absorption of L-tryptophan, the major precursor in the
synthesis of serotonin.

The phenylalanine from the dipeptide component of the aspartame
molecule, is a major precursor in the norepinephrine-dopamine
synthetic
pathway.

Recent research demonstrated that aspartame reduces
acetylcholinesterase, an enzyme which breaks down acetylcholine -- a
key
player in the central nervous system, with an important role in
cognition and memory, and with a reciprocal, inhibitory relationship
with dopamine.

We are not sophisticated enough at this point in time to fully
understand all the implications of the neurochemical changes induced
by
aspartame, but as a busy clinician I see the profound impact on
patients' lives on a daily basis.

It can both produce and aggravate depression.

In certain patients it can trigger manic episodes.

It can produce or aggravate panic attacks.
Some of my patients have experienced a complete cessation of panic
attacks and needed no further treatment after they completely
eliminated
aspartame from their diet.

Certain schizophrenic patients have experienced fewer auditory
hallucinations or needed less antipsychotic medication after the
elimination of aspartame.

It is essential that there be much greater awareness of the hazards of
this highly toxic substance!

Ralph G. Walton, M.D.,
Medical Director, Safe Harbor Behavioral Health
500 Gypsy Lane, P.O. Box 240 Youngstown,
OH 44501 330-740-3621 rwalton193@aol.com,

http://www.neoucom.edu/DEPTS/Psychiatry/walton.htm
Professor of Clinical Psychiatry,
Northeastern Ohio Universities College of Medicine
Adjunct Professor Of Psychiatry,
Lake Erie College of Osteopathic Medicine

Dr. Walton's aspartame study:
"Adverse Reactions to Aspartame: Double-Blind Challenge in Patients
from
a Vulnerable Population:
http://www.mindfully.org/Health/Aspartame-Adverse-Reactions-1993.htm

Dr. Walton's research on Scientific Peer Reviewed Studies and Funding:
http://www.dorway.com/doctors.html#walton

http://groups.yahoo.com/group/aspartameNMmessage/1443
Food Safety wants ban on aspartame in schools in New Zealand: Murray
2007.06.21

www.stuff.co.nz/print/4103631a6479.html

Friday, 22 June 2007

Campaign to outlaw sweetener in schools

Food Safety campaigners are calling for a ban on diet drinks and other
artificially sweetened products in schools after a Wellington woman
said she was poisoned by sugar-free chewing gum.

Abigail Cormack, 25, said she began suffering muscle cramps, heart
palpitations, anxiety, depression and skin rashes after chewing gum
that contained the artificial sweetener aspartame.

Her symptoms disappeared when she stopped her four-pack-a-day habit.

A spokeswoman for the Wrigley company, which makes Extra chewing gum,
said aspartame -- which is used in more than 6000 products consumed by
200 million people worldwide -- was the "most tested food additive in
history".

More than 200 studies supported the safety of aspartame, the company
said.

"Wrigley Australia and New Zealand is committed to ensuring that all
safety food standards are met for all of our confectionery products,
including gum," it said.

Since aspartame was 200 times sweeter than sugar, it was only used in
"minuscule" amounts, and was composed of ingredients found naturally
in food.

However, Green MP Sue Kedgley -- who is campaigning to have fizzy
drinks containing aspartame removed from schools -- said the
Government had a responsibility to warn the public.

"The problem is that products containing aspartame are being touted as
a healthier alternative and this means that many children are being
exposed to potentially large doses of this artificial sweetener," she
said.

"While it's important to reduce the sugar intake of children and
adults, to replace that sugar with a controversial additive is just
not the answer."

Safe Food Campaign spokeswoman Alison White said the use of this
"questionable" additive had more to do with "power, politics and
money" than science.

"It is interesting and predictable that the research showing problems
with aspartame is all independently funded," she said.

Ms Cormack's case was likely to be "the tip of the iceberg".

Khandallah man Clive Bennett said he believed he had aspartame
poisoning while living in Britain five years ago. He suffered muscle
pains and dizzy spells while taking sugar substitutes in three coffees
a day.

After reading about aspartame poisoning, he stopped using artificial
sweetener and his problems disappeared.

"It annoys me when scientists and food companies say there is no
proven link to anything bad. More likely, they know there's a problem
but they won't admit it."

Auckland woman Cathy Norman blames aspartame used to sweeten soft
drinks for her heart palpitations, blackouts and unexplained seizures.

At one time, she was drinking two litres or more of diet soft drink a
day.

"I think the doctors thought I was making it all up ... But when I
changed my diet and I cut out aspartame from my diet altogether, I
have not been sick like that since."

Clinical pharmacologist Professor Carl Burgess, from the Wellington
School of Medicine, said to get aspartame poisoning from a diet soft
drink, one would have to drink 28 cans in one sitting.

However, he said some people were more sensitive to additives than
others.

"You might test a product on 5000 people but if it causes an adverse
reaction in one in 100,000 people, you're unlikely to find it."

You may not copy, republish or distribute this page or the content
from it without having obtained written permission from the copyright
owner. To enquire about copyright clearances contact
clearance@fairfaxnz.co.nz.

www.safefood.org.nz/

Do additives affect you or your children?
Do you have any good stories to tell about this?
A documentary about additives in food is going to be made.
Top Shelf Productions, an Auckland, New Zealand, based television
production company, is currently preparing a documentary that will
discuss the widespread use of food additives in our everyday food
products. To support the documentary, the Top Shelf team is looking
for individuals or families that can contribute interesting experience
and help discuss the problems that are connected to some of the
substances.

Interested readers, please contact Sigrun on (09) 377 8774 or
sigrun.l@topshelfproductions.co.nz,
November 2006

The Safe Food Campaign is a nationwide organisation which campaigns
for safer, healthier food.
We provide consumers with information so that they can make up their
own minds about what is safe to eat.
We lobby government to make our food safer.

How to Contact the Safe Food Campaign:
By Post: PO Box 9206, Wellington, New Zealand
By Telephone: +64 (0)4 476 8607 Alison +64 (0)4 562 8664 Jacky
By email: info@safefood.org.nz,

To become a member of the Safe Food Campaign send an email with your
contact details to: Member@SafeFood.org.nz
Membership Rates:
Unwaged/Low waged NZ$ 10.00
Waged NZ$ 25.00
group/small business NZ$35
business (incl.15 newsletters) NZ$50
corporate (incl.30 newsletters) NZ$100
Donations of any size gratefully accepted.

Other Safefood Contacts in New Zealand:
Auckland,   Anne Dubois - (09) 441 2358
Waiheke Island,   Wendy Johnson - (09) 372 9680
Hamilton,   Phil Evans - (027) 697 0374
Thames,   Alia Steward-Finn - (07)868 1030
Napier / Hawkes Bay,   Odile Balas - (06) 835 0141
New Plymouth,   Nina Vink - (06)758 8174
Levin,   Lynnette Attwell - (06)367 8042
Wanganui,   Ali Martin - (06) 343 2346
Kapiti Coast,  Brigit Howitt - (04) 904 3681
Nelson,  Lorraine Leader - (03) 547 0195
Christchurch,  Jayne Green - (03) 381 4551
Oamaru,   Waitaki Environment Centre - (03) 434 8330

www.wrigley.co.uk/
The Wrigley Company Limited
Estover, Plymouth, Devon PL6 7PR UK
Tel.: +44 (0) 1752 701107  Tel.: +44 (0) 1752 778850
consumer.affairs@wrigley.co.uk,
//////////////////////////////////////////////////////////

http://groups.yahoo.com/group/aspartameNM/message/1442
Wellington, NZ lady, 25, free by 24 hours of severe muscle cramps (5
months) after quitting 4-8 packs daily aspartame chewing gum (past few
years): Murray 2007.06.20

[ 6-8 mg aspartame per stick chewing gum, so 8 packs, 5 sticks each,
gives 240-320 mg, while a 12 oz can aspartame diet soda has 200 mg --
however, aspartame from gum is absorbed directly into the mucosal
membranes in the mouth, close to the brain. ]

http://ww2.abc13.com/Global/story.asp?S=6514064

www.scoop.co.nz/stories/print.html?path=PA0706/S00418.htm

Scoop Independent News

www.scoop.co.nz/stories/PA0706/S00418.htm

Chewing gum case strengthens school diet drink ban
Thursday, 21 June 2007, 11:37 am
Press Release: Green Party

Chewing gum case strengthens call for school diet drink ban

The case of a Wellington woman who became seriously unwell after
consuming excessive amounts of the controversial additive aspartame in
chewing gum underlines the urgent need for consumer information and
warnings about potential side effects, Green Party MP Sue Kedgley
says.

"This case also leads me to repeat the call for fizzy drinks
containing aspartame to be removed from schools," Ms Kedgley says.

Abigail McCormack began suffering
crippling muscle cramps and tingling in her hands and feet,
heart palpitations,
anxiety attacks,
depression
and skin rashes,
she thought she was dying after consuming excessive amounts of chewing
gum containing aspartame.

Ms McCormack is concerned that there were no warnings to alert her to
the fact that aspartame could cause harm.

These health problems stopped when Ms McCormack stopped chewing
aspartame sweetened gum.

"Like Ms McCormack, many consumers have no idea that aspartame is a
controversial additive, or that it has been linked to a significant
number of side-effects, especially if it is frequently consumed in
large quantities.

Aspartame, once ingested, breaks down into aspartic acid,
phenylalanine and methanol, which in turn converts into formaldehyde
which is a deadly neurotoxin," Ms Kedgley says.

"Given the large number of products containing aspartame and the
marketing focus on diet foods and drinks containing the additive,
it is essential that consumers are alerted to any potential side
effects.

"The Government has a responsibility to require that this information
is provided, through warning labels on products and public information
campaigns.

"The problem is that products containing aspartame are being touted as
a healthier alternative and this means that many children are being
exposed to potentially large doses of this artificial sweetener."

While, it's important to reduce the sugar intake of children and
adults, to replace that sugar with a controversial additive is just
not the answer.

"There are now credible international studies suggesting a link
between aspartame and cancer in animals. Such studies, along with the
health difficulties experienced by Ms McCormack, demand action by the
Government."

www.newswire.co.nz/main/viewstory.aspx?storyid=378970&catid=30

Warning Over Artificial Sweeteners
1:15 pm, 21 Jun 2007

A Wellington GP says more research is needed into artificial
sweeteners after a patient became sick from too much sugar-free
chewing gum.

Wellington woman Abigail McCormack went to her doctor suffering severe
cramps and other symptoms, but initial tests couldn't find the cause.

The woman's GP, Penny Rowley, says she then discovered Miss McCormack
was eating up to eight packs of a sugar-free chewing gum a day,
which contain the artificial sweetner aspartame.

Dr Rowley says more needs to be known about the impact of ingesting
large quantities of the sweetener.

However, the Food Safety Authority says aspartame has been through
rigorous testing and is safe.

Â(c) NewsRoom 2007

www.tv3.co.nz/News/Womanpoisonedby4packadaychewinggumhabit/tabid/209/articleID/2
9322/Default.aspx

Woman poisoned by 4-pack-a-day chewing gum habit
Thu, Jun 2007 2:13p.m.
Abigail McCormack [ photo ]

Chewing gum has become more than just a dirty habit for one Wellington
woman.

Abigail McCormack thought she was dying from a mystery illness when
she began suffering crippling muscle cramps and tingling in her limbs
four months ago.

Those symptoms escalated to heart palpitations, skin rashes and
difficulty sleeping.

Then the 25-year-old realised it was the four packets of gum she was
chewing daily that was causing her problems.

Ms McCormack told 3 News giving up has been the same as kicking any
habit.

Listen to Andre Patterson's full interview wtih Professor Carl Burgess
on RadioLIVE's World at Noon.

http://news.ninemsn.com.au/article.aspx?id=274460

New questions over artificial sweetener
Thursday Jun 21 12:53 AEST

New questions have been raised about the potential effects of
artificial sweetener after a New Zealand woman fell ill, blaming her
daily consumption of four packs of sugar-free chewing gum.

Abigail Cormack, 25, of Wellington, went to her doctor complaining of
crippling muscle cramps, anxiety attacks, depression and skin rashes,
and was forced to take sick leave, the Dominion Post newspaper
reported.

Cormack's doctor Penny Rowley told AAP it was a "strong possibility"
her patient had been made ill by the artificial sweetener aspartame,
which is used in NutraSweet and Equal, as well as thousands of other
products.

Cormack's symptoms disappeared within 24 hours of her giving up the
gum, which she had been chewing for a few years.

"She stopped having the gum and things resolved, so it looks like
there was a cause and effect there," Rowley said.

Cormack admits her chewing gum consumption was "excessive", but says
there were no warnings it could do her harm.

Food Standards Australia New Zealand (FSANZ) says aspartame is safe
for human consumption.

Pharmacologist Professor Carl Burgess, from the Wellington School of
Medicine, said most people were not affected, but some people did
react to artificial sweeteners.

"On a personal basis I have not seen it but it is certainly in the
literature. Some people do react to these substances, particularly
with headache and feeling tired, weary, that sort of stuff, and
occasionally depression," he said.

"Anxiety and panic attacks are described with these sort of
compounds," Burgess said.

Last year an Italian team which conducted a controversial seven-year
study into the substance linked it to a range of cancers.

However the Italian team's findings were later disputed in a review by
the European Food Safety Authority, prompting FSANZ not to change the
acceptable daily intake of 40 mg/kg.

New Zealand's Green Party wants all fizzy drinks containing aspartame
to be removed from schools in light of the Wellington case.

"Many consumers have no idea that aspartame is a controversial
additive, or that it has been linked to a significant number of side-
effects, especially if it is frequently consumed in large quantities,"
said Green MP Sue Kedgley.

A public relations firm representing Wrigley, makers of Extra sugar-
free gum, which contains aspartame, could not immediately comment on
the reports.

Â(c)AAP 2007

www.stuff.co.nz/print/4102292a6000.html

Thursday, 21 June 2007  12:53 AEST

Chewing gum habit `poison'

Abigail Cormack thought she was dying from a mystery illness. She
never realised her daily chewing gum habit was probably poisoning her.

The sugar-free gum contained aspartame, a food additive widely used in
thousands of products, including gum, diet soft-drinks and tea and
coffee.

The additive is prompting debate in the international medical world
about its safety.

When Ms Cormack, 25, of Wellington, began suffering crippling muscle
cramps and tingling in her hands and feet about five months ago, she
feared she was having a heart attack.

She started suffering heart palpitations, anxiety attacks, depression
and skin rashes, was unable to sleep and had to take sick leave.

But, despite a battery of tests, doctors could not pinpoint the cause.
"They thought it might be a salt imbalance, maybe I was over-training
at the gym.

"I was prescribed anti-inflammatories and Valium to help me sleep but
it just got worse and worse. I thought I was dying."

Finally, an Internet site alerted her to the possibility of aspartame
poisoning.

Under the brand name NutraSweet, aspartame is used in more than 5000
foods and beverages worldwide.

For the past few years, Ms Cormack has chewed through up to four
packets of chewing gum a day.

She did not suspect the seemingly innocuous habit could be slowly
poisoning her.

Aspartame is digested into aspartic acid, phenylalanine and methanol,
which converts into formaldehyde -- a deadly neurotoxin used as
embalming fluid.

The food industry says these are all "naturally occurring" substances
in foods and the amounts are too small to be harmful. No study has
found a definitive link between the compounds and serious effects in
humans, but some research has found higher incidences of chronic
fatigue, migraines and other conditions.

Ms Cormack admits her chewing gum consumption was "excessive".

"But there were no warnings it could be doing me harm."

Her GP, Penny Rowley, was at the point of referring her to a
neurologist when she heard about the gum habit.

She confirmed aspartame poisoning as the likely culprit, and within 24
hours of giving up gum, Ms Cormack's symptoms disappeared.

Dr Rowley said it was the first case she had seen. "I was certainly
surprised but it seems to have worked."

Clinical pharmacologist Professor Carl Burgess, from the Wellington
School of Medicine, said that though someone would have to take
"megadoses" of aspartame for it to be toxic, some people were more
susceptible to allergic reactions.

The New Zealand Food Safety Authority says there is no scientific
evidence of any significant harm from a large daily intake of
aspartame.

You may not copy, republish or distribute this page or the content
from it without having obtained written permission from the copyright
owner. To enquire about copyright clearances contact
clearance@fairfaxnz.co.nz.

www.greens.org.nz/people/kedgley_s.asp  Sue Kedgley, MP
Parliamentary Contacts
Phone:       04-470 6717  Fax:     04-472 7116
Email:     sue.kedgley@parliament.govt.nz,
Wellington Office
Phone:       04-381 4640  Fax:     04-381 2876
Email:     greenmps.wellington@greens.org.nz,

8 Dekka St is the site of the Khandallah Medical Centre. A suburban,
community-focused general practice with the four partners of Drs Anne
Marie Cullen, Sally Talbot, Alistair Young and Richard Hogg.
Dr Penny Rowley is the associate doctor. +64-4-479-7157

Prof. Carl Burgess: Head of Department:
General Medicine & Clinical Pharmacology carlb@wnmeds.ac.nz,

Prof. Julian Crane: Clinical Epidemiology crane@wnmeds.ac.nz,

http://ww2.abc13.com/Global/story.asp?S=6514064

Headache Prevention Diet  June 20 2007
From iVillage.com

Headaches can be caused by many things, including illness, stress and
lack of sleep. They may also be triggered by several common foods, and
simply changing your diet could be the most effective treatment. Once
you and your doctor have ruled out other potentially more serious
causes for your headaches, take a look at what you eat every day and
see if eliminating common trigger foods eliminates your headaches.

Here's how the Headache Prevention Diet can help:

Dietary modifications that exclude common food triggers may help you
pinpoint just what is causing your headaches. Although the list of
potential food triggers is long, the most common are chocolate, red
wine, caffeine, MSG, Aspartame, cured meats, aged cheese, nuts,
nitrate, sulfites, alcohol and ice cream. This diet excludes all
common headache triggers, yet is still nutritionally balanced. Try
following it for several weeks to see if it doesn't help reduce the
number and severity of your headaches.

Recent studies show that omega-three fatty acids, the kind found in
fish oil, may help prevent migraines. This diet includes plenty of
fish options that may reduce the frequency of your headaches.

# Caffeine, found in coffee, tea and colas, as well as more "hidden"
sources like chocolate and some medications including Anacin, Excedrin
and Actifed, can exacerbate headaches. This meal plan excludes foods
that are high in caffeine and suggests alternatives (like herb tea and
juices).

Start eating the breakfasts, lunches, dinners and snacks that will
help prevent head pain!

BREAKFAST
Option one:
Non-citrus juice such as apple, pear or peach
Whole grain, calcium fortified cereal topped with skim milk or soy
milk and fresh berries
Herb tea

Option two:
Scrambled eggs (purchase those high in omega-three fatty acids) or add
in some fresh cooked salmon or canned salmon and fresh herbs such as
basil or cilantro
Fresh Blueberry Muffin or toasted whole grain bread
Herb tea
Melon

Option three:
French toast recipe such as Seattle Apple French Toast (using skim
milk)
100% juice
Herb tea

LUNCH
Option one:
Vegetable cottage cheese (low fat) in whole-wheat pita with lettuce or
sprouts
Fresh fruit
Herb tea

Option two:
Homemade soup that doesn't contain prohibited foods, such as Asparagus
and Sesame Chicken Soup (substituting cider vinegar for the rice wine
vinegar)
Crusty roll
Calcium fortified juice
Salad

Option three:
Tuna salad sandwich on whole grain bread with lettuce
Baby carrots
Strawberry Sports Shake
Oatmeal Cookies

DINNER
Option one:
Pasta stir-fry, such as Linguini Honey-Sauced Prawns
Steamed broccoli
Garlic bread sticks
Fresh fruit salad

Option two:
Broiled fish, such as salmon or tuna
Baked potatoes
Sauteed zucchini
Microwave Rhubarb Crisp

Option three:
Gingered Pork and Peaches (made without the lemon juice or peel)
Mashed potatoes
Mixed green salad
Cinnamon-Scented Raspberry Rice Pudding

SNACKS

1/2 cup cottage cheese topped with canned peaches and sprinkling of
cinnamon

1/2 whole-wheat bagel with light cream cheese

Hard-boiled egg and whole-wheat crackers

Small bowl of high fiber cereal topped with skim milk or low-fat soy
milk

Soft and Chewy Molasses Cookie

Healthy Dos and Don'ts

Do:
Take ginger at the first sign of a headache (1/3 teaspoon or 500 mg).
According to the National Headache Foundation, ginger has a small
amount of antihistamine and is an anti-inflammatory

Get plenty of sleep. Although the reasons are not well understood,
studies show that sleep deprivation can cause headaches

Take a multivitamin supplement that includes the B vitamins and
antioxidants. Deficiencies of these vitamins are a possible cause of
migraines

Read all labels very carefully to avoid trigger foods

Avoid stress, which is considered a key headache trigger

DO NOT! --

Go long periods without eating or forget to drink enough fluids. Low
blood sugar or dehydration may be other dietary causes of headaches

Consume artificial flavorings and preservatives, especially MSG,
sulfites and nitrites. Most wines, many dried fruits and preserved
fruits contain sulfites. Many canned foods contain the flavor enhancer
MSG, particularly Chinese foods.Don't eat processed foods, and focus
only on all natural, fresh foods. Also avoid cured meats including
bacon, bologna, corned beef, ham, salami, sausage, hot dogs and smoked
fish due to the nitrate content

Eat foods containing artificial sweeteners, especially Aspartame,
found in diet beverages, candy or gum. Be skeptical of foods labeled
"diet" or "light"

Eat legumes and broad beans, and pods of broad beans, including lima,
navy, pinto, garbanzo, pole, fava, string and navy beans, lentils,
snow peas and pea pods

Consume hot, fresh, yeast-containing breads, including coffee cakes or
doughnuts (okay if allowed to cool and okay toasted)

Eat certain dairy products, including ripened cheeses (e.g., cheddar,
brie, camembert, gruyere), whole milk, sour cream and yogurt

Eat nuts, including peanuts, and seeds such as pumpkin or sunflower

Eat fermented, pickled or marinated foods -- no pickles, olives,
sauerkraut, chili peppers, miso, tempeh or soy sauce

Eat particular fruits -- papayas, passion fruit, figs, dates, raisins,
citrus fruits. Limit bananas to one a day. Limit tomatoes to 1/2 cup
per day

Use vinegars, except white and cider vinegar. Also avoid most mustard,
mayonnaises and ketchups

Eat food containing Brewer's yeast, large amounts of onion, chocolate
and alcohol or red wine

All content Â(c) Copyright 2003 - 2007 WorldNow and KTRK.
All Rights Reserved.
//////////////////////////////////////////////////////////

details on 6 epidemiological studies since 2004 on diet soda (mainly
aspartame) correlations, as well as 14 other mainstream studies on
aspartame toxicity since summer 2005: Murray 2007.11.21
http://groups.yahoo.com/group/aspartameNM/message/1490
http://rmforall.blogspot.com/2007_11_01_archive.htm
Wednesday, November 14, 2007

"Of course, everyone chooses, as a natural priority, to enjoy peace,
joy, and love by helping to find, quickly share, and positively act
upon evidence about healthy and safe food, drink, and environment."

Rich Murray, MA Room For All rmforall@comcast.net
505-501-2298 1943 Otowi Road, Santa Fe, New Mexico 87505

http://RMForAll.blogspot.com  new primary archive

http://groups.yahoo.com/group/aspartameNM/messages
group with 112 members, 1,493 posts in a public,
searchable archive

http://rmforall.blogspot.com/2007_09_01_archive.htm
Saturday, September 15, 2007
http://groups.yahoo.com/group/aspartameNM/message/1472
bias, omissions, incuriosity = opportunity, aspartame safety
evaluation, Magnuson BA, Burdock GA, Williams GM, 7 more, 2007 Sept,
Ajinomoto funded 98 pages  html [$ 32 781888262_content.pdf]: Murray
2007.09.15
////////////////////////////////////////////////////////////

http://groups.yahoo.com/group/aspartameNM/message/1491
industry scientists praise aspartame safety and benefits in Paris on
2006.05.30, Herve Nordmann, Andrew G. Renwick, Carlo La Vecchia, Tommy
Visscher, Jaap Seidell, France Bellisle, Adam Drewnowski, Margaret
Ashwell, Anne de la Hunty, Sigrid A. Gibson, Alan R. Boobis: Murray
2007.11.18

[ This layman review gives detailed access to the gist of six
epidemiological studies since 2004, two in 2007, that show
correlations of diet soda (largely aspartame) with health issues.

Probably studies of the correlations at the top 0.1 to 1.0 % level of
use over periods of years by people in vulnerable groups are needed.

http://groups.yahoo.com/group/aspartameNM/message/1141
Nurses Health Study can quickly reveal the extent of aspartame
(methanol, formaldehyde, formic acid) toxicity: Murray 2004.11.21

The Nurses Health Study is a bonanza of information about the health
of
probably hundreds of nurses who use 6 or more cans daily of diet soft
drinks -- they have also stored blood and tissue samples from their
immense pool of subjects, over 100,000 for decades.

In total, there are 20 mainstream studies about negative effects with
aspartame since summer, 2005, listed in this review, included many
about the detailed biochemistry involved. ]
////////////////////////////////////////////////////////////

http://RMForAll.blogspot.com September 21, 2007
http://groups.yahoo.com/group/aspartameNM/message/1475
19,000 people, the 4% of users of aspartame who drink average 5 cans
daily, have more problems in NIH AARP study of 474,000 people: Murray
2007.09.21

This is the first good data about the percentage of aspartame users
who
use over 3 cans daily, averaging 5 cans daily at 200 mg per 12 oz can
diet soda.

About 4% of 473,984 is 19,000 people, with a peak intake of 17 cans
daily, and average 5 cans daily.

It would be worthwhile to investigate a wide variety of symptoms for
the
0.1% of highest level users, about 500 people.

For about 200 million USA aspartame users, this would be 200,000
people.

Table 1 reveals consistent increase in problems from

--------------------- zero to (400 - 600) to (over 600) mg/d
aspartame intake:

% of cohert ---------- 46 -------- 5 -------- 4 %

mean aspartame mg/d --- 0 -------441 ------ 986

16+ education -------- 37 ------- 40 ------- 34 %

diabetes history ------ 3 ------- 22 ------- 26 %

alcohol g/d ---------- 14 ------- 11 ------- 13

never smoke ---------- 36 ------- 31 ------- 29 %

Body Mass Index ------ 26 ------- 29 ------- 29

18.5 - 25 ------------ 42 ------- 21 ------- 19 %

30 - 35 -------------- 13 ------- 23 ------- 26 %

over 35 --------------- 4 ------- 10 ------- 13 %

Physical activity %:

under 3-4/mo --------- 32 ------- 32 ------- 37 %

under 1-2/wk --------- 22 ------- 21 ------- 19 %

over 3-4/wk ---------- 45 ------- 45 ------- 43 %

Calories kcal ----- 1,919 ---- 1,855 ---- 2,044 %

Caffeine mg/d ------- 393 ------ 364 ------ 424

There do seem to be many increases of problems
from the second to third row, as mean aspartame use doubles.

Granted, this is cherry picking the data, selecting interesting
patterns.

Correlations alone do not prove any direction of causation.

Nevertheless, it may be of value to study the correlations for
increasing aspartame intake among the 4 % using over 600 mg, the
equivalent of 3 cans 12-oz cans diet soda daily.
The average use for this group is 5 cans daily.

For instance, are a minority of these heavy users displaying the great
majority of the problems that are reflected in the mean for each level
of use, with most users only having little or no increase in problems?

This is a group of about 20,000 people.

"We cannot exclude the possibility that higher aspartame consumption
than that observed in this study may be associated with an elevated
risk
of hematopoietic or brain cancers."

http://cebp.aacrjournals.org/cgi/content/full/15/9/1654 free full text
http://cebp.aacrjournals.org/cgi/reprint/15/9/1654 free full text pdf

Cancer Epidemiology Biomarkers & Prevention Vol. 15, 1654-1659,
September 2006
(c) 2006 American Association for Cancer Research

Consumption of Aspartame-Containing Beverages and Incidence of
Hematopoietic and Brain Malignancies

Unhee Lim 1,
Amy F. Subar 2, subara@mail.nih.gov,
Traci Mouw 1,
Patricia Hartge 1,
Lindsay M. Morton 1,
Rachael Stolzenberg-Solomon 1,
David Campbell 3,
Albert R. Hollenbeck 4
and Arthur Schatzkin 1

1 Division of Cancer Epidemiology and Genetics,

2 Division of Cancer Control and Population Sciences, National Cancer
Institute, NIH, Department of Health and Human Services;

3 Information Management Services, Inc., Rockville, Maryland; and

4 AARP, Washington, District of Columbia

Requests for reprints: Amy Subar,
Division of Cancer Control and Population Sciences,
National Cancer Institute,
6130 Executive Boulevard, EPN 4005, Rockville, MD 20852-7344.
Phone: 301-594-0831; Fax: 301-435-3710. E-mail: subara@mail.nih.gov,

BACKGROUND:
In a few animal experiments, aspartame has been linked to
hematopoietic
and brain cancers.

Most animal studies have found no increase in the risk of these or
other
cancers.

Data on humans are sparse for either cancer.

Concern lingers regarding this widely used artificial sweetener.

OBJECTIVE:
We investigated prospectively whether aspartame consumption is
associated with the risk of hematopoietic cancers or gliomas
(malignant
brain cancer).

METHODS:
We examined 285,079 men and 188,905 women ages 50 to 71 years in the
NIH-AARP Diet and Health Study cohort

Daily aspartame intake was derived from responses to a baseline
self-administered food frequency questionnaire that queried
consumption
of four aspartame-containing beverages (soda, fruit drinks, sweetened
iced tea, and aspartame added to hot coffee and tea) during the past
year.

Histologically confirmed incident cancers were identified from eight
state cancer registries.

Multivariable-adjusted relative risks (RR) and 95% confidence
intervals
(CI) were estimated using Cox proportional hazards regression that
adjusted for age, sex, ethnicity, body mass index, and history of
diabetes.

RESULTS:
During over 5 years of follow-up (1995-2000), 1,888 hematopoietic
cancers and 315 malignant gliomas were ascertained.

Higher levels of aspartame intake were not associated with the risk of
overall hematopoietic cancer
(RR for >/=600 mg/d, 0.98; 95% CI, 0.76-1.27),
glioma (RR for >/=400 mg/d, 0.73; 95% CI, 0.46-1.15;
P for inverse linear trend = 0.05),
or their subtypes in men and women.

CONCLUSIONS:
Our findings do not support the hypothesis that aspartame increases
hematopoietic or brain cancer risk. PMID: 16985027

"We cannot exclude the possibility that higher aspartame consumption
than that observed in this study may be associated with an elevated
risk
of hematopoietic or brain cancers.

In the laboratory study with positive findings, animals were fed doses
starting from 4 mg up to 5,000 mg per kg body weight.

Significantly elevated lymphomas and leukemias were observed in female
rats fed 20 mg of aspartame and higher (e.g., 1,200 mg for humans
weighing 60 kg or 132 lb; refs. 13, 14).

The reported aspartame intake in our data ranged from 0 to 3,400 mg/d
with sparse numbers in the upper intake categories
(1,200 or 2,000 mg/d, which is equivalent to ~7 to 11 cans of soft
drinks daily) compared with the lowest categories,
and the associations were similarly null in both men and women."
////////////////////////////////////////////////////////////

http://RMForAll.blogspot.com October 12, 2007
http://groups.yahoo.com/group/aspartameNM/message/1479
13,620 seniors using more than 1 can/week artificially sweetened
[aspartame] soft drinks had 8% higher death risk, 1981-2004,
Paganini-Hill A, Kawas CH, Corrada MM, U. Southern Cal., Prev. Med.
2007
April 44(4) 305-10: Murray 2007.10.12

"Individuals who drank more than 1 can/week of artificially sweetened
(but not sugar-sweetened) soft drink (cola and other) had an 8 %
increased risk (95 % CI: 1.01-1.16)."

"The increased death risk with consumption of artificially sweetened,
but not sugar-sweetened, soft drinks suggests an effect of the
sweetener
rather than other components of the soft drinks, although residual
confounding remains a possibility."

Prev Med. 2007 Apr; 44(4): 305-10. Epub 2006 Dec 29.
Non-alcoholic beverage and caffeine consumption and mortality: the
Leisure World Cohort Study.
Paganini-Hill A, annliahi@usc.edu,
Kawas CH, ckawas@uci.edu,
Corrada MM. mcorrada@uci.edu,
Department of Preventive Medicine, Keck School of Medicine of the
University of Southern California, CA, USA.

OBJECTIVE:
To examine the effects of non-alcoholic beverage and caffeine
consumption on all-cause mortality in older adults.

METHODS:
The Leisure World Cohort Study is a prospective study of residents of
a
California retirement community.

A baseline postal health survey included details on coffee, tea, milk,
soft drink, and chocolate consumption.

Participants were followed for 23 years (1981-2004).

Risk ratios (RRs) of death were calculated using Cox regression for
8644
women and 4980 men (median age at entry, 74 years) and adjusted for
age,
gender, and multiple potential confounders.

RESULTS:
Caffeine consumption exhibited a U-shaped mortality curve.

Moderate caffeine consumers had a significantly reduced risk of death
(multivariable-adjusted RR = 0.94, 95 % CI: 0.89, 0.99 for 100-199 mg/
day
and RR = 0.90, 95 % CI: 0.85, 0.94 for 200-399 mg/day
compared with those consuming <50 mg/day).

Individuals who drank more than 1 can/week of artificially sweetened
(but not sugar-sweetened) soft drink (cola and other) had an 8 %
increased risk (95 % CI: 1.01-1.16).

Neither milk nor tea had a significant effect on mortality after
multivariable adjustment.

CONCLUSIONS:
Moderate caffeine consumption appeared beneficial in reducing risk of
death.

Attenuation in the observed associations between mortality and intake
of
tea and milk with adjustment for potential confounders suggests that
such consumption identifies those with other mortality-associated
lifestyle and health risks.

The increased death risk with consumption of artificially sweetened,
but
not sugar-sweetened, soft drinks suggests an effect of the sweetener
rather than other components of the soft drinks, although residual
confounding remains a possibility. PMID: 17275898

Age Ageing. 2007 Mar; 36(2): 203-9.
Type of alcohol consumed, changes in intake over time and mortality:
the
Leisure World Cohort Study.
Paganini-Hill A, Kawas CH, Corrada MM.
Department of Preventive Medicine,
Keck School of Medicine of University of Southern California, USA.
annliahi@usc.edu

BACKGROUND:
modifiable behavioural risk factors including smoking and alcohol
consumption are major contributing or actual causes of mortality.

OBJECTIVE:
to examine the effect of alcohol intake on all-cause mortality in
older
adults.

Design and SETTING:
prospective population-based cohort study of residents of a
California,
United States retirement community.

SUBJECTS:
8,877 women and 5,101 men (median age, 74 years) who in the early
1980s
completed a postal health survey incluing details on alcohol
consumption.

METHODS:
participants were followed for 23 years (1981-2004) including two
follow-up questionnaires (in 1992 and 1998) asking about current
alcohol
intake.

Age-adjusted and multivariate-adjusted risk ratios of death and 95 %
confidence intervals were calculated separately for men and women,
using
proportional hazard regression.

RESULTS:
of the 8,644 women and 4,980 men with complete information on the
variables of interest and potential confounders,
6,930 women and 4,456 men had died (median age, 87 years).

Both men and women who drank alcohol had decreased mortality compared
with non-drinkers.

Those who drank two or more drinks per day had a 15 % reduced risk of
death.

The reduced risk was not limited to one type of alcohol.

Stable drinkers (those who reported drinking both at baseline and
follow-up) had a significantly decreased risk of death compared with
stable non-drinkers.

Those who started drinking at follow-up also had a significantly lower
risk.

Women who quit drinking were at increased risk of death.

CONCLUSION:
in elderly men and women, moderate alcohol intake exhibits a
beneficial
effect on mortality.

Those who quit may do so for health reasons that affect mortality.
PMID: 17350977
////////////////////////////////////////////////////////////

" Analyses that used food frequency questionnaire data suggested that
intake of over 1 drink per day of either regular or diet soft drinks
was
associated with a over 50% higher incidence of metabolic syndrome
compared with intake of under 1 soft drink per week.

" Although the association of high fructose corn syrup intake and
insulin resistance may be a contributory mechanism, 31 in the present
study, both regular and diet soft drinks appeared to pose similar
metabolic hazards,
which suggests that other factors may be operational. "

" The caramel content of both regular and diet drinks may be a
potential
source of advanced glycation end products, 5 which may promote insulin
resistance 36 and can be proinflammatory. 37 "

" It is conceivable, though,
that there may be residual confounding caused by lifestyle factors not
adjusted for in the present analyses. "

" As noted above, it is conceivable that residual confounding by
lifestyle/dietary factors not adjusted for may have contributed to the
metabolic risks associated with soft drink intake. "

" The similar metabolic hazard posed by both regular and diet soft
drinks is noteworthy given the lack of calories in the latter;
however, other studies have also reported associations of diet soft
drinks with weight gain in boys 29 and with hypertension in adult
women. 7 "

29. Berkey CS, Rockett HRH, Field AE, Gillman MW, Colditz GA.
Sugar-added beverages and adolescent weight change.
Obesity Res. 2004; 12: 778-788.[Abstract/Free Full Text]

7. Winkelmayer WC, Stampfer MJ, Willett WC, Curhan GC.
Habitual caffeine intake and the risk of hypertension in women.
JAMA. 2005; 294: 2330-2335.[Abstract/Free Full Text]

http://circ.ahajournals.org/cgi/content/full/116/5/480 free full text
[ Extracts ]

doi:10.1161/CIRCULATIONAHA.107.689935
CLINICAL PERSPECTIVE
Circulation. 2007; 116: 480-488.
(c) 2007 American Heart Association, Inc.
Epidemiology

Circulation. 2007 Jul 31; 116(5): 480-8. Epub 2007 Jul 23.
Soft drink consumption and risk of developing cardiometabolic risk
factors and the metabolic syndrome in middle-aged adults in the
community.
Ravi Dhingra, MD;
Lisa Sullivan, PhD;
Paul F. Jacques, PhD;
Thomas J. Wang, MD;
Caroline S. Fox, MD;  foxca@nhlbi.nih.gov,
James B. Meigs, MD, MPH;
Ralph B. D'Agostino, PhD;
J. Michael Gaziano, MD, MPH;
Ramachandran S. Vasan, MD  vasan@bu.edu,

From the National Heart, Lung, and Blood Institute's Framingham Heart
Study (R.D., T.J.W., C.S.F., R.S.V.), Framingham, Mass;

Massachusetts Veterans Epidemiology Research and Information Center
(R.D., J.M.G.), VA Boston Healthcare System, Boston, Mass;

Division of Aging (R.D., J.M.G.), Brigham and Women's Hospital,
Harvard
Medical School, Boston, Mass; Alice Peck Day Memorial Hospital (R.D.),
Lebanon, NH;

Department of Biostatistics (L.S., R.B.D.), Boston University School
of
Public Health, Boston, Mass;

Jean Mayer USDA Human Nutrition Research Center on Aging (P.F.J.),
Tufts
University, Boston, Mass; Division of Cardiology (T.J.W.) and
Department
of Medicine (J.B.M.), Massachusetts General Hospital, Harvard Medical
School, Boston, Mass;

National Heart, Lung, and Blood Institute (C.S.F.), Bethesda, Md;
Divisions of Preventive Medicine and Cardiovascular Medicine (J.M.G.),
Brigham and Women's Hospital, Boston, Mass;

and Cardiology Section and the Department of Preventive Medicine and
Epidemiology (R.S.V.), Boston University School of Medicine, Boston,
Mass.

Correspondence to Ramachandran S. Vasan, MD, Framingham Heart Study,
73
Mount Wayte Ave, Suite 2, Framingham, MA 01702-5803.  vasan@bu.edu,

Received January 12, 2007; accepted May 15, 2007.

BACKGROUND:
Consumption of soft drinks has been linked to obesity in children and
adolescents, but it is unclear whether it increases metabolic risk in
middle-aged individuals.

METHODS AND RESULTS:
We related the incidence of metabolic syndrome and its components to
soft drink consumption in participants in the Framingham Heart Study
(6,039 person-observations, 3,470 in women; mean age 52.9 years) who
were free of baseline metabolic syndrome.

Metabolic syndrome was defined as the presence of over of the
following:

waist circumference over 35 inches (women) or over 40 inches (men);
fasting blood glucose over 100 mg/dL;
serum triglycerides over 150 mg/dL;
blood pressure over 135/85 mm Hg;
and high-density lipoprotein cholesterol under 40 mg/dL (men)
or under 50 mg/dL (women).

Multivariable models included adjustments for age, sex, physical
activity, smoking, dietary intake of saturated fat, trans fat, fiber,
magnesium, total calories, and glycemic index.

Cross-sectionally, individuals consuming over 1 soft drink per day had
a
higher prevalence of metabolic syndrome
(odds ratio [OR], 1.48; 95 % CI, 1.30 to 1.69)
than those consuming under 1 drink per day.

On follow-up (mean of 4 years), new-onset metabolic syndrome developed
in 765 (18.7 %) of 4095 participants consuming under 1 drink per day
and
in 474 (22.6 %) of 2059 persons consuming over 1 soft drink per day.

Consumption of over 1 soft drink per day
was associated with increased odds of developing
metabolic syndrome (OR, 1.44; 95% CI, 1.20 to 1.74),
obesity (OR, 1.31; 95 % CI, 1.02 to 1.68),
increased waist circumference (OR, 1.30; 95 % CI, 1.09 to 1.56),
impaired fasting glucose (OR, 1.25; 95% CI, 1.05 to 1.48),
higher blood pressure (OR, 1.18; 95 % CI, 0.96 to 1.44),
hypertriglyceridemia (OR, 1.25; 95 % CI, 1.04 to 1.51), and
low high-density lipoprotein cholesterol
(OR, 1.32; 95 % CI 1.06 to 1.64).

CONCLUSIONS:
In middle-aged adults, soft drink consumption is associated with a
higher prevalence and incidence of multiple metabolic risk factors.
PMID: 17646581

Key Words: diabetes mellitus * metabolic syndrome * epidemiology *
obesity * risk factors * carbonated beverages

*        Introduction

Several reports from the United States and Europe indicate increasing
consumption of soft drinks among children, adolescents, and adults
over
the past 3 decades. 1,2

Many clinical studies have linked the rising consumption of soft
drinks
to the present epidemic of obesity and diabetes mellitus among
children
and adolescents 3-6 and to the development of hypertension in adults.
7

Furthermore, added sweeteners in soft drinks have been linked to an
increase in serum triglycerides levels in some reports 8,9 but not in
others. 10,11

The association of soft drink consumption with obesity and higher
insulin resistance has been attributed to multiple factors, including
greater caloric intake, the high fructose corn syrup content, 12 less
satiety and compensation, and a general effect of consuming refined
carbohydrates (see review by Drewnowski and Bellisle 13).

The aforementioned data raise the possibility that the consumption of
soft drinks can fuel metabolic derangements, including insulin
resistance, that can translate into a greater risk of developing
abdominal obesity, high triglyceride levels, low levels of high-
density
lipoprotein cholesterol (HDL-C), elevated blood pressure, and impaired
glucose tolerance; this constellation of metabolic traits has been
collectively referred to as the metabolic syndrome. 14

Higher prevalence of the metabolic syndrome poses greater risk for
cardiovascular disease in the community, 15 although the independent
contribution of this entity to vascular risk beyond its components has
been questioned 16

In the present prospective investigation, we tested the hypothesis
that
greater soft drink consumption increases the risk of developing
metabolic risk factors (alone and in combination [metabolic syndrome])
in middle-aged adults in the community.

Additionally, we evaluated whether metabolic risk varied on the basis
of
consumption of sugar-sweetened ("regular") versus artificially
sweetened
("diet") soft drinks.

*        Methods

Study Sample

The Framingham Heart Study began in 1948 with the enrollment of 5,209
participants into the original study cohort. 17

In 1971, children of the original cohort participants and the spouses
of
the children were enrolled into the Framingham Offspring Study
(n=5,124). 18

Offspring study participants are evaluated approximately every 4
years.

Information on daily consumption of soft drinks was collected via a
physician-administered questionnaire at each study visit from the
fourth
(1987-1991) through the sixth (1995-1998) examination cycles.

That examination questionnaire did not elicit information regarding
consumption of regular versus diet soft drinks; however, such
information was available from the self-administered food frequency
questionnaires (FFQ; Willett questionnaire) 19 completed by
participants
at the fifth (1992-1995) and sixth examination cycles (see below).

For the present investigation, we selected offspring cohort
participants
who attended any 2 consecutive examinations from the fourth through
the
seventh (1998-2001) examination cycles.

We excluded participants with missing data on covariates (n = 207) and
those with prevalent cardiovascular disease (n = 926).

After exclusions, a total of 8997 person-observations (4871 in women)
were eligible for the cross-sectional analyses.

For prospective analyses, we excluded individuals with baseline
metabolic syndrome (n = 2897 person-observations; metabolic syndrome
as
defined below) and those with any missing metabolic syndrome
components
on follow-up (n = 61 person-observations).

The schema for selection of individuals eligible for cross-sectional
and
longitudinal analyses is displayed in the Figure.

All participants provided written informed consent, and the protocol
for
the study was approved by institutional review board of Boston Medical
Center.

Figure 1185095

     Selection of study sample from baseline examinations using the
examination cola questionnaire and from the sample with available FFQ
data (within parentheses, for examinations 5 and 6).
Eligible participants and exclusions are indicated in the Figure.
CVD indicates cardiovascular disease.

Measurement of Covariates

At each Framingham Heart Study examination, participants provided a
medical history and underwent a complete standardized physical
examination that included anthropometry, blood pressure measurements,
and laboratory assessment of vascular risk factors.

Fasting levels of blood glucose, triglycerides, and HDL-C were
measured
with standard assays.

Blood pressure was measured by a physician using a mercury
sphygmomanometer and with the participant resting in a seated position
for 5 minutes; the average of 2 readings obtained on the participant's
left arm constituted the examination blood pressure.

Physical activity was assessed by calculating a "physical activity
index"; participants were asked specific questions regarding how many
hours in a typical day they spent sitting, sleeping, or performing
light-moderate or heavy physical activities. 20

Alcohol intake was assessed by averaging the number of alcoholic
beverages consumed per week.

Participants who reported smoking 1 or more cigarettes per day in the
year before the Framingham Heart Study examination were considered
current smokers.

Assessment of Soft Drink Consumption and Dietary Intake of Other Foods

At the index examinations, participants reported the average number of
12-oz servings of soft drinks (Coke, Pepsi, Sprite, or other
carbonated
soft drinks, separately categorized into caffeinated or decaffeinated
drinks) consumed per day in the year preceding the examination.

The responses to the questions were entered as integers (0 or more)
separately for caffeinated and decaffeinated soft drinks.

This questionnaire (referred to as the "examination cola
questionnaire")
did not separate nondrinkers from infrequent drinkers (<1 drink per
day).

Accordingly, we compared individuals who reported consuming 1, over 1,
or over 2 soft drinks per day with attendees who reported consuming
under 1 soft drink per day (infrequent drinkers and nondrinkers, who
served as the referent).

Intake of regular and diet soft drinks was assessed from FFQs 19 that
were administered at the fifth and sixth examinations.

We also assessed the dietary information on consumption of total
calories, saturated fat, trans fat, fiber, magnesium, and glycemic
index
from the FFQ. 19

Because a FFQ was not administered at the fourth examination cycle,
dietary covariate data from the fifth examination cycle were used for
analyses using information from the examination cola questionnaire at
all 3 examinations.

Data from the FFQ were considered valid only if total energy intakes
reported were over 2.51 MJ/d (600 kcal/d) for men and women but under
17.54 MJ/d (4200 kcal/d) for men or under 16.74 MJ/d (4000 kcal/d) for
women and if fewer than 13 food items were left blank.

Each food item was categorized in 9 categories that ranged from never
or
under 1 serving per month to over 6 servings per day.

For assessment of saturated fat, trans fat, or dietary fiber, the
nutrient intakes from all specific food items were multiplied by the
frequency of consumption.

The validity of the FFQ has been demonstrated previously. 21

Definition and Components of the Metabolic Syndrome

The metabolic syndrome was considered present if 3 or more of the
following individual components were present 14,22:
waist circumference over 35 inches (88 cm) for
or over 40 inches (102 cm) for men;
fasting blood sugar over 100 mg/dL (5.5 mmol/L) or treatment with oral
hypoglycemic agents or insulin;
blood pressure over 135/85 mm Hg or treatment for hypertension;
serum triglycerides over 150 mg/dL (1.7 mmol/L)
or treatment for hypertriglyceridemia (with niacin or fibrates);
and HDL-C under 40 mg/dL (1.03 mmol/L) in men
or under 50 mg/dL (1.3 mmol/L) in women.

Statistical Analyses

Age- and sex-adjusted baseline characteristics of the participant
groups
defined according to the number of soft drinks consumed in 1 day
(under 1, 1, or over 2 per day) were compared by multiple linear and
multiple logistic regression analysis for continuous and categorical
characteristics, respectively.
Data on consumption of soft drinks at each of the 3 eligible baseline
examinations (examination cola questionnaire) were used for this
purpose.
Tests for trend in baseline characteristics across soft drink
consumption categories were performed with multiple regression.
We also assessed the baseline characteristics after excluding
participants with prevalent metabolic syndrome at baseline
examinations (sample used for incidence analyses; see below).

Soft Drink Consumption and Prevalence of the Metabolic Syndrome

We used data from examinations 4, 5, and 6 (examination cola
questionnaire) and generalized estimating equations to compare the
prevalence of metabolic syndrome in participants who consumed over 1
soft drink per day with those who consumed under 1 soft drink per day
(referent).
Each participant could contribute up to 3 person-examinations of data
for analysis.
We also evaluated a dose response by comparing individuals
who consumed 1 soft drink per day and those who consumed over 2 soft
drinks per day with the referent group.
We constructed multivariable models in hierarchical fashion with
adjustment for age and sex (model I)
and for age, sex, physical activity index, smoking, dietary
consumption of saturated fat, trans fat, fiber, magnesium, total
calories, and glycemic index (model II).

We used soft drink consumption data from FFQs at examinations 5 and 6,
which yielded a smaller sample (Figure), to relate the prevalence of
metabolic syndrome across the following categories of intake of
regular
versus diet soft drinks using generalized estimating equations:
(1) under 1 diet or regular soft drink per week (referent),
(2) 1 to 6 diet soft drinks per week,
(3) over 1 diet soft drink per day,
(4) 1 to 6 regular soft drinks per week,
(5) 1 to 6 regular or diet soft drinks per week,
and (6) over 1 regular soft drink per day.
Individuals reporting consumption of both diet and regular soft drinks
over 1/d (n = 16) were grouped into the last category empirically.
We evaluated the 2 sets of models (I and II) noted above.

Soft Drink Consumption and Incidence of the Metabolic Syndrome

To assess the relations of soft drink consumption to the incidence of
metabolic syndrome, we excluded participants with prevalent metabolic
syndrome at each of examination cycles 4, 5, and 6 (n = 2,897
person-observations).
Then, we used pooled logistic regression analyses
by combining each 4-year follow-up period of observations to relate
the
number of soft drinks consumed per day (examination cola
questionnaire)
to the incidence of metabolic syndrome (from examination cycles 4 to
5,
5 to 6, and 6 to 7).23
The eligible participants were free of metabolic syndrome
at each baseline examination,
and in this setting, pooled logistic regression has been shown to
provide risk estimates similar to time-dependent Cox models.24
We compared the consumption of soft drinks  over 1 per day with
infrequent drinkers (under 1 per day; referent) and also
tested for a dose response by comparing groups consuming 1 and over 2
soft drinks per day with the referent group.
We evaluated 2 sets of models
(covariates as in models I and II above),
which paralleled the analyses of prevalence of metabolic syndrome.

Consumption of soft drinks varies with age and by sex.25
It has also been suggested that the effects of soft drinks and
carbohydrates on  metabolic traits may vary according to age, sex,26
and baseline body  weight.27
Therefore, we assessed for effect modification by age (modeled
as a continuous variable), sex, and body mass index
(under 30 versus over 30 kg/m2) by incorporating appropriate
interaction terms in the multivariable models.
We repeated analyses with additionally adjustment
for alcohol consumption and baseline levels of systolic and diastolic
blood pressure, blood glucose, serum triglycerides, and HDL-C.
These models were constructed to account for baseline levels of
metabolic traits.
Additionally, we repeated analyses to examine the association
between consumption of caffeinated and decaffeinated soft drinks,
considered separately, and incidence of the metabolic syndrome.
Because individuals with diabetes mellitus are a particularly high-
risk group for developing metabolic abnormalities, we also repeated
our analyses after excluding those with prevalent diabetes mellitus at
baseline.

To compare the risk of new-onset metabolic syndrome according to the
type of soft drink consumed (regular versus diet),
we used data from the FFQs at examinations 5 and 6
and evaluated the incidence of the metabolic syndrome across
categories of soft drinks consumed.
The 6 categories of regular and diet soft drinks were those noted
above (for the analyses of the prevalence of metabolic syndrome),
and 2 sets of models were evaluated
(models I and II, as described above).

Incidence of Individual Components of Metabolic Syndrome

We used multivariable logistic regression to evaluate the relations of
soft drink consumption to the incidence of each individual component
of
metabolic syndrome using data from the examination cola questionnaire.
We excluded participants who had the specific metabolic trait
prevalent
at baseline; for example, we excluded individuals with blood glucose
over 100 mg/dL (5.5 mmol/L) from the "at-risk" group for analysis that
examined the incidence of impaired fasting glucose.
Thus, we examined the incidence of increased waist circumference,
impaired fasting glucose, high blood pressure, hypertriglyceridemia,
and low HDL-C (all defined as above) according to the number of soft
drinks consumed per day.

We evaluated 2 sets of models (I and II, as noted above) and compared
the risk of developing metabolic traits associated with consumption of
over 1 soft drinks per day
with that in infrequent drinkers (under 1 soft drinks per day).
We also evaluated for a dose response as detailed above.
We did not perform analyses of development of individual metabolic
syndrome components in relation to regular versus diet soft drink
intake using the FFQ data at examinations 5 and 6 because the grouping
of incident events into 6 categories resulted in modest numbers of
events in each category.

All analyses were performed with SAS software version 9.0 (SAS
Institute, Cary, NC). A 2-sided probability value of under 0.05 was
considered statistically significant.

The authors had full access to and take full responsibility for the
integrity of the data. All authors have read and agree to the
manuscript
as written.

Results

The baseline characteristics of participants according to the
categories
of soft drinks consumed per day are presented in Table 1.

Approximately 35 % of the participants reported consuming over 1 soft
drink per day in response to the examination cola questionnaire
(data based on all 3 examinations).

In comparison, only 22 % of participants reported intake of at least 1
soft drink (diet or regular) per day in response to the FFQ (data
available for examinations 5 and 6 only).

The lower proportion reporting daily intake on the FFQ may be related
to
the greater number of options available to indicate soft drink intake;
participants drinking 1 to 6 soft drinks per week (also 22 % on the
FFQ)
may have rounded their responses on the examination cola questionnaire
to the nearest integer.

View this table:

     TABLE 1. Baseline Characteristics of Participants According to
Soft Drink Consumption (n = 8997)

In age- and sex-adjusted models, the prevalence of obesity (assessed
both by body mass index and by waist circumference), high blood
pressure, glucose intolerance, low HDL-C, and hypertriglyceridemia was
significantly higher in those who consumed a greater number of soft
drinks per day.

Serum total cholesterol, low-density lipoprotein cholesterol, physical
activity index, and alcohol consumption did not vary across categories
of soft drinks consumed.

Similar trends were obtained when we excluded individuals with
prevalent
metabolic syndrome (Data Supplement, Table I).

Prevalence of the Metabolic Syndrome

There was a 48 % higher adjusted prevalence of metabolic syndrome
among
those who consumed 1 or more soft drinks per day relative to
individuals
with infrequent soft drink consumption (Table 2).

We observed a rising prevalence of metabolic syndrome across
categories
of 1 and over 2 soft drinks per day

In parallel analyses with the data from the FFQ (Table 2),
participants
who consumed over 1 diet or regular soft drink per day had nearly a
1.8-fold adjusted prevalence of metabolic syndrome compared with
infrequent drinkers (under 1 per week).

TABLE 2. Cross-Sectional Relationships of Soft Drink Consumption With
Prevalence of Metabolic Syndrome

Incidence of the Metabolic Syndrome

Individuals who consumed at least 1 soft drink per day had a 44 %
higher
adjusted risk (95 % CI, 20 % to 74 %) of developing metabolic syndrome
compared with infrequent drinkers in multivariable-adjusted analyses
(Table 3).

There was no effect modification by age, body mass index, or sex
(interaction terms were not statistically significant).

After additional adjustment for baseline levels of covariates (blood
sugar, systolic and diastolic blood pressure, triglycerides, and HDL-
C)
and alcohol consumption in our models, the association of consumption
of
over 1 soft drink per day with incidence of metabolic syndrome
remained
robust (odds ratio [OR], 1.44; 95 % CI, 1.19 to 1.74).

Further exclusion of individuals with diabetes mellitus at baseline (n
=
138) attenuated the association (OR for over 1 soft drink per day,
1.16;
95% CI 1.00 to 1.34).

After stratification of analyses by caffeinated versus decaffeinated
drinks, results were consistent with the primary analyses; consumption
of over 1 soft drink per day was associated with incident metabolic
syndrome for both types of beverages (Data Supplement, Table II).

TABLE 3. Multiple Logistic Regression Examining Soft Drink Consumption
and Incidence of Metabolic Syndrome (n = 6154)

In analyses with FFQ data (Table 3), intake of at least 1 regular or
diet soft drink per day was associated with a over 50 % higher
incidence
of metabolic syndrome than among those who drank under 1 soft drink
per
week, although the association was borderline significant for intake
of
over 1 regular soft drink per day ( P = 0.07 ).

We also observed a graded increase in the risk of metabolic syndrome
from those who were consuming 1 to 6 diet or regular soft drinks per
week to those who drank over 1 soft drinks per day (diet or regular).

Incidence of Individual Components of the Metabolic Syndrome

Compared with infrequent drinkers, individuals who consumed over 1
soft
drink per day had a 25 % to 32 % higher adjusted risk of incidence of
each individual metabolic trait (Table 4), with the exception of
development of high blood pressure, for which there was a borderline
significant 18 % higher adjusted odds ( P = 0.10).

TABLE 4. Multiple Logistic Regression Analysis Examining the Relations
of Incidence of Individual Components of Metabolic Syndrome According
to
Soft Drink Consumption (Data From All 3 Examinations [4, 5, and 6])

Discussion

In the present study, we observed a significantly higher prevalence of
metabolic syndrome among middle-aged adults who consumed over 1 soft
drink per day.

This association was consistent for intake of both regular and diet
soft
drinks.

Our prospective analyses corroborated the cross-sectional findings;
we observed an increase in the incidence of metabolic syndrome among
adults consuming at least 1 soft drink per day, regardless of whether
it was of the regular or diet type.

Additionally, consumption of soft drinks daily was associated with a
higher incidence of each metabolic syndrome component.

The present study extends results from prior studies that reported
that
a greater intake of soft drinks is associated with increased
prevalence
of metabolic syndrome, 28 higher risk of obesity, 4-6 high blood
pressure, 7 and diabetes mellitus. 5

The similar metabolic hazard posed by both regular and diet soft
drinks
is noteworthy given the lack of calories in the latter; however, other
studies have also reported associations of diet soft drinks with
weight
gain in boys 29 and with hypertension in adult women. 7

Mechanisms

There are several mechanisms that can explain the higher risk of
metabolic abnormalities associated with greater consumption of soft
drinks.

These can be broadly grouped under physiological effects, dietary
behavior, and the economics of food choice. 13

There are several physiological effects of soft drinks that may pose
an
adverse metabolic risk.

Larger consumption of added nutritive sweeteners such as high fructose
corn syrup (the primary sweetener in soft drinks) can lead to weight
gain, increased insulin resistance, 30,31 a lowering of HDL-C, 32 and
an
increase in triglyceride levels. 27

Typically, in the United States, the high fructose corn syrup added to
the beverages contains about 55 % fructose. 30,31

Although the association of high fructose corn syrup intake and
insulin
resistance may be a contributory mechanism, 31 in the present study,
both regular and diet soft drinks appeared to pose similar metabolic
hazards, which suggests that other factors may be operational.

Consumption of liquids is associated with a lesser degree of dietary
compensation (the adjustment in energy intake made in subsequent meals
in response to food intake).

Some investigators believe that intake of sugar-sweetened beverages
induces less compensation than intake of artificially sweetened soft
drinks, 33 but others disagree. 34

The high sweetness of diet or regular soft drinks may lead to
conditioning for a greater preference for intake of sweetened items,
35
although this explanation also has been questioned by some experts. 13

The caramel content of both regular and diet drinks may be a potential
source of advanced glycation end products, 5 which may promote insulin
resistance 36 and can be proinflammatory. 37

Dietary behavior among individuals consuming soft drinks may account
in
part for the clustering of metabolic risk factors in these people. 13

Individuals with greater intake of soft drinks also have a dietary
pattern characterized by greater intake of calories and saturated and
trans fats, lower consumption of fiber 38 and dairy products, 39 and a
sedentary life. 40

These observations were corroborated by the our findings of increased
consumption of saturated and trans fat, lower consumption of dietary
fiber, and higher rates of smoking in those with greater intake of
soft
drinks.

Nonetheless, in the present investigation, we adjusted for saturated
fat
and trans fat intake, dietary fiber consumption, smoking, and physical
activity in multivariable analyses and still observed a significant
association of soft drink consumption with the risk of developing
metabolic syndrome and its component traits.

It is conceivable, though, that there may be residual confounding
caused
by lifestyle factors not adjusted for in the present analyses.

Last, it has been suggested that the obesity-promoting effects of soft
drinks may be related in part to their costs, with less expensive
drinks
being associated with greater hazard by virtue of their preferential
selection for economic reasons. 13

The present investigation could not explore this explanation.

Strengths and Limitations

The strengths of the present study include the large community-based
sample of men and women and the adjustments for potential confounders;
however, several limitations merit comment.

We chose to use the modified definition of metabolic syndrome
recommended by the National Cholesterol Education Program 14 and did
not
use other criteria for the syndrome (such as those suggested by the
World Health Organization 41 or the European panel).

Researchers have found high correlation between these guidelines. 42

Given the observational nature of the present study, we cannot infer
that the observed associations are causal.

As noted above, it is conceivable that residual confounding by
lifestyle/dietary factors not adjusted for may have contributed to the
metabolic risks associated with soft drink intake.

Finally, participants in the present study were all white Americans,
which may limit the generalizability of our results to nonwhites.

Conclusions

In our large community-based sample of middle-aged adults, soft drink
consumption was associated with higher risk of developing adverse
metabolic traits and the metabolic syndrome.

The present observational data raise the possibility that public
health
policy measures to limit the rising consumption of soft drinks in the
community may be associated with a lowering of the burden of metabolic
risk factors in adults.

Acknowledgments

Sources of Funding

This work was supported through National Institutes of Health/National
Heart, Lung, and Blood Institute contracts N01-HC-25195, 1R01HL67288,
and 2K24HL04334 (Dr Vasan) and K23HL74077 (Dr Wang) and by a career
development award from the American Diabetes Association (Dr Meigs).

Disclosures

None.

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p 488 CLINICAL PERSPECTIVE

Consumption of soft drinks among children, adolescents, and middle-
aged
adults has risen in the United States and Europe during the past 3
decades.

Prior studies have shown a higher prevalence of obesity and diabetes
mellitus in children who consume more soft drinks, although these
associations are less clear for adults.

We evaluated the relations of metabolic syndrome and its components to
soft drink consumption in Framingham participants.

Cross-sectionally, individuals consuming at least 1 soft drink per day
had about 50 % higher prevalence of the metabolic syndrome than those
consuming under 1 drink per day.

During a follow-up period of about 4 years, consumption of over 1 soft
drink per day was associated with a higher incidence of metabolic
syndrome and a higher incidence of each of its components, ie,
obesity,
increased waist circumference, impaired fasting glucose, higher blood
pressure, hypertriglyceridemia, and low high-density lipoprotein
cholesterol.

Analyses that used food frequency questionnaire data suggested that
intake of over 1 drink per day of either regular or diet soft drinks
was
associated with a over 50% higher incidence of metabolic syndrome
compared with intake of under 1 soft drink per week.

We conclude that consumption of more than 1 soft drink per day is
associated with a higher prevalence and incidence of multiple
metabolic
risk factors in middle-aged adults.

Our observational data raise the possibility that public health
measures
to limit consumption of soft drinks may be associated with a lowering
of
the burden of cardiometabolic risk factors in adults.

Footnotes

The online-only Data Supplement, consisting of tables, is available
with
this article at
http://circ.ahajournals.org/cgi/content/full/CIRCULATIONAHA.107.689935/DC1.

Guest Editor for this article was Gregory L. Burke, MD, MSc.

[ Dr. Gregory L. Burke is Professor and Chair of the Department of
Public Health Sciences at the Wake Forest University School of
Medicine. His research interests include epidemiology and
cardiovascular disease, atherosclerosis and subclinical CVD,
measurement issues in epidemiology, clinical trials of chronic disease
prevention, women's health, translation of scientific data for
physicians and the general public, and alternative strategies for
chronic disease prevention. Dr. Burke received his M.D. from the
University of Iowa in 1981.

Departments of Public Health Sciences, Pathology, and Obstetrics and
Gynecology, Wake Forest University School of Medicine,
and Lyndhurst Gynecology Associates, Winston-Salem, NC 27157, USA.
gburke@wfubmc.edu, ]

Find additional patient-related information at:
http://www.americanheart.org/presenter.jhtml?identifier=3050553

Related Article:
Issue Highlights
Circulation 2007 116: 457. [Full Text]

Related Internet Resources:
   Podcast
   Press Release
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////////////////////////////////////////////////////////////

" When studying individual classes of caffeinated beverages, habitual
coffee consumption was not associated with increased risk of
hypertension.

By contrast, consumption of cola beverages was associated with an
increased risk of hypertension, independent of whether it was sugared
or
diet cola (P for trend <.001).

Conclusion
No linear association between caffeine consumption and incident
hypertension was found.

Even though habitual coffee consumption was not associated with an
increased risk of hypertension, consumption of sugared or diet cola
was
associated with it.

Further research to elucidate the role of cola beverages in
hypertension
is warranted. "

" The findings were consistent between the cohorts and were present
across types of soda beverages:
both sugared cola and diet cola beverages were associated with an
increased risk of hypertension (Table 5 and Table 6).

Hence, we speculate that it is not caffeine but perhaps some other
compound contained in soda-type soft drinks that may be responsible
for
the increased risk in hypertension.

If these associations are causal, they may have considerable impact on
public health. "

" Finally, an examination of the possible associations between
caffeinated cola beverages and the risk of hypertension
showed that
sugared caffeinated cola (NHS I, P for trend = .03; NHS II, P for
trend <.001) (Table 5)
and diet caffeinated cola (NHS I, P for trend = .02; NHS II, P  for
trend <.001) (Table 6)
were positively associated with hypertension in both cohorts. "

" Table 6. Age-Adjusted and Multivariate Relative Risks for Incident
Hypertension According to Frequency of Diet Cola Intake

Glasses or Cans of Diet Cola per Day
under 1 ------- 1 ----------- 2-3 ------- 4 and more --- P for Trend


Nurses' Health Study I (1990-2002) 53,175 nurses, ages 44-69 in 1990

No. of cases of Incident Hypertension
17,268 ------- 1,154 ---------- 662 --------- 130
% 100 ---------- 6.7 ---------- 3.8 -------- 0.75
#% 32.5 -------- 2.2 ---------- 1.3 -------- 0.25 #% of 53,175

Person-years
479,890 ----- 30,579 --------17,316 ------- 3,173
% 100 -----------6.4 ---------- 3.6 -------- 0.66

Age-adjusted relative risk (95% CI)
1.00 -- 1.16(1.10-1.24)-- 1.23(1.13-1.33)-- 1.37(1.15-1.62)-- under .
001

Multivariate relative risk (95% CI)*
1.00 -- 1.07(1.00-1.13) -- 1.06(0.98-1.15) -- 1.16(0.97-1.37)------ .
02

Nurses' Health Study II (1991-2003) 87,369 nurses, ages 27-44 in 1991


No. of cases of Incident Hypertension
10,192 -------- 1,452 -------- 1,358 --------- 449
% 100 ---------- 14.3 ----------- 13.3 --------- 4.4
#% 11.7 --------- 1.7 ------------ 1.6 --------- 0.51 #% of 87,369

Person-years
713,971 ----- 91,144 ------- 77,398 ------- 21,265
% 100 --------- 12.8 --------- 10.8 ---------- 3.0

Age-adjusted relative risk (95% CI)
1.00 -- 1.16(1.10-1.23) -- 1.33(1.26-1.41) -- 1.63(1.49-1.80) under .
001

Multivariate relative risk (95% CI)*
1.00 -- 1.05(0.99-1.11) -- 1.09(1.03-1.15) -- 1.19(1.08-1.32) under .
001

Abbreviation: CI, confidence interval.
*Adjusted for age, body mass index, intake of alcohol, family history
of
hypertension, oral contraceptive use (in Nurses'Health Study II only),
physical activity, and smoking status, as well as the other classes of
beverage. "

http://jama.ama-assn.org/cgi/reprint/294/18/2330?ijkey=ff7fa86b688f2c2e23d9b6185
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JAMA Vol. 294 No. 18, November 9, 2005

Online Features
Original Contribution

Habitual Caffeine Intake and the Risk of Hypertension in Women
Wolfgang C. Winkelmayer, MD, ScD;  wwinkelmayer@partners.org,
Meir J. Stampfer, MD, DrPH;  stampfer@hsph.harvard.edu,
Walter C. Willett, MD, DrPH;  walter.willett@channing.harvard.edu,
Gary C. Curhan, MD, ScD  gary.curhan@channing.harvard.edu,
JAMA. 2005; 294: 2330-2335.

Context
Caffeine acutely increases blood pressure, but the association between
habitual consumption of caffeinated beverages and incident
hypertension
is uncertain.

Objective
To examine the association between caffeine intake and incident
hypertension in women.

Design, Setting, and Participants
Prospective cohort study conducted in the Nurses' Health Studies
(NHSs) I and II of 155,594 US women free from physician-diagnosed
hypertension followed up over 12 years
(1990-1991 to 2002-2003 questionnaires).

Caffeine intake and possible confounders were ascertained from
regularly
administered questionnaires.

We also tested the associations with types of caffeinated beverages.

Main Outcome Measure
Incident physician-diagnosed hypertension.

Results
During follow-up, 19.541 incident cases of physician-diagnosed
hypertension were reported in NHS I and 13,536 in NHS II.

In both cohorts, no linear association between caffeine consumption
and
risk of incident hypertension was observed after multivariate
adjustment
(NHS I, P for trend = .29; NHS II, P for trend = .53).

Using categorical analysis, an inverse U-shaped association between
caffeine consumption and incident hypertension was found.

Compared with participants in the lowest quintile of caffeine
consumption, those in the third quintile had a 13 % and 12 % increased
risk of hypertension, respectively (95 % confidence interval in NHS I,
8
% - 18 %; in NHS II, 6 % - 18 %).

When studying individual classes of caffeinated beverages, habitual
coffee consumption was not associated with increased risk of
hypertension.

By contrast, consumption of cola beverages was associated with an
increased risk of hypertension, independent of whether it was sugared
or
diet cola (P for trend <.001).

Conclusion
No linear association between caffeine consumption and incident
hypertension was found.

Even though habitual coffee consumption was not associated with an
increased risk of hypertension, consumption of sugared or diet cola
was
associated with it.

Further research to elucidate the role of cola beverages in
hypertension
is warranted.

Author Affiliations:
Division of Pharmacoepidemiology and Pharmacoeconomics (Dr
Winkelmayer),
Renal Division (Drs Winkelmayer and Curhan),
and Channing Laboratory (Drs Stampfer, Willett, and Curhan),
Department of Medicine, Brigham and Women's Hospital, Harvard Medical
School,
and Departments of Epidemiology (Drs Stampfer, Willett, and Curhan)
and
Nutrition (Drs Stampfer and Willett), Harvard School of Public Health,
Boston, Mass.

RELATED LETTERS

Caffeine and Incident Hypertension in Women
Joe A. Vinson
JAMA. 2006;295:2135.

Caffeine and Incident Hypertension in Women
Johanna M. Geleijnse
JAMA. 2006;295:2135-2136.

Caffeine and Incident Hypertension in Women
Paolo Palatini
JAMA. 2006;295:2136.

Caffeine and Incident Hypertension in Women
Dae Hyun Kim
JAMA. 2006;295:2136-2137.

Caffeine and Incident Hypertension in Women--Reply
Wolfgang C. Winkelmayer and Gary C. Curhan
JAMA. 2006;295:2137.

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What's new in hypertension?
Mann
Nephrol Dial Transplant 2007;22:47-52.

Caffeine and incident hypertension in women.
Vinson
JAMA 2006;295:2135-2135.

Caffeine and incident hypertension in women.
Palatini
JAMA 2006;295:2136-2136.

Caffeine and incident hypertension in women.
Geleijnse
JAMA 2006;295:2135-2136.

Caffeine and incident hypertension in women.
Kim
JAMA 2006;295:2136-2137.

Cola, but Not Coffee, Appears to Raise Hypertension Risk
JWatch Women's Health 2006;2006:1-1.

Make That a Double Espresso!
Journal Watch Cardiology 2005;2005:4-4.

What's new in the other general journals
Tonks
BMJ 2005;331:1165-1166.

INTRODUCTION

Approximately 50 million people in the United States have
hypertension,
and the prevalence is increasing. 1

Hypertension is a major risk factor for coronary heart disease,
stroke,
and congestive heart failure. 2-3

Therefore, even small reductions in the prevalence of hypertension
could
have a potentially large public health and financial impact.

Much clinical lore about the possible association between caffeine
intake and the risk of hypertension is available.

Short-term studies have demonstrated that caffeine intake acutely
increases blood pressure, but over time, attenuation of this effect
does
occur. 4

Experimental studies have shown that caffeine can raise plasma levels
of
several stress hormones, such as epinephrine, norepinephrine, 5-6 and
cortisol, all of which can lead to an increase in blood pressure. 6-7

However, these experiments have been limited to relatively short
periods of observation, typically less than 1 week; information on a
more sustained neuroendocrine response to regular exposure to caffeine
is not available.

A long-term effect of caffeine intake on the risk of developing
hypertension would be of substantial public health importance given
the
widespread consumption of beverages containing caffeine, but
currently,
studies of this association are scarce.

A recent longitudinal study in 1,017 men found a positive association
between coffee consumption and blood pressure and incident
hypertension
in unadjusted analyses. 8

Although the association with blood pressure level was significant in
multivariate analyses, a nonsignificant 40 % increase in the risk of
incident diagnosis of hypertension (95 % confidence interval [CI], -6
%
to 109 %) for 3 to 4 cups per day and a 43 % increase (95% CI, -6 % to
118 %) for 5 or more cups per day vs no coffee consumption was found.

No published studies to date of the association between caffeine
intake
and the risk of hypertension in women are available.

To prospectively elucidate whether caffeine intake or consumption of
certain caffeine-containing beverages is associated with the risk of
incident hypertension in women, we examined these questions in 2 large
cohort studies of women, the Nurses' Health Studies (NHSs) I and II.

METHODS

Study Populations

The NHS I cohort was assembled in 1976 when 121,700 female registered
nurses, aged 30 to 55 years, completed and returned a mailed
questionnaire. 9

Follow-up questionnaires have been mailed every 2 years to update
information on health-related behaviors and medical events.

The NHS II began in 1989, when 116,671 female registered nurses, aged
25
to 42 years, completed and returned a mailed questionnaire.

Questionnaires have been mailed every 2 years to update exposure
information and diagnosis of new diseases.

The follow-up for both cohorts exceeds 90 %.

In this analysis, all participants who had not been diagnosed with
hypertension before the return of the 1990 NHS I or 1991 NHS II
questionnaires were included.

This study was approved by the institutional review board at Brigham
and
Women's Hospital, Boston, Mass.

Receipt of each questionnaire implies participant's consent.

Dietary Assessment

Food frequency questionnaires were used to measure dietary intake and
were completed in 1990, 1994, and 1998 for NHS I and 1991, 1995, and
1999 for NHS II.

Participants were asked about their usual intake of foods and
beverages
during the past year.

The response options for specified serving sizes were the following:
never or less than once per month;
1 to 3 times per month;
1 per week;
2 to 4 per week;
5 to 6 per week;
1 per day;
2 to 3 per day;
4 to 5 per day;
and 6 or more per day.

The relevant beverages included on the questionnaire were the
following:
low-calorie cola (eg, Diet Coke or Diet Pepsi with caffeine),
regular cola (eg, Coke, Pepsi,
or other cola beverages with sugar),
tea with caffeine, tea without caffeine,
coffee with caffeine, and decaffeinated coffee.

Total caffeine intake was calculated primarily using US Department of
Agriculture food composition sources.

In these calculations, it was assumed that the content of caffeine was
137 mg per cup of coffee, 47 mg per cup of tea, 46 mg per can or
bottle
of cola beverage, and 7 mg per serving of chocolate candy. 10

This method of measuring coffee intake was shown to be valid in both
the
NHS I cohort and a similar cohort study of male health professionals.
11-13

Assessment of Other Variables

Data on height and family history of hypertension were collected at
baseline in both cohorts.

Information on weight was updated every 4 years.

Using each participant's updated weight, body mass index was
calculated
by dividing the weight in kilograms by height in meters squared.

Also, an updated variable for weight difference between baseline and
the
time of respective follow-up questionnaire was generated.

Information on oral contraceptive use in the NHS II cohort also was
updated every 4 years.

The same semiquantitative food frequency questionnaires were used to
determine intake of alcohol, sodium, potassium, magnesium, calcium,
and
phosphorus. 14

Physical activity was assessed in NHS I (1988, 1992, and 1996) and NHS
II (1989, 1993, and 1997) cohorts; energy expenditure was expressed in
metabolic equivalent tasks. 15

In addition, the frequency of analgesic drug use (aspirin,
nonsteroidal
anti-inflammatory drugs, and acetaminophen) was ascertained. 16-17

Outcome Definition

The baseline and biennial follow-up questionnaires inquired about
physician-diagnosed hypertension and the year of diagnosis.

Self-reported diagnosis of hypertension was found to be reliable in
the
NHS I cohort. 18

In a subset of women who reported hypertension, review of medical
records confirmed a documented systolic and diastolic blood pressure,
respectively, higher than 140 mm Hg and 90 mm Hg in 100 % and higher
than 160 mm Hg and 95 mm Hg in 77 % of participants.

Additionally, self-reported hypertension was predictive of subsequent
cardiovascular events. 18

A study participant was considered to have a history of hypertension
if
she reported a diagnosis of high blood pressure on any questionnaire
up
to and including the 1990 questionnaire in NHS I and the 1991
questionnaire in NHS II, and therefore was excluded from the study.

Among the remaining women in each cohort, incident cases were included
as those who first reported hypertension on any of the subsequent
biennial questionnaires and whose date of diagnosis was after the
return
of the 1990 NHS I or the 1991 NHS II questionnaire.

This method recently has been used in a study of folate intake and the
risk of hypertension in women. 19

Statistical Methods

The time of observation was between return of the 1990 NHS I and 1991
NHS II and the 2002 NHS I and 2003 NHS II questionnaires.
Participants who did not return the baseline questionnaires for this
study were allowed to contribute person-time for later time intervals,
provided that they had not been diagnosed with hypertension prior to
return of the respective questionnaire.
Participants were censored after being diagnosed with hypertension or
at the time of death.
Each cohort was analyzed separately.
Age-adjusted Cox proportional hazards regression models were used to
estimate relative risks and 95% CIs.
In addition, multivariate models were constructed that adjusted for
other known risk factors of the study outcome:
age (continuous), body mass index (continuous), alcohol use (6
categories), physical activity (quintiles of metabolic equivalent
tasks), smoking status (current, past, or never), family history of
hypertension (yes/no), and current oral contraceptive use (yes/no;
only in NHS II).
In additional analyses, we ensured that sodium, magnesium, calcium,
potassium, and phosphorus intake (quintiles) did not confound the
estimates from these multivariate models.
All variables were updated to reflect the most recent value provided
by the participants on the biennial questionnaires.
Participants with missing data were assigned to a missing category for
that specific time period.
We determined P values for trend for each of the exposures of interest
by using the median for each category.
Level of significance for P values for trend was <.05.
Also the interaction between caffeine intake and the other variables
was
tested.
We used SAS version 8.2 for UNIX statistical software package
(SAS Institute Inc, Cary, NC).

RESULTS

In NHS I, 53,175 women had not been diagnosed with hypertension at
baseline in 1990.

Another 7,916 participants who did not respond to the 1990
questionnaire
but who did respond to a later questionnaire disclosing that they
previously had not been diagnosed with hypertension allowed them to
contribute person-time from that point in time.

Over the 12 years (539,388 person-years of follow-up), 19,541 incident
cases of physician-diagnosed hypertension were reported.

In NHS II, 94,503 participants who were free of hypertension (87,369
in
1991 and an additional 7,134 at a later point in time) were included
in
the analyses of younger women.

During 909,199 person-years of observation, 13,536 participants
responded that they were diagnosed with hypertension by a physician.

Participant characteristics by quintile of caffeine intake are
presented
in Table 1.

In both cohorts, mean caffeine consumption ranged from less than 20 mg/
d
in the lowest quintile to approximately 600 mg/d in the highest
quintile.

Caffeine intake was correlated positively with alcohol consumption and
smoking status
r = 0.12, P < .001 for NHS I; r = 0.23, P < .001 for NHS II),
whereas all other relevant characteristics did not differ
materially across quintiles of caffeine consumption.

Table 1. Baseline Characteristics of Cohort by Quintile of Caffeine
Intake in Nurses' Health Study I (N = 53,175)
and Nurses' Health Study II (N = 87,369)*

Age-adjusted analyses demonstrated an inverse U-shaped relation
between
caffeine intake and the incidence of hypertension in both cohorts.

Compared with participants in the lowest quintile of caffeine
consumption, the risk of incident hypertension was increased by 14 %
(95
% CI, 9 % -19 % for NHS I) and 15 % (95 % CI, 9 % - 21 % for NHS II)
for
those in the third quintile, whereas those in the highest quintile
were
not at an increased risk of hypertension (Table 2).

Multivariate adjustment did not materially change these findings
(Table 2).

Table 2. Age-Adjusted and Multivariate Relative Risks for Incident
Hypertension According to Quintile of Caffeine Intake

To further examine this inverse U-shaped association, the frequency of
use of different caffeine-containing beverages in relation to the risk
of incident hypertension was evaluated.
In multivariate models including beverage type, rather than actual
caffeine intake, no association between frequency of intake of
caffeinated coffee and incident hypertension was observed in either
cohort.
Compared with NHS I participants drinking less than 1 cup per day of
caffeinated coffee, the relative risks were
1.06 (95% CI, 1.01-1.10) for those consuming 1 cup per day,
1.00 (95% CI, 0.97-1.04) for those drinking 2 to 3 cups per day,
0.93 (95% CI, 0.88-0.99) for those drinking 4 to 5 cups per day,
and 0.88 (95% CI, 0.80-0.98) for those drinking 6 or more cups per day
(Table 3).
The trend for the NHS I cohort was marginally significant for
an inverse association between coffee intake and the risk of
hypertension (Table 3; P for trend = .02).
The findings in the NHS II cohort were practically identical (P for
trend = .03).
The results for intake of decaffeinated coffee also were similar to
the data for caffeinated coffee intake (data not shown);
the trend suggested an inverse association of risk of hypertension in
the NHS I cohort (P for trend = .08)
but not in the NHS II cohort (P for trend = .67).

Table 3. Age-Adjusted and Multivariate Relative Risks for Incident
Hypertension According to Frequency of Coffee Intake

An association between caffeinated tea intake and incident
hypertension
in the NHS I cohort (Table 4; P for trend = .79) was not found.
However, in the cohort of younger women in NHS II, a moderate increase
in risk of hypertension (P for trend = .01; Table 4) was detected.

Table 4. Age-Adjusted and Multivariate Relative Risks for Incident
Hypertension According to Frequency of Caffeinated Tea Intake

Finally, an examination of the possible associations between
caffeinated
cola beverages and the risk of hypertension
showed that
sugared caffeinated cola (NHS I, P for trend = .03; NHS II, P for
trend <.001) (Table 5)
and diet caffeinated cola (NHS I, P for trend = .02; NHS II, P  for
trend <.001) (Table 6)
were positively associated with hypertension in both cohorts.

Table 5. Age-Adjusted and Multivariate Relative Risks for Incident
Hypertension According to Frequency of Sugared Cola Intake

Table 6. Age-Adjusted and Multivariate Relative Risks for Incident
Hypertension According to Frequency of Diet Cola Intake

Glasses or Cans of Diet Cola per Day
under 1 ------- 1 ----------- 2-3 ------- 4 and more --- P for Trend


Nurses' Health Study I (1990-2002) 53,175 nurses, ages 44-69 in 1990

No. of cases of Incident Hypertension
17,268 ------- 1,154 ---------- 662 --------- 130
% 100 ---------- 6.7 ---------- 3.8 -------- 0.75
#% 32.5 -------- 2.2 ---------- 1.3 -------- 0.25 #% of 53,175

Person-years
479,890 ----- 30,579 --------17,316 ------- 3,173
% 100 -----------6.4 ---------- 3.6 -------- 0.66

Age-adjusted relative risk (95% CI)
1.00 -- 1.16(1.10-1.24)-- 1.23(1.13-1.33)-- 1.37(1.15-1.62)-- under .
001

Multivariate relative risk (95% CI)*
1.00 -- 1.07(1.00-1.13) -- 1.06(0.98-1.15) -- 1.16(0.97-1.37)------ .
02

Nurses' Health Study II (1991-2003) 87,369 nurses, ages 27-44 in 1991


No. of cases of Incident Hypertension
10,192 -------- 1,452 -------- 1,358 --------- 449
% 100 ---------- 14.3 ----------- 13.3 --------- 4.4
#% 11.7 --------- 1.7 ------------ 1.6 --------- 0.51 #% of 87,369

Person-years
713,971 ----- 91,144 ------- 77,398 ------- 21,265
% 100 --------- 12.8 --------- 10.8 ---------- 3.0

Age-adjusted relative risk (95% CI)
1.00 -- 1.16(1.10-1.23) -- 1.33(1.26-1.41) -- 1.63(1.49-1.80) under .
001

Multivariate relative risk (95% CI)*
1.00 -- 1.05(0.99-1.11) -- 1.09(1.03-1.15) -- 1.19(1.08-1.32) under .
001

Abbreviation: CI, confidence interval.
*Adjusted for age, body mass index, intake of alcohol, family history
of
hypertension, oral contraceptive use (in Nurses'Health Study II only),
physical activity, and smoking status, as well as the other classes of
beverage.

Additional analyses adjusting for intake of sodium, magnesium,
potassium, phosphorus, and calcium or analgesic drug use did not
change
the results materially for the caffeine intake or specific beverage
intake analyses. When testing the robustness of the results, such as
by
limiting the analysis to those women who reported having had a routine
physical examination during the time interval or by using baseline
body
mass index and updated change in weight rather than updated body mass
index, the results were virtually unchanged (data not shown).

COMMENT

In this prospective study of the association between caffeine intake
and
the risk of physician-diagnosed hypertension in 2 large cohorts of
women, we found a modest inverse U-shaped association between caffeine
intake and hypertension in both cohorts.

The magnitude of the highest multivariate relative risk was 1.13 in
NHS
I and 1.12 in NHS II.

To better understand this nonlinear relation between caffeine intake
and
the risk of hypertension, we evaluated the individual associations of
several caffeine-containing beverages.

Neither caffeinated nor decaffeinated coffee demonstrated a positive
association with incident hypertension in either cohort.

The results for consumption of caffeinated tea were inconclusive:
although no association was observed in the NHS I cohort, a positive
trend was shown in the NHS II cohort.

By contrast, we found a highly significant association between cola
intake (sugared or low-calorie cola) and incident hypertension that
was
consistent across the cohorts.

To our knowledge, this study is the first to prospectively evaluate
the
putative effect of caffeine consumption on the long-term risk of
hypertension in women.

The speculation that coffee may cause hypertension was supported by
several small experiments over short periods of observation ( under 80
days). 20

If the short-term effects of caffeine on blood pressure persist, then
habitual coffee drinking might contribute to an excess risk of
hypertension.

Such an effect would be of great public health importance given the
widespread use of coffee and other caffeinated beverages.

In this study with more than 1.4 million person-years of follow-up,
the
relevant exposures and outcomes have been found valid and accurate,
11-13,18 and coffee intake was updated to reflect changes in
individual
behavior.

We found strong evidence to refute speculation that coffee consumption
is associated with an increased risk of hypertension in women.

The associations found between caffeinated tea consumption and the
risk
of hypertension differed between the 2 cohorts.

In the NHS I cohort, no association was found; however, in the NHS II
cohort, a significant positive trend was observed.

A recent study conducted among 711 men and 796 women in Taiwan found a
strong inverse association between both frequency and duration of tea
intake and hypertension. 21

Since the types of tea (green or oolong) consumed in that study are
likely different from those consumed in our study of US women, the
comparability of the findings from these 2 studies appears uncertain.

In both NHS cohorts we found a positive association between frequency
of
caffeinated soft drink consumption and the risk of hypertension.

The findings were consistent between the cohorts and were present
across
types of soda beverages: both sugared cola and diet cola beverages
were
associated with an increased risk of hypertension (Table 5 and Table
6).

Hence, we speculate that it is not caffeine but perhaps some other
compound contained in soda-type soft drinks that may be responsible
for
the increased risk in hypertension.

If these associations are causal, they may have considerable impact on
public health.

Recent studies have found an effect of the intake of cola beverages on
insulin resistance in a rat model 22; in humans, the intake of cola
beverages was associated with an increased risk of diabetes in the NHS
II cohort. 23

These studies have attributed these associations to the glycemic load
of
corn syrup, which is used as sweetener in these beverages, and the
caramel coloring, which is rich in advanced glycation end products.

Further studies on the possible mechanisms underlying these
associations
clearly are needed.

We acknowledge the limitations of this study.

We cannot rule out that individuals susceptible to adverse effects of
caffeinated coffee intake on their blood pressure in the past may have
reduced their consumption of beverages containing caffeine.

Patients were asked about the frequency of their food intake, but no
information was available on the daily timing of such ingestion.

We did not directly measure the participants' blood pressure and the
diagnosis of hypertension was self-reported.

Nonetheless, self-reported blood pressure has been validated and
demonstrated to be a strong predictor of actual values. 18

Furthermore, we do not know whether these findings are generalizable
beyond populations of predominantly white women.

We also cannot exclude the possibility that the associations found are
residually confounded.

Lastly, no statement can be made on the effect of coffee intake on the
control of blood pressure among individuals already diagnosed with
hypertension.

In conclusion, consumption of coffee in women does not appear to
increase the risk of developing hypertension.

Whether caffeinated soft drinks are causally related to the risk of
hypertension and its underlying mechanism will require further study.

AUTHOR INFORMATION

Corresponding Author: Wolfgang C. Winkelmayer, MD, ScD, Division of
Pharmacoepidemiology and Pharmacoeconomics and Renal Division, Brigham
and Women's Hospital, 1620 Tremont St, Suite 3030, Boston, MA 02120
wwinkelmayer@partners.org,

Author Contributions: Dr Winkelmayer had full access to all of the
data
in the study and takes responsibility for the integrity of the data
and
the accuracy of the data analysis.

Study concept and design: Winkelmayer, Willett, Curhan.

Acquisition of data: Stampfer, Willett, Curhan.

Analysis and interpretation of data: Winkelmayer, Stampfer, Willett,
Curhan.

Drafting of the manuscript: Winkelmayer.

Critical revision of the manuscript for important intellectual
content:
Winkelmayer, Stampfer, Willett, Curhan.

Statistical analysis: Winkelmayer, Willett, Curhan.

Obtained funding: Willett, Curhan.

Administrative, technical, or material support: Stampfer, Willett,
Curhan.

Study supervision: Curhan.

Financial Disclosures: None reported.

Funding/Support:
This study was funded by National Institutes of Health grants DK52866,
DK66574, CA87969, and CA050385.

Dr Winkelmayer is a 2004 T. Franklin Williams Scholar in Geriatric
Nephrology and a recipient of the American Society of
Nephrology-ASP-Junior Development Award in Geriatric Nephrology,
jointly
sponsored by the Atlantic Philanthropies, the American Society of
Nephrology, the John A. Hartford Foundation, and the Association of
Subspecialty Professors.
He is also supported by an American Heart Association Scientist
Development grant (0535232N).

Role of the Sponsors:
None of the funding organizations had any role in the design and
conduct
of the study; collection, management, analysis, and interpretation of
the data; or preparation, review, or approval of the manuscript.

Author Affiliations
Division of Pharmacoepidemiology and Pharmacoeconomics (Dr
Winkelmayer),
Renal Division (Drs Winkelmayer and Curhan), and Channing Laboratory
(Drs Stampfer, Willett, and Curhan), Department of Medicine, Brigham
and
Women's Hospital, Harvard Medical School, and Departments of
Epidemiology (Drs Stampfer, Willett, and Curhan) and Nutrition (Drs
Stampfer and Willett), Harvard School of Public Health, Boston, Mass.

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