WellnessOptions 025

WellnessOptions
DIGESTION &
ABSORPTION
The interconnected gut
Stress is indigestible
What is important
for gut health
Vitamin Ds story
of twists & turns
Plant remedies
No.25
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PM 1807935
Science News | Health Perspectives | Nutrition Trends | Body & Emotional Fitness
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WellnessOptions No.25
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2 a WellnessOptions No.25
CANADIAN EDITORIAL
ADVISORS
Dr. Hilde Vandenberghe
Toxicologist, Gamma-Dynacare
Laboratories, London, ON
Dr. Alykhan S. Abdulla
Director, Kingsway Health
Center, Sports and family
physician, Toronto, ON
Dr. Earl Berger
Managing Director, The Berger
Medical Monitor, Toronto, ON
Dr. Maureen M. Chan
Pharmacologist, Toronto, ON
Dr. Peter Chang
Psychiatrist, Chang &
Associates, Toronto, ON
Dr. Hilda A. Donhoffer
Medical Biochemist,
Toronto, ON
Dr. Raymond Edge
President, The Toronto School
of Homeopathic Medicine, ON
Dr. Michael F. Filosa
Cell biologist, University of
Toronto, ON
Dr. Martin J. Gibala
Associate professor,
Kinesiology, McMaster
University, ON
Dr. David M. Goldberg
Professor Emeritus, Laboratory
Medicine & Pathobiology,
University of Toronto, ON
Dr. Tibor F. Heim
Professor of Pediatrics &
Nutrition, University of
Toronto, ON
Dr. Arif Manuel
Nephrologist, York Central
Hospital, Richmond Hill, ON
Dr. Manny W. Radomski
Professor Emeritus, Faculty
of Medicine and Faculty of
Physical Education and
Health, University of
Toronto, ON
Dr. Cory Ross
Manager, Organisation Health
& Wellness, Mount Sinai
Hospital, Toronto, ON
Dr. Paul Saunders
Naturopathic doctor,
Toronto, ON
Dr. Gord Surgeoner
President, Ontario Agri-Food
Tech. Guelph, ON / Professor
of Plant Agriculture, University
of Guelph, ON
Dr. Jake J. Thiessen
Professor and Associate Dean,
Faculty of Pharmacy,
Dr. Zul Verjee
Clinical Biochemist, Hospital
for Sick Children, Toronto, ON
Dr. Pui-Yee Wong
Professor of Pathology &
Laboratory Medicine,
Dr. Mary X. Wu
Director, Toronto School of
Traditional Chinese
Medicine, ON
Dr. Michael Zitney
Director, Headache and Pain
Relief Centre, Toronto, ON
Dr. Larry Chan
Chiropractor and Naturopathic
Doctor, Anti-Aging and
Chinese Medicine Specialist,
Vancouver, BC
Dr. Stanley Coren
Professor of Psychology,
University of British Columbia,
Vancouver, BC
Dr. Imre Csapo
Family Physician, Vancouver, BC
Dr. C. Chan Gunn
President, The Institute for the
Study and Treatment of Pain,
Vancouver, BC
Dr. Nicholas Lee
Gynecologist, Vancouver, BC
Dr. Henry Lu
Principal, International College
of Traditional Chinese
Medicine, Vancouver, BC
Dr. Stuart M. MacLeod
Executive Director, BC Institute
for Children and Womens
Health, Vancouver, BC
Dr. Anthony M. Ocana
Physician, Department of
Family and Community
Medicine, University of British
Columbia, Vancouver, BC
Dr. Andrew Woolfenden
Neurologist, University of
British Columbia, BC
Dr. Jacqueline J. Shan
Adjunct professor, Food and
Nutritional Sciences,
University of Alberta, AB
Dr. Lyle Redman
Director, Clinical Biochemistry,
Brandon Medical Centre,
Brandon, MB
Dr. Ian Landells
Assistant Professor, Faculty of
Medicine, Memorial University
of Newfoundland, NL
Dr. David Brookman
Microbiologist and President,
Consultant, David Brookman
& Associates, Montreal, PQ
Dr. John Hooper
President, Oakleigh
Enterprise, Hudson, PQ
INTERNATIONAL EDITORIAL
ADVISORS
Dr. Jorge Cerani
Former Medical Manager,
Roche Consumer Health &
Representative, International
Institute of Health Promotion,
American University,
Argentina
Dr. Alain Buguet
Deputy Director, Institute
of Tropical Medicine,
Marseille, France
Dr. Kelvin Chan
Director, Institute for the
Advancement of Chinese
Medicine, Baptist University,
Hong Kong
Dr. Daniel Y.T. Fong
Research Assistant Professor,
Senior Medical Statistician,
Clinical Trial Centre, The
University of Hong Kong
Dr. Kwok-Pui Fung
Professor of Biochemistry,
The Chinese University of
Hong Kong
Dr. Pak-Chung Ho
Professor and Chair,
Obstetrics & Gynecology,
The University of Hong Kong
Dr. David Higgins
Professor, Department of
Pathology, The University
of Hong Kong
Dr. David Paul Johns
Chairman, Department of
Sports Science & Physical
Education, The Chinese
University of Hong Kong
Dr. Cyrus R. Kumana
Professor and Chair, Clinical
Pharmacology & Therapeutics,
Dr. William W. Mak
Manager, Genome Research
Centre, The University of
Hong Kong
Dr. Ricky K.Y. Man
Professor and Head,
Department of Pharmacology,
Dr. Sidney Tam
Consultant Chemical
Pathologist, Queen Mary
Hospital, Hong Kong
Dr. Lap-Chee Tsui
Vice-Chancellor, The University
of Hong Kong, Hong Kong
Dr. Ikuo Takeuchi
Chairman of the Board of
Trustees, Novartis Foundation;
Professor Emeritus, Faculty of
Science, Kyoto University,
Japan
Dr. George Chan
Director of Hematology,
Auckland Health Care
Services, Auckland,
New Zealand
Dr. Ram Swaminathan
Professor of Chemical
Pathology, St. Thomas
Hospital/Guys Hospital,
London, United Kingdom
Dr. Majid Ali
Professor of Medicine,
The Institute of Integrative
Medicine, New York, NY, USA
Dr. Daniel W. Chan
Professor of Pathology,
Oncology, Radiology &
Urology, Johns Hopkins
Medical Institutions,
Baltimore, MD, USA
Dr. Ka-Kit Hui
Director, Center for East-West
Medicine, David Geffen School
of Medicine, University of
California, LA, USA
Dr. Joseph A. Knight
Professor and Head of
Education, Department of
Pathology, University of
Utah, USA
Dr. Steven Soldin
Director, Department of
Biochemistry, Childrens
National Medical Center,
Washington D.C., USA
Editorial Advisors
Cover photo: istockphoto.com/Slobo Mitic
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WellnessOptions No.25 b3
WellnessOptions
No.25 Digestion & Absorption
Trends
Bird u & cat u 6
Can diet control cholesterol? 6
Why avian u is not spreading
rapidly among humans? 7
Green Tea and the Brain 8
Trace metals in bottled water 8
Erectile dysfunction drugs protect stomach? 9
Woody medicine 9
Amazing gut 10
Finding the stress-gut connection 10
Direct to the gut 10
Taste sensitivity in smoking 11
Adult testis stem cells to
replace embryonic stem cells ? 11
A growing line up 12
Cover Feature
The interconnected gut 14
A passage of connection 16
Nutrient absorption 18
Vitamin D: a story of unexpected turns 22
Learning on an empty stomach 25
Stress is indigestible:
the mind and stomach link 26
Body
What is important for gut health 28
How acid reux happens 30
Common upper gut problems 32
Medications for stomach disorders 33
Are plant polyphenols
helpful for gut problems? 34
Stomach Flu 36
Gastroenteritis outbreaks on ships 37
Yoga for back pain 38
Food & Nutrition
Every day good and bad fats 40
For a better mood/Good fat in bacon? 43
Back to the roots 44
Cocoa & chocolate health treats 46
Garlic wonders 49
Regulars
Editorial Advisors 2
Contents 3
Contributors 4
Editorial 5
Distribution 48
Subscription forms 50
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Stanley Coren,
PhD, FRSC
Stanley Coren is a
Professor of Psychology
at the University of
British Columbia. He
received his doctorate
at Stanford University
and has published over
300 reports in professional scientic journals. His
research includes studies on sleep, human vision
and hearing, effects of birth stress, creativity,
behaviour genetics, and human-canine
relationships. He is a Fellow of the Royal Society of
Canada. The best-seller books that he has written
include Sleep Thieves, The Left-hander Syndrome,
The Intelligence of Dogs, and The Pawprints of
History. He is regularly seen on TV programs such
as Oprah, Larry King Live, Good Morning America,
and the Today Show in Canada and the US.
Flavio Habal,
MD, PhD, FRCPC
Flavio Habal received
his MD and his PhD in
Pathology from the
University of Toronto.
He subsequently
trained in Internal
Medicine and in
Gastroenterology at the University of Toronto. He is
currently an Associate Professor of Medicine and
staff physician at the Toronto General Hospital, and
the Education Chair of the Canadian Digestive
Health Foundation. His clinical interests are in the
areas of acid related disorders, inammatory bowel
disease in pregnancy, hepatitis C and liver disease.
He was the winner of the 2004 American College of
Gastroenterology/ Naomi Nakao Gender Based
Research Award for his work entitled Inammatory
Bowel Disease and Pregnancy: A 20 Year
Prospective Case Control Study.
Bruce J Holub, PhD
Bruce Holub is
University Professor
Emeritus in the
Department of Human
Health & Nutritional
Sciences at the
University of Guelph.
He graduated from the
University of Guelph and obtained his PhD in
Biochemistry and Nutrition from the University of
Toronto before receiving further training at the
University of Michigan Medical School. He has
served as President of the Nutrition Society of
Canada and Chair of the Nutrition Task Force of the
Heart & Stroke Foundation of Ontario.
He has authored over 200 papers in scientic
journals, book chapters, and conference
proceedings. His research is focused on dietary
omega-3 fatty acids from sh/sh oils (DHA/EPA),
plant oils, their resulting nutraceuticals, and the
health effects of functional foods on humans,
especially for the prevention/ management of
cardiovascular disease and other chronic
disorders. He is also involved with the evaluation
of nutraceuticals and agri-foods for cost-savings
to the healthcare system. He maintains active
collaborative research with clinical groups at
various Canadian medical schools, the Mayo
Clinic in the US, Japan, Greenland, and the agri-
food sectors.
Richard H. Hunt,
MD, FRCP, FRCPC, FACG
Richard Hunt qualied
from Edinburgh
University, and is
presently a Professor of
Medicine and
Gastroenterology at
McMaster University,
where he was the rst Director of the Intestinal
Disease Research Unit, and of the Division of
Gastroenterology. He has received many prizes and
medals for his work in Gastroenterology including
the Canadian Association of Gastroenterology
Distinguished Service Award in 2002. He was the
President of the Canadian Association of
Gastroenterology 1992-1993 and President of the
Canadian Helicobacter Study Group 1997-2001. He
is currently Vice President of the Canadian
Digestive Health Foundation.
His professional interests focus on acid related
disorders and clinical pharmacology of treatment of
gastrointestinal disease. He has published over
600 papers and abstracts, authored or edited 8
books and 50 chapters, and produced 20 TV video
lms on peptic ulcer disease, reux esophagitis,
and colonoscopy.
William G. Paterson,
MD, FRCPC
William Paterson
received his MD from
Queens University and
subsequently trained
in Internal Medicine at
Queens and the
University of Western
Ontario. Following a clinical gastrointestinal
fellowship at Queens, he was awarded an MRC
Research Fellowship to study esophageal
physiology under the mentorship of Dr. Raj Goyal
at Harvard University. He then returned to a faculty
position at Queens, where he is currently
Professor in the Departments of Medicine, Biology
and Physiology and the Chair of the Division of
Gastroenterology. He currently holds a Queens
University Research Chair and is President of the
Canadian Association of Gastroenterology.
Contributors
4a WellnessOptions No.25
NEXT
ISSUE
NO.26
DIGESTION &
ELIMINATION
Some topics in the
June 2006 issue of
WellnessOptions are:
Inammatory bowel diseases
Irritable bowel syndrome
Colon cancer
Probiotics
Electrolytes and energy drinks
ADHA (Attention Decit/
Hyperactivity Disorders)
Pain management
Food allergy
Vitamin D and calcium
Omega-3 fatty acids
Glycemic index
WellnessOptions
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Editorial
Before the invention of synthetic strings, both
violin and tennis racket strings were made of
sheep intestines.
A 10th century doctor, al-Zahrawi, reportedly
discovered that sheep intestines could be used
as self-dissolving sutures when the gut strings
of his lute were eaten by a monkey. Sheep
intestines (called catgut) were used for surgery
until after World War II when bovine intestines
replaced them. They have since mostly been
replaced by synthetic sutures.
Highway congestion is not unlike gut
indigestion. They are both hassles we have to
live with from time to time, annoying and
inconvenient.
Gut connection
What really connects highways and the
digestive tract is stress. Trafc jams cause
frustration behind the wheels and stress.
Stress depresses gut function, causing
indigestion. This in turn affects our general
sense of well-being, further lowering our level
of tolerance on and off the road. Science is
beginning to discover that the gut-brain-gut
axis is more intimate than we previously
realized. Serving meals with relaxing music
probably soothes both the mind and the gut.
The environment is us
Digestion is a body function. But it occurs in an
external space that runs through the center of
our body like a main highway of lifeline. This
environment deep within us is constantly being
subjected to the outside world through the
foods, drinks, microbes, and toxins that we
introduce to it. Research is nding out how
inseparable we are from our gut environment.
The microbial communities in our gut actually
contribute to dening how and what we are.
Perhaps we are, after all, our inner and
external environments.
Flow through
The highways are an integral part of our life in
Western societies. Even if we do not live near
one, most of us depend on the highway
network for delivery of foods, goods, and
services. Trafc levels and road conditions are
important for smooth delivery of the
necessities of life.
Likewise, the condition of the digestive tract
and what and how much we put through the
system are important for the smooth
processing of the food. A healthy diet with less
fat and red meat, more vegetables and fruits,
and an adequate intake of essential nutrients
ensures that our gut is not overworked.
Speed and pace
It takes time for the body to effectively break
down the foods after ingestion and to absorb
as many nutrients as possible. It normally
takes 24 to 72 hours for food to pass through
the system. Unlike pythons that must lay still
while digesting a meal, we can perform other
tasks when our gut is processing food. But this
also makes it easy for us to neglect and abuse
the digestive systemeating on the run and
forgetting to eat are examples.
Travelling speed and driving rules are
important for highway trafc. Likewise, pace
and rhythm are important for effective
digestion and absorption. For example,
stomach emptying is an orderly and highly
regulated process. Many factors can affect the
rate of emptying. Fried foods, fear, and ice
cream are examples of foods and emotions
that slow it down. Eating too fast can also
make bloating and acid reux symptoms worse.
Interplay
Studies have found that genetics, diet, our
inner and external environments, emotions,
how we sleep, and stress all play signicant
roles in gut function. A highway can benet or
create havoc for the communities along it. Our
digestive tract can also nourish life or cause
great suffering. It helps to understand how
highways and our gut work.
This issue of WellnessOptions is on digestion
and nutrient absorption. Please enjoy.
Lillian Chan, Editor
Highways and the digestive tract
How is a violin related to a tennis racket?
What has catgut got to do with surgical procedures?
What is the connection between highways and the digestive tract?
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Bird u & cat u
Even though the H5N1 virus is still considered fundamentally a bird
u virus, an increasing number of feline infection fatalities have
been reported worldwide. Some scientists monitoring the situation
are alarmed.
In the April 6, 2006 issue of the scientic journal Nature, a
commentary warns the scientic community that feline and other
mammals may serve as host for the avian u virus H5N1.
Cats and tigers are victims too
The rst report of domestic cats dying from H5N1 came in February
2004. In a household near Bangkok, 14 out of 15 cats died. One of
the cats had eaten a chicken carcass in a farm where there was an
H5N1 virus outbreak. Eleven of these cats were subjected to
necropsies, with H5N1 infection conrmed in every case.
Three months prior to this event, two tigers and two leopards died
suddenly in a zoo in Suphanburi, Thailand, after feeding on fresh
chicken carcasses. The incidence occurred during a local outbreak of
H5N1 in poultry. The deaths were attributed to H5N1 infection.
Later in the same year, 147 tigers died in another zoo in Thailand
during a different H5N1 outbreak. The cause was again the
consumption of virus-infected chicken.
It is generally believed that both domestic and wild cats are
resistant to inuenza A infection, of which H5N1 is a subtype. In fact,
both the WHO and the World Organization for Animal Health have
recently stated that there is no evidence of domestic cats playing a
role in the transmission of H5N1 virus and the virus is basically an
avian pathogen.
However, latest evidence shows that fatal infections among cats are
common in countries such as Indonesia, Thailand, and Iraq, where the
virus seems to be endemic in poultry. Shortly after H5N1 was detected
in wild birds in Germany, the same virus was also found in dead or
moribund cats recently.
Laboratory studies
Infected cats excrete H5N1 virus from the pharynx, nose and rectum,
but the amount of virus excreted by cats is much lower than by
chickens. Laboratory investigations of H5N1 suggest that cats could
be infected via the respiratory tract, by feeding on virus-infected
chicks, or through close contact with other infected cats.
Although humans can be infected, further spread of the virus in its
present form is unlikely. However, other mammals, such as cats, can be
involved in helping the virus adapt and mutate into a new form that
can transmit efciently among humans. Studies have shown that H5N1
infects cats in a similar way as it infects humans. The virus attaches to
cells in the lining of the lungs, not the upper respiratory tract
Preventive guidelines
Most international guidelines have not considered the potential role
of cats in a H5N1 pandemic. The commentary suggests that ofcial
guidelines for controlling the spread of avian virus infection in cats are
necessary. It proposes that in areas where H5N1 virus has been
detected in either poultry or wild birds, contacts between cats and
infected birds or their droppings should be prevented. Domestic cats
should be kept indoor, and those suspected to have had contacts with
infected birds should be quarantined.
Recently, H5N1 virus infection has been detected in Germany in a
stone marten, a nocturnal mammal belonging to the weasel family. The
commentary further warns that some other animals that are vulnerable
to H5N1 avian u infection may include domestic and wild carnivores
such as dogs, foxes, weasels, and seals. It suggests increased
surveillance and precautions in areas where H5N1 is endemic.
For more on infectious diseases, u and avian u, refer to
WellnessOptions issue 14, 20 and 23.
Reference:
Kuiken T et al. (2006) Feline friends or potential foe? Nature 440: 741-742.
Can diet control
cholesterol?
Cholesterol-lowering foods such as soy protein, almonds, plant sterol
enriched margarines, oats, and barley may reduce cholesterol levels
more effectively when eaten in combination.
A study led by David Jenkins, a professor at the University
of Toronto, found that this combination of foods reduces low-density
lipoprotein cholesterol (bad cholesterol) in ways similar to a rst
Trends News & Notes
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For over 60 years, women around the world have passionately
recommended Floradix Formula Liquid Iron to their closest friends for
its ability to prevent common iron deficiency symptoms such as fatigue,
poor concentration, brittle hair and nails, dark circles under the eyes,
restlessness, and cold hands and feet. It has long been embraced by
women because of their requirement for consistent dietary iron intake
due to monthly blood loss. Beloved by thousands of women who find
they are able to remain free from constipation commonly caused by
iron supplementation, Floradix is the natural iron solution.
Highly soluble iron gluconate for maximum absorption
No preservatives, alcohol, artificial additives or pesticides
No sugar, artificial sweeteners or colourings
Vitamin C and whole food concentrates for enhanced absorption
Easy on the digestive tract
Recommended during
pregnancy and breastfeeding
Delicious fruit juice base
Suitable for vegans/vegetarians
Contains strengthening herbal

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For a tried and true long-term
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generation statin, a cholesterol lowering drug. It suggests that
these changes in diet can boost the success rate of statins in
general while providing additional health benets. They may
also offer an alternative to those for whom drugs are not a
viable option.
Researchers prescribed a seven-day menu high in viscous
bres, soy protein, almonds, and plant sterol margarine to 66
people with an average age of 59.3 and within 30% of their
recommended cholesterol targets. Of this group, 55 participants
managed to follow the menu for a year in real-life conditions.
After 12 months, more than 30% of the participants had
successfully adhered to the diet and lowered their cholesterol
levels by 20%. This rate is comparable to the results achieved by
29 of the participants who took a statin for one month under
metabolically controlled conditions before the real-life diet study.
The study suggests that it may be viable to use diet as the
primary means to control cholesterol levels for some people.
Reference:
Jenkins DJA et al. (2006) Assessment of the longer-term effects of a dietary portfolio of cholesterol-
lowering foods in hypercholesterolemia. Am J Clin Nutr. 83: 582-591.
Why avian u is not
spreading rapidly
among humans?
The avian H5N1 inuenza A virus has infected more than 100
people. Although this virus can replicate efciently in the lungs,
human-to-human transmission is still considered rare.
Different inuenza viruses prefer different binding molecules
along the respiratory tract. A recent publication coauthored by
researchers in Japan and the US suggests that this low infection
rates might be associated with the distribution of binding
molecules in the human airway.
The study shows that several different strains of human
inuenza A viruses preferentially recognize and infect epithelial
cells lining the bronchi and alveolar deep at the end of the
respiratory tract in the lungs. Whereas avian inuenza virus
including a H5N1 strain preferentially recognizes and infects
alveolar cells only.
They suggest that although the H5N1 virus can be transmitted
from birds to humans, it can replicate efciently only in cells in
the lower region of the respiratory tract. Transmission by coughing
and sneezing from human to human is therefore not as efcient
as with some other u viruses.
However, if the H5N1 virus evolves or mutates and acquires the
ability to recognize receptors higher up along the human
respiratory tact, it could be readily spread by sneezing and
coughing from human to human.
For more on avian u, refer to WellnessOptions issue 14 and 20.
Reference:
Shinya K et al. (2006) Inuenza virus receptors in the human airway. Nature 440: 435-436.
Green Tea and
the Brain
In developed countries, dementia has a
reported prevalence of 1.5% at age 65,
doubling every 4 years and reaching 30%
by age 80.
Experimental studies have shown that
tea and tea polyphenols (which include
catechins and their derivatives) may protect
against neurodegenerative diseases such as
Alzheimers (AD) and Parkinson disease (PD).
A recent human study on 1,000 Japanese
seniors aged 70 and older examined the
association between green tea, black tea,
and coffee consumptions and cognitive
functions. Participants took tests of mental
status, including memory, orientation, ability
to follow commands, and attention. Green
tea, black tea, and coffee drinkers scored
differently. Those who reported drinking the
most green tea were found to be least likely
to show cognitive impairment, based on
their test scores.
Researchers suggest that a higher
consumption of green tea is associated with
a lower prevalence of cognitive impairment
in humans, and this might partly explain the
relatively lower prevalence of dementia,
especially AD, in Japan compared to Europe
and North America.
Reference:
Kuriyama S et al. (2006) Green tea consumption and cognitive
function: a cross-sectional study from the Tsurugaya Project. Am J
Clin Nutr 83: 355-361.
Trace metals in
bottled water
A recent report from the University of
Heidelberg presented evidence that there is
substantial leakage of metal antimony (Sb),
a potentially toxic trace element, into bottled
water from plastic containers made of
polyethylene terephthalate (PET).
Antimony has no known physiological
function and is found in natural deposits.
Under very strict laboratory conditions
and with precise instruments, a
concentration of Sb as low as 0.03 ng/L
can be detected reliably.
Previous studies have reported that the
natural abundance of Sb in uncontaminated
ground waters is very low, at about 2 ng/L
(2 parts per 10
9
). In pristine ground waters
from a calcareous aquifer in southern Ontario,
Canada, the average Sb concentration is
reported to average 2.2 ng per L.
In contrast, the concentrations of Sb
have been found to be about 100 times
higher for mineral waters (42 samples
tested) and spring waters (102 samples
tested) bottled in Canada. The averaged
Sb concentrations were 320 ng/L and
300 ng/L respectively.
Similarly, high concentration of Sb
were reported for bottled water
from Europe at 165 ng/L and
Japan with 16 out of 55 brands
with Sb levels above 500 ng/L.
Most bottled water is
shipped in bottles made from
PET. Currently, an estimated
150 billion PET bottles are
produced annually. About 90%
of the PET manufactured
worldwide uses antimony
trioxide as a catalyst. Antimony
trioxide is a suspected
carcinogen, and it is listed as a
priority pollutant by the US
EPA, the EU, and the German
Research Foundation.
This report found that 12
brands of bottled natural
waters from Canada contained
Sb at 70 to 242 ng/L, and 3
brands of deionized water
contained on an average 162 ng/L; all of
these were bottled in PET containers. On the
other hand, natural water from Ontario
bottled in polypropylene contained an
average of 8.2 ng/L. Comparison of three
German brands of water available in both
glass bottles and PET containers also showed
that water Sb levels in PET containers was up
to 30 times higher.
To conrm that the elevated Sb
concentrations are due to leaching from the
PET containers, water was collected in acid-
cleaned, low density polyethylene bottles
from a commercial source in Germany. It was
tested prior to bottling and found to contain
an average Sb level of 3.8 ng/L. The same
brand of water in PET bottles purchased and
tested locally contained Sb level of 359 ng/L,
and after an additional three months of
storage at room temperature, the same
bottle yielded 626 ng/L.
Similar test results were obtained when
pristine groundwater from Canada was
collected from the source using PET bottles.
After 37 days of refrigeration in a PET bottle,
Sb levels in the water rose to 50 ng/L. Six
months after storage at room
temperature, Sb concentration rose to
556 ng/L.
The report emphasises that all of
the waters measured in this study were
found to contain Sb levels well below
the guidelines commonly
recommended for drinking water:
WHO 20 ug/L; US EPA, Health
Canada, and the Ontario
Ministry of Environment 6 ug/L;
German Federal Ministry of
Environment 5 ug/L; Japan 2
ug/L (1ug/L is 1,000 ng/L).
However, given that
there appears to be a continual
release of Sb from the
containers to the water, further
investigation of the extent and
intensity of contamination is
warranted. Also, since the Sb
concentrations in the water
mainly reects the duration of
storage, perhaps bottled water
should be dated for expiry.
Reference:
Shotyk W et al. (2006) Contamination of
Canadian and European bottled waters with
antimony from PET containers. J. Environ. Monit.
8: 288-292.
Trends News & Notes
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Erectile
dysfunction
drugs protect
stomach?
Nonsteroidal anti-inammatory drugs
(NSAIDs) reduce swelling and inammation
and relieve pain and fever. Aspirin (acetyl
salicylic acid) is the best-known and most
widely used NSAIDs.
These drugs work by inhibiting an enzyme
called cyclooxygenase (COX). This enzyme is
responsible for the bodys production of
prostaglandins, hormone-like substances
involved in inammation and pain.
At least two forms of the enzyme exist:
COX-2 is found in activated inammatory
cells and is associated with inammation.
Suppression by NSAIDs reduces
inammation and pain.
COX-1 is responsible for the generation of
prostaglandins, PGE
2
. Supressing COX-1 and
gastric PGE
2
productions result in decreased
blood ow and increased leukocyte adhesion
in the stomach. This leads to erosion of the
stomach lining and cause bleeding and ulcers.
Specic NSAIDs that suppress only COX-2
produce the desirable anti-inammatry
effect. Since they do not inhibit COX-1, they
do not cause gastric complications. However,
most COX-2 selective inhibitors have been
withdrawn from the market after being linked
to adverse effects on the cardiovascular
system, including increased risk of heart
attack and stroke, and severe skin reactions.
Sildenal (Viagra), a phosphodiesterase V
(PDE V) inhibitor, is used for the treatment of
erectile dysfunction. A recent animal
investigation found that sildenal protects
experimental rats from stomach
complications casused by indomethacin, a
NSAID. The drug reduces indomethacin-
induced gastric damage by increasing gastric
blood ow and limiting leukocyte adhesion
in the stomach.
This study suggests that administration of
a PDE V inhibitor with an NSAID may prevent
the unwanted stomach side effects of
NSAIDs. Further clinical research in humans
is required to support this nding.
In addition to sildenal, other PDE V
inhibitors such as vardenal (Levitra) and
tadalal (Cialis) share similar mechanisms
and may offer similar protection against
gastric side effects from NSAIDs. Other than
being a prescription drug for erectile
dysfunction, the use of PDE V inhibitors are
currently being evaluated for treatment of
hypertension, heart attack, stroke, diabetes,
and congestive heart failure in clinical and
pre-clinical studies.
References:
Santos CL et al. (2005) Sildenal prevents indomethacin-induced
gastropathy in rats: role of leukocyte adherence and gastric blood
ow. British Journal of Pharmacology 146: 481486.
Sawatzky, DA et al. (2005) Sildenal offers protection against
NSAID-induced gastric injury. British Journal of Pharmacology 146:
477478.
Woody medicine
Creosote describes a variety of products: wood
creosote, coal tar creosote, coal tar, coal tar
pitch, and coal tar pitch volatiles. These
products are mixtures of chemicals created
from high-temperature treatment of woods,
coal, or from the resin of the creosote bush.
Wood creosote was rst prepared and used
for medicinal purposes in 1830 in Germany.
There are four major active components in
wood creosote: guaiacol, creosol, o-cresol,
and 4-ethylguaiacol. Wood creosote is listed
in the Japanese Pharmacopoeia and is used
for the treatment of diarrhea.
A recent review published in Yakugaku
Zasshi, the Journal of Pharmaceutical Society
of Japan, attributes the antidiarrheal effects
of wood creosote to its antimotility and
antisecretory actions. By blocking the
chloride channel on the intestinal
epithelium, wood creosote inhibits intestinal
secretion induced by enterotoxins. It also
inhibits the inux of calcium ions into
gastrointestinal smooth muscle cells, thus
reducing intestinal motility accelerated by
mechanical, chemical, or electrical stimulus.
A laboratory study compared the
antisecretory effects of wood creosote with
a popular medication used for the relief of
acute and chronic diarrhea, loperamide.
In experiments on acetycholine induced
responses in the jejunum and colon, it was
found that loperamide is most potent in the
jejunum, while wood creosote showed equal
potency in both jejunum and colon.
A multicenter, double-blind, randomized
study with adult patients with acute, non-
specic diarrhea concluded that wood
creosote and loperamide had comparable
antidirrheal effects. Wood creosote appears
more effective in improving or resolving
stomach cramping, whereas loperamide
appears more effective in improving
diarrhea. Both treatments were well
tolerated. The dose of wood creosote used
in this study was up to 5 doses of 135 mg
per day, for up to 3 days.
Like all medications, dosage is important.
The Agency for Toxic Substances and Disease
Registry (ATSDR) of the U.S. Department of
Health and Human Services warns that,
Eating large amounts of creosote (any form)
may cause a burning in the mouth and throat
and stomach pains. Eating large amounts of
herbal remedies containing creosote bush
leaves may cause liver damage.
References:
Ataka, K et al. (2005) New views on antidiarrheal effect of wood
creosote: is wood creosote really a gastrointestinal antiseptic?
Yakugaku Zasshi 125: 937-50.
Greenwood-Van Meerveld, B et al. (2000) Comparison of the
antidiarrheal effects of wood creosote and loperamide in the rat
jejunum and colon in vitro. Biol Pharm Bull 23: 952-6.
Kuge, t et al. (2004) Multicenter, double-blind, randomized
comparison of wood creosote, the principal active ingredient of
Seirogan, an herbal antidiarrheal medication, and loperamide in
adults with acute nonspecic diarrhea. Clin Ther 26: 1644-51.
Agency for Toxic Substances and Disease Registry, Wood creosote,
coal tar creosote, coal tar, coal tar pitch, and coal tar pitch volatiles.
http://www.atsdr.cdc.gov/tfacts85.html
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Trends News & Notes
Amazing gut
Is longer better?
Longer guts are more efcient in digesting
food and absorbing nutrients. They force
food to spend more time passing through,
providing more chances for the gut to digest
and absorb nutrients. But there may be a
link between gut length and environment.
Experiments on tadpoles conducted at
the University of Pittsburg show that the
greater the competition for food, the longer
the gut grows. Food may not come by as
easily when competition is erce, so the gut
needs to be able to extract as much nutrient
from the food as possible.
However, studies on the same tadpoles
also show that in an environment where
quick escape from predators is necessary,
gut length is reduced. This accommodates a
longer tail that is needed for a fast get away.
The gut length of some animals seems to
be related to an effective balance between
environmental factors important for survival.
Rapid gut change to accommodate
a travelers diet
Migrating birds have to cope with seasonal
changes in food supply and diet. A
researcher at the Royal Netherlands
Institute for Sea Research found that the
gizzard of the migrating bird red knots
grows rapidly and triples in organ weight
when their diet changes from soft foods
(e.g. shrimps) to hard foods (e.g. mussels).
This and other studies have also found
that depending on the ying distance,
fueling-stopping frequency, and feeding
needs of the migrating birds, their gut may
grow in size or shrink at different phases of
their ight. The extent and efciency of this
kind of intestinal plasticity is amazing.
The hibernating gut
It seems that in some hibernating animals,
their gut shrinks dramatically to maintain
minimal function and preserve body
resources during hibernation. As much as
70% gut mass can be lost in the rst 3
months of hibernation in an Australian green
strip burrowing frog.
But efcient digestive capability is also
preserved so that they can quickly digest and
absorb nutrients upon awakening.
Findings show that even though the gut
lining of these animals atrophies, there is
limited tissue damage as the genes that
curtail cell death are active at the same time.
The surviving nutrient absorbing cells from
the hibernating animals have actually been
found to be more efcient than those from
similar non-hibernating species.
Reference:
Pennisi E, (2005) The dynamic gut. Science 307:1896-1899
Finding the
stress-gut
connection
Gut dysfunction and diseases are related
to stress and early life events. But the
mechanisms involved are not well-dened.
Studies show that severe or chronic stress
induces long-term alterations in stress
response. Stress hormones mediate
increased colonic motor activity and slowed
gastric emptying in response to stress.
Researchers from the Intestinal Disease
Research Program at McMaster University are
among those examining the gut-brain
connections. They report that in animal
studies, stress has been shown to induce
mucosal barrier dysfunction (increased
epithelium permeability to large antigen
molecules), and increase gut motility and
secretion of chloride.
There is also evidence that early life
trauma and chronic stress affect the clinical
course of intestinal disorders and reactivate
inammation in colitis. Both genetics and
environmental factors are important in
determining how the gut mucosal response
to stress.
References:
Bhatia V & Tandon RK (2005) Stress and the gastrointestinal tract. J
Gastroenterol Hepatol 20(3): 332-339
Soderholm JD et al (2002) Chronic psychological stress induces
mast cell-dependent bacterial adherence to epithelium and
initiates mucosal inammation in rat intestine. Gastroenterology
123:1099-1108
Soderholm JD et al (2002) Neonatal maternal separation
predisposes adult rats to colonic barrier dysfunction in response to
mild stress. Am L Physiol 283:G1257-1263
Direct to the gut
The immune system is compartmentalized
into primary, secondary, and tertiary organs.
Current theory maintains that lymphocytes
(immune cells) are produced in primary
lymphoid organs (thymus and bone marrow).
These new lymphocytes then travel to
secondary lymphoid organs, such as the
spleen, lymph nodes, and Peyers patch
(located in the submucosa of the intestine),
where they are exposed to antigens and
become activated (learn to recognize specic
foreign antigens). Then they enter the
tertiary nonlymphoid sites, such as the skin
and intestine, and contribute to the bodys
defense system.
A team of US scientists recently demon-
strated that this concept might not be
complete. They show that a type of lympho-
cytes (CD8+ T) from mice have a unique surface
composition that allows them to migrate
directly from the blood to the small intestine
epithelium and engage in immune function.
Reference:
Staton TL et al. (2006) CD8+ recent thymic emigrants home to and
efciently repopulate the small intestine epithelium. Nature
immunology advanced online publication; 2 April 2006;
doi:10.1038/ni1319.
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Reasons why you can trust
Shaklee products:
Guaranteed potency all products are
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the nutrients it needs
Shaklees commitment to research
over $250-million has been invested in
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standards assurance that each product
delivers the correct dosage of key
ingredients based on clinical research
Exemplary quality control over 83,000
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annually to guarantee quality and purity
Backed by c|rnrca| studres, over 100
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All Shaklee formulations are based on
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Company has 50 years of experience
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So how do your products compare?
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Since/Depuis 1956
Adult testis
stem cells to
replace
embryonic
stem cells ?
Researchers have now isolated stem cells
from adult mouse testis that can develop
into different kinds of cells, much like
embryonic stem cells (ESC).
Scientists at the Georg-August-
University of Goettingen in Germany have
isolated spermatogonial (sperm-
producing) stem cells from the adult
mouse testis. Under certain laboratory
conditions, some of these cells have
grown into colonies much like embryonic
stem cells, capable of differentiating into
multiple organ tissue cells. They call
these cells multipotent adult germline
stem cells (maGSCs).
Finding adult stem cells that can be
easily harvested has important
implications. At present, therapeutic
experiments with stem cells to grow
genetically matched cells or to regenerate
organ tissue require the use and harvesting
of ESCcells. This has created both technical
difculties and ethnical controversies.
If human adult stem cells with
properties similar to embryonic stem
cells can be extracted from men using a
simple testicular biopsy, they could
replace the need to grow humanESC for
theraputic or research purposes.
Furthermore, these easily harvested adult
stem cells may provide new opportunities
to study genetic diseases.
For more on stem cells, harvesting
embryonic stem cells, technical and
ethnical problems of using embryonic stem
cells, and germline cells for genetic re-
search, refer to WellnessOptions issue 19.
References:
Guan K et al. (2006) Pluripotency of spermatogonial stem cells
from adult mouse testis. Nature, 440, doi: 10, 1038.
Kubota H and Brinster RL (2006) Technology insight: in vitro
culture of spermatogonial stem cells and their potential
therapeutic uses. Nature Clinical Practice Endocrinology &
Metabolism 2: 99-108.
Taste
sensitivity
in smoking
Bitter taste perception is the most
complex of the basic tastes. The
ability to taste the bitter compounds
phenylthiocarbamide (PTC) and 6-n-
propylthiouracil (PROP) in humans is
well-studied.
Recent research indicates that the
ability to taste bitter taste may protect
against cigarette smoking. There seems
to be lower PROP taste sensitivity and
fewer PROP taster buds among smokers
than nonsmokers. Furthermore, the
ability to taste PTC is less prevalent
among heavier smokers compared to
nonsmokers or people who smoke less
than 8 cigarettes a day.
A study examining the association
between bitter-taste PTC gene
polymorphisms and cigarette smoking
also found that smokers who are less
sensitive to bitter taste were more likely to
smoke for the taste of cigarettes.
Blood samples from the participants
were examined for the PTC genes two
most common sets of alleles-PAV and AVI,
named for the amino acids at their three
genetic-pair locations. Those with only
PAV are most sensitive to bitter taste,
while those with only AVI are less
sensitive. AVI non-tasters were more
likely than the PAV tasters to smoke for
the taste of the cigarettes.
Researchers suggest that inherited taste
sensitivity and the taste of the cigarettes
may be factors in nicotine dependence. A
similar relationship between bitter taste
perception and alcohol consumption has
also been reported.
For more on how the senses of taste
and smell work, refer to WellnessOptions
issue 20.
References:
Cannon DS et al. (2005) Associations between
phenylthiocarbamide gene polymorphisms and cigarette
smoking. Nicotine Tob Res 7: 853-58
Enoch MA et al. (2001) Does a reduced sensitivity to bitter
taste increase the risk of becoming nicotine addicted?
Addictive Behavior 26:399 - 404.
Trends News & Notes
Canada is almost at the bottom
among Western countries in terms of
how long a patient has to wait to
consult a specialist for digestive
system probelms.
As the crisis of GI specialist
(gastrointestinal specialist, or
gastroenterologist) shortage worsens,
the already long waiting line for
diagnosis and treatment of gut
problems is getting even longer.
According to William Paterson,
President of the Canadian Association
of Gastroenterology (CAG), there are
about 550 gastroenterologists
currently in the country. This
amounts to 1.83 GI specialists per
100,000 people, putting Canada
behind the US (3.9), France (3.1), and
Australia (2.2).
Among Western countries, only the
UK (1.5) is behind Canada, But they
already recognized the crisis and have
plans in place to double or triple the
number of GI specialist in the country.
While Canada has not recognized
the crisis, and has no plan to improve
the service level, Paterson points out.
Shortage crisis
A GI specialist is a physician who
specializes in diseases of the stomach,
intestines, and associated organs in
the digestive system. According to
Paterson, at the present time, about
60% of GI specialists in Canada are in
the 45-61 age range.
If trainees continue to come in at
the present rate, Canada will have
10% fewer GI specialists in 10 years
time. There is a 2 to 3 years lag time
in training, so governments need to
respond quickly to the problem.
CAG report
The CAGs Gastroenterology Wait Time
Program Report, based on data from
5,500 patient visits to about 200 GI
specialists across Canada, was released
in September 2005. It shows that:
Half of the patients referred to a GI
specialist by family doctors have to
wait for more than 2 months; one
in four waits for more than 4 months.
Half of them have to wait for
another 6 weeks for a diagnostic
test; one in four waits for another 4
months for tests.
Over one third of the patients have
alarm symptoms, which may
indicate serious underlying disease
such as cancer.
Half of the patients with alarm
symptoms have to wait nearly 2
months to see a specialist and have
tests performed. One in four of
them waits for more than 4 months.
Half of the patients classied as
urgent who required consultation in
7 days have to wait for 2 weeks,
while one in four of them waits for
more than 5 weeks.
Even though approximately 20,000
new cases of colon cancer are
diagnosed each year, and colon
cancer is 95% preventable with
timely and thorough testing, the
wait for a screening colonoscopy is
long. More than half of all patients
who are at average risk for colon
cancer have to wait from 2 months
to a year for a colonoscopy.
Prevalence
The most common reasons why
Canadians are referred to a GI specialist
include lower gastrointestinal bleeding
(19%), abdominal pain (17%),
dyspepsia (9%), and irritable bowel
syndrome (8%). Upper gastrointestinal
bleeding, diarrhea, inammatory
bowel disease, and screening
colonoscopy each accounted for 7%
of the total referrals. While chest pain,
dysphagia (difculty swallowing),
reux, and constipation each
accounted for 5% of the referrals.
Data from the CAG indicates that
digestive diseases are responsible for
15% of the total direct economic
burden of Canadian health costs.
Digestive diseases cause frequent short-
term loss of productivity, costing $1.14
billion/year and exceeding the cost of
mental, cardiovascular, respiratory, and
central nervous system diseases.
Recommendations
The CAG has set targets for maximal
medically acceptable wait times for 24
different GI conditions such as acute
gastrointestinal bleeding, rectal
bleeding, hepatitis etc., which require
consultation and treatment by a GI
specialist.
These targets aim to advance
gastroenterology care in Canada.
Wait time targets fall into 4 main
catagories. Target wait time for
consultation and screening of cases
classied as emergency is 24 hours,
for urgent cases is 2 weeks. For
common chronic diseases, target wait
time is 2 months, and for preventive
carecolon cancer screening in
patients with family historyis 6
months.
Some medical disicplines are able to
generate tremendous support from the
public and politicians, and attract
more media attention. In spite of the
signicant demand for healthcare and
treatment, there is relatively less
government funding available for
research in digestive diseases in
Canada. Similarly, there are fewer
university staff and hospital resident
doctors training for gastroenterology.
Improvement in gastroenterology
care requires prompt support from
both the federal and provincial
governments.
It may not always be feasible for
government and research agencies to
provide enough funding to meet the
expectations of medical professionals
and patients. However, funding
allocation should be balanced to
reect the healthcare needs of the
general public.
References:
Paterson GW, President of the Canadian Association of
Gastroenterology, personal communication.
Canadian Association of Gastroenterologist. Gastroenterology wait-
times program: result. http://www.cag-acg.org/mediaroom/pdf/
GASTROENTEROLOGY%20WAIT-TIMES%20PROGRAM%20
RESULTS%20-%20ENG.pdf
Canadian Association of Gastroenterologist. Canadian consensus on
medically acceptable wait-time targets: 24 recommendations.
http://www.cag-acg.org/mediaroom/pdf/CANADIAN%20
CONSENSUS%20ON%20MEDICALLY%20ACCEPTABLE%20-20ENG.pdf
A growing
line up
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Perspectives Cover Story
by Lillian Chan
H
ow an individual digests
and absorbs nutrients is
inuenced by genetic,
environment, and
psychological factors,
resulting in individual differences in
food metabolism, energy storage, and
nutritional status.
Research suggests that even
though the calorie value of food
items are listed on the food label,
there are individual differences in
the amount of energy harvested from
them. The length of time food
materials stay in the gut, gut motility
and secretion, and the composition
of an individuals gut microbial ora
can all inuence the efciency of
harvest. High harvest efciency
promotes fat storage and low
efciency leads to leanness.
Interplay with emotions, social
cues, and learned behaviours
Food intake, digestion, and absorption
are also inuenced by emotions,
social cues, and learned behaviours.
The guts intrinsic nervous system
(enteric nervous system) contains
about 100 million sensory neurons, as
many as found in the spinal cord, and
is very sensitive to our emotional states.
Excitement hastens stomach
emptying, and fear slows it. Stress
depresses gut function, compromises
gut defenses against pathogens, and
increase susceptibility to inammation.
New studies have found that both
early life trauma and on-going
psychological stress can affect the
onset and the course of intestinal
diseases. For example, scientists have
found that newborn mice separated
from their mothers are more prone as
an adult to gut barrier permeability
dysfunction, and are therefore more
susceptible to inammation when
exposed to even mild stress. (See
other articles in this issue for more).
On the other hand, gut disease can
also alter brain function. New animal
studies have shown that chronic
helicobacter pylori infection produces
changes in gastric motor-sensory
The
inter
connected
gut
Effective gut function is essential for well-being.
Many factors impact gut function, which in turn affects
our physical health, mood, brain function, and energy status.
025_14_21_Persp_Absorb_V6.qxd 4/6/06 11:00 PM Page 1
mechanisms and food intake
behaviour. This indicates that a
localized bacterial infection in the gut
can produce changes in brain function.
We tend to eat faster when our
companions are eating quickly. We
also tend to eat more when dining
out, especially at a buffet. Researchers
are beginning to nd out more about
how social cues and learned
behaviours affect diet, food
preferences, and gut function.
For example, meal frequency, and
therefore how much food and how
much time we give our gut to digest
a meal, is inuenced by many factors
besides the availability, amount and
type of foods. They include cultural
differences, income level, employment,
physical activity levels, mood, gender,
age, education, climate, and family
tradition.
Roles in regulating food intake,
energy store, and nutrition status
In addition to digestion and absorption,
the gut and its associated visceral
organsliver, pancreas, and adipose
(fat) depotsalso play important roles
in the communications involved with
the regulation of food intake, energy
storage, and nutrient status. The gut
employs both neural and hormonal
pathways to sense and send signals to
the brain, where other signs of energy
and nutrition requirements are
integrated.
The interplay between gut function
and regulation of food intake, energy
storage and nutrition status, and how
that interact with emotions and
psychological factors, are being
actively investigated. Findings may
have implication in prevention or
treatment of some health conditions.
For example, the gut hormone leptin
is involved with the regulation of
appetite. Its interaction with the brain
and other body systems may have
implications for ghting obesity.
A community inside the gut
It is estimated that there are 100
trillion microorganisms in the gut.
This is more than the total number of
cells in our body and far more than
all the microbial communities
associated with our bodys surfaces
such as skin and hair. The density of
bacteria living in the gut is the
highest among all known ecosystems.
The microbial community of the gut
plays important roles in gut function.
Colonization of our gut starts at birth
and continue through life. It provides
us with metabolic advantages
including the ability to access some
nutrients that we are unable to access
and absorb otherwise.
Some of the microbes are essential
for food digestion and fermenting
processes. Some are harmful to our
body. New studies are nding out
how gut microbial ora maintains
balance and how members can
complement or harm us.
For example, scientists compared
mice raised with germ-free (GF) gut
(without exposure to any micro-
organism) to those conventionally
raised (CR) that had acquired a normal
microbial gut environment after birth.
They found that young CR adult
mice have 40% more total body fat
than GF mice even though they were
all fed the same diet with the same
calories. The researchers concluded
that some indigestible sugars were
made accessible by gut microbes in
the CR mice.
Inammation and allergyupset
connections?
Our gut requires a large surface area
for optimal absorption. But the
environment in the lumen is harsh
and threatening, causing lining cells
to die and be replaced rapidly. Also,
the gut lining consists of only a single
layer of cells. So the gut immune
system is constantly being challenged
while trying to defend this long, thin
line of defense.
The gut immune system also has
to be sensitive to pathogens while
remaining unresponsive to normal
food components and members of
the guts normal microbial ora.
Many infectious diseases involve the
gut. In western countries, most of these
diseases are under control. However,
the integrity of the gut immune
system appears to be increasingly
compromised. Food allergies and
chronic inammation diseases
(inammation without infection)
are becoming more common.
The cause for this is not clear.
However, scientists are nding that
in both human and animal studies,
mutations in genes that control
immune recognition, adaptive
immunity, and gut epithelium
permeability are all associated with
gut inammation. An optimal balance
between gut antigen and gut
immunity may be an important factor
in the development of gut
inammation and allergy.
The prevailing hypothesis is that
the absence of infection may have
upset this balance between normal
healthy gut microbial ora and the
mucosal immune system. New
research ndings on the interplay
between genetics, microbial ora, and
the gut lining will have implications
for treatments of gut inammatory
diseases and allergy.
For more on Stress and gut function,
refer to p.26; How we eat and
Hormones and appetite refer to
WellnessOptions issue16; Gut
microora, refer to WellnessOptions
issue 11, 20; Stress, immune response
and allergy, refer to WellnessOptions
issues 3, 14, 20; How early
development affect us, refer to
WellnessOptions issue 24
References:
Badman MK & Flier JS (2005) The gut and energy balance. Science
307:1909-1914.
Bhatia V & Tandon RK (2005) Stress and the gastrointestinal tract. J
Gastroenterol Hepatol 20(3): 332-339.
Ganong WF (2003) Review of Medical Physiology 21st ed. Lange
Medical Publications
MacDonal TT & Monteleone G (2005) Immunity, inammation, and
allergy in the gut. Science 307: 1920-1925.
McPhee S, Lingappa VR, Ganong WF, Lnage JD (1997)
Pathophysiology of Diseases
Soderholm JD et al (2002) Chronic psychological stress induces
mast cell-dependent bacterial adherence to epithelium and
initiates mucosal inammation in rat intestine. Gastroenterology
123:1099-1108.
Soderholm JD et al (2002) Neonatal maternal separation
predisposes adult rats to colonic barrier dysfunction in response to
mild stress. Am L Physiol 283:G1257-1263.
Staton TL et al. (2006) CD8+ recent thymic emigrants home to and
efciently repopulate the small intestine epithelium. Nature
immunology advanced online publication; 2 April 2006.
A
passage of
connection
A
n average North American consumes about
36.3 metric tones (40 tones) of food in a lifetime.
This amounts to about 9.5 litres (2.5 gallons) of
processing a day. Most of the food is not in a form that
the body can readily use as nourishment.
Carbohydrates, proteins and fats must be broken down
into small absorbable units (digestion). They must pass
from the gut into the blood circulation and be carried to
different parts of the body (absorption) to nourish cells,
sustain life, and provide energy.
The types of food we eat have a direct impact on
digestion and absorption. For example, the rate of
digestion in the stomach is fastest for carbohydrates.
Proteins take longer, and fats are the slowest.
Digestion and absorption make heavy demands on the
circulatory system, increasing blood ow to the gut by
about 50% after eating. Thats why we may feel sleepy
after a big meal, as more blood is drawn to the gut.
by Lillian Chan
THE TUNNEL
The gastrointestinal tract (GI tract or
gut) is the passage through which
foods are digested and absorbed into
the body. Although gut lumen, the
inside of the GI gut, seems to be
inside the body, it is actually an
external space through the body. It is
a series of hollow organs (like rooms)
connected in a long, twisting tube
(like joining corridors) from the mouth
to the anus, about 10 meters (30 feet)
in length when completely relaxed.
Food undergoes mechanical and
chemical changes in the mouth,
esophagus, stomach and the rst part
the small intestine, the duodenum,
before it is rendered suitable for
absorption.
PERISTALSIS
It is a reex response that moves
food along. It occurs in all parts
of the gut from the esophagus
to the rectum (see gure).
Propelling rates vary from 2 to
25 cm/second. The wave of
contraction can be increased
or reduced by food intake
and emotional state.
BASIC ELECTRICAL RHYTHM
The function of this rhythm (similar
to heart beat) is to co-ordinate
peristaltic contraction and other
motor activities. Contraction only
occurs when muscles are tensed
during the depolarized part of the
rhythmic wave.
SALIVA AND CHEWING
About 1,500 mL of saliva are secreted
everyday. It makes chewing and
swallowing easier and more efciency and
kills some bacteria. Enzymes in the saliva
attack carbohydrates and fats. The optimal
number of chews depends on the food, but
usually ranges from 20 to 25. The chewing
period also allows the food to warm to the
temperature optimal for digestion.
SWALLOWING
Swallowing is a reex response. It
continues between meals. Total number
of swallowing average 600 times a day:
200 while eating and drinking, 350 wile
awake but not eating, and about 50 while
sleeping. Food is swept down the
esophagus at about 4 cm/second. In an
upright position, liquid and semi-solid
foods can usually falls by gravity faster,
ahead of the peristaltic movement.
STOMACH
It is behind the rib cage under the
diaphragm on the left side of the body.
Because of the way the stomach with its
liquid contents is positioned, acid reux
occurs much more commonly when a
person lies on the right side of the body.
An adult stomach can hold about 1.2
litres (2.5 pints) of materials. The stomach
lining contains about 35 million glands
that secret about 2.5 litres of gastric juice
everyday. Enzymes in the stomach attack
proteins and fats.
Food is stored, mixed with gastric acid,
mucus, and digestive enzymes and digested
for about 3-6 hours in the stomach. The
release of food from the stomach is tightly
controlled, with just the right amount
steadily entering the duodenum (rst
section of the small intestine). Fluids
empty quickly. Large chunks and solids take
longer. Carbohydrates empty rst. Proteins
take longer and fats are the slowest.
The consumption of milk, butter or olive
oil before alcohol slows down its effect.
Fats keep the alcohol in the stomach
longer where absorption is slower than in
the small intestine. Fats also slow down
stomach emptying, releasing smaller
amounts of the alcohol to the small
intestine for absorption. This gives more
time for the body to metabolize and
eliminate the alcohol.
Other factors that slowed stomach
emptying include low temperature (e.g. ice
cream), exercise after a meal that divert
blood ow from the stomach to the heart
and muscle, and strong emotions that
depress gut function
SMALL INTESTINE
This is the longest section of the gut, and
consists of the duodenum, the jejunum,
and the ileum. While we are alive, the
small intestine is just short of 3 meters.
After death, it relaxes to become about
7 meters long.
As food enters the duodenum,
it stimulates four organs to release
chemicals to complete the digestion
processes. The small intestine secretes
mucus to protect the duodenum from the
gastric acid. It also produces hormones to
stimulate the liver, the pancreas and the
gallbladder to release digestive juices
such as bile. The pancreas secretes
digestive enzymes that attack carbo-
hydrates, proteins and fats. It also
secretes hormones such as insulin, which
regulates the use of glucose in the body.
When food is in the small intestine, the
muscles encircling the gut contract rapidly
at about 7 to 12 times per minute. This
movement churns and kneads the food
back and forth. Peristaltic movement here
is weaker, so the food stays in one place
longer for nutrient absorption. But toxic
substances can stimulate strong propelling
movements to expel the guts conents.
3
D
C
l
i
n
i
c
S
everal enzymes are located in
the brush border of the small
intestine, where digestion of
food into simple molecules is
completed and the task of absorption
kicks into full gear.
Most nutrients are absorbed in the
upper small bowel. An exception is
vitamin B12 which is absorbed
exclusively in the lower end of the
small bowel.
Absorption
Most of our knowledge about nutrient
absorption was gathered by classical
investigations, in which elementary
diets of different sugars, amino acids,
and lipids were fed to people and
their manifestations in the blood
circulation measured.
It is only with the more recent
advance of biochemical, molecular, and
histological research tools that we are
able to gain insight into the workings
of enterocytes, the absorbing cells.
In order to get from the gut to the
blood or lymph, nutrients must enter
into the enterocyte, travel through it
unchanged or changed, and leave the
enterocyte to enter blood circulation.
Food molecules enter from the
intestinal lumen through the apical
end (tip), and exit at the opposite
end through the basal membrane.
Absorption at the cellular level is a
complex process.
Some health implications of
absorption
Glucose and fructose are both sugars
but because their absorption is
through different mechanisms, their
rates of absorption and metabolism
are different. The glycemic index for
fructose is lower than that of glucose,
indicating that fructose raises blood
sugar levels slower than glucose.
The solution used for rehydration
(e.g. people suffering from diarrhea)
always contains sodium because
sodium helps to absorb the glucose
that provides energy.
Medium chain fatty acids (e.g.
coconut oil) are well absorbed and
can satisfy energy needs when certain
diseases inhibit long chain fatty acid
(e.g. animal fats) absorption.
High cholesterol diets do not affect
everybody in the same way. How
cholesterol transfer proteins work may
explain the difference.
Vegetarians are at higher risk of
iron deciency since non-haem iron
from plant food is poorly absorbed.
Vitamin B12 deciency is common
in patients with gastric problems (e.g.
lack of intrinsic factor) and in Crohns
disease when the site of vitamin B12
absorption is affected.
Epithelium
The gut lumen is surrounded by the
gastro-intestinal tract wall. In general,
the layers that make up this wall
include the longitudinal muscle, the
circular muscle, the submucosa
(connecting tissue), and the mucosa.
The epithelium (outer top layer
of cells in the mucosa), like the
epidermis (top layer of cells) of the
skin, makes up a barrier between
the body and the outside world in
the lumen.
While the skin epidermis is made
up of several layers of cells, the gut
epithelium is made up of only a single
layer of cells. These single-layered
cells not only digest food and absorb
the resulting mix of nutrients, they
must also keep indigestible food bulk
and pathogens from getting through
into the body interior.
The mucosal immune system keeps
tight surveillance of the gut lining.
A new report published this month
estimates that over 1 billion immune
T cells are found in the human small
intestine. They are posted to patrol
and defend the gut lining. Researchers
have also discovered a unique route
by which immune T cells home in to
the small intestine. (See note).
Enterocytes: absorbing cells
The gut lumen is surrounded by the
mucosa, which forms 0.5-1.0 mm
long ngerlike projections called villi.
Capillaries and lymph vessels run in
the centre of the villi. In the crypts
between the villi, stem cells
differentiate into enterocytes
(absorbing cells). As they mature,
they move up the villus.
Matured enterocytes reach the tip
in 48-72 hours. Their lifespan is short
due to the harsh environment in the
gut. After 2-5 days, they are sloughed
off into the lumen. We lose 17 billion
absorbing cells each day.
The enterocytes form a single layer
and are tightly attached to each other.
No nutrient can pass between the
cells. At its apical surface, an
enterocyte has about 1,000 microvilli.
The villous structure of the small
intestine enhances the absorptive
surface area by about 600 times
compared to what it would be if its
walls were smooth.
Nutrient
absorption
by Hilda Donhoffer, MD, FRCPC
025_14_21_Persp_Absorb_V6.qxd 4/10/06 1:36 AM Page 5
Entry into enterocyte Example
No energy required:
Simple diffusion oxygen, carbon dioxide, alcohol
Facilitated diffusion
facilitative proteins fructose
ion channels* sodium, potassium
Energy required:
co-transporter glucose, amino acids
endocytosis vitamin B12
*To be discussed in a future issue
In enterocyte Example
Unchanged glucose, fructose
Bound to carrier protein vitamin B12
Chemical change fatty acids
Forming complex particles triglycerides, cholesterol
Storage iron
Exit from enterocyte Example
Simple diffusion oxygen, carbon dioxide, alcohol
Facilitated diffusion glucose, fructose
Sodium pump sodium
Carrier protein iron
Exocytosis vitamin B12, lipoproteins
MECHANISMS OF ABSORPTION
LAYERS OF THE GI TRACT WALLS WALL OF SMALL INTESTINE EPITHELIUM
(TOP LAYER OF CELLS
IN THE VILLI)
Submucosa
connective
tissue
Mucosa Villi
Crypt
Mucosa
Microvilli Muscle
Enterocyte
(absorbing
cell)
Submucosa
Nucleus
Circular
muscle
Longtitudinal
muscle
025_14_21_Persp_Absorb_V6.qxd 4/10/06 10:59 AM Page 6
Inside of cell
Outside of cell
Fructose Fructose
DIFFUSION OF FRUCTOSE
Inside of cell
Low Na
+
/ High glucose
Intestinal lumen
High Na
+
/ Low glucose
Glucose 2 Na
+
Glucose 2 Na
+
ACTIVE TRANSPORT OF GLUCOSE
To blood
Enterocyte
Lumen
To lymphatics
Esterification
Uptake
Lipoprotein
formation
Exocytosis
Fatty acid
Short &
medium chain
fatty acid
Long chain
fatty acid
Triglycerides
ABSORPTION OF FATS
Inside
of cell
Outside
of cell
Gases
CO
2
H
2
O
O
2
Ethanol
Glucose
Protein
(Amino Acids)
H
+
Ions
Cl
-
Small
molecules
Large
molecules
Charged
molecules
PERMEABILITY OF ENTEROCYTE
How are nutrients absorbed?
Different nutrients have different
chemical structures and are absorbed
differently. There are several known
mechanisms by which nutrients enter
into the enterocyte.
Oxygen, carbon dioxide
and alcohol absorption
Simple diffusion
Molecules tend to move from an area
of higher concentration to an area of
lower concentration, or along their
concentration gradient. Only oxygen,
carbon dioxide, and alcohol can pass
into the enterocyte by simple diffusion.
Fructose (carbohydrate) absorption
Facilitated diffusion
Fructose is a simple sugar found in
fruits. It enters with the help of a
transporter protein embedded into the
apical membrane of the enterocyte.
After passing through the cell, fructose
leaves by a similar mechanism and is
taken up by the blood.
Glucose (carbohydrate) absorption
Na+ dependent glucose transporter
Glucose enters the enterocyte arm-in-
arm with sodium (Na+) through a
special protein transporter (Na+ -
glucose co-transporter). Na+
concentration in the cell is low. Na+
therefore moves from the high
concentration intestinal lumen into
the cell, taking glucose with it.
After glucose passes through the
cell, it moves out alone through
another transporter protein (by
facilitated diffusion) at the basal end.
The Na+ is pumped out actively. Both
enter the capillary blood circulation.
Protein (amino acids) absorption
Na+ dependent amino acid
transporters
Amino acids are also dragged along by
sodium, similarly to glucose. However,
there are at least 7 transporter proteins
due to the varied chemical structure of
different amino acids. Outbound trafc
of amino acids goes through 5 known
transport systems. Amino acids are
also taken up by the blood circulation.
Fat (triglyceride) absorption
Transporter proteins
This is a complex process. Trigly-
cerides are compounds in which 3
fatty acids of variable length are
bound to a glycerol (an alcohol).
Digestive enzymes split off two fatty
acids so glycerol is left with one
(monoglyceride). Monoglycerides and
all fatty acids use trans-port proteins
to enter into the enterocyte.
Fatty acids that have a carbon chain
of less than 12 carbons (short chain)
leave the cells and enter the blood
circulation.
The fate of long chain fatty acids is
more complex. Within the enterocyte,
they are attached again to glycerol and
form triglycerides (re-esterication).
Then they are combined with proteins
and form lipoprotein particles. These
are transported in vesicles to the basal
membrane and ejected from the
enterocyte by exocytosis (binds to a
cell surface receptor and leaves).
Lipoproteins do not enter the blood
but are taken up by the lymphatic
system that drains later into the blood
circulation.
For more on fats, triglycerides,
lipoprotein, and fatty acids refer to
WellnessOptions issue 21.
Cholesterol absorption
Transfer protein
In spite of the attention this molecule
receives as a cardiovascular risk factor,
the absorption of cholesterol from the
intestinal lumen has only been recently
claried. In 2004, a gene (NPC1L1)
was identied. It codes for a special
cholesterol transfer protein that is located
at the apical end of the enterocyte. The
intracellular biochemical pathway has
not been dened yet. However, we
know that cholesterol, packaged into
lipoproteins together with triglycerides
and phospholipids, leaves the
enterocyte by exocytosis.
Iron absorption
Metal transporter protein
Two different transporters are involved.
One for haem iron and another for
non-haem iron.
Haem is a large molecule with an
iron atom in its centre. Haem iron is
exclusively of animal origin. It is part
of hemoglobin in red blood cells and
myoglobin in muscle, and it transports
oxygen. Haem is efciently taken up
into the enterocyte where the iron is
released. Plants contain only non-
haem iron. This is poorly absorbed.
From the enterocyte, some of the
iron moves out with the help of
another transporter into the blood.
The rest is stored in the enterocyte,
bound to protein.
Iron absorption is tightly regulated
at the enterocyte level. When the
need increases, more transporters
appear at the apical membrane. When
the iron stores in the enterocyte are
saturated, no more iron is absorbed.
This is called the mucosal block.
The stored iron is lost when the
enterocyte cell dies.
Vitamin B12 absorption
Endocytosis
Vitamin B12 binds to intrinsic factor
(IF), a protein that is produced by the
stomach. This vitamin-IF complex is
protected from the digestive enzymes
so that it can travel unharmed until it
reaches the far end of the small
intestine where it can be absorbed.
Here it is bound to a cell surface
receptor and taken in (internalized by
endocytosis). In the enterocyte,
vitamin B12 is removed from the IF
and binds to a transporter protein.
This newly formed complex leaves the
cell to enter blood circulation.
References:
Altmann SW et al (2004) Niemann-Pick C1-like protein is critical for
intestinal cholesterol absorption. Science 303(5661): 1149-1150.
Brody T (1999) Nutritional Biochemistry 2nd ed. Academic Press
Ganong WF (2003) Review of Medical Physiology 21st ed. Lange
Medical Publications
Gunshin H et al (1977) Cloning and characterization of a
mammalian proton-coupled metal-ion transporter. Nature
388(6641): 482-488.
Murray RK et al (eds) (2003) Harpers Illustrated Biochemistry 26th
ed. Lange Medical Books/McGraw-Hill
Seetharam B and Yammani RR (2003) Cobalamin transport proteins
and their cell-surface receptors. Expert Reviews in Molecular
Medicine 5: 1-18.
T
he story of vitamin D has many
unexpected turns. Today,
scientists are still unraveling the
many different roles it plays in
sustaining life and maintaining health.
Gut absorption of vitmin D and its
regulation is affected by other body
functions, the environmental
conditions that in turn regulate these
functions, and genetics. The interplay
of many factors leads to the different
health states and consequences.
Vitamin D not only regulates the
absorption of dietary calcium and
phosphorus in the intestine, it may
also be involved in the regulation of
more than 50 genes, in neuromuscular
function, brain activity, prevention of
cancer, effectiveness of the immune
system, cardiovascular health, and
insulin production.
This is the rst part of a two-part
story on vitamin D.
History
Rickets, a disease in which bones fail
to harden resulting in knock-knees,
bowed legs, rib deformities, painful
muscle spasms in hands and feet,
breathing difculties, and convulsions,
was rst described in the 1600s.
The incidence of rickets increased
dramatically during the industrial
revolution. By 1900, it was estimated
that more than 90% of the children in
Leiden, Netherlands and 80% of
children in Boston were affected. The
geographical distribution of rickets
seemed to be related to the amount of
sunshine in a region.
By 1921, it was conclusively
demonstrated that rickets could be
successfully treated by sunbathing or
exposure to ultraviolet light. It was
found around 1927 that a lipid
molecule, sterols, in plants and animal
skins could be converted to vitamin D
by ultraviolet light. Not long thereafter,
vitamin D was chemically synthesized,
and many foods were fortied.
What is vitamin D?
Vitamins are substances necessary to
sustain life and maintain health, which
are not synthesized by the human
body and are thus required from the
diet. It has become clear now that
vitamin D is not really a vitamin. It is
synthesized in the body and is not
obtained solely or directly from foods.
The active form of vitamin D is a
hormone, a compound synthesized in
organs or tissue, which has distinct
effects on specic cells or organs in
the body.
The synthesis of vitamin D is com-
plex. The precursors are metabolized
rst in the liver and then in the kidney.
The active vitamin D
3
hormone
molecule, 1, 25-dihydroxyvitamin D
3
(Active D
3
) is then released into the
blood and reaches various tissues in
the body where it exerts specic
functions.
Working as a hormone
Some hormones act by associating
with a receptor (a molecule, usually a
specic protein, found in cells). This
combination of hormone and receptor
may then bind to specic regions of
the DNA in the cell, activating specic
genes to trigger a specic cell
function.
When a hormones receptor is
present in a cell, chances are the
hormone can affect the function of
that cell. The receptor for the vitamin
D hormone is found in cells of the
intestine and bones as expected. It
was a surprise to scientists to discover
that the same vitamin D receptor is
also present in more than 30 other
cell types in the body including skin,
nerves, prostate, colon, and pituitary
cells. In addition, some of these cells
are capable of making Active D
3
.
In fact, vitamin D hormone is
involved in the regulation of more
than 50 different genes, and probably
affects many more functions than just
calcium and bone metabolism.
by Michael F. Filosa, PhD
Vitamin D:
a story of
unexpected
turns
025_22_25_Persp_VitaminD.qxd 4/10/06 1:37 AM Page 1
DIET
salmon, mackeral,
sardines, milk, orange juice,
bread, cereal fortified with
chemically synthesized vitamin D
Liver
Pre-vitamin D
3
Vitamin D
3
25-hydroxyvitamin D
3
(OH-D
3
)
1,25-dihydroxyvitamin D
3
(Active D
3
)
Calcium
Kidney
Bone Intestine
Parathyroid
Gland
ULTRAVIOLET RAYS
in sunlight or
produced artificially
q w
e
r
t
y
i
s
k
d
f
g
h
j
u
o
a
Only small amounts are obtained
from the diet. More than 90% of
the total vitamin D we utilize
everyday was made in the skin
when exposed to ultraviolet rays
of sunlight c. The substance 7-
dehydrocholesterol in the
membranes of skin cells dis
converted to pre-vitamin D e.
Both pre-vitamin D and dietary
vitamin D are inactive forms of
the vitamin.
They are carried in blood to the
liver fwhere cell enzymes convert
them to another inactive form, 25-
hydroxyvitamin D3 (OH-D3) g.
This is carried to the kidneys h
where enzymes convert it to the
active form of vitamin D, 1,25-
hydroxyvitamin D3 (Active D3) i.
The active vitamin D is transported
to the various tissues such as the
intestine jand bones 1!.
The parathyroid gland regulates
the amount of calcium in the body
by producing a hormone that
affects the kidneys synthesis of
Active D3.
The parathyroid hormone (PTH)
in the blood stimulates the
kidneys 1# to make Active D3,
which in turn induces the intestine
1$ to transfer calcium from food to
the blood for bone formation 1^.
Calcium is not only required for
bone formation, but for other
processes as well. If the level of
dietary calcium is too low to
satisfy requirements, both the PTH
1@ and Active D3 will trigger the
removal of calcium from bones 1%
for other uses, especially by nerve
and muscle cells 1&.
Vitamin D enables the intestine
to absorb about 30% of the
calcium in our diet. During periods
of high calcium demand such as
growth or pregnancy and lactation,
as much as 60% can be absorbed.
Active D3 also stimulates the
intestinal absorption of dietary
phosphorous.
025_22_25_Persp_VitaminD.qxd 4/6/06 11:08 PM Page 2
Factors affecting synthesis and
deciency
Any interference with skin exposure
to UV sunrays affects this synthesis.
Sunscreen with a protective blocking
factor of 8 reduces the amount of
vitamin D produced in skin by almost
95%. But studies show that there is
still sufcient UV radiation reaching
the skin so that regular use of
sunscreen does not seem to result in
vitamin D deciency.
Skin cells contain melanin, a
pigment that absorbs UV rays. Dark
skin requires about a 5 to 10 times-
longer sun exposure to make the same
amount of vitamin D as fair skin.
Clothing shields the skin from direct
sunlight and also reduces synthesis.
The amount of UV reaching the skin
is also related to the time of day, the
season, air pollution, and
geographical location.
Skin can most effectively produce
vitamin D between the hours of 10 am
and 3 pm in the spring, summer, and
autumn when the sun is at 45 degrees
or more to the earth. One study found
that in June, a fair-skinned person in
Boston could maximize vitamin D
synthesis in less than 5 minutes. With
a SPF-15 sunscreen, it would take
about 20 minutes.
Since vitamin D is fat-soluble, the
excess made during sunny periods
can be stored in body fat and used in
the winter when there is less direct
sunlight. Individuals with health
conditions that interfere with fat
absorption such as cystic brosis or
Crohn's disease are at increased risk
for vitamin D deciency.
It also appears that abdominal fat
can bind much of vitamin D in an
irreversible way. Obese individuals are
therefore at risk for vitamin D
deciency. Age is also a factor. At age
70, only about 25% of vitamin D is
made compared to at age 20 with the
same amount of sun exposure.
How much is needed?
Measurement
Blood concentration of Active D
3
is
difcult to analyse. Vitamin D status
is usually determined by measuring
the amount of its precursor, 25-
hydroxyvitamin D
3
(OH-D
3
) as
an indicator.
The level of this precursor necessary
for bone health is 32 ng/mL (nanograms
per milliliter blood serum, 1 gram
equals 1,000,000,000 nanogram).
For protection against cancer and
autoimmune disease, neuromuscular
function, and cardiovascular health,
future research needs to conrm
respective effective levels.
For example, one study showed that
blood glucose is related to vitamin D
level. The optimal level for OH-D
3
to
handle glucose in non-diabetic
individuals is about 46 ng/mL,
signicantly higher than the level
needed for bone health.
Standards
What constitutes vitamin D
insufciency differs widely.
Taking into consideration the
amount of sunshine an average North
Americans is exposed to, the most
effective way to increase the level of
vitamin D is via intake of fortied
foods and/or supplements.
One study estimated that for 97%
of the US population to maintain a
sufcient level of OH-D
3
at 32ng/mL,
the intake of vitamin D per day must
be an average of 2,600 International
Units (IU) in addition to what is
synthesized by the skin. It is also
known that excess vitamin D has
adverse effects, and the toxic level is
above 6,000 IU per day.
Status and recommendations
A study of children and adolescents
aged 2 to 16 in Edmonton found that
at the end of winter, 34% were
vitamin D insufcient and 6% were
decient, with OH-D
3
levels at less
than 15 ng/mL and less than 10
ng/mL respectively. Among those
aged 9 to 16, 69% of the boys and
35% of the girls had vitamin D
insufciency.
A study on a healthy Calgary adult
population was conducted with blood
samples taken from the participants at
different seasons of the year. Using
15ng/mL of OH-D
3
as reference, it
reported that 34% of the participants
had insufcient levels at least once
during the study. If the denition of
insufciency is raised to 32 ng/mL,
then 97% of the participants had
vitamin D insufciency.
Currently, Health Canada sets the
daily adequate intake (AI) for vitamin
D for population aged 51-70 as 400 IU,
200 IU for younger persons, and 600
IU for those over 70. The upper safe
limit for all ages is 2,000 IU.
The AI is based on the amount that
healthy individuals are known to
obtain from their daily diet. It does
not necessarily reect the amount
actually required for most to achieve
optimum health benets according to
the recommended daily allowance
(RDA). No RDA for vitamin D exists
in Canada.
A Canadian researcher has proposed
that to maintain a sufciency level of
OH-D
3
in Canadian adults at about
15ng/mL, 1,000 IU per day would
be needed.
References:
Bertone-Johnson, E et al (2005) Plasma 25-hydroxyvitamin D and
1,25-dihydroxyvitamin D and risk of breast cancer. Cancer
Epidemiology, Biomarkers and Prevention 14: 1991-1997.
Chen, T and M Holick (2003) Vitamin D and prostate cancer
prevention and treatment. Trends in Endocrinology and Metabolism
14: 423-430.
Conlan, R and E. Sherman (2000) National Academy of Sciences of the
United States. http://www.beyonddiscovery.org/
VITAMIN D
deciency
insufciency
sufciency
25-(OH) D
3
BLOOD LEVEL
8 to 10 ng/mL
< 15 to < 20ng/mL or <32 to <40
ng/mL depending on researcher
above insufciency level and not
reaching toxic level
CHARACTERISTICS
rickets or osteomalacia
may not produce obvious
manifested signs of disease
no bone problems and optimum
health benet
ng = nanogram; mL = milliliter
Learning
on an empty
stomach!
Ghrelin is a gut hormone, which is known
to regulate the release of growth hormone
and stimulate appetite. It is secreted by an
empty stomach into the blood.
A new study suggests that ghrelin may
also control higher brain functions and
may represent a molecular link between
learning capabilities and energy
metabolism.
This study shows that in mice and rats,
circulating ghrelin enters the hippocampus,
a brain region critical for learning and
memory, where it binds to neurons
promoting new connections between
nerve cells, enhancing spatial learning
and memory.
The evidence that a hormone produced
in the stomach directly stimulates the
higher brain functions of learning and
memory implies that the brain may be
affected in unexpected ways by what is
going on in other parts of the body.
Based on these ndings in the animal
study, researchers suggests that since
ghrelin levels are usually highest in the
blood during the day when the stomach
is empty, learning may be most effective
on an empty stomach!
The study also found that mice lacking
the ghrelin gene have 25% fewer neuron
synapses in the hippocampus and that
injecting extra ghrelin increases synapses
and improve their learning and memory
scores.
Since aging and obesity are associated
with a decline in ghrelin levels and an
increased risk of memory loss, researchers
also suggest that administration of ghrelin-
like drugs may protect against certain
forms of dementia.
For more on the physiology of hunger,
refer to wellnessOptions issue 16, on brain
and memory, refer to issue 18.
References:
Diano S et al. (2006) Ghrelin controls hippocampal spine synapse density
and memory performance. Nature Neuroscience 9: 381-8.
Kojima, M, Kangawa, K. (2005) Ghrelin: structure and function. Physiol.
Rev. 85: 495522.
content/view.article.asp?a=414
DeLuca, H (2004) Overview of general physiologic features
and functions of vitamin D American Journal of Clinical
Nutrition 80 (suppl) : 1689S-1696S.
Garland, C et al. (2006) The role of vitamin D in cancer
protection American Journal of Public Health 96: 252-261
Garland, C and F. Garland (2005) Do sunlight and vitamin D
reduce the likelihood of colon cancer? International Journal
of Epidemiology.
Giovannucci, E. (2006) The epidemiology of vitamin D and
colorectal cancer: recent ndings. Current Opinion in
Gastroenterology 22:24-29.
Health Canada (2005) Dietary Reference Intakes for Vitamins
http://www.hc-sc.gc.ca/fn-an/nutrition/reference/table/
ref_vitam_tbl_e.html
Heaney, R (2005) The Vitamin D requirement in health and
disease Journal of Steroid Biochemistry & Molecular Biology
97: 13-19.
Holick, M (2004) Sunlight and vitamin D for bone health and
prevention of autoimmune disease, cancers and
cardiovascular disease. American Journal of Clinical Nutrition
80 (suppl) : 1678S-1688S.
Holick, M (2006) High prevalence of vitamin D inadequacy
and implications for health. Mayo Clinic Proceedings 81:
353-373.
Liu, P. et al. (2006) Toll-Like Receptor Triggering of a Vitamin
DMediated Human. Antimicrobial Response Science 311:
1770-1773.
Mark, B and J. Carson (2006) Vitamin D and autoimmune
diseaseimplications for practice from the multiple sclerosis
literature. Journal of the American Dietetic Association 106:
418-424.
McGrath, J (1999) Hypothesis: Is low prenatal vitamin D a
risk-modifying factor for schizophrenia? Schizophrenia
Research 40: 173-177.
Roth, D et al (2005) Are national vitamin D guidelines
sufcient to maintain adequate blood levels in children?
Canadian Journal of Public Health 96: 443.
Ruck, D et al. (2002) Vitamin D insufciency in a population
of healthy western Canadians. Canadian Medical Association.
Journal 166: 1517-1524.
Vieth, R and D. Fraser (2002) Vitamin D insufciency: no
recommended dietary allowance exists for this nutrient
Canadian Medical Association. Journal 166: 1541-1542.
Wactawski-Wende, J et al., (2006) Calcium plus vitamin D
supplementation and the risk of colorectal cancer. New
England Journal of Medicine 354: 684-696.
Wolpowitz, D and B. Gilchrest (2005) The vitamin D questions:
how much do you need and how should you get it? Journal of
the American Academy of Dermatology 54: 301-317.
Young, A and S. Walker (2005) Symposium-in-print UV
radiation, vitamin D and human health: an unfolding
controversy Photochemistry and Photobiology 81: 1243-1245.
Zittermann, A (2003) Vitamin D in preventive medicine: are
we ignoring the evidence ? British Journal of Nutrition 89:
552-572.
Sources of
vitamin D
Source Per common serving size
IU g*
Diary foods
Milk, whole, fortied, 1 cup 99 2.5
Edam cheese, 1 oz 10 0.3
Parmesan cheese (hard), 1 oz 8 0.2
Swiss cheese, 1 oz 12 0.3
Eggs and soy
Egg, whole fresh chicken, 1 large 17 0.4
Soy millk, fortied, 1 cup 100 2.5
Seafood
Fish oil, cod liver, 1 Tbsp 1,360 34.0
Mackeral, Atlantic, canned in oil, 3 oz 205 5.1
Herring, pickled, 3 oz 612 15.3
Salmon, canned pink, 3 oz 562 14.0
Sardines, canned in oil, drained solids with bone 77 1.9
Oysters, 3 oz 320 8.0
Shrimp, 3 oz 137 3.4
Meat
Braunschweiger, 1 oz 12 0.3
Olive loaf, 1 oz 12 0.3
Salami, Cotto beef, 1 oz 14 0.3
Vegetables
Mushrooms, shitake, dried, 4 mushrooms 249 6.2
Data from: US Department of Agriculture. National Nutrient database for standard reference, version 17.
http://www.ars.usda.gov/fnic/foodcomp/search/index.html
Provisional table on the vitamin D content of foods. http://www.nal.usda.gov/fnic/foodcomp/Data/Other/vit_d99.pdf
*Micrograms, 40 IU=1g
W
e owe our rst
conrmation of the fact
that stress and emotions
affect our digestive
processes to the bad temper of a
French-Canadian trapper. In June
1822, William Beaumont, a U.S. army
surgeon serving at Fort Mackinac
(now in Michigan), was summoned to
nearby Michilimackinac to treat Alexis
St. Martin, a 19-year-old trapper.
The patients temper had gotten
him into an argument, which ended
when he was wounded at close range
by a shotgun blast. The shot removed
a portion of his abdominal wall and
left a hole in the front wall of his
stomach.
During the year it took for the
wound to heal, the hole in his
abdominal wall never sealed correctly.
Instead, it was held closed by the odd
growth of a sort of a ap, leaving a
passage (called a gastric stula).
When Beaumont pressed his nger
against the ap, the passage opened
and he could see the activities going
on within St. Martins stomach.
The rst scientic report
Beaumont used the trappers unique
condition to benet medical science,
and his studies ultimately led to a few
discoveries about digestion. What
surprised him the most was how
anger, fear, or any strong emotion
seemed to affect the stomach, causing
the normal ow of uids to diminish
to such a degree that the stomach wall
would lose its healthy appearance.
Since the 1833 publication of
Beaumonts results, there has been
a large amount of research that
establishes a denite connection
between activities in the brain and
in the gastrointestinal system.
Functional disorders
The three common functional diseases
affecting digestion that often bring
people to seek medical help are
excessive gas, functional dyspepsia,
and irritable bowel syndrome.
The term functional disease refers
to a disorder in which the only
observable change is in the way the
systems in the body work, rather than
an observable inammatory condition,
infection, or structural abnormality
that can be conrmed by common
examination procedures, x-rays, or
laboratory tests.
It is now apparent that these three
functional problems are associated with
a mind-body link and are, to some
degree, consequences of psychological
stress and intense emotions.
Excessive gas
Excessive gas is the simplest and least
threatening of the three, although it
can sometimes accompany other
problems. A common source of upper
intestinal gas is air that is swallowed.
Each time we swallow, a small amount
of air enters the stomach and is
usually passed into the small intestine.
Any remaining gas travels into the
colon (large intestine) and is passed
out through the rectum. In some
people, part of the gas is belched out
instead of being passed from the
stomach into the intestine.
There is a simple relationship
between gas and emotion. People
by Stanley Coren, PhD, FRSC
Stress is
indigestible:
the mind and
stomach link
025_26_27_Persp_Stress.qxd 4/6/06 11:12 PM Page 1
under a lot of stress tend to breathe
more with their mouths and tend to
swallow large amounts of airmuch
more than the intestines can absorb.
Too much gas is annoying and
uncomfortable, and its release can be
embarrassing.
Dyspepsia and irritable bowel
syndrome
The other two functional problems
associated with digestion are more
serious. The symptoms of functional
dyspepsia include upper abdominal
pain (above the navel), belching,
nausea (with or without vomiting), a
sensation that the stomach is
uncomfortably full (often coming after
eating only a very small amount of
food), and there may also be abdominal
distention (swelling).These symptoms
are most often triggered by eating.
Irritable bowel syndrome is a
disorder most commonly characterized
by cramping, abdominal pain, bloating,
constipation, and diarrhea. It occurs
more often in women than in men
and begins before the age of 35 in
about half of the cases.
Pyschological stress
Both functional dyspepsia and irritable
bowel syndrome are connected to
psychological stress and intense
emotions. Together, these problems
affect more than one out of four
people in North America to some
extent. There are numerous studies,
which show that individuals whose
lives are undergoing major upsets
(divorce, death of a spouse or child,
loss of a job, and so forth) are much
more likely to develop symptoms.
Individuals with a history of childhood
abuse, sexual abuse, or spousal
violence are at higher risk as well.
It is also clear that personality
factors play a role. Individuals who
are emotionally reactive, score high
on neuroticism tests, have sleep
difculties, or have tendencies toward
depression are all more likely to have
both of these digestive difculties.
Many people often experience
cramps or butteries when they are
nervous or upset. In people with
irritable bowel syndrome, the colon
can be overly responsive to even
slight conict or stress. For such
people, the stress makes them more
aware of the sensations that arise in
the colon, which in turn adds to the
unpleasantness of the episodes.
How stress affects digestion
We have a pretty good idea as to how
stress affects digestion. The body has
four different major nervous systems.
The somatic nervous system controls
muscles. The central nervous system
includes the brain and spinal cord.
There is also the autonomic nervous
system, which consists of two
competing nervous systems--the
sympathetic nervous system and the
parasympathetic nervous system.
The parasympathetic nervous
system handles many basic life
maintaining functions, including
digestion. Under parasympathetic
control, digestive uids are generated
in the stomach, the stomach contracts
to move food along, and other
contractions assist movement, further
digest food in the intestines, and
nally remove waste material by
passing it through the colon.
In times of stress, the sympathetic
nervous system takes over. It is
concerned with immediate survival
from threats, so it speeds the heart,
increases oxygen consumption, and
generates stress related hormones
like cortisol.
You get much the same stress
response from the sympathetic nervous
system whether the stressor is a tiger
that you must run from, or a hostile
comment from your boss or lover.
When the sympathetic nervous system
goes into high gear, it commands all of
the resources that it can.
This requires shutting down much of
the parasympathetic activities. In
effect, digestion stops. Digestive uids
stop owing. Movement of materials
through the gastrointestinal system
stalls. If this response continues for
any signicant period of time, irritation
develops in the stomach walls. When
this occurs frequently, stomach upset
and even ulcers may result.
The mucous membranes that line the
intestines can also become damaged.
Partially digested materials at a stand
still in the gastrointestinal system upset
the normal intestinal bacteria ora
(concentrations of the bacteria, mainly
Lactobacilli and E. coli).
The parasympathetic nervous
system seems to recognize that this
is not a good state of affairs, so it
tries to restore normal digestion as
soon as possible. However, if the
sympathetic nervous system is still
responding to stress, conicting
messages may be sent to the gut that
can exaggerate the irritability of the
digestive system.
Treatments
With such a large component of
gastrointestinal difculties dependent
upon psychological factors associated
with stress response, treatment
approaches often include psychological
therapies proven successful for stress
management.
Cognitive therapies, for example,
are quite helpful in alleviating
symptoms. More recently, hypnotherapy
has shown to be quite useful. Given
the link between stress and depression,
the use of antidepressant drugs,
including some of the serotonin
reuptake inhibitors (Prozac-like
drugs), have also shown to reduce
stomach upset and gastric pain in
patients with functional dyspepsia
and irritable bowel syndrome.
I often think of my grandfather
Jake who always tried to tell a funny
story at the beginning of supper. If
people laughed or smiled, he would
triumphantly announce, Thats
good! Happiness improves digestion.
It appears that science is proving
him right.
References:
Bhatia, V. and Tandon, R.K. (2005). Stress and the gastrointestinal
tract. Journal of Gastroenterology and Hepatology, 20, 332339.
Mawdsley, J.E. and Rampton, D.S. (2005). Psychological stress in
IBD: new insights into pathogenic and therapeutic implications.
Gut, 54; 1481-1491.
Smith M. L. (2005). Functional dyspepsia pathogenesis and
therapeutic optionsImplications for management. Digestive and
Liver Disease, 37, 547558.
025_26_27_Persp_Stress.qxd 4/6/06 11:12 PM Page 2
What are the nutritional,
psychological and environmental
factors that are important for
digestive health?
The principle factors that inuence
gut health are diet, infection,
environment, and genetics.
Physical tness and exercise are
important for general health. Obesity
is increasingly associated with cancer
including cancers in the digestive
system. Stress aggravates symptoms of
digestive system diseases, especially
in functional gastrointestinal (GI)
disorders.
Many changes have occurred over
human evolution particularly in the
last approximately 150 years:
increased calorie intake, increasing
salt intake, increased consumption of
rened sugar, reduced insoluble bre
intake, and the use of food additives
and chemicals. Also since the middle
of the last century, the widespread
use of antibiotics has altered our
normal bowel ora.
Our gut environment has changed
dramatically, with potentially serious
digestive health consequences. A
balanced diet with less red meat and
fat, and more bre, fruits and
vegetables is important for gut health.
The digestive system is a major
sensory organ of the body, with a
surface area that is 10-20 times larger
than the bodys skin. Thus, we
believe that digestive tract events have
a major inuence on brain activity,
and the gut-brain-gut axis effects
regulatory control of gut function with
local control through the enteric
nervous system.
Other important factors are the
local neurohormonal control pathways
in the gut wall, which modulate
motility and secretion. Stress is not
likely a cause of GI disease, but there
is no doubt that stress can increase
susceptibility to gut disease or make
symptoms worse in some people.
Genetic differences between people
may account for some of the differences
seen in gut function in a number of
diseases. However, it is likely that
environmental and dietary factors are
at least as important as genetic
expression in most GI conditions.
What are the most common gut
disorders?
Digestive disorders ranks forth highest
of diseases leading to productivity loss
in Canada, ahead of mental disorders
and second only to cardiovascular
diseases. Among Canadians with
dyspepsia symptoms (upper gastro-
intestinal symptoms of indigestion
such as heartburns, bloating, early
satiety, and nausea), the most
common disorder is gastroesophageal
reux disease (GERD).
In Canada, about 38% of people
have symptoms of gastroesophageal
reux. A survey of 195 family doctors
reported that they spent 7.5% of their
time seeing patients with just these
symptoms. Another survey of GERD
patients found that 41% had lost
work days due to their disease.
In the US, more than 60 million
American adults experience GERD
at least once a month, and about
25 million adults suffer daily from
heartburn.
About 6-10% of the population has
functional bowel disorders, for which
no clear cause has been found
although a signicant proportion of
patients have a history of a prior
enteric infection. There are usually
several symptoms including abdominal
discomfort or pain, bloating and altered
bowel function. These symptoms are
related to digestive system function
rather than any structural problems.
There are some 25,000 new cases of
digestive tract cancers diagnosed each
year in Canada. Among all the
digestive system cancers, colorectal
cancer is the most common,
accounting for approximately 17,000
new cases diagnosed each year.
Potential years of life lost due to
colorectal cancers in Canada is about
107,000 and our life time chance of
getting a large bowel cancer is about
6%. Canadians over age 50 should
undergo screening for colon cancer,
and those with a family history
should be screened at 10 years earlier
than the year of diagnosis of the
youngest case in the family.
What are some of the challenges GI
specialists face in advancing
digestive health?
Anti-inammatory drug induced
ulcers
Over the past few decades, the
incidence of peptic ulcers has
decreased dramatically due to very
effective treatments with the H2-
receptor antagonists (H2RA) and the
proton pump inhibitors (PPI). They
reduce stomach acid very effectively.
Over the past 15-20 years eradication
of Helicobacter pylori infection in the
stomach has led to a permanent cure
for many with peptic ulcer.
However, despite these dramatic
improvements in ulcer disease
generally, bleeding from complicated
Body Condition
by Lillian Chan
What is important for gut health?
A discussion with Richard Hunt, Professor of Medicine
and Gastroenterology at McMaster University and
Vice president of the Canadian Digestive Health Foundation
025_28_33_Body_Reflux.qxd 4/10/06 12:59 PM Page 1
ulcers has remained static or
increased slightly due to the
increasing widespread use of anti-
inammatory drugs (NSAIDs) for pain
and arthritis.
In the US there are about 300,000
hospital admissions for a bleeding
ulcer and up to 10% of patients die of
this complication. Drug-induced
peptic ulcer and ulcer complications,
especially bleeding, remain a serious
clinical challenge and NSAIDs are
now the most common cause for
peptic ulcer in western countries.
As high as 40-50% of those taking
NSAIDs, including aspirin, experience
upper GI symptoms, such as
indigestion and GERD. Development
of gut complications including peptic
ulcers is found in about 20% of users
and bleeding is seen in 1 to 4%.
It is important to note that low dose
aspirin, which is often given for
cardiovascular protection after a
myocardial infarction or thrombotic
stroke, is a common cause of GI
bleeding. Since half of the population
over 65 are taking one NSAID or
aspirin a day, the population exposure
to risk of gastrointestinal ulcer and
bleeding is huge. Patients are
therefore encouraged to discuss with
their doctors the best drug and
therapy for their problems.
Most medications have some side
effects, and taking a drug always
poses some risks. It is important to
balance the benets against possible
risks, and consider whether the
adverse events can be managed.
Helicobacter pylori infection
Helicobacter pylori infection is also a
common cause of peptic ulcer
although in western countries the
prevalence of this infection is falling
and is now about 30% in Canada.
Both this infection and the NSAIDs
are independent risk factors for ulcer
and ulcer complications with a similar
magnitude of effects. Together, they
amplify the damaging effects of injury
to the mucosa of the stomach,
accounting for more than 90% of
peptic ulcers.
Other issues
Resource issues are the most serious.
The general public needs to realize
that digestive disorders are at least as
serious as other chronic diseases, and
the impact is particularly serious as
digestive diseases affect people of all
ages, including younger people who
are important to the work force and
have immediate family
responsibilities. Waiting times for
consultation and investigation have
become seriously long. Moreover, we
anticipate a serious shortage of
gastroenterologists over the next ten
years. Shortage of consultants will
lead to a serious manpower crisis.
Medication is relatively expensive
but has led to a dramatic reduction in
surgery for ulcer and esophageal
disease. In Canada, over $670 million
is spent on prescription PPI and H2RA
treatments for reux disease annually,
and GI specialists often have to spend
time justifying the use of effective
drugs to the payers.
What direction is research
heading?
There are 3 main areas of research in
the development of new drugs to
control acid reux disease. The most
effective acid suppressing drugs are
the PPI but not all patients respond to
these drugs and 20-30% of patients
require twice daily treatment.
Thus, researchers are trying to nd
new drugs that are both effective and
provide a longer duration of drug
effect. This is especially important for
patients with symptoms at night.
Another focus of drug research aims
to provide a better environment for
antibiotics to work, so that
Helicobacter pylori infection can be
eradicated more efciently.
As mentioned above, GI bleeding is
another important clinical problem.
Much work is being undertaken to
produce safer anti-inammatory drugs
and better treat patients with
complications particularly GI bleeding.
Interface between key regulators of
digestive function and the microbial
ora of the digestive tract is an
important area of fundamental
research. This interface and the
consequences of associated changes
dene how and what we are.
For example, infection by just one
bacterium, Helicobacter pylori, which
has developed highly sophisticated
survival mechanisms allowing it to
colonize the stomach, modies
stomach function extensively.
It is probable that other bacteria act
similarly throughout our intestines.
Studying animals raised in a controlled
germ-free environment with no
bacteria in their gut will enhance our
understanding of digestive health. We
have just established such a facility at
McMaster where we can explore the
mechanisms involved in colonization
and infection with a variety of gut
bacteria.
025_28_33_Body_Reflux.qxd 4/10/06 10:39 AM Page 2
Body Condition
by Lillian Chan
The understanding of normal anti-
relux mechanisms is important. If the
defective mechanisms can be corrected,
acid reux can be controlled, making
suppression of normal amounts of
gastric acid unnecessary.
However, medications currently
available to control defective reux
mechanisms have side-effects and
are not for most patients. Further
research on reux regulation and
control is important. At the present
time, acid suppression remains the
main therapy for acid reux.
Q: What is LES and how does it
prevent acid reux?
At the lower end of the esophagus,
there is a strong muscular ring called
the lower esophageal sphincter (LES).
Unlike other muscles, which are
normally relaxed, the LES muscles
are contracted all the time. They
form a one way valve so that the
LES normally remains tightly closed.
When one swallows, the muscles
here relax to let food and drink pass
through into the stomach.
Pressure in the stomach is higher
than in the chest, so if this valve is not
closed properly, there is a tendency for
the stomach contents to go back up
the esophagus. The resting pressure of
a properly closed LES is normally
slightly higher than that of the
stomach, keeping the contents down.
If the LES opens when it should
not, or if the muscles here are weak,
stomach and LES pressure become
the same, thus allowing acid reux
to occur.
The resting pressure of the LES
depends not only on muscle
contraction, but also on inhibitory
and excitatory neurotransmitters and
circulating hormones in the blood.
Stress and emotions can inuence LES
function. The effect and mechanism
of stress on LES is not well-studied,
but there is good evidence that stress
affects gut muscle function.
LES is the most important
component of the bodys normal anti-
reux barrier. But there are also other
factors involved.
Q: What are other factors?
Diaphragm and stomach position
The anatomic relation between the
stomach-esophagus junction and the
diaphragm plays a signicant role.
When the diaphragm is appropriately
positioned right beside the LES, it
bolsters the LES from the outside.
The top part of the stomach can
migrate up into the chest through a
hole in the diaphragm when the tissue
is weakened due to aging, or in
obesity and pregnancy when the
pressure in the abdomen is increased.
This condition is called hiatus hernia
and, when present, also weakens the
pressure barrier of the LES. Acid reux
triggers shortening of the esophagus,
so reux itself may also contribute to
the formation of a hiatus hernia by
pulling the stomach up into the chest.
The stomach relaxes as it
accommodates food to the back and
the left side of the abdominal cavity.
This anatomic feature keeps the acid
contents away from the LES. Acid
reux is much more likely to occur
when lying down after a meal or lying
on the right side when stomach acid
moves closer to the LES. The hiatus
hernia sac also provides a reservoir
for stomach acid with ready access to
the LES.
Acid clearance and neutralization
Some degree of acid reux occurs in
all people, but effective esophageal
clearance of acid contents and acid
neutralization protect the esophagus
lining and LES from injuries.
Normally, when reux occurs,
additional peristaltic waves are
induced to sweep the reux contents
Lifestyle factors affecting acid reux
Studies have shown that fried and fatty
foods, chocolate, peppermint, coffee,
alcohol, and perhaps onions and garlic
may worsen acid reux. Some foods such
as citrus fruits that irritate damaged
esophageal lining can make symptoms
worse. Smaller meal portions may help.
Taking no food 2 to 3 hours before
bedtime and elevating the head of the
bed 10-15 cm (4-6 inches) reduces acid
reux. Bending over or lying down after a
meal makes symptoms worse. It is better
to walk or sit down after meals.
GERD is worse when under stress.
Tight clothing may also aggravate
symptoms. Obesity and pregnancy are
risk factors. Losing weight can help
reduce acid reux.
Acid reux is also more common when
an individual lie on their right side
versus the left side.
How acid reux happens
William G Paterson, Professor of Medicine, Research Chair of the Division of
Gastroenterology at Queens University and President of the Canadian
Association of Gastroenterologist, explains how the bodys natural defensive
mechanisms protect us against stomach acid reux.
Esophagus
Stomach
Acid
Tightly closed LES Weak Sphincter Muscles
Stomach
Acid
Diaphragm
Esophagus
LES
Diaphragm
Stomach
At the stomach-esophagus junction, the Lower Esophagus Sphincter (LES) is normally cloased tight.
Esophagus muscles are contracted all the time. They only relaxe when one swallows. The diaphragm
bolsters the LES from the outside when positioned properly next to it. This is a back up that helps to
keep the stomach-esophageal barrier closed properly. Acid reux can occur when LES muscles are weak.
Body Condition
back into the stomach. This also
brings bicarbonate-rich saliva down
from the mouth to neutralize the
remaining acid.
Those with a compromised
swallowing reex, impaired salivation
or defective peristalsis are more
susceptible to prolonged acid contact
and esophageal problems. Medications
that lead to dry mouth, patients with
Sjogrens syndrome, and patients who
reux during sleep are at risk.
Q: Is there any other protective
strategy besides acid suppression
against GERD and peptic diseases?
Many people use anti-inammatory
drugs (NSAID), but these agents are a
major cause of peptic ulcers and
bleeding in Western countries.
NSAIDs dont appear to damage the
esophageal mucosa, which is made of
cells different from those in the
stomach. But NSAIDs upset the
protective mechanism in the stomach,
leading to stomach ulcer and ulcer
complications.
The environment in the stomach is
nasty and its lining has natural
mechanisms to protect itself. A side
effect of NSAIDs is the suppression of
the enzyme COX-1, which is involved
in the generation of prostaglandins.
When theses substances are inhibited,
the normal stomach lining defenses
are compromised (e.g. by decreased
protective mucus production and blood
ow). One strategy is to develop
medications that counter balance these
effects. Another is to use coxibs,
which have an antiinammatory
effect by suppressing the COX-2
enzyme, while having little effect on
the COX-1 enzyme.
References:
Habal F, Associate Professor of Medicine University of Toronto, and
Education Chair of the Canadian Digestive Health Foundation.
Material contribution.
Hunt RH, Professor of Medicine and Gastroenterology at McMaster
University and Vice president of the Canadian Digestive Health
Foundation. Personal communications.
Paterson, WG, Professor of Medicine and Research Chair of the
Division of Gastroenterology at Queens University, and President of
the Canadian Association of Gastroenterologist. Personal
communications.
Armstrong D et al.; Canadian Association of Gastroenterology GERD
Consensus Group (2005) Canadian consensus on the management
of GERD. Review. Canadian J Gastroenterology (1): 15-35.
Devault KR et al. (2005) Updated guidelines for the diagnosis and
treatment of gastroesphageal reux diseases. Am J
Gastroenterology (100):190-200.
Peura D (2004) Prevention of nonsteroidal Anti-inammatory Drug-
associated gastrointestinal symptoms and ulcer complications. Am
J Medicine (117):63S-71S.
Talley N et al (2005) Guidelines for the management of Dyspepsia.
Am J Gastroenterology 100: 2324-2337.
Yuan Y, Padol IT, & Hunt RH (2006) Peptic ulcer disease today.
Nature Clinical Practice Gastroenterology & hepatology (2): 80-89.
Canadian Association of Gastroenterologist: http://www.cag-acg.org
Canadian cancer statistics: http://www.cancer.ca/vgn/images/
portal/cit_86751114/48/28/401594768cw_2005stats_en.pdf
Canadian Digestive Health Foundation website:
http://www.cdhf.ca/disease_diorder/GERD.htm
Common upper
gut problems
Bloating
Some air being swallowed when eating or
drinking is unavoidable. Gases are also
produced when food breaks down or fer-
ments in the gut. The daily production of
gas in the gut is about 500-1,500 mL, the
volume normally found is about 200 mL.
Some of the gases are belched, some
are absorbed, and much is passed to the
colon. Oxygen is absorbed in the colon,
but other gases including hydrogen,
hydrogen sulde, carbon dioxide, and
methane are expelled as atus. The smell
is usually due to the suldes.
To avoid bloating, avoid chewing gum,
gas producing foods and carbonated
drinks, and eat slowly. Beans contain
certain sugars that cannot be digested by
the body that are fermented, giving off
gases. For those who are sensitive to
lactose, diary products also produce gas.
Excess gas in the gut can cause
cramps, rumbling noises, or abdominal
pain. Lying on ones side or sitting in a
knee-chest position until the gas passes
can relieve symptoms. Frequent belching
with accompanying symptoms such as
heartburn, a sour taste in the mouth, or
vomiting may indicate other gut problems
such as acid reux disease. Bloating can
also be a symptom of ovarian cancer.
Nausea and vomiting
Nausea is the subjective feeling of a need
to vomit. The mechanism underlying
nausea is poorly understood. There
doesnt seem to be a single brain area
that controls nausea. Rather, several brain
areas are involved in initiating it.
Vomiting is the oral expulsion of upper
gastrointestinal contents, resulting from
contractions of gut and thoracoabdominal
wall muscles. It is a neuromuscular
response coordinated by the brain.
Nausea and vomiting can be caused by
conditions and factors within or outside
the gut and by drugs or toxins circulating
in the body.
Indigestion
Indigestion (dyspepsia) is a general
term referring to chronic or recurring
discomfort or pain in the upper abdomen.
The feeling may include a variety of
symptoms such as early satiety, bloating,
upper abdominal fullness, heartburn,
and nausea.
Heartburn
The hydrochloric acid in our stomach kills
many germs, provides an effective
environment for enzymes to digest food,
and stimulates the ow of bile. But, it is
concentrated enough to cause tissue
damage. Even with a layer of protective
coated mucus, about half a million cells in
the stomach lining still need to be
replaced every minute. and Stomach
lining is completely replaced about every
three days. Gastric acid is normally kept
within the stomach barrier.
Heartburn is a burning sensation felt
behind the breastbone and sometimes in
the neck and throat. It is caused by
stomach acid reuxing (contents
splashing up) into the esophagus, which
connects the throat to the stomach.
Almost everyone has this occasionally.
However, severe or chronic reux of
acid can injure esophageal lining. This is
referred to as gastroesophageal reux
disease (GERD). If left untreated, Barretts
esophagus, in which abnormal cells grow
in the esophagus, may develop. This may
lead to cancer of the lower esophagus
(adenocarcinoma).
Body Rx
by Manny W Radomski, PhD, with material
contribution from F. Habal MD, PhD
Medications for Peptic Disorders
Proton pump inhibitors
Lansoprazole (Prevacid)
Omeprazole (Prilosec)
Pantoprazole (Protonix, Pantoloc)
Rabeprazole (Aciphex)
Esomeprazole (Nexium)
Others
Bismuth subsalicylate
(Pepto bismol)
Misoprostol (Cytotec)
Sucralfate (Carafate)
DRUG ACTION SIDE EFFECTS
Antibiotics
Amoxicillin
Clarithromycin
Metronidazole
Tetracycline
Antacids
Aluminum hydroxide (Amphogel)
Calcium carbonate
Magnesium hydroxide
(Milk of magnesia)
Sodium bicarbonate
Histamine-2 blockers
Cimetidine (Tagamet)
Famotidine (Pepcid)
Nizatidine (Axid)
Ranitidine (Zantac)
Most potent drug that reduces stomach acid
production. PPI promote healing of ulcers in a
greater percentage of people within a shorter
period of time than do H2 blockers. Available
for use by people taking aspirin, NSAIDs, or
corticosteroids.
Diarrhea, constipation, headache
Reduces production of stomach acid and
strengthens the stomach lining to become more
resistant to acid. Available for people who are at
higher risk of developing an ulcer caused by
NSAIDs or other reasons. Sometimes used in
combination with antibiotics.
Diarrhea (bismuth subsalicylate, misoprostol),
darkening of the tongue and stool (bismuth
subsalicylate), spontaneous abortion
(misoprostol), constipation (bismuth
subsalicylate), may reduce effectiveness of other
drugs (sucralfate)
For treating peptic ulcers caused by Helicobacter
pylori infection
Diarrhea (amoxicillin, clarithromycin,
tetracycline), altered taste, nausea
Used to relieve occasional symptoms not cure.
Neutralize stomach acid. Effectiveness varies
with the amount taken and amount of acid
produced. Magnesium hydroxide is a more
effective antacid than aluminum hydroxide.
Almost all antacids are over the counter drugs.
Generally not effective in healing ulcers.
Nausea, headache, weakness, loss of appetite,
constipation (aluminum hydroxide) or diarrhea
(magnesium hydroxide). Continual use of
calcium carbonate and sodium bicarbonate may
make the blood too alkaline resulting in nausea,
headache, and weakness.
Relieve symptoms and promote ulcer healing by
reducing stomach acid. H2 blockers usually do
not cause serious side effects. Some histamine-
2 blockers like Zantac and Pepcid AC are
available without prescriptions.
Rash, fever, muscle pains; may cause breast
enlargement and erectile dysfunction in men,
may interfere with elimination of certain drugs
(cimetidine), maay cause confusion (cimetidine,
ranitidine)
References:
Armstrong D et al. (2005) Canadian consensus conference on the management of gastroesophageal reux disease in adults update 2004. Can J Gastroenterol 19: 15-35
DeVault KR and Castell DO (2005) Updated guidelines for the diagnosis and treatment of gastroesophageal reux disease. Am J Gastroenterol 100: 190-200.
Talley NJ and Vakil N (2005) Guidelines for the management of dyspepsia. Am J Gastroenterol 100: 2324-2337.
Vigneri S et al. (1995) A comparison of ve maintenance therapies for reux esophagitis. N Engl J Med. 333:1106-1110.
Medications for stomach disorders
Over the counter antacids and antireuxants are useful for milder forms of acid reux. H2RAs (histamine 2-receptor
blockers) have much longer drug action duration than antacids. They are not as effective as PPI (proton pump inhibitors)
in acid suppression, but less expensive. It is clear from research that PPI therapy results in the most effective symptom
control and esophagitis healing. They block the release of hydrochloric acid from the parietal cells in the stomach.
NSAID-induced upper gastrointestinal problems may or may not show symptoms. More serious signs include
indigestion associated at times with nausea and vomiting, black, tarry stools that indicate bleeding, and sudden pain
throughout the abdomen suggesting perforation of an ulcer.
Body Disorder
Polyphenols and avonoids
There are numerous studies
suggesting that plant polyphenols,
mainly by virtue of their antioxidant
activities, have health benets.
Polyphenols can be chemically
divided into a number of different
classes. The largest group is the
avonoids, of which there are about
6,000 different kinds.
One important subclass of
avonoids is the avanols, found
abundantly in the fruits and leaves of
various plants. Flavonols can be
extracted and consumed when plants
are used to make beverages such as
tea and wine.
The common avonol found in tea
is catechin, and for red wine, it is
quercetin. Quercetin is also found in
apples, broccoli, and onions. Another
source of avonoids is cocoa.
For the most part, the expected
health benets of polyphenols are
based on animal studies, studies of
human cells in tissue cultures and
epidemiological surveys. Positive
effects in clinical human trials are
fewer in number.
Polyphenols are known to exist in
high concentrations in the digestive
tract, which may be the most likely
site for any dramatic effects they
might have. A recent review examined
the literature dealing with the effects
of polyphenols on disorders of the
digestive tract. These are the ndings.
Review: effects on GI disorders
Inammatory bowel disease (IBD)
Rats with colitis similar to the
condition found in humans improved
when treated with a polyphenol-rich
extract of green tea leaves. Mice with
colitis that were fed green tea
polyphenols also showed improvement.
Acute diarrhea
Polyphenols extracted from immature
apples were found to inhibit the
diarrhea induced by cholera in mice.
An alcoholic extract of avanols
from the leaves of an African plant,
the Christmas bush, inhibited diarrhea
in mice. In a clinical trial on children
with acute diarrhea, carob powder
rich in polyphenols ended symptoms
of diarrhea 1.5 days sooner than in
children not given the powder.
Peptic ulcer
Helicobacter pylori is a bacterium
known to play a role in causing peptic
ulcers. Using human stomach cells in
tissue cultures, researchers found that
a catechin (type of polyphenol) from
green tea could block the bacterial
toxic effect on the cells. It was
speculated that continuous drinking of
green tea may prevent the effects of
Helicobacter infection.
Cancer of the digestive tract
Mice on a high fat diet (similar to
human diets associated with colon
cancer) were injected with a chemical
known to induce colon cancer. The
number of precancerous lesions in the
colon of these mice was reduced if
they drank green tea for 10 weeks
after the chemical injection.
Liver disease
Milk thistle is a daisy-like plant that
has been used for over 2,500 years
and is still used for liver conditions in
naturopathic medicine. The active
ingredient, silymarin, is a collection
of four avonoids from the seeds of
the plant.
Animal studies indicate that
silymarin protects the liver from
damage from a number of different
toxins, and studies are underway to
test its effectiveness against cancer.
Human studies using silymarin as a
treatment for cirrhosis of the liver
have produced contradictory results.
Some studies have found that
silymarin may have some benet for
alcohol-caused cirrhosis, but others
have not. Studies of hepatitis B and C
liver disease indicate no benecial
effect of silymarin. But investigators
suggest more carefully controlled
trials should be done. Some adverse
effects of silymarin have occured.
Carbon tetrachloride is known to
cause liver damage. The liver of rats
that are treated with this chemical
undergo distinct biochemical and
structural changes. Studies with such
rats found that green tea polyphenols,
in particular an epicatechin, can
reduce the severity of the toxic effects.
Liver damage in humans may respond
in a similar way.
References:
Agbor, G et al (2004) The Antidiarrhoeal Activity of Alchornea
cordifolia Leaf Extract Phytotherapy Research. 18: 873876.
Dryden, G et al (2006) Polyphenols and gastrointestinal diseases
Current Opinion in Gastroenterology 22: 165-170.
Lee, K-M et al (2004) Protective Mechanism of Epigallocatechin-3-
Gallate against Helicobacter pylori-Induced Gastric Epithelial Cyto-
toxicity viathe Blockage of TLR-4 Signaling Helicobacter 9: 632-642.
Rambaldi, A et al (2005) Milk Thistle for Alcoholic and/or Hepatitis
B or C Liver DiseasesA Systematic Cochrane Hepato-Biliary Group
Review with Meta-Analyses of Randomized Clinical Trials American
Journal of Gastroenterology 100: 25832591.
Are plant polyphenols helpful
for gut problems?
025_34_Body_Polyphenols.qxd 4/6/06 11:15 PM Page 1
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Gastroenteritis is a general term that
describes the inammation of the
lining of the gastrointestinal tract (the
pathway for digestion that includes
the mouth, esophagus, stomach, and
intestines). Gastroenteritis is some-
times referred as stomach u, even
though it is not related to inuenza.
Cause
Gastroenteritis may result from
bacterial, viral, parasitic (protozoa)
infection. It could also be associated
with toxic substances, side effect from
medications or of unknown etiology.
Many different types of bacteria
can cause bacterial gastroenteritis
including salmonella, staphylococcus,
shigella, E. coli, and others. Each
organism causes slightly different
symptoms but all result in diarrhea.
Viral gastroenteritis is often the
cause of severe diarrhea in both
adults and children. The most
common are: rotavirus, which is the
leading cause of severe gastroenteritis
in children and in nursing homes, and
Norwalk virus, which often causes
diarrhea outbreaks.
Gastroenteritis can be associated
with ingestion of toxic substances:
plant toxins (e.g. from some mushrooms
and potatoes), contaminated sea foods
(sh, clams, mussels), or heavy-metals
(e.g. arsenic, lead, mercury, cadmium).
Many drugs, including broad-spectrum
antibiotics, can also have gastro-
intestinal tract side effects causing
gastroenteritis.
Risks
Some common sources of infection
include improperly prepared foods,
contaminated foods, contaminated
water or ice cubes, contact with
infected person, unwashed hands,
dirty utensils, and travel or residence
in areas of poor sanitation. Travellers
diarrhea and food poisoning are
common examples of gastroenteritits.
In healthy persons, the illness is
usually mild and self-limited, but in
immuno-compromised patients
(elderly and those with chronic
diseases) the condition may be severe,
causing substantial electrolyte and
uid loss. People who are at a higher
risk include children in day care,
students living in dormitories, military
personnel, and travellers.
Symptoms
The characteristic and severity of
symptoms depends on the nature of
the causative agent, the duration of its
action, the patients immune response,
and the extent of gastrointestinal
involvement. Onset is often sudden
and sometimes dramatic. The main
symptom is diarrhea.
Other symptoms may include
vomiting, anorexia, nausea,
borborygmi (growling stomach),
bloating, abdominal cramps, fever,
malaise, muscular aches, exhaustion,
and fatigue.
Vomiting may lead to excessive loss
in uid and stomach acid, resulting in
metabolic alkalosis (when the body
has too much alkaline substance).
On the other hand, if diarrhea is more
prominent, acidosis (too much acid in
the body) is more likely.
Excessive vomiting or diarrhea
may also cause hypokalemia (low
circulating potassium). If hypotonic
uids are used in replacement therapy,
hyponatremia (low circulating sodium)
may develop. Persistent vomiting and
diarrhea may also result in severe
dehydration and shock.
Signs of dehydration include:
Extreme thirst
Urine that is darker in colour
Dry skin
Dry mouth
Sunken cheeks or eyes
In infants, dry diapers (for more
than 4-6 hours)
Treatment
Supportive treatment and bed rest are
the most important. It is essential to
replace uids and electrolytes that are
lost because of diarrhea and vomiting.
Special uids are not usually
necessary for mild illness.
For more serious cases, a home
made oral glucose-electrolyte
solutions can be prepared by mixing
1 tsp table salt, 1 tsp baking soda,
4 tsp table glucose (or table sugar)
in 1 L water (about 1 qt). Strained
broth or salted bouillon may be taken
to prevent dehydration or treat mild
dehydration. Even if vomiting, the
patient should take frequent but small
sips of these uids.
Children may become dehydrated
more quickly and should be given an
appropriate rehydration solution
(available from any drug store).
Carbonated beverages or sports drinks
lack the correct ratio of glucose to
sodium and are not appropriate for
children younger than 5 years old.
If vomiting is severe or last more
than 2 days, if diarrhea persists or
turns bloody, if a high fever of more
than 39C (102F) is present, or if
dehydration is prominent, seek
medical attention promptly.
Medicines that stop diarrhea are
helpful in some cases, but they are not
recommended for people whose
diarrhea is caused by a bacterial
infection or parasite. Stopping diarrhea
may trap infecting organism in the
Body Condition
by Y. Michael Chan, PhD, CChem, FRSC(UK), FACB
Stomach Flu
025_36_37_Body_StomachFlu.qxd 4/6/06 11:16 PM Page 1
intestines, prolonging the problem.
When the patient can tolerate
uids without vomiting, bland foods
(cereal, gelatin, bananas, toast) may
be added to the diet gradually. Other
foods such as potatoes, lean meats
(e.g. chicken meat), and whole grains
can help replace nutrient loss. Avoid
milk and dairy products, caffeine,
alcohol, nicotine, citrus juice, and
fried, fatty, or highly seasoned foods
for a few days.
Most children should continue to
eat a normal diet including formula or
milk while they have mild diarrhea.
Breastfeeding should continue. In
some cases, children develop a mild
and temporary lactose intolerance,
which may necessitate a switch from
regular milk to a soy formula. For
children who are on solid foods, the
B.R.A.T. diet is a common diet for
diarrhea. B.R.A.T. is an acronym for
bananas, rice (or other starchy food),
applesauce and toast.
Probiotics, available as supplements
and in some yogurts as active bacteria
culture, have shown particular
promise in improving symptoms of
acute infectious diarrhea and in the
prevention of antibiotic-associated
diarrhea. Other conditions that
probiotics may potentially help include
chronic diarrhea, inammatory bowel
disease, irritable bowel syndrome, and
some food allergies.
References:
Beers, MH & Berkow, RM (eds) (1999) The Merck Manual of
Diagnosis and Therapy, Seventeenth Edition, Chapter 28,
Gastroenteritis.
Managing Acute Gastroenteritis Among Children. Centre for Disease
Control. November 21, 2003. MMWR/Vol. 52/No. RR-16.
Van Niel CW (2005) Probiotics: Not Just for Treatment Anymore.
Pediatrics 115: 174-177.
American Academy of Pediatrics, Treating diarrhea and dehydration.
http://www.aap.org/healthtopics/gastroenterology.cfm
The Cleveland Clinic Health Information Center, Gastroenteritis.
http://www.clevelandclinic.org/health/health-info/docs/3900/
3901.asp?index=1241ed
Gastroenteritis
outbreaks on ships
The US Centers for Disease Control and
Prevention (CDC) reported on 22
gastroenteritis outbreaks aboard 18
cruise ships in the year 2002. Of these
outbreaks, three were blamed on
bacteria, and seven could not be traced
with certainty. But the remaining 12 were
conrmed to be associated with
noroviruses - Norwalk-like viruses that
cause gastroenteritis.
The CDC believes that poor personal
hygiene is the most likely cause of
infection. Some people probably went on
board with the virus. Since a cruise ship
is an enclosed community with lots of
public areas, virus could be deposited on
various surfaces that could be easily
picked up and spread. Furthermore,
those who are sick may not want to stay
in their cabins. As a result, virus can
spread around in a ship rapidly.
The best prevention against
gastroenteritis on a ship is frequent and
thorough hand washing with warm,
soapy water. Travellers who dont have
ready access to soap and water may
want to carry along a hand gel sanitizer,
found in most supermarkets and
drugstores.
While going on shore excursions,
travellers should also choose foods and
beverages carefully. Foods should be
thoroughly cooked and served hot. As a
precaution, try to avoid raw meat, raw
seafood, green salads, raw sprouts, tap
water that is not boiled, and ice cubes
made with tap water.
Reference:
Bren L (2003) Cruising with condence.
FDA Consumer magazine, May-June.
http://www.fda.gov/fdac/features/2003/303_virus.html
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025_36_37_Body_StomachFlu.qxd 4/6/06 11:16 PM Page 2
Body Exercise
by Manny W Radomski, PhD
Tasty Ways
to get your EFAs
2 1/4 lb new potatoes, scrubbed well,
quartered, skin left on
2 Tbsp red onion, diced
2 Tbsp parsley, chopped
2 Tbsp vinegar
2 Tbsp water
2 tsp prepared mustard
2 tsp sugar
1/4 tsp salt
1/4 cup Udos 369 Oil Blend
salt and pepper to taste
For more recipe ideas, pick up a copy of
our free booklet at your local specialty
natural health food retailer.
1 To make dressing: In a bowl, mix vinegar, water,
mustard, sugar and salt. Slowly whisk in Udos 369
Oil Blend. Add onion and parsley.
2 Boil potatoes in salted water until tender
(approximately 10-15 minutes). Drain well.
3 Add hot potatoes to dressing. Toss until well coated.
4 Season to taste. Set aside for a few minutes to let
potatoes absorb dressing. Serve warm or at room
temperature.
Makes six servings.
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Wellness Opt Udo Oil ad Apr 06 3/2/06 3:02 PM Page 1
Yoga for
back pain
Most treatments for chronic lower
back pain have modest efcacy at
best. Exercise is one of the few
proven treatments for chronic lower
back pain; however, its effects are
often small, and few studies have
shown that one form is clearly better
than another.
A recent clinical study of 101
patients with chronic lower back pain
that persisted for at least 12 weeks
compared the effects of three
treatments: 12-week session of yoga
classes, conventional exercise classes,
and a self-care book.
It reports that yoga patients had a
better improvement in function and
were less bothered by their pain than
patients in the other two groups.
Also, 6 months after the beginning
of their yoga exercise treatment,
patients still reported improvement of
symptoms. The yoga exercise used in
this study is viniyoga, a therapeutically
oriented style of yoga that emphasizes
safety and is relatively easy to learn.
Yoga is one of the most popular
forms of mindbody therapy. An
estimated 14 million Americans
practiced yoga in 2002, including
more than 1 million who used it as a
treatment for back pain.
There is little research on the
mechanisms by which yoga practice
might relieve back pain. Researchers
suggest that the practice places as
much emphasis on mental focus and
breathing as on physical movements,
probably providing both physical and
psychological benets.
References:
Bogduk N. (2004) Management of chronic low back pain. Med J
Aust. 180:79-83.
Hayden JA, et al. (2005) Meta-analysis: exercise therapy for
nonspecic low back pain. Ann Intern Med. 142:765-75.
Sherman KJ, et al. (2005) Comparing yoga, exercise, and a self-care
book for chronic low back pain: a randomized, controlled trial. Ann
Intern Med. 143:849-56.
Sovik R. (2000) The science of breathingthe yogic view. Prog Brain
Res. 122:491-505.
Yoga postures for back pain
Cobra Knee to chest Wheel
Bridge Extended leg Warrior
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New potatoes... Boiled or
steamed, these nuggets are
worth their weight in gold;
potatoes are rich in potassium
and fibre, and the skin provides
additional nutrients such as
vitamin C and other anti-
oxidants. Plus, the nutritional
value of this or any dish is easily boosted
with the addition of Udos 369 Oil Blend.
You are probably aware of the necessity of
Omega-3 and -6 essential fatty acids (EFAs)
in the diet. With todays busy lifestyle, who
has the time to plan for the proper balance of
EFA-rich foods such as nuts, seeds, flax and
fish? Udo has made it easy with his 369 Oil
Blend its the fast and tasty way to get your
daily EFAs in your favourite recipes, from
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Dont just take Udos 369 Oil Blend use it!
New Potatoes with
Mustard Dressing
Instead of the usual butter, try this tasty
dressing made with Udos 369 Oil Blend.
RECI PES TO I NSPI RE THE USE OF UDO S 369 OI L BLEND I N YOUR EVERYDAY MEALS
Tasty Ways
to get your EFAs
2 1/4 lb new potatoes, scrubbed well,
quartered, skin left on
2 Tbsp red onion, diced
2 Tbsp parsley, chopped
2 Tbsp vinegar
2 Tbsp water
2 tsp prepared mustard
2 tsp sugar
1/4 tsp salt
1/4 cup Udos 369 Oil Blend
salt and pepper to taste
For more recipe ideas, pick up a copy of
our free booklet at your local specialty
natural health food retailer.
1 To make dressing: In a bowl, mix vinegar, water,
mustard, sugar and salt. Slowly whisk in Udos 369
Oil Blend. Add onion and parsley.
2 Boil potatoes in salted water until tender
(approximately 10-15 minutes). Drain well.
3 Add hot potatoes to dressing. Toss until well coated.
4 Season to taste. Set aside for a few minutes to let
potatoes absorb dressing. Serve warm or at room
temperature.
Makes six servings.
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Wellness Opt Udo Oil ad Apr 06 3/2/06 3:02 PM Page 1
Standing forward bend Kneeling forward bend Chair
Swimmers
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025_38_39_Body_Yoga.qxd 4/10/06 1:59 AM Page 2
Background
Not all fats are created equal
Our body needs lipids (oils and fats)
for energy and for building structures
such as cell membranes. From a
calorie perspective, all oils and fats
provide the same amount of energy,
which is 9 calories per gram. This is
about twice the energy compared to
an equivalent amount of carbohydrate
or protein.
Even though all oils and fats are
triglycerides with similar chemical
structures - having fatty acids
(hydrocarbon chains) bound to a
glycerol (an alcohol), their length and
how the fatty acid chains are shaped
can be very different. Those packed
tightly are solid at room temperature
and are saturated fats. Oils have
unsaturated fatty acids and are liquid
at room temperature.
Trans fatty acids (trans fats) behave
like saturated fatty acids. They are
formed when hydrogen is added to
turn oils into a more solid form. They
are found in small amounts naturally
in the fat, milk and cheese of
ruminating animals, and in much
larger amounts in some manufactured,
hydrogenated products such as
shortenings and margarines.
From a health perspective, there
are big differences between oils, fats
and trans fats. An increase in
the intake of saturated fats/trans
fats can lead to an increase of bad
(LDL) cholesterol. It is generally
recommended that no more than
30% of daily energy intake should be
from fats, of which no more than
10% from saturated plus trans fats.
Essential fatty acids
Our body can made fatty acids with
the exception of the polyunsaturated
oils omega-3 and omega-6 fatty acids.
These are essential to maintain health
and have to come from our diet.
Omega-3 fatty acids
There are many health benets of
omega-3 fatty acids.
The most readily available omega-3
fatty acid in our diet is ALA (alpha-
linolenic acid) from axseeds, canola
oil, and walnuts. Some of it can be
converted into two other important
omega-3 fatty acids DHA
(docosahexaenoic acid) and EPA
(eicosapentaenoic acid) by the body,
but not in sufcient amounts. DHA
and EPA are consumed almost
exclusively from marine products
especially fatty sh.
An adequate intake of omega-3
fatty acids, particularly DHA/EPA, is
associated with reduced risks for
coronary heart disease and strokes,
enhanced brain and retina development
and functioning, lower risks for age-
related memory loss, and some
protections against inammation.
Q&A
Nutrition gap
Q: What are the fats in our diet? Are
we eating the right fats?
Ive compiled a table here to show the
composition of fat components in our
diet. In general, we are deriving too
much energy from fats, and from fats
that are not healthy (see table below).
Food & Nutrition Omega 3
by Lillian Chan
Every day good and bad fats
Interview with Bruce Holub, Professor Emeritus,
Department of Human Health & Nutritional Sciences,
University of Guelph
What are the fats in our diet?
Composition of daily fat consumption for an average Canadian adult
Fat Component Common Food Source gm/day % of energy (avg)
Total fat mixed (animal/plant) 75-105 30-35
Saturated FAs dairy products, fatty meats, palm/coconut oils 30-40 14.0
Monounsaturatd FAs (natural) canola oil, olive oil, animal fat 21-30 10.0
Trans fatty acids (monounsaturated) hydrogenated, vegetable oils, shortenings,
processed and fast foods
9-13 4.5
Polyunsaturated FA (mostly omega-6 as linoleic acid) corn, safower and sunower oils 10-17 6.0
Polyunsaturated FA (omega-3 as alpha-linolenic) canola oil, soybean oil, axseed 1.4-2.0 0.6
Polyunsaturated FA (omega-3 as EPA/DHA) sh/sh oil 0.13-0.15 0.06
Cholesterol animal foods/fats 0.35-0.40 0 (not an energy source)
Source: Data compiled by Bruce Holub, Department of Human Health & Nutritional Sciences, University of Guelph.
025_40_41_Food_Interview.qxd 4/10/06 2:01 AM Page 1
Q: Are we taking enough omega-3
fatty acids?
No, there is a huge nutritional gap
between the current intake of an
average North American adult and
recommended levels (see chart).
The current average North
American adult intake is only 80 DHA
and 50 EPA, for a combined level of
130 mg/day. This is the equivalent of
only one serving of sh every 10 days.
The International Society for the
Study of Fatty Acids and Lipids
(ISSFAL) recommends that for normal
adult health and heart protection,
intake of omega-3 fatty acids should
be 650 mg/day of combined DHA and
EPA, of which at least one third
should be DHA. This is approximately
5 servings of sh a week.
For patients with heart problems,
the American Heart Association
(AHA) recommends a combined DHA
and EPA level of 900 mg/day. Their
guidelines report that one fatty sh
meal per day (or supplement) can
result in an omega-3 fatty acids intake
of 900 mg/day, an amount shown to
benecially affect coronary heart
disease mortality rates in patients with
the disease. They also recommend the
use of supplementation for those not
consuming sufcient amount of sh.
The AHA recommends the
consumption of 2 servings of sh per
week for those who are healthy and
free of heart disease. This provides an
average daily intake of 250-300 mg of
combined DHA and EPA.
The US Food and Nutrition Board in
collaboration with Health Canada
established an AI (Acceptable Intake)
for ALA omega-3 fatty acids of 1.1-
1.6g/day, but no specic
recommendation for DHA and EPA.
Vegetarian diets
Q: How do people on a vegetarian diet
obtain their DHA and EPA omega-3
fatty acids, which are mainly from sh?
Particularly at risk are the vegans who
do not eat any animal products
including milk and eggs. Their DHA
daily intake will be zero. They are
encouraged to increase consumption
of axseeds, canola oil, walnuts and
chia oil. Even then, conversion is a
concern because omega-6 fatty acids
from corn oil and sunower oil
compete with omega-3 fatty acids for
metabolic conversion of ALA to DHA
and EPA.
They can take algae oil rich in DHA
as a dietary supplement. The goal is
to push DHA omega-3 fatty acid
intake to the level of 0.1% of daily
energy intake as recommended by the
ISSFAL workshop in 1999.
For pregnant and lactating women
in general, adequate intake of 300
mg/day of DHA is important. DHA is
essential for the babys brain and
retina development and function.
Those on a vegetarian diet can get
limited DHA from diary products and
eggs if these are included in their diet.
They may also increase intake from
functional foods enriched with omega-
3 fatty acids or supplements.
Anti-inammation
Q: Are omega-3 fatty acids effective
for reducing gut inammation?
Recent studies have shown that
consumption of omega-3 fatty acids
is associated with some reducing
effects on biomarkers of
inammation in the blood.
Intake seems to have modifying
effects, reducing the activation of
endothelial white blood cells and
lowering the levels of inammation.
The effect is systemic and not specic
to the gut, so may affect skin and
arthritis too. Further investigation is
required and worthwhile.
This is the third regular interview
column on omega-3 fatty acids with
Bruce Holub, a Canadian expert on
omega-3 fatty acids at the Department
of Human Health & Nutritional
Sciences, University of Guelph.
For more on different types of fat, oil
and fatty acids and their health effects
refer to WellnessOptions issues 15, 20,
21, 23, and 24. Omega-3 fatty acid
website: www.dhaomega3.org
References:
Denomme J et al. (2005) Direct quantitated dietary (n-3) fatty acid
intakes of pregnant Canandian women are lower than current
dietary recommendations. J Nutri 135: 206-211.
Lopez-Garcia E et al. (2004) Consumption of (n-3) fatty acids is
related to plasma biomarkers of inammation and endothelial
activation. J Nutr 134: 1806-1811.
Are we meeting our need for omega-3 fatty acids?
Combined DHA and EPA intakes (mg/day)
North American current
intake
For normal health
and heart protection
Recommended intake by
the International Society
for the Study of Fatty
Acids and Lipids
For those with
coronary heart disease
Recommended intake by
the American Heart
Association
130
650
900
025_40_41_Food_Interview.qxd 4/10/06 2:02 AM Page 2
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For a better
mood
Both Omega-3 and Omega-6 fatty acids are
required for normal membrane structure and
function and for normal nerve transmission.
A number of studies have linked low levels
of omega-3 to major depressive disorder,
bipolar disorder, schizophrenia, substance
abuse, and attention decit disorder.
Two new studies from Milan and
Pittsburgh have now shown that omega-3
fatty acids are also associated with better
mental health in healthy adults.
Normal, healthy participants in the
studies consumed eight capsules (4 g) of sh
oil per day before meals for at least one
month. The amount of eicosapentaenoic
acid (EPA) per capsule was 200 mg, and
docosapentaenoic acid (DHA) per capsule
was 100 mg.
The Milan study shows a positive central
nervous system effect, with improvements of
reactivity, attention and cognitive
performances, improvement of mood state,
and modications of some neuro-electrical
parameters.
The Pittsburgh study shows that omega-3
fatty acids may also inuence mood,
personality, and behaviour. Healthy
participants with lower blood levels of
omega-3s were found to be more likely to
report mild or moderate symptoms of
depression, a more negative outlook, and be
more impulsive. Conversely, those with
higher blood levels of omega-3s were found
to be more agreeable.
Reference:
Conklin SM et al. (2006) Plasma fatty acids are associated with
normative variation in mood, personality and behaviour. Proc 64th
Am Psychosomatic Soc. March 2006, Denver, CO, USA.
Good fat in
bacon?
Meat products usually contain large amounts
of omega-6 fatty acids and small amount of
omega-3 fatty acids. The high omega-6 to
omega-3 fatty acids ratio in meat is mainly
due to the extensive use of grains rich in
omega-6 fatty acids as animal feed.
Livestock cannot convert omega-6 fatty acids
into omega-3 fatty acids efciently because
they lack the gene required to synthesis the
enzyme needed for such a conversion.
Scientists have already produced omega-3
fatty acid-enriched pork by feeding pigs with
axseed, sh oil, or shmeal. This resulted
in a increase in total omega-3 fatty acids in
muscle fat from 1% to 6%.
Studies have also shown that if only ALA,
alpha-linolenic acid (mostly from seeds and
nuts) is increased, the porks sensory
qualities (e.g. avour and texture) can be
affected negatively. But, increasing omega-3
fatty acids EPA and DHA (mostly from sh
and sh oil) does not affect the quality of
cooked pork.
Now, researchers have produced piglets
with an extra gene that encodes a protein
capable of converting omega-6 fatty acids
into omega-3 fatty acids.
The concentrations of total omega-3 fatty
acids (ALA, EPA, DPA, and docosahexaenoic
acid DHA) in the tail tissues of these
experimental piglets were found to be three
times higher than usual. On the other hand,
the concentration of total omega-6 fatty
acids was reduced by 23%. This resulted in
an overall ve times reduction in the
omega-6 to omega-3 ratio.
Similar levels were found in all major
tissues, including muscle, liver, heart,
spleen, tongue, brain, and skin. Also, the
total omega-3 fatty acid in the muscle fat of
these piglets was about 8%, which is much
higher than the levels in other pigs (1-2%).
Adding an extra gene seems to be an efcient
way to produce omega-3-enriched pork.
However, additional research is needed
before omega-3 pork could be considered for
human consumption. The long-term health of
the pigs, whether omega-3 fatty acid levels
will remain high when the animals reach
adulthood, and how the meat tastes are only
some questions that remain unanswered.
As the public has become more aware of
the benecial effect of omega-3 fatty acids,
the food industry has been rushing to
introduce products enriched with omega-3
fatty acids to consumers. So far, the only way
to enrich animal tissues with omega-3 fatty
acids is via diet.
Animals must be fed with axseed,
shmeal, or other marine products. Not only
is the feed more costly than conventional
feed, but the shing industry is also being
challenged by a decline in sh stocks and
contamination issues. A land-based
alternative source of dietary omega-3 fatty
acids may become necessary sometime in
the future.
For more on omega-3 fatty acids, see
WellnessOptions issue 16, 21, 23, 24 and
other articles in this issue.
References:
Fontani G et al (2005) Cognitive and physiological effects of Omega-
3 polyunsaturated fatty acid supplementation in healthy subjects.
Eur J Clin Invest. 35(11):691-9.
Lai L et al (2006) Generation of cloned transgenic pigs rich in
omega-3 fatty acids. Nature Biotechnology, Advanced Online
Publication, March 26, 2006.
Food & Nutrition Updates
by Y. Michael Chan, PhD, CChem, FRSC(UK), FACB
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Ginger
Ginger rhizome (Zingiber ofcinale) is well
known in the form of ginger sticks or ginger
ale. It is used worldwide as a spice and in
herbal remedies, with a long history of
safety. The US FDA (Food and Drug
Administration) classies ginger as
Generally Recognized as Safe (GRAS), and
the German Commission E monographs
reports that ginger has no known side effects
and no known drug/herb interaction.
In traditional Chinese medicine, ginger is
used for dyspepsia, nausea, diarrhea,
rheumatism, and toothache. The principal
active pharmacological ingredients of ginger
are gingerols and shogaols and volatile oils
(sesquiterpenes and monoterpenes).
Health benets
Nausea and Vomiting during Pregnancy
Four well-controlled, double-blind,
randomized clinical studies have been
published, providing convincing evidence for
the effectiveness of ginger for nausea and
vomiting during pregnancy. These studies
used a daily 1-g dose in capsule or syrup
form for 4 days to 3 weeks, with no adverse
outcomes or side effects.
Another study compared the use of one
capsule of ginger (350 mg) with one capsule
of vitamin B6 (25 mg) 3 times a day for 3
weeks. It shows that symptoms of nausea,
dry retching, and vomiting in early pregnancy
were reduced to a similar extent. The
researchers conclude that the use of ginger
can reduce the severity of symptoms.
Motion sickness
A study on 80 naval cadets unaccustomed to
sailing found that ginger reduced the tendency
to vomit and the incidence of cold sweats. In
another study, ginger at a dose of 1,000 mg
effectively reduced the severity of nausea
evoked by circular motion on a rotating chair,
Food & Nutrition Herbs
by Manny W. Radomski, PhD & Y. Michael Chan, PhD, CChem, FRSC(UK), FACB
Dosage Information for Various Forms of Ginger
1000 mg
standardized extract =
1 teaspoon fresh grated rhizome
2 droppers liquid extract (2 mL)
2 teaspoons syrup (10 mL)
4 cups (8 oz each) ginger tea prepackaged
4 cups (8 oz each) ginger tea, steeping 1/2 teaspoon
grated ginger for 5-10 min
8-oz cup ginger ale, made with real ginger
2 pieces crystallized ginger, each 1 inch square, 1/4 inch thick
Ginger product preparation may vary, check labels for ginger content (mg ginger per dose/serving),
and adjust accordingly to reach 1000 mg ginger/day.
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025_44_45_Food_Ginger.qxd 4/6/06 11:18 PM Page 1
prolonged latency before the onset of nausea,
and shortened the recovery time from nausea
after the cessation of motion.
Postoperative nausea and vomiting
This is one of the most common side effects
associated with surgical procedures, with
incidence rates ranging from 1% to 43%. A
meta-analysis study shows that a xed dose
of 1 g of ginger is more effective than
placebo for the prevention of postoperative
nausea and vomiting.
In another study on postoperative nausea
and vomiting after major gynaecological
surgery, no signicant difference was found
between the effect of ginger and an
antiemetic (against vomiting and nausea)
agent, metoclopramide.
Anti-inammatory
The original discovery of gingers inhibitory
effects on prostaglandin biosynthesis in the
early 1970s has been repeatedly conrmed.
This discovery identied ginger as sharing
pharmacological properties with non-steroidal
anti-inammatory drugs, which suppresses
prostaglandin synthesis through inhibition of
cyclooxygenase-1 and cyclooxygenase-2. An
important extension of this early work is the
observation that ginger also suppresses
leukotriene biosynthesis by inhibiting 5-
lipoxygenase.
Recent studies suggest that dual
inhibitors of cyclooxygenase and 5-
lipoxygenase may have a better therapeutic
prole and have fewer side effects than non-
steroidal anti-inammatory drugs.
The characterization of the pharmacological
properties of ginger entered a new phase
with the discovery that a ginger extract
(EV.EXT.77) derived from Zingiber ofcinale
(family Zingiberaceae) and Alpina galanga
(family Zingiberaceae) inhibits the
expressions of several genes involved in the
inammatory response. These include genes
encoding cytokines, chemokines, and the
inducible enzyme cyclooxygenase-2. This
discovery provides the rst evidence that
ginger modulates biochemical pathways
activated in chronic inammation.
The identication of the molecular targets
of individual ginger constituents provides an
opportunity to optimize and standardize
ginger products. Such preparations will be
useful in experimental animals studies and
human clinical trials on the effects of
specic biomarkers of inammation.
References:
Afzal M et al. (2001) Ginger: an ethnomedical, chemical and
pharmacological review. Drug Metabol Drug Interact 18: 159-90.
Chaivakunapruk N et al. (2006) The efcacy of ginger for the
prevention of postoperative nausea and vomiting: a meta-analysis.
Am J Obstet Gynecol 194: 95-9.
Chrubasik S et al. (2005) Zingiberis rhizoma: a comprehensive
review on the ginger effect and efcacy proles. Phytomedicine 12:
684-701.
Ernst E and Pittler MH (2000) Efcacy of ginger for nausea and
vomiting: a systematic review of randomized clinical trials. Br J
Anaesth 84: 367-371.
Grzanna R et al. (2005) Ginger--an herbal medicinal product with
broad anti-inammatory actions. J Med Food 8: 125-32.
Langner E et al. (1998) Ginger: history and use. Adv Ther 15: 25-44.
Lien H-J et al. (2003) Effects of ginger on motion sickness and
gastric slow-wave dysrhythmias induced by circular vection. Am J
Physiol Gastrointest Liver Physiol 284: 481.
Smith C et al. (2004) A randomized controlled trial of ginger to treat
Nausea and vomiting in pregnancy. Obstet Gynecol 103: 639-645.
Curcumin
The turmeric (Curcuma longa) plant, a
perennial herb belonging to the ginger
family, is cultivated extensively in south and
southeast tropical Asia. The rhizome or root
of this plant is used for culinary and
medicinal purposes in Ayurvedic and
traditional Chinese medicine. The most
active component of turmeric is curcumin,
which makes up 2-5% of the spice.
In Chinese medicine curcumin is used
for abdominal pain, whereas in Indian
medicine, it is used for inammation,
including sprains and swellings caused by
injury, wound healing, and abdominal
problems. There are over 1,500 citations in
Medline, a medical website, relating to the
biological effects of curcumin. At doses of 8
grams a day, curcumin is not known to show
any adverse effects.
Recent animal and clinical human studies
have shown that curcumin may be used for a
variety of health conditions.
Target disease and Curcumin action
Anti-inammatory and antioxidant
As an antioxidant, it is 10 times more active
than vitamin E. Curcumin prevents the
oxidation of hemoglobin and inhibits lipid
peroxidation.
Anticancer
It blocks tumour initiation, tumour promotion,
invasion, angiogenesis, and metastasis.
Curcumin inhibits the proliferation of a wide
variety of tumour cells including B-cell and T-
cell leukemia, colon carcinoma, epidermoid
carcinoma, and various breast carcinoma
cells. It also suppresses carcinogenesis of
the skin, stomach, colon, and liver in mice.
Cardioprotective
Curcumin inhibits the proliferation of
peripheral blood mononuclear cells and
vascular smooth muscle cells, hallmarks of
atherosclerosis. It prevents oxidation of low-
density lipoproteins (LDLs), inhibits platelet
aggregation, and reduces the incidence of
myocardial infarction.
Skin diseases
It may have effects on psoriasis, scleroderma,
and dermatitis. Curcumin may ccelerate
wound healing.
Rheumatoid Arthritis
Curcumin possesses anti-rheumatic and
anti-arthritic effects, most likely through the
down-regulation of COX2, tumor necrosis
factor (TNF), and other inammatory cytokines.
Multiple Sclerosis
It inhibits experimental allergic
encephalomyelitis by blocking interleukin
(IL)-12 signaling in T cells, suggesting it
might have effects on multiple sclerosis
Alzheimers Disease
Curcumin can suppress oxidative damage,
inammation, cognitive decits, and amyloid
accumulation in Alzheimers disease
Inammatory Bowel Disease
Pretreatment of experimental mice with
curcumin for 10 days ameliorated diarrhea
and the disruption of the colonic architecture.
References:
Aggarwal BB et al. (2003). Anticancer potential of curcumin:
preclinical and clinical studies. Anticancer Res. 23: 363-398.
Aggarwal BB et al. (2005). Curcumin derived from turmeric
(Curcuma longa): a spice for all seasons. In Phytochemicals in
Cancer Chemoprevention. P.D. Debasis Bagchi & H.G. Preuss, Eds.:
349-387. CRC Press. New York.
Egan ME et al. (2004). Curcumin, a major constituent of turmeric,
corrects cystic brosis defects. Science 304: 600-602.
Ohtsu H et al. 2002. Antitumor agents. 217. Curcumin analogues
as novel androgen receptor antagonists with potential as anti-
prostate cancer agents. J. Med. Chem. 45: 5037-5042.
Shishodia S et al. (2005) Curcumin: getting back to the roots. Ann
NY Acad Sci 1056: 206-17.
Ukil A et al. (2003) Curcumin, the major component of food avour
turmeric, reduces mucosal injury in trinitrobenzene sulphonic acid-
induced colitis. Brit J Pharmacol 139: 209-18.
025_44_45_Food_Ginger.qxd 4/6/06 11:18 PM Page 2
Polyphenols include avonoids,
and a rich source of favonoids is
cocoa. Chocolate and other products
made from cocoa contain avonoids
such as catechin, epicatechin, and
procyanidin. There is some evidence
that cocoa has a protective effect on
the cardiovascular system.
Testing chocolates effects
Up until now, evidence for cocoas
protective effects came from two types
of research. Test tube studies using
extracts of cocoa or avanols isolated
from cocoa found, for example,
antioxidant activities that protect red
blood cells from damage or blocked
the oxidation of DNA. But what
avanols do in a test tube may not
take place in the human body.
Some intervention studies that
involve feeding cocoa or cocoa
avanols to people have shown that
cocoa, and in particular the avanols
of cocoa, have effects that could
benet cardiovascular health.
What studies show
The avanols present in cocoa indeed
enter the blood stream after ingestion,
a necessary rst step if they are to
have an effect. It has also been found
that individuals who eat 75 grams of
Food & Nutrition Cocoa
Cocoa & chocolate
health treats
There are increasing reports that plant
polyphenols with their antioxidant
properties may offer protection against
certain cancers and cardiovascular
disease (CVD).
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025_46_47_Food_Cocoa.qxd 4/6/06 11:19 PM Page 1
dark chocolate or chocolate enriched
with cocoa polyphenols daily for 3
weeks show about a 12% increase in
good (HDL) cholesterol, while those
eating white chocolate (which has no
cocoa polyphenols) show a 3%
decrease in HDL.
One human study on blood vessel
dysfunction showed that blood ow
increases signicantly due to dilation
of an artery when individuals are fed
a cocoa drink enriched with cocoa
avanols. The effect peaks 2 hours
after drinking and returns to baseline
after 4 hours.
Another human study on healthy
individuals examined the difference
between eating 100 grams of
commercially available dark chocolate
bars containing polyphenols and white
chocolate bars without polyphenols,
both with the same energy content.
Participants ate one dark chocolate
bar per day for 14 days. Blood
pressure and insulin sensitivity were
measured at the beginning and the
end of the test period. Participants
then repeated the test with white
chocolate bars.
The study shows that the dark
chocolate decreased systolic blood
pressure between 4.1 and 11.9 mm Hg
and signicantly improved insulin
sensitivity. But white chocolate had
no effect on either parameter.
Similar studies in which a smaller
amount (46 grams instead of 100
grams) of dark chocolate were
consumed daily showed that this
amount did not result in lowered
blood pressure.
The studies mentioned were short
term and employed small numbers of
individuals. The rst large
epidemiological study was reported
recently and is described below:
Recent update on cocoa benets
A study in the Netherlands examined
the protective effects of chocolate in
470 elderly men over 15 years. At the
start of the study, none of these men
had a history of CVD, cancer, or high
blood pressure. They were examined
for various health parameters in 1985,
1990, and 1995 and were also inter-
viewed on the composition of their diet.
Researchers prepared a list of 24
cocoa-containing foods (drinks,
puddings, nutritional supplements,
etc.) and calculated the amount of
cocoa consumed each day by the
participants based on the estimated
cocoa contents in the foods. The men
were divided into 3 groups depending
on the amount of chocolate they
consumed daily: non-consumption,
lower, and higher consumption.
Results show that in 1985, about
one-third of the men did not eat
cocoa. The lower consumption group
took an average 0.92 g/d of cocoa.
The higher consumption group ate
4.18 g/d of cocoa, which is the
equivalent of 10 g/d of dark
chocolate. Cocoa consumers were
more likely to eat candies, cookies,
nuts and seeds, and drink alcohol. It
also seems that the more cocoa they
ate, the less meat and coffee they
consumed.
The study shows that a higher
intake of cocoa is associated with
lower systolic and diastolic blood
pressure. Those with the highest
cocoa consumption (> 2.25 g/d)
were an average 3.7 mm Hg lower in
their blood pressure than those who
ate less cocoa (<0.05g/d).
Statistics on mortality and cause of
death of this group of men were also
examined. Between 1985 and 2000,
314 (66.8%) of the men had died,
with CVD accounting for 152 deaths.
Analysis of data indicates that those
with the highest cocoa intake had the
lowest number of deaths from CVD.
Men in the high consumption group
were half as likely to die from CVD as
the others.
This reduced risk was not associated
with a higher consumption of nuts,
seeds, or cookies and was
independent of other factors such as
weight, smoking, physical activity
levels, calorie intake, and alcohol
consumption. Furthermore, the higher
consumption group was also less
likely to die of other causes.
Researchers suggest that long-term
daily intake of a small amount of
cocoa equivalent to only 10 g/d of
dark chocolate lowers blood pressure
and reduces the risk of death from
heart disease.
Continued study of cocoa and its
avonoids as signicant protectors of
cardiovascular health is warranted.
References:
Buijsse B et al. (2006) Cocoa intake, blood pressure, and
cardiovascular mortality: the zutphen elderly study. Archives of
internal medicine 166:411-417.
Engler MB and Engler MM (2004) Vasculoprotective effects of
avonoid-rich cocoa and chocolate. Nutrition Research 24: 695-706.
Grassi D et al (2005) Short-term administration of dark chocolate is
followed by a signicant increase in insulin sensitivity and a
decrease in blood pressure in healthy persons. American Journal of
Clinical Nutrition 81:611 614.
Heiss C et al. (2003) Vascular effects of cocoa rich in avan-3-ols.
Journal of the American Medical Association 290:1030-1031.
Keen C et al. (2005) Cocoa antioxidants and cardiovascular health.
American Journal of Clinical Nutrition 81(suppl):298S-303S.
Mursu J et al. (2004) Dark chocolate consumption increases HDL
cholesterol concentration and chocolate fatty acids may inhibit lipid
peroxidation in healthy humans. Free Radical Biology & Medicine
37: 1351-1359.
Sies H et al. (2005) Cocoa polyphenols and inammatory mediators.
American Journal of Clinical Nutrition 81(suppl):304S-312S.
Taubert D et al. (2003) Chocolate and blood pressure in elderly
individuals with isolated systolic hypertension. Journal of the
American Medical Association 290:1029-1030.
Not all chocolates are created equal
Dark chocolate usually contains more antioxidant avanols than milk chocolate.
White chocolate usually has very little or no avanoids.
The amount of avonoids in cocoa products depends on the type of cocoa bean,
the processing of the beans, and the processing of the cocoa for use in specic
products. In some cases, as much as 90% of the original avanol content may be
lost during processing.
An analysis shows that 40 grams of a milk chocolate contains 395 milligrams of
avonoids, while the same amount of dark chocolate contains 951 milligrams. As for
hot cocoa drinks, 240 milliliters contains about 45 milligrams of avonoids.
025_46_47_Food_Cocoa.qxd 4/6/06 11:20 PM Page 2
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Food & Nutrition Remedy
by Manny W. Radomski, PhD
The health benets of garlic in
preventing and improving a wide
variety of diseases have been known
for centuries. Garlics protective
effects are largely due to its high
content of organosulfur compounds
and antioxidant activity.
Fresh garlic, however, may cause
indigestion, and its pungent odour
that lingers on the breath and skin
can be a social deterrent. These
disagreeable effects of fresh garlic are
due to allicin, an oxidant released
upon cutting or chewing the clove.
Common garlic preparations include
powder, tablets, oil of steam-distilled
garlic, oil of oil-macerated garlic,
ether-extracted oil of garlic, and aged
garlic extract (AGE).
The best and most stable garlic
preparation for research purposes is
aged garlic extract (AGE). This
standardized and highly bioavailable
form is odourless and still rich in anti-
oxidants. It is produced by prolonged
extraction and aging of organic fresh
garlic at room temperature.
The process converts unstable
compounds, such as allicin, to stable
substances and produces high levels
of water-soluble organosulfur
compounds that are antioxidants.
AGE can be taken for a long time
without toxic side effects or
contraindications with medications. It
has been widely used to study cancer,
cardiovascular, immunological,
metabolism, and other diseases.
Health benets for heart and brain
Over the last one-quarter century, the
role of garlic in preventing and
improving cardio-vascular conditions
and protecting against dementias has
received much attention.
AGE has been shown to modulate
cardiovascular risk factors in both
clinical (improving) and preclinical
(preventive) settings. It can reduce
blood pressure, inhibit platelet
aggregation and adhesion, lower LDL
and elevate HDL cholesterol, reduce
smoking-related oxidative damage,
inhibit the production of prostaglandins
involved in inammation, and lower
homocysteine levels.
It has been shown to increase micro-
circulation, protecting endothelial cells
from oxidative damage. This is important
in diabetes where the microvasculature
in the brain may be damaged, leading
to an increased risk of dementia.
Oxidative damage is a major factor
in cardiovascular disease and
dementia. AGE can also temporarily
increase by 30-40% the synthesis of
constitutive nitric oxide, a protective
factor against myocardial ischemic or
reperfusion injury (that increases the
risk for heart problems and dementia
after stroke). AGE has been found to
inhibit the progression of coronary-
artery calcication, reducing the risk
of a heart attack.
AGE has the potential to protect the
brain against neurodegenerative
conditions. It may also help prevent
cognitive decline by protecting
neurons. Additional research on
humans is needed to conrm these
benets, but compelling evidence
supports the benecial health effects
of AGE in cardiovascular diseases and
reduced risk of dementia.
References:
Borek C. (2006) Garlic reduces dementia and heart-disease risk. J
Nutr. 136:810S-2S.
Borek C. (2001) Antioxidant health effects of aged garlic extract. J
Nutr.131:10103-53.
Rahman K, Lowe GM. (2006) Garlic and Cardiovascular Disease: A
Critical Review. J Nutr 136: 736S-41S.
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Garlic
wonders
025_49_Food_Garlic.qxd 4/6/06 11:45 PM Page 1
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