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Abilify 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 dependent. Optimum Solace is so much more than weight loss!

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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) signaling 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 MiceAbstractThis 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.