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The Willner Window Product Reference Catalog, Winter 2014
since 1911
• Willner Chemists •
the nutritional supplement professionals
Stevia: New Flavors Now Available
Extracts of leaves from Stevia rebaudiana have been used for many years in traditional treatment of diabetes in South America. Various compounds in stevia has been
concentrated, and used as natural sweeteners. These compounds possess up to 250 times the sweetness intensity of sucrose, and they are noncaloric and noncariogenic.
Stevioside, a natural plant glycoside isolated from the plant Stevia rebaudiana, has been commercialized as a noncaloric sweetener in Japan for more than 20 years.
Some studies have shown that stevia may be beneficial to those with hypertension, and those with type-2 diabetes. Dosage: Add 2-8 drops, as needed. Each ml is equiv-
alent to 300 mg of Stevia. Willner Chemists has offered stevia as a liquid herbal concentrate, providing Stevia Leaf Extract, standardized to 90% Steviosides, in 1, 2 and 4
oz sizes:
Phyto-Tech™ Stevia Extract 90
1 fl oz, prod code: 56943. ~ 4 fl oz, prod code: 56942. 2 fl oz, prod code: 56940.
~~~~~~~~~~~~~~~~~~~
Now, Willner Chemists is pleased to offer six new stevia leaf extracts, in flavored form:
Phyto-Tech™ Stevia Extract - Chocolate, 2 oz, Alcohol Free (#60140)
Phyto-Tech™ Stevia Extract - Cinnamon, 2 oz, Alcohol Free (#60139)
Phyto-Tech™ Stevia Extract - Lemon, 2 oz, Alcohol Free (#60141)
Phyto-Tech™ Stevia Extract - Orange, 2 oz, Alcohol Free (#60144)
Phyto-Tech™ Stevia Extract - Peppermint, 2 oz, Alcohol Free (#60143)
Phyto-Tech™ Stevia Extract - Vanilla, 2 oz, Alcohol Free (#60142)
These new Stevia liquids are 100% Gluten Free, and contain only organic stevia leaf extract, veg-
etable glycerin, purified water and natural flavors/essential oils. .
Suggested Use: As a dietary supplement, add 5-8 drops to a beverage or food. Shake well before
using.
~~~~~~~~~~~~~
To listen to an interview on stevia and other therapeutic herbal supplements, go to www.willner.com
and look up the May 22, 2011
Willner Window Radio Program
another four weeks. The probiotics combina-
tion included several lactobacilli and bifi-
dobacteria varieties.
During the probiotics phases, nearly half of
those taking probiotics reported having no
respiratory or gut illness symptoms compared
to 20 percent of those during the placebo
phases. Also during the probiotics phases,
those taking probiotics reported 42 percent
fewer days of illness compared to the place-
bo phases.
Reference: Journal of Dietary Supplements;
2013, Vol. 10, No. 3, 171-83
Yeast beta glucan increased
immunity
After strenuous exercise, the natural
immune capacity of mucous membranes that
line the air passageways and digestive tract
can deteriorate for up to 24 hours, increasing
chances for infection.
In the first of two studies, 182 marathon
runners took 250 mg of yeast beta glucan per
day, or a placebo, for 28 days immediately
after a marathon. Compared to placebo,
those who took yeast beta glucan had 37
percent fewer cold or flu symptoms overall.
In the second study, 60 men and women
took a placebo or 250 mg of yeast beta glu-
can per day 10 days before attempting a
strenuous 50-minute cycling exercise. Two
hours after completing the cycling test, com-
pared to placebo, the yeast beta glucan
group had 32 percent higher levels of a sali-
vary antibody, signaling the mucous mem-
branes were stronger, and could resist infec-
tion better.
Reference: Journal of Dietary Supplements;
2013, Vol. 10, No. 3, 171-83
See information on Mushroom Complex on
page 90, Immune Acute on page 44, and
Immune Complex on page 44.
of conversion to dementia. MCI is quite vari-
able in the population at large, ranging from
6-30%, according to different studies. And
Alzheimer’s disease ranges from 5-30%,
depending on age.
Focus:
In one of your studies, you found
that lower levels of both tocopherols and
tocotrienols are associated with cognitive
impairment. Do you think levels are lower
because of genetic vulnerabilities, such as
less ability to utilize Vitamin E forms? Or is
oxidative stress actually “using” up the
Vitamin E?
Mecocci:
Both are possibilities. Lower plas-
ma levels of different vitamin E forms in sub-
jects with AD and MCI could be due to
changes in metabolism and/or dietary habits
promoted by AD. However, clinical informa-
tion about the study participants allowed us
to exclude malnourishment in all subjects.
Furthermore, in our population reduced
levels of
α
- and
γ
-tocopherol were associated
with increased indices of their utilization due
to reaction with free radicals. This suggests
that vitamin E depletion was due, at least in
part, to increased utilization in
oxidative/nitrosative stress (OS/NS) events.
Higher plasma levels of total tocopherols,
total tocotrienols and total vitamin E were
associated with a 50% reduced risk of devel-
oping Alzheimers Disease over six years fol-
low-up. Overall, our data support the
hypothesis of a causal role of deficiency of
vitamin E forms in development and clinical
expression of AD.
In support of this oxidative stress hypothe-
sis, we did a longitudinal study, in which we
examined plasma levels of all eight vitamin E
forms in relation to the incidence of AD in
Swedish octogenarians. In this study we
found that higher plasma levels of total toco-
pherols, total tocotrienols and total vitamin E
were associated with a 50% reduced risk of
developing AD over six years follow-up.
Overall, our data support the hypothesis of a
causal role of deficiency of vitamin E forms in
development and clinical expression of AD.
As for genetic mechanisms regulating
bioavailability of different forms of vitamin E
in humans, very few studies have been done
so far to clarify this issue, and such studies
mainly focus on genetic factors affecting plas-
ma levels of vitamin E alpha-tocopherol. We
still do not know which genes regulate plas-
ma levels and tissue distribution and cellular
use of the eight vitamin E congeners. The
apolipoprotein E (APOE) gene has been sug-
gested as potential candidate for this role.
This gene is a well-known risk factor for late-
life AD: people who are carriers of the allele
ε
4 have an increased risk of developing AD
than those who carry the alleles
ε
2 or
ε
3.
Some studies suggested that APOE
ε
4 can
affect serum levels and cell delivery of lipids
and
α
-tocopherol, promoting the retention of
Vitamin E in plasma lipoproteins and Vitamin
E deficiency in peripheral tissues (see for
instance Mas et al., Dementia and Geriatric
Cognitive Disorders, 2006). However, few
studies have investigated this issue and con-
clusive data on the effect of the APOE geno-
type on tissue delivery of vitamin E con-
geners is still lacking.
Focus:
How does vitamin E “damage”
show up?
Mecocci:
We found significantly higher
levels of the ratio of
α
-tocopherylquinone/
α
-
tocopherol and the ratio of 5-nitro-
γ
-
tocopherol/
γ
-tocopherol in subjects with AD
and MCI in comparison to cognitively normal
. . . continued on page 88
Vitamin E and Cognitive
Impairment
The Importance Of Looking At All
Forms Of Vitamin E.
An Interview with Patrizia Mecocci, MD,
PhD., reprinted from “Focus on Allergy
Research Group”
Focus:
You have done some remarkable
work on tocotrienols and the aging brain. But
before we get to that, can you tell us about
the scope of the multicenter AddNeuroMed
Project that you are involved in?
Mecocci:
AddNeuroMed is a multicenter
European longitudinal study focused on the
detection of biomarkers for Alzheimer’s dis-
ease (AD), which can assist diagnosis, prog-
nosis, drug discovery and treatment monitor-
ing. The project includes six countries
(Finland, France, Greece, Italy, Poland and
the UK). More than 700 older individuals
were recruited. These subjects included
those individuals over 65 years of age who
were cognitively normal, those who suffered
mild cognitive impairment, or they had actu-
al dementia due to AD.
Focus:
What are the symptoms of mild
cognitive impairment?
Mecocci:
The term mild cognitive impair-
ment (MCI) describes a clinical syndrome
which can be caused by several diseases.
Among neurodegenerative diseases, AD is
among the most common brain disorders
causing MCI. MCI is a condition in which
memory or other cognitive abilities (e.g.,
executive function, language, visuospatial
skills) are slightly abnormal but they coexist
with predominantly normal functions in the
activities of daily living and absence of
dementia. MCI is related to an increased risk
. . . continued from page 78
Patrizia Mecocci, MD, PhD, received her MD from
the University of Perugia School of Medicine
where she completed a residency program in
geriatrics. She also earned a PhD in biology and
physiopathology of aging at the University of
Modena (Italy). After receiving a grant from the
Italian National Research Council (CNR), she spent
three years as a research fellow first at the
Department of Psychiatry and Neurochemistry at
the University of Lund (Sweden) and then at the
Department of Neurology, MGH-Harvard Medical
School in Boston. She is now Full Professor in
Gerontology and Geriatrics and Director of the
Geriatric Clinic at the University of Perugia. She
has a specific interest the role of oxidants and
antioxidants in neurodegenerative and
cardiovascular diseases. She has been PI or co-
investigator in research projects funded by the
European Commission and by the Italian Ministry
of Research. She is author of more than 180
papers in peer-reviewed scientific journals and 30
books and book chapters.