Abilify Aripiprazole Weight Gain
Abilify is also associated with metabolism problems. This can lead to weight gain
and dangerously high blood sugar levels.
Aripiprazole is prescribed to treat schizophrenia, bipolar disorder, and other mental
health disorders. Abilify can ease your symptoms and help you avoid a relapse
(when your symptoms come back), but it also cause weight gain.
Patients often put on weight soon after starting Aripiprazole and keep gaining over
time. Children are more likely to gain weight. Overweight raises your risk of
diabetes, heart attack, stroke, high blood pressure, arthritis, sleep apnea, and some
cancers.
Abilify can make you hungrier, so you might eat more. Abilify changes the way
your brain and hormones (T3-T4) work together to control your appetite. You will
likely crave sweets or fatty foods. They can also raise the amount of sugar and fat
in your blood.
The Harper Method is a method which helps reduce or completely eliminate
Abilify weight gain so you may receive the most benefit from the Abilify and not
suffer the health consequences.
Aripiprazole disrupts the part of the brain called the hypothalamus. In doing so the
balance of thyroid hormones are disrupted, the pituitary axis is thrown off and this;
is the beginning of the Abilify weight gain. This is also why diet and exercise
alone will not help you keep the weight off or lose the weight you have gained.
The Harper Method addresses a gene and several proteins that are associated with
that gene and helps bring them back in balance again. This action helps the
hypothalamus and pituitary axis function normally again.
The gene is called the JNK gene and the proteins are known as JNK1, JNK2, and
JNK3. The JNK1 is the one mainly addressed in the program. We do address JNK2
and JNK 3 but only slightly. WE reduce the activation of the JNK gene and the
protein JNK1 as a main course of action. This is done in a natural manner so you
do not disrupt the metabolism rate of the Abilify.
The 2 supplements used to help reduce the activation of the JNK are called
JNK5 and Optimum Solace
The ingredients of the JNK 5 and what they do:
Raspberry Ketone 98% extract - This nutritional supplement reduces the
activation of the JNK gene as well as the upstream proteins (MAPKs) that activate
the JNK gene. (1)
Green tea 98% - Green tea has a compound called Quercetin within. Quercetin is
a potent inhibitor of the JNK gene as well as the upstream proteins MAPKs. Green
tea was used instead of only quercetin so you receive it in a more natural manner.
(2)
Caffeine Anhydrous 50% extract - Anhydrous means without water. Water has
been dehydrated from the caffeine in this formula. Caffeine is great for JNK
activity reduction. The amount of caffeine used in the JNK 5 is relatively small and
should not cause caffeine agitation, anxiety or nervousness. (3)
Green Coffee Bean 50% extract - Green coffee bean reduces the activation of the
JNK. That is one slight example of its purpose in this supplement. It also helps
reduce fat accumulation, insulin resistance and much more. (4)
Garcinia Cambogia 50% extract - Garcinia Cambogia has been used as a weight
loss supplement for several years. A great product but as a standalone weight loss
supplement it is not effective. It does inhibit the JNK gene activation but only of 1
JNK pathway which renders it ineffective for weight loss in most individuals. In
combination with the other supplements found in the JNK 5, it is a catalyst to help
make the JNK 5 very effective. (5)
The supplement Optimum Solace
Saffron - With 88.5mg of saffron per capsule the Optimum Solace has been
manufactured to give the most potential of saffron. All saffron is not the same. The
parts that make up saffron are different in most supplements and even the area of
the world saffron was grown makes a huge difference in the effectiveness of
saffron. Crocin is the active part of saffron and the Optimum Solace is very high in
crocin. It is also the most expensive part of saffron but when done correctly, worth
ever penny with its ability to reduce the activation of the JNK gene and so much
more. The reference we are using here shows the JNK gene inhibition is with
treating osteoporosis which is JNK activation dependant. Optimum Solace is so
much more than weight loss! (6)
References
(1) Hepatoprotective effects of raspberry (Rubus coreanus Miq.) seed oil and its
major constituents.
Abstract
Raspberry seed is a massive byproduct of raspberry juice and wine but usually
discarded. The present study employed a microwave-assisted method for extraction
of raspberry seed oil (RSO). The results revealed that omega-6 fatty acids (linoleic
acid and γ-linolenic acid) were the major constituents in RSO. Cellular antioxidant
enzyme activity such as superoxide dismutase (SOD), glutathione peroxidase
(GPx), and catalase (CAT) were investigated in HepG2 cells treated with RSO.
Induction of the synthesis of several antioxidants in H
2
O
2
-exposed HepG2 cells
was found. RSO increased the enzyme activity of SOD, CAT, and GPx in H
2
O
2
-
exposed HepG2. Furthermore, RSO inhibited the phosphorylation of upstream
mitogen-activated protein kinases (MAPK) such as c-Jun N-terminal kinase (c-
JNK) and extracellular signal-regulated kinase (ERK). Taken together, the possible
mechanisms to increase antioxidant enzyme activities in HepG2 may through the
suppression of ERK and JNK phosphorylation. Raspberry seed oil exhibited good
effects on the activities of the intracellular antioxidant enzymes and seems to
protect the liver from oxidative stress through the inhibition of MAPKs.
(2) Molecular mechanisms underlying protective role of quercetin in attenuating
Alzheimer's disease.
Abstract
Quercetin belongs to the flavonoids family, which is present in most of the plants
including fruits, vegetables, green tea and even in red wine having antioxidant
activities. It is available as a food supplement in the market and has physiological
health effects. Quercetin has anti-inflammatory, anticancer and anti-prostate
activities along with its beneficial effects on high cholesterol, kidney
transplantation, asthma, diabetes, viral infections, pulmonary, schizophrenia and
cardiovascular diseases. Quercetin possesses scavenging potential of hydroxyl
radical (OH
-
), hydrogen peroxide (H
2
O
2
), and superoxide anion (O
2
-
). These
reactive oxygen species (ROS) hampers lipid, protein, amino acids and
deoxyribonucleic acid (DNA) processing leading to epigenetic alterations.
Quercetin has the ability to combat these harmful effects. ROS plays a vital role in
the progression of Alzheimer's disease (AD), and we propose that quercetin would
be the best choice to overcome cellular and molecular signals in regulating normal
physiological functions. However, data are not well documented regarding exact
cellular mechanisms of quercetin. The neuroprotective effects of quercetin are
mainly due to potential up- and/or down-regulation of cytokines via nuclear factor
(erythroid-derived 2)-like 2 (Nrf2), Paraoxonase-2, c-Jun N-terminal kinase (JNK),
Protein kinase C, Mitogen-activated protein kinase (MAPK) signalling cascades,
and PI3K/Akt pathways. Therefore, the aim of the present review was to elaborate
on the cellular and molecular mechanisms of the quercetin involved in the
protection against AD.
(3) Caffeine induces beneficial changes in PKA signaling and JNK and ERK
activities in the striatum and cortex of Alzheimer's transgenic mice
Abstract
Caffeine intake has been associated with a lower incidence of Alzheimer's disease
(AD) in humans. In AD mouse models, caffeine significantly decreases senile
plaques and amyloid beta (Aβ) levels while also protecting against or reversing
cognitive impairment. To understand the mechanism(s) underlying the protective
effects of caffeine against AD pathology, we investigated the effects of a two-week
treatment with caffeine (3mg/day) in transgenic (APPswe) mice and non-
transgenic (NT) mice on signaling factors involved in neuronal plasticity and
survival. We evaluated cAMP-dependent protein kinase A (PKA), phospho-cyclic
AMP response-element binding protein (phospho-CREB), and the pro-apoptotic
protein kinases extracellular signal-regulated kinase 1/2 (phospho-ERK) and
phospho-c-Jun N-terminal kinase 1 (phospho-JNK) in the striatum and frontal
cortex of caffeine-treated mice. In the striatum, APPswe control mice exhibited a
significant decrease in phospho-CREB, as well as significant increases in phospho-
JNK and phospho-ERK in comparison to NT mice. Caffeine treatment stimulated
PKA activity, increased phospho-CREB levels, and decreased phospho-JNK and
phospho-ERK expression in the striatum of APPswe mice, all of which are thought
to be beneficial changes for brain function. Even caffeine-treated NT mice
exhibited some of these changes in striatum. In the frontal cortex, caffeine did not
significantly increase phospho-CREB and PKA activity, but significantly reduced
phospho-JNK and phospho-ERK expression in both APPswe and NT mice. These
results suggest that caffeine shifts the balance between neurodegeneration and
neuronal survival toward the stimulation of pro-survival cascades and inhibition of
pro-apoptotic pathways in the striatum and/or cortex, which may contribute to its
beneficial effects against AD.
(4) Decaffeinated Green Coffee Bean Extract Attenuates Diet-Induced Obesity and
Insulin Resistance in Mice
Abstract
This study investigated whether decaffeinated green coffee bean extract prevents
obesity and improves insulin resistance and elucidated its mechanism of action.
Male C57BL/6N mice (N = 48) were divided into six dietary groups: chow diet,
HFD, HFD-supplemented with 0.1%, 0.3%, and 0.9% decaffeinated green coffee
bean extract, and 0.15% 5-caffeoylquinic acid. Based on the reduction in HFD-
induced body weight gain and increments in plasma lipids, glucose, and insulin
levels, the minimum effective dose of green coffee bean extract appears to be
0.3%. Green coffee bean extract resulted in downregulation of genes involved in
WNT10b- and galanin-mediated adipogenesis and TLR4-mediated
proinflammatory pathway and stimulation of GLUT4 translocation to the plasma
membrane in white adipose tissue. Taken together, decaffeinated green coffee bean
extract appeared to reverse HFD-induced fat accumulation and insulin resistance
by downregulating the genes involved in adipogenesis and inflammation in
visceral adipose tissue.
(5) Gambogic acid inhibits growth, induces apoptosis, and overcomes drug
resistance in human colorectal cancer cells
The emergence of chemoresistance is a major limitation of colorectal cancer
(CRC) therapies and novel biologically based therapies are urgently needed.
Natural products represent a novel potential anticancer therapy. Gambogic acid
(GA), a small molecule derived from Garcinia hanburyi Hook. f., has been
demonstrated to be highly cytotoxic to several types of cancer cells and have low
toxicity to the hematopoietic system. However, the potential role of GA in
colorectal cancer and its ability to overcome the chemotherapeutic resistance in
CRC cells have not been well studied. In the present study, we showed that GA
directly inhibited proliferation and induced apoptosis in both 5-fluorouracil (5-FU)
sensitive and 5-FU resistant colorectal cancer cells; induced apoptosis via
activating JNK signaling pathway. The data, therefore, suggested an alternative
strategy to overcome 5-FU resistance in CRC and that GA could be a promising
medicinal compound for colorectal cancer therapy.
(6) Crocin inhibits RANKL-induced osteoclastogenesis by regulating JNK and NF-
κB signaling pathways
Abstract
Receptor activator of nuclear factor-κB ligand (RANKL), a member of the tumor
necrosis factor receptor-ligand family, is a crucial factor involved in osteoclast
differentiation. Crocin, a pharmacologically active component of Crocus sativus
L., has been reported to attenuate ovariectomy-induced osteoporosis in rats.
However, the molecular mechanism underlying the effect of crocin on osteoclast
formation remains to be determined. The present study aimed to investigate the
effect of crocin on RANKL-induced osteoclastogenesis and its underlying
molecular mechanism. Results demonstrated that crocin decreased
osteoclastogenesis in bone marrow-derived macrophages (BMMs). In addition, the
expression levels of osteoclast marker proteins were downregulated by crocin.
Mechanistically, crocin inhibited RANKL-induced activation of nuclear factor-κB
(NF-κB) by suppressing inhibitor of κBα degradation and preventing NF-κB p65
subunit nuclear translocation, and by activating c-Jun N-terminal kinase (JNK) in
BMMs. In summary, the results of the present study suggested that crocin
downregulates osteoclast differentiation via inhibition of JNK and NF-κB signaling
pathways. Thus, crocin may be a potential therapeutic agent for the treatment of
osteoclast-associated diseases, including osteoporosis.
Abilify Aripiprazole Weight Gain
Abilify is also associated with
metabolism problems. This can lead
to weight gain and dangerously high
blood sugar levels.
Aripiprazole is prescribed to treat
schizophrenia, bipolar disorder, and
other mental health disorders. Abilify
can ease your symptoms and help you
avoid a relapse (when your symptoms
come back), but it also cause weight
gain.
Patients often put on weight soon
after starting Aripiprazole and keep
gaining over time. Children are more
likely to gain weight. Overweight
raises your risk of diabetes, heart
attack, stroke, high blood pressure,
arthritis, sleep apnea, and some
cancers.
Abilify can make you hungrier, so
you might eat more. Abilify changes
the way your brain and hormones
(T3-T4) work together to control your
appetite. You will likely crave sweets
or fatty foods. They can also raise the
amount of sugar and fat in your blood.
The Harper Method is a method
which helps reduce or completely
eliminate Abilify weight gain so you
may receive the most benefit from the
Abilify and not suffer the health
consequences.
Aripiprazole disrupts the part of the
brain called the hypothalamus. In
doing so the balance of thyroid
hormones are disrupted, the pituitary
axis is thrown off and this; is the
beginning of the Abilify weight gain.
This is also why diet and exercise
alone will not help you keep the
weight off or lose the weight you have
gained.
The Harper Method addresses a gene
and several proteins that are
associated with that gene and helps
bring them back in balance again.
This action helps the hypothalamus
and pituitary axis function normally
again.
The gene is called the JNK gene and
the proteins are known as JNK1,
JNK2, and JNK3. The JNK1 is the
one mainly addressed in the program.
We do address JNK2 and JNK 3 but
only slightly. WE reduce the
activation of the JNK gene and the
protein JNK1 as a main course of
action. This is done in a natural
manner so you do not disrupt the
metabolism rate of the Abilify.
The 2 supplements used to help
reduce the activation of the JNK
are called JNK5 and Optimum
Solace
The ingredients of the JNK 5 and
what they do:
Raspberry Ketone 98% extract -
This nutritional supplement reduces
the activation of the JNK gene as well
as the upstream proteins (MAPKs)
that activate the JNK gene. (1)
Green tea 98% - Green tea has a
compound called Quercetin within.
Quercetin is a potent inhibitor of the
JNK gene as well as the upstream
proteins MAPKs. Green tea was used
instead of only quercetin so you
receive it in a more natural manner.
(2)
Caffeine Anhydrous 50% extract -
Anhydrous means without water.
Water has been dehydrated from the
caffeine in this formula. Caffeine is
great for JNK activity reduction. The
amount of caffeine used in the JNK 5
is relatively small and should not
cause caffeine agitation, anxiety or
nervousness. (3)
Green Coffee Bean 50% extract -
Green coffee bean reduces the
activation of the JNK. That is one
slight example of its purpose in this
supplement. It also helps reduce fat
accumulation, insulin resistance and
much more. (4)
Garcinia Cambogia 50% extract -
Garcinia Cambogia has been used as a
weight loss supplement for several
years. A great product but as a
standalone weight loss supplement it
is not effective. It does inhibit the
JNK gene activation but only of 1
JNK pathway which renders it
ineffective for weight loss in most
individuals. In combination with the
other supplements found in the JNK
5, it is a catalyst to help make the
JNK 5 very effective. (5)
The supplement Optimum Solace
Saffron - With 88.5mg of saffron per
capsule the Optimum Solace has been
manufactured to give the most
potential of saffron. All saffron is not
the same. The parts that make up
saffron are different in most
supplements and even the area of the
world saffron was grown makes a
huge difference in the effectiveness of
saffron. Crocin is the active part of
saffron and the Optimum Solace is
very high in crocin. It is also the most
expensive part of saffron but when
done correctly, worth ever penny with
its ability to reduce the activation of
the JNK gene and so much more. The
reference we are using here shows the
JNK gene inhibition is with treating
osteoporosis which is JNK activation
dependant. Optimum Solace is so
much more than weight loss! (6)
References
(1) Hepatoprotective effects of
raspberry (Rubus coreanus Miq.) seed
oil and its major constituents.
Abstract
Raspberry seed is a massive
byproduct of raspberry juice and wine
but usually discarded. The present
study employed a microwave-assisted
method for extraction of raspberry
seed oil (RSO). The results revealed
that omega-6 fatty acids (linoleic acid
and γ-linolenic acid) were the major
constituents in RSO. Cellular
antioxidant enzyme activity such as
superoxide dismutase (SOD),
glutathione peroxidase (GPx), and
catalase (CAT) were investigated in
HepG2 cells treated with RSO.
Induction of the synthesis of several
antioxidants in H
2
O
2
-exposed HepG2
cells was found. RSO increased the
enzyme activity of SOD, CAT, and
GPx in H
2
O
2
-exposed HepG2.
Furthermore, RSO inhibited the
phosphorylation of upstream mitogen-
activated protein kinases (MAPK)
such as c-Jun N-terminal kinase (c-
JNK) and extracellular signal-
regulated kinase (ERK). Taken
together, the possible mechanisms to
increase antioxidant enzyme activities
in HepG2 may through the
suppression of ERK and JNK
phosphorylation. Raspberry seed oil
exhibited good effects on the
activities of the intracellular
antioxidant enzymes and seems to
protect the liver from oxidative stress
through the inhibition of MAPKs.
(2) Molecular mechanisms underlying
protective role of quercetin in
attenuating Alzheimer's disease.
Abstract
Quercetin belongs to the flavonoids
family, which is present in most of the
plants including fruits, vegetables,
green tea and even in red wine having
antioxidant activities. It is available as
a food supplement in the market and
has physiological health effects.
Quercetin has anti-inflammatory,
anticancer and anti-prostate activities
along with its beneficial effects on
high cholesterol, kidney
transplantation, asthma, diabetes, viral
infections, pulmonary, schizophrenia
and cardiovascular diseases.
Quercetin possesses scavenging
potential of hydroxyl radical (OH
-
),
hydrogen peroxide (H
2
O
2
), and
superoxide anion (O
2
-
). These reactive
oxygen species (ROS) hampers lipid,
protein, amino acids and
deoxyribonucleic acid (DNA)
processing leading to epigenetic
alterations. Quercetin has the ability
to combat these harmful effects. ROS
plays a vital role in the progression of
Alzheimer's disease (AD), and we
propose that quercetin would be the
best choice to overcome cellular and
molecular signals in regulating
normal physiological functions.
However, data are not well
documented regarding exact cellular
mechanisms of quercetin. The
neuroprotective effects of quercetin
are mainly due to potential up- and/or
down-regulation of cytokines via
nuclear factor (erythroid-derived 2)-
like 2 (Nrf2), Paraoxonase-2, c-Jun N-
terminal kinase (JNK), Protein kinase
C, Mitogen-activated protein kinase
(MAPK) signalling cascades, and
PI3K/Akt pathways. Therefore, the
aim of the present review was to
elaborate on the cellular and
molecular mechanisms of the
quercetin involved in the protection
against AD.
(3) Caffeine induces beneficial
changes in PKA signaling and JNK
and ERK activities in the striatum and
cortex of Alzheimer's transgenic mice
Abstract
Caffeine intake has been associated
with a lower incidence of Alzheimer's
disease (AD) in humans. In AD
mouse models, caffeine significantly
decreases senile plaques and amyloid
beta (Aβ) levels while also protecting
against or reversing cognitive
impairment. To understand the
mechanism(s) underlying the
protective effects of caffeine against
AD pathology, we investigated the
effects of a two-week treatment with
caffeine (3mg/day) in transgenic
(APPswe) mice and non-transgenic
(NT) mice on signaling factors
involved in neuronal plasticity and
survival. We evaluated cAMP-
dependent protein kinase A (PKA),
phospho-cyclic AMP response-
element binding protein (phospho-
CREB), and the pro-apoptotic protein
kinases extracellular signal-regulated
kinase 1/2 (phospho-ERK) and
phospho-c-Jun N-terminal kinase 1
(phospho-JNK) in the striatum and
frontal cortex of caffeine-treated
mice. In the striatum, APPswe control
mice exhibited a significant decrease
in phospho-CREB, as well as
significant increases in phospho-JNK
and phospho-ERK in comparison to
NT mice. Caffeine treatment
stimulated PKA activity, increased
phospho-CREB levels, and decreased
phospho-JNK and phospho-ERK
expression in the striatum of APPswe
mice, all of which are thought to be
beneficial changes for brain function.
Even caffeine-treated NT mice
exhibited some of these changes in
striatum. In the frontal cortex,
caffeine did not significantly increase
phospho-CREB and PKA activity, but
significantly reduced phospho-JNK
and phospho-ERK expression in both
APPswe and NT mice. These results
suggest that caffeine shifts the balance
between neurodegeneration and
neuronal survival toward the
stimulation of pro-survival cascades
and inhibition of pro-apoptotic
pathways in the striatum and/or
cortex, which may contribute to its
beneficial effects against AD.
(4) Decaffeinated Green Coffee Bean
Extract Attenuates Diet-Induced
Obesity and Insulin Resistance in
Mice
Abstract
This study investigated whether
decaffeinated green coffee bean
extract prevents obesity and improves
insulin resistance and elucidated its
mechanism of action. Male
C57BL/6N mice (N = 48) were
divided into six dietary groups: chow
diet, HFD, HFD-supplemented with
0.1%, 0.3%, and 0.9% decaffeinated
green coffee bean extract, and 0.15%
5-caffeoylquinic acid. Based on the
reduction in HFD-induced body
weight gain and increments in plasma
lipids, glucose, and insulin levels, the
minimum effective dose of green
coffee bean extract appears to be
0.3%. Green coffee bean extract
resulted in downregulation of genes
involved in WNT10b- and galanin-
mediated adipogenesis and TLR4-
mediated proinflammatory pathway
and stimulation of GLUT4
translocation to the plasma membrane
in white adipose tissue. Taken
together, decaffeinated green coffee
bean extract appeared to reverse
HFD-induced fat accumulation and
insulin resistance by downregulating
the genes involved in adipogenesis
and inflammation in visceral adipose
tissue.
(5) Gambogic acid inhibits growth,
induces apoptosis, and overcomes
drug resistance in human colorectal
cancer cells
The emergence of chemoresistance is
a major limitation of colorectal cancer
(CRC) therapies and novel
biologically based therapies are
urgently needed. Natural products
represent a novel potential anticancer
therapy. Gambogic acid (GA), a small
molecule derived from Garcinia
hanburyi Hook. f., has been
demonstrated to be highly cytotoxic to
several types of cancer cells and have
low toxicity to the hematopoietic
system. However, the potential role of
GA in colorectal cancer and its ability
to overcome the chemotherapeutic
resistance in CRC cells have not been
well studied. In the present study, we
showed that GA directly inhibited
proliferation and induced apoptosis in
both 5-fluorouracil (5-FU) sensitive
and 5-FU resistant colorectal cancer
cells; induced apoptosis via activating
JNK signaling pathway. The data,
therefore, suggested an alternative
strategy to overcome 5-FU resistance
in CRC and that GA could be a
promising medicinal compound for
colorectal cancer therapy.
(6) Crocin inhibits RANKL-induced
osteoclastogenesis by regulating JNK
and NF-κB signaling pathways
Abstract
Receptor activator of nuclear factor-
κB ligand (RANKL), a member of the
tumor necrosis factor receptor-ligand
family, is a crucial factor involved in
osteoclast differentiation. Crocin, a
pharmacologically active component
of Crocus sativus L., has been
reported to attenuate ovariectomy-
induced osteoporosis in rats.
However, the molecular mechanism
underlying the effect of crocin on
osteoclast formation remains to be
determined. The present study aimed
to investigate the effect of crocin on
RANKL-induced osteoclastogenesis
and its underlying molecular
mechanism. Results demonstrated that
crocin decreased osteoclastogenesis in
bone marrow-derived macrophages
(BMMs). In addition, the expression
levels of osteoclast marker proteins
were downregulated by crocin.
Mechanistically, crocin inhibited
RANKL-induced activation of nuclear
factor-κB (NF-κB) by suppressing
inhibitor of κBα degradation and
preventing NF-κB p65 subunit
nuclear translocation, and by
activating c-Jun N-terminal kinase
(JNK) in BMMs. In summary, the
results of the present study suggested
that crocin downregulates osteoclast
differentiation via inhibition of JNK
and NF-κB signaling pathways. Thus,
crocin may be a potential therapeutic
agent for the treatment of osteoclast-
associated diseases, including
osteoporosis.