| |
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 H2O2-exposed
HepG2 cells was found. RSO increased the enzyme activity
of SOD, CAT, and GPx in H2O2-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 (H2O2), and
superoxide anion (O2-). 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.
|
|