Arabinogalactan Benefits and Dosage

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Arabinogalactan (AG), is a fermentable fiber found in high concentrations in North American larch trees. It is also the active constituent of echinacea. Using a patent-protected, water-based extraction process, the larch AG can be extracted from the plant cell in its natural state. Arabinogalactans are thought to contribute to the possible immune-enhancing activities of ganoderma lucidum and echinacea. Arabinogalactan may be an important adjunct to cancer treatments due to its capability to stimulate Natural Killer Cell cytotoxicity, stimulate the immune system, and block metastasis of tumor cells to the liver.

Arabinogalactan Benefits

Larch AG are a class of long, densely branched polysaccharides of the 3,6-beta-D-galactan type with molecular weights ranging from 10,000-120,000. Arabinogalactan has showed the capability to activate immune cells involved with the body’s first line of defense and to promote cytokine production, the communication and signaling compounds of immune cells.

Scientific experiments have indicated arabinogalactan can stimulate natural killer cell cytotoxicity, develop other functional aspects of the immune system, and inhibit the metastasis of tumor cells to the liver. Natural Killer Cell activity is a important marker for health. A number of chronic diseases are characterized by decreased natural killer cell activity, including viral hepatitis, HIV/AIDS, chronic fatigue syndrome, and autoimmune diseases such as multiple sclerosis. In prostate cancer, changes in natural killer cell activity were found to be associated with boththe likelihood of metastasis and tumor response to therapy. Actually, it was found to be as reliable as the specific tumor markers reflective of prostate cancer.

Natural killer cells are a type of lymphocyte and a component of innate immune system. Natural killer cells play a critical role in the host-rejection of both tumours and virally infected cells. Natural killer cells circulate through the blood, lymphatic and tissues, on patrol for the presence of transformed or pathogen-infected cells. Since NK cells are possible to kill cancer cells, experts are studying ways to increase the number or boost the function of these cells in the body as a method to treat cancer stronger.

Arabinogalactans  may be substantial in cancer cure  protocols due to its capability to block the metastasis of tumor cells to the liver, and to stimulate natural killer cell cytotoxicity. Metastatic disease most commonly spreads to the liver, in preference to other organ sites. This has been theorized to be the result of a reaction between the galactose-based glycoconjugate on the metastatic cells and a hepatic-specific lectinlike receptor found in liver parenchyma. Some experiments  have reported that arabinogalactan may alter this reaction by inhibiting the attachment of metastatic cells to liver parenchyma via competitive binding to liver hepatic galactose receptors. A study involving animal with liver carcinoma treatment with larch arabinogalactan reported a reduced amount of liver metastasis and also had prolonged survival times, although all test animals eventually succumbed to liver metastasis. Modified Citrus Pectin has also been mentioned as a possible anti-metastatic agent in cancer however, arabinogalactan, while having the same anti-metastatic activity of action as  Modified citrus pectin, also offers immunemodulating activity not offered by this other natural substance.

Larch Arabinogalactan Dosage

Dose of general use 400 mg, 4 times a day. Available medical literature indicates that this dietary supplement should be standardized to at least 98 % arabinogalactan. Antioxidants, such as vitamin C, may boost arabinogalactan effect.

Serratiopeptidase Dosage and Benefits

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Serrapeptase, also known as serratiopeptidase, is an enzyme isolated from a non-pathogenic bacteria called enterobacter Serratia E15. This enzyme is naturally processed commercially through fermentation. In other words, serratiopeptase is produced by purification from culture of Serratia E-15 bacteria. This immunologically active enzyme is entirely bound to the alpha 2 macroglobulin in biological fluids. Various researches reveal strong anti-inflammatory properties of this naturally occurring enzyme.

Serratiopeptidase Benefits

Particularly in Asia and Europe, it is clinically used for anti-inflammatory conditions such as arthritis, atherosclerosis, fibrocystic breast disease and carpal tunnel syndrome. Researches in Japan and Germany has shown serratiopeptidase can dissolve ovarian and breast cysts, case symptoms of arthritis, speed the healing of torn ligaments and sports injuries and aid post operative healing. Serratiopeptidase just dissolves non-living tissue, leaving living tissue alone. Blood clots, cysts and arterial plaque are all slowly dissolved.

Clinical Trials

The German doctor, Dr. Hans Nieper, used serratiopeptidase on patients who were candidates for chelation therapyserratiopeptidase and surgery to remove the plaque from arteries. Especially, advises the use of this enzyme to treat blocked carotid arteries when classic surgery is too risky. The formation of plaque involves deposits of fatty substances, cholesterol, calcium, cellular waste products,  and fibrin  on the inner lining of the arteries. In his researches, Dr. Nieper proved that serratiopeptidase was capability of dissolving and digesting the substances that cause plaque formation on the arterial walls, such as cholesterol, calcium, cellular wastes, various fats, and fibrin, a clotting agent. Excessive plaque results in partial or complete blockage of blood flow through an artery, resulting in arteriosclerosis  which could cause a heart attack or stroke. Dr. Nieper explained that serratiopeptidase digests non-living tissue, blood clots, cysts, arterial plaque and inflammation in all forms. It protects against strokes and has been found to be more effectual and fast than EDTA chelation therapies in removing arterial plaque.

Serratiopeptidase anti-inflammatory effects are similar to those of the ibuprofen, salicylates and non-steroidal anti-inflammatories. Unlike these drugs, serratiopeptidase is a naturally occurring enzyme and that does not irritate the digestive system. Besides reducing inflammation, one of serratiopeptidase most important effects is decrease of pain, due to its capability to block the release of pain-inducing amines from inflamed tissues.

In a study 2008; compared serrapeptase and its anti-inflammatory effect with aspirin and two human pancreatic proteolytic enzymes ( chymotrypsin and trypsin). Though all groups were effective at reducing inflammation, serrapeptase  was the most effective.

Serratiopeptidase reduces the viscosity of the mucus, improving the elimination of bronchopulmonary secretions. Early research findings suggests that patients with sinusitis who take serratiopeptidase have important reduced pain, nasal secretions, and nasal obstruction after 3-4 days of therapy. People taking  the serratiopeptidase experienced a significant reduction in severity of pain, amount of secretion, purulence of secretions, difficulty in swallowing,  nasal obstruction, and body temperature after only three or four days. A study in Japan investigated the efficacy of serratiopeptidase on sputum properties and symptoms in individuals with chronic airway diseases. After four weeks of serratiopeptidase therapy, sputum output, viscosity and sputum neutrophil count decreased significantly. Also, the frequency of expectoration and of coughing decreased.

Serratiopeptidase has been approved as a standard solution in many European countries for swelling and inflammation. A study was conducted on the effect of serratiopeptidase on post-operative pain of the ankle and swelling. In the serratiopeptidase group, the swelling decreased by 50 percent on the third post-operative day, while in the control groups no reduction in swelling occurred. Another double-blind study, reported in the “Pharmatherapeutica“, found that serratiopeptidase reduced swelling in patients who underwent surgery to treat empyema.

In a double-blind study, serratiopeptidase was found to decrease breast pain, breast swelling and induration in 85.7 percent of the patients taking the supplement. Experts concluded that serratiopeptidase is a  influential and  safe remedy for the therapy of breast engorgement.

Scientists in India conducted a study to assess the response of serratiopeptidase in people with carpal tunnel syndrome. 20 patients with carpal tunnel syndrome were evaluated clinically after six weeks taking serratiopeptidase. 65 % demonstrated significant clinical development, which was supported by improvement in electrophysiological parameters. While surgery had been considered the first  therapy,  new researches  reveal that the use of serratiopeptidase in conjunction with bromelain and Vitamins B2 and B6 is also useful.

Serratiopeptidase Dosage

The general recommended dose is 10 mg to 30 mg per day. According to Dr. Nieper, just 3 three 5 mg tablets of serratiopeptidase daily for twelve to eighteen months are sufficient to remove fibrous blockages from constricted coronary arteries, as confirmed in many of his patients by ultrasound examination. For pain, start with 10 mg daily and work up to 20 mg if necessary. The enzyme activity is measured in units and are based on the ratio of 10 mg of serratiopeptidase equaling 20,000 units of activity.

Serratiopeptidase is taken on an empty stomach 1 hour before of 2 hours after meals. Serratiopeptidase capsules and tablets  are enteric coated and are taken on an empty stomach to ensure that they are activated in the small intestine, rather than in the stomach. Non-enteric coated capsules or  tablets  are rapidly destroyed by the stomach acid.

Magnesium Anxiety Dosage

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Magnesium ions regulate over 300 biochemical reactions in the body through their function as enzyme cofactors. Helps maintain healthy muscle and nerve function, keeps heart rhythm steady, supports a normal immune system, and keeps bones potent. Also, plays an momentous role in the central nervous system, regulating neurotransmitter metabolism and modulating the sensitivity of nerve receptors, including those related in the “fight or flight” stress response. A deficiency of magnesium can present common psychiatric symptoms including anxiety, depression, restlessness and irritability.  Experts estimate that the average person’s body contains about 25 gr of magnesium, and about  half of that is in the bones. Only 1 percent of magnesium in the body is essentially found in blood, and just 3 percent is found in blood serum. Hypomagnesemia (magnesium deficiency) is defined as having magnesium levels that are less than 1.8 mg/dL.

Magnesium and Anxiety Problems

Magnesium is a calming mineral that helps avoid anxiety, fear, nervousness, restlessness and irritability. Some studies it was shown that magnesium therapy resulted in faster improvement from major depression including symptoms of headache, anxiety, irritability, insomnia and short-term memory loss. Symptoms of chronic magnesium deficiency include paranoia, anxious behavior,  apprehension, depression, confusion, anger, nervousness, insomnia. Magnesium is the first mineral to be depleted when the body is under external or  internal stress; it is furthermore the first mineral to help recovery from, stress, anxiety and mineral imbalances.

Magnesium is an inhibitor of the N-methyl-D-aspartate, receptor in the brain. Inhibition of the N-methyl-D-aspartate (NMDA) activity may be associated with anti-anxiety activity, according to a 2004 research reported by Ewa Poleszak. Magnesium ions regulate calcium ion flow in neuronal calcium channels, helping to regulate neuronal nitric oxide production. In MG inability, neuronal requirements for magnesium may not be met, causing neuronal injury which could manifest as depression. Magnesium therapy is hypothesized to be influential in treating major depression resulting from intraneuronal mg deficits. CSF (Cerebral spinal fluid) magnesium has been found low in treatment-resistant suicidal depression and in people that have attempted suicide.

AnxietyCatecholamines cause general physiological changes that prepare the body for physical activity. Some characteristic effects are increases in heart rate, blood pressure, blood glucose levels, and a reaction of the sympathetic nervous system. The important catecholamines are dopamine, norepinephrine, and epinephrine. Catecholamines activate an area inside the brain named the amygdala , which appears to trigger an emotional response to a stressful event. When there is a perceived danger or stress, the brain releases these hormones, which by leaps and bounds speed up the heart rate, increase the blood pressure, and put the body in a state of readiness for physical action. Also, during the stressful condition catecholamines suppress activity in areas at the front of the brain concerned with short-term memory, concentration, inhibition, and rational thought.  Increased catecholamines lead to excretion of magnesium in urine, which reduces the concentration of magnesium in the body. Catecholamine secretion is suppressed in the presence of sufficient magnesium levels.

“Brain Derived Neurotrophic Factor” (BDNF) is produced inside brain neurons or nerve cells, especially in learning centres. The experts found that elevated brain magnesium was able to induce the production of “Brain Derived Neurotrophic Factor“, your brains rejuvenation compound. Scientists from the “School of Medicine at the University of Texas” in Austin found that elevating brain levels of magnesium can help undo the bad programming from prior stress experiences by helping to create new brain response patterns not influenced by anxiety or fear. Experts included supplementary magnesium to a group of volunteers and found that elevated brain magnesium was able to induce the production of BDNF, a compound used by the brain to rejuvenate cellular function. This led to an increase in synaptic plasticity, enabling the learned fear response to essentially change.

In an 1992 study reported in Ceskoslovenská Psychiatrie, 20 women with anxiety revealed that a combination of anxiety medicines and magnesium led to a more quick recuperation of anxiety when compared to standard therapy alone. A study in France of 264 people with generalized anxiety disorder found that a statistically significant number of women and men reported developments on a magnesium treatment. An epidemiological study found  correlate between low magnesium levels and symptoms of depression in Norway. In a 2008 clinical trial showed that magnesium was as effectual as the tricyclic antidepressant imipramine in treating depression in diabetics and without any of the negative effects of imipramine (Magnesium Research 2008-December). A study reported in the October 2010 edition of “Psychology and Behaviour” showed that low magnesium levels in blood serum and brain were amply related with behavior symptoms associated to anxiety.

Magnesium Anxiety Dosage

General magnesium dosage for adults involves 270 mg to 400 mg per day for men and 280 mg to 300 mg per day for women. A study described by “National Institutes of Health” demonstrated a reduce in symptoms of anxiety and depression in people who took 125 mg to 300 mg of magnesium, as taurinate and glycinate, daily with each meal and  at bedtime. Vit B6 in the helps determine how much magnesium absorbs into cells. High doses of zinc in interfere with the absorption of magnesium.

Niacinamide Benefits and Side Effects

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Vitamin B3 as Niacinamide and B3 as Niacin are both generally considered one of the 8  essential B Complex vitamins that can‘t be made by the body. It is an substantial precursor to the co-factors nicotinamide adenine dinucleotide (NADH) and nicotinamide adenine dinucleotide phosphate (NADPH). Along with their reduced forms  NADPH and NADH  these enzymes participate in numerous enzymatic reactions and act as antioxidants. Nicotinic acid (niacin) and niacinamide (nicotinamide) are similarly effective as a vitamin because they can be converted into each other within the organism. The blanket term vit B3 is used for both.

Niacinamide Benefits

Niacinamide is a biologically active form of vitamin B3 found widely in many  yeasts and root vegetables. Niacinamide can be made from niacin in the body. Niacin is converted to niacinamide when it is taken in amounts more than what is needed by the body. Niacin, as niacinamide or nicotinic acid , is converted in the body to the active forms,  nicotinamide adenine dinucleotide) and a phosphorylated form. Nicotinic acid and nicotinamide have similar vitamin effects, however they have very different  pharmacological activities. Nicotinamide, via its major metabolite nicotinamide adenine dinucleotide, is involved in a spacious range of biological processes including the production of energy, the synthesis of fatty acids, cholesterol and steroids, signal transduction, and the maintenance of the integrity of the genome.

Antioxidant

Nicotinamide has been shown to have antioxidant effect. In vitro, it has been found to inhibit protein oxidation and lipid peroxidation. It stops reactive oxidants that induce apoptosis or cell death.

Tryptophan

NiacinamideDietary tryptophan is  converted to niacin in the body. Approximately 2/3 of your body’s niacinamide is made from the amino acid, tryptophan. Because dietary tryptophan can be metabolized to niacin, nutritions rich in tryptophan can compensate for inadequate dietary niacin. A double-blind, placebo controlled study that was reported in “Acta Psychiatrica Scandinavica” compared 3 different therapy approaches in 25 serious depressed patient aged 18-60. One group was given a combination of tryptophan and nicotinamide, one group was given imipramine and a other group was given a combination of imipramine with the nicotinamide and tryptophan. In the group given the medicine and the supplements, there was a negative correlation between tryptophan levels and response to the treatment suggesting that the tryptophan levels were too high.The data suggest that nicotamide-tryptophan may be as efficient as imipramine in unipolar patients providing the dose is kept within the therapeutic window, and that at low doses it could also potentiate the action of tricyclic antidepressants.

Insulin

In diabetics, delays the destruction of insulin-producing pancreatic cells, avoids cell damage and improves regeneration, reduces levels of glycated haemoglobin and develops parameters of glycaemia. Nicotinamide is being investigated as an substance for the possible delaying or prevention  of the onset of type 1 diabetes mellitus. In vitro experiments have showed that nicotinamide can prevent macrophage or interleukin-1beta-induced beta-cell damage. An study in New Zealand using nicotinamide therapy demonstrated a 50 percent decrease in the development of IDDM (insulin-dependent diabetes mellitus) over a 5-year period. In a meta-analysis of ten randomized controlled trials, niacinamide  promoted wholesome C-peptide levels, insulin metabolism and beta cell function. Nicotinamide has been shown to decrease the production of IL-12 and TNF-alpha in cultures of whole blood from prediabetic and diabetic people and in healthy people.

Arthritis

In the 1950s, doctor W. Kaufman published findings from numerous of case results  the useful of niacinamide for arthritis pain in a variety of scientific journals. In a twelve-week randomized double-blind trial involving 72 participant, niacinamide provided statistically significant support for healthy inflammatory response and joint flexibility. Reduces joint inflammation by mediating interleukin I and inhibiting nitricoxide free radicals. The findings of a study reported in the July 1996 edition of Inflammation Research demonstrate that niacinamide develops joint flexibility, reduces inflammation and permits the dose of anti-inflammatory drugs to be reduced in individuals suffering from osteoarthritis.

Sir2p Activity

Niacinamide enhances Sir2p activity by increasing NAD (Nicotinamide adenine dinucleotide). New researches, show that Nicotinamide adenine dinucleotide (NAD) a plays substantial roles in transcriptional regulation, longevity, calorie-restriction-mediated life-span extension and age-associated illness. Study has revealed a longevity gene known as Sir2  that produces the protein Sir2p that has been shown to extend cell life. If Sir2 is removed from the cell’s DNA, lifespan is sharply curtailed. If an extra copy of the gene is inserted into the DNA, lifespan is extended, sometimes by as much as 50 percent.

Side Effects

Side effects associated with high-dose niacinamide include nausea, heartburn, vomiting, dizziness, decrease in insulin sensitivity, liver toxicity, irregular heartbeat, and diarrhea.

Define Acetylcholine

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Define Acetylcholine Neurotransmitter. Acetylcholine (chemical formula C 7 H 16 N O 2) is an organic, polyatomic cation that acts as a neurotransmitter in both the peripheral nervous system and central nervous system in many organisms including humans.  Acetylcholine (ACh) carries nerve impulses across a gap between neurons, known as a synapse. When a nerve impulse arrives at the nerve ending, acetylcholine, which is stored there in vesicles, is released and combines with a receptor molecule in the postsynaptic membrane or the end-plate membrane of a muscle fibre. Once released from a nerve terminal, it reacts instantly to a specific receptor, producing a particular response. Acetylcholine plays a critical task in the peripheral nervous system by activating muscle cells.

There are 2 Important Types of Acetylcholine receptor (AChR);

There are 2 basic types of cholinergic receptors, mAChR (muscarinic acetylcholine receptors) and nAChR (nicotinic acetylcholine receptors). Both of these receptors respond to acetylcholine. Nicotinic receptors are located at synapses between 2 neuron and at synapses between neurons and skeletal muscle cells. Upon activation a nicotinic receptor acts as a channel for the movement of ions into and out of the neuron, directly resulting in depolarization of the neuron. Muscarinic receptors, located at the synapses of nerves with smooth or cardiac muscle, trigger a chain of chemical events referred to as signal transduction.

Acetylcholine Food Sources

Acetylcholine is not found in foods; body synthesizes it from a molecule named Acetyl CoA, which combines with choline. Foods that contain choline; Raw egg yolks, beef liver, milk, low-fat cheese, wheat germ, shrimp,  salmon,  soy protein, oat bran, pine nuts. An approximate diet supplies 200 mg-600 mg of choline daily. Choline supplement dosage; Researchers recommend 550 mg per day for men and 425 mg a day for women.

Acetylcholine Function in The Body

BrainAcetylcholine is a substance that transmits nerve impulses in both the peripheral nervous system and central nervous system. In the central nervous system (CNS), acetylcholine acts as part of a neurotransmitter system and plays a role in attention and arousal. In the peripheral nervous system (PNS), this neurotransmitter is a important part of the autonomic nervous system and works to activate muscles. As a neuromodulator, it can exist in the cerebrospinal fluid and regulate a series of neurons directly as opposed to through a single synaptic connection.

ACh is a chemical messenger, a neurotransmitter, released by nerve cells in numerous parts of the peripheral nervous system. As a essential neurotransmitter, acetylcholine helps nerve impulses communicate with one other by moving messages across the synaptic cleft. Acetylcholine is closely associated with cognitive functions, most especially memory. Also, acetylcholine is necessary in both voluntary and involuntary processes in the body such as slowing the heart beat and contraction in the skeletal muscle. ACh is responsible for opening several sodium channels in the cell membrane by binding the skeletal muscles and the acetylcholine receptors. Subsequently the sodium ions are then triggered to penetrate the muscle cells which cause the muscles to contract.

Alzheimer’s Disease

Alzheimer’s, first described by the German neurologist Alois Alzheimer, is a physical disease affecting the brain. Symptoms generally develop slowly and get worse over time, becoming severe enough to interfere with daily work. During the course of the disease, protein plaques and tangles develop in the structure of the brain, leading to the death of brain cells. Short-term memory fails when Alzheimer’s disease first destroys nerve cells in the hippocampus, and language skills and judgment decline when neurons die in the cerebral cortex. Today, 26 million people worldwide have this dementia, and over 15 million Americans will be affected by the year 2050.

The level of acetylcholine decreases as you age. In Alzheimer’s disease, acetylcholine reduces much faster than normal because of the accumulation of 2 abnormal proteins. These proteins kill acetylcholine-transmitting cells. The gradual death of cholinergic brain cells, cells that transmit acetylcholine, results in a progressive and important loss of brain function. ACh lack can display as Alzheimer’s, MS, dementia, speech problems, slow movement, learning disorders, verbal memory problems, memory lapses, attention problems, carelessness, and decreased creativity. A 1998 research in the “Journal of Clinical Psychiatry” found that individuals who do not have sufficient level of acetylcholine have an increased possibility of developing Alzheimer’s disease.

Though there is no cure for Alzheimer’s disease, there are a few medicine on the market which can help to ease some of the symptoms of the disease. Cholinesterase inhibitors are designed to protect the cholinergic system, which is necessary for memory and learning and is progressively destroyed in Alzheimer’s disease. Cholinesterase inhibitors slow the metabolic breakdown of acetylcholine and make more of this chemical available for communication between cells. It helps slow the progression of cognitive impairment and can be useful for some Alzheimer’s patients in the early to middle stages. The first cholinesterase inhibitor drug, tacrine, was approved in 1993, but is rarely prescribed at the present time  due to safety concerns. The 3 most commonly prescribed cholinesterase inhibitors are donepezil, rivastigmine, and galantamine.