By O. Dawson. Lesley University. 2018.
It’s the only over-the-counter nutraceutical treatment for low progesterone proven to be effective isoptin 40 mg with amex. At doses of 750 mg/day order 40mg isoptin overnight delivery, vitamin C has been shown to raise progesterone in women with both low progesterone and luteal phase defect. Within three menstrual cycles, the group receiving vitamin C saw progesterone levels increase on average from 8 to 13 ng/mL. Taking 750 mg/day is completely safe, even though the recommended daily allowance is an abysmally low 75 to 90 mg/day. Incidentally, a daily dose of 500 to 1,000 mg of vitamin C also helps prevent cancer and stroke, keeps your eyes working well, boosts immunity, and increases longevity. Progesterone is another stress-related hormone, and affiliation helps women to calm down. I’m guessing the answer is no, because many American physicians are addicted to caffeine themselves. Sorry to be the bearer of bad news, but one of the first steps I recommend in treating low progesterone is weaning yourself from caffeine. Caffeine boosts energy temporarily by raising cortisol, but as we’ve seen, high cortisol can block progesterone receptors: your daily jolt may be decreasing the ability of your progesterone to bind to its receptor and do its job. I have a systematic approach: switching from regular coffee to yerba mate or green tea, and from yerba mate or green tea to decaffeinated green tea, and then to flavorful herbal teas, such as rooibos and fruit teas. While you are abstaining from coffee and nonherbal tea, consider ditching other drinks that can adversely affect your hormonal balance. Alcohol intake is associated with premenstrual anxiety, mood problems, and headache. This sidetracks your fat-burning mechanism and may slow down your rate of fat burning by more than half. Step 2: Herbal Therapy There are several herbs worth mentioning, but chasteberry is the most effective and safe. Other botanical therapies that raise progesterone include bladderwrack and saffron. Also known by several other terms, including chaste tree, chaste tree berry, and vitex, this herb is available as capsules or liquid tincture, and the average dose is 500 to 1,000 mg/day. Chasteberry, used by the ancient Greeks more than two thousand years ago, restores normal progesterone levels in the body. Most researchers believe that chasteberry increases the release of luteinizing hormone from the pituitary, which raises progesterone and normalizes the second half of the menstrual cycle. The progesterone boost stimulated by chasteberry has been demonstrated in blood- hormone levels, in endometrial biopsies documenting progesterone effect on the uterine lining, and in analysis of vaginal secretions. After six months of treatment, 32 percent of the women taking chasteberry became pregnant, compared with 10 percent of the group taking a placebo. Among this small percentage, the most common complaints are malaise and gastrointestinal complaints, including nausea and diarrhea. Chasteberry has been proven to help low progesterone in more than sixty years of clinical research, including five randomized trials. When performed properly, they allow the least amount of bias and demonstrate causation—unlike lesser- quality study approaches, such as observational studies or case-control studies. As we try to find what truly, effectively helps women with hormone imbalances, any kind of bias is the enemy. The number of products out there can seem dizzying; it’s hard to know what to look for and where to find it. I’ve spent twenty years testing products, following the studies, and experimenting for the benefit of my patients. I recommend it even if you don’t have an issue with fertility but have symptoms of low progesterone. One nonrandomized but large study found that chasteberry increases fertility, which led to a well- designed randomized trial that documented increased fertility in women taking 31 chasteberry. A company in Cologne, Germany, makes this proprietary blend of chasteberry fruit tincture, which contains 9 grams of 1:5 tincture for each 100 grams of aqueous alcoholic solution. Most herbalists are able to create a tincture with this formula, or you can purchase the proprietary blend from Europe. Bladderwrack, an edible brown seaweed, has been used for thousands of years in Ayurveda, the traditional medicine of India. If your low progesterone symptom is a shortened menstrual cycle, consider bladderwrack, which has been shown in one study to raise progesterone levels and lengthen a shortened menstrual cycle. It peaks a few days before my period and I can go from zero to sixty in a nanosecond if, for instance, my fiancé picks a fight or does anything annoying. Along with premenstrual anxiety, Lucinda can routinely gain five or more pounds in her luteal phase, the time from ovulation until the start of her period. She calls the premenstrual bloat her “belly goiter” but, joking aside, feels the amount of bloating is rather freakish. Lucinda and her fiancé are planning their wedding, and once the ring is on her finger, she is eager to get pregnant. She and her fiancé are currently using condoms, which I favor—when used correctly and consistently, they provide reasonable contraception and, unlike birth control pills, do not delay fertility. Treatment protocol: Lucinda came to me not long after she’d purchased progesterone cream. I recommended she try chasteberry for three months, because progesterone cream can sometimes prevent ovulation, which is not helpful if you want to proceed rapidly to baby- making. Results: Within six weeks, Lucinda had reverted to a regular cycle, every thirty days. Her anxiety resolved, which was particularly useful as she made plans for her wedding. But we worked on her food plan and tried a modified elimination diet of cutting out dairy, refined carbohydrates, alcohol, and gluten. Together with the boosted progesterone, the modified elimination diet resolved Lucinda’s bloating completely. Five years of birth control pill use is associated with a 90 percent reduction in future ovarian cancer. You need B vitamins, especially vitamins B1, B2, and B6, to keep your neuroendocrine system working as an ally.
Upon ligand binding buy discount isoptin 240mg online, the receptor may phosphorylate itself on a tyrosine or serine residue proven isoptin 40 mg, or the ligand-induced conformational change may make the receptor a substrate for a phosphorylase kinase. Sulfhydryl redox reactions, seen in the nicotinic cholinoceptor, result in alteration of relative ligand sensitivities; in the insulin receptor, they lead to affinity changes. Thus covalent modifications of receptors, whether homospecific or heterospecific, lend biochemical significance to the pharmacological terms affinity and intrinsic activity. They can also influence the receptor environment, causing a change in membrane potential or receptor distribution (clustering, patching). A notable example is the effect of Na+ ions on the relative affinity of opiate receptors toward agonists and antagonists. The lateral mobility of the ligand–receptor complex, a phenomenon still not well understood, is further regulated by an alteration in membrane fluidity triggered by the ligand–receptor complex itself. Peptide hormone receptors in particular are known to form clus- ters that are observable microscopically by use of fluorescent receptor probes. Clustering is a necessary but insufficient prerequisite for the pharmacological effect. Ligand bind- ing to clustered receptors is still necessary for cell activation in such instances as insulin receptor-mediated lipolysis in adipocytes (fat cells). As implied earlier, clustering could explain receptor cooperativity in a positive sense, as well as in a negative sense. These pits are apparent in electron micro- graphs as membrane invaginations coated on the inner (cytoplasmic) side with a web of the protein clathrine. It has been suggested that certain receptor proteins have structural domains that allow them to react with coated pits. Perhaps the most important role of internalization is the removal of receptors from the plasma membrane, the down-regulation of a receptor population. Cellular function may be conceptualized into three very broad categories of activity: 1. Transmitting information from one cell to an adjacent cell (via voltage-gated and ligand-gated ion channels). Transmitting information from the exterior of the cell to the interior of the cell (via G-protein coupled receptors). Biosynthetic activity within the interior of the cell (in the nucleus and cytosol via enzyme-catalyzed activities). Accordingly, receptor types may be categorized into five types, which address these broad categories of cellular function: 1. Protein synthesis-regulating receptors Voltage-gated ion channels (Na+,Ca2+, and K+ ion channels) are large transmembrane proteins whose conformation is dependent upon the transmembrane voltage gradient. By controlling transmembrane transport of ions they control electrical activity (e. Ligand-gated ion channels are large transmembrane proteins whose conformation is dependent upon the presence or absence of particular ligands bound to the protein; ligand binding causes the channel to open and ions to cross the cellular membrane, thereby influencing cellular function. G proteins (discussed in detail in the next section) are proteins that permit a ligand binding to the exterior of the cell to influence metabolic processes, such as enzymatic activity, within the cell. Since enzymes are catalysts that promote biosynthesis within the cell, they are logical receptors for drug action. Finally, protein synthesis-regulating receptors are found in both the cytosol and the nucleus and are capable of binding steroid and thyroid hormones. The hormone binds to a domain on the receptor protein, which in turn binds to a particular nucleotide sequence on a gene, thereby regulating its transcription. This list of potential receptors encompasses the majority of receptors that permit drug regulation of endogenous biochemical processes. However, this list of receptors is not comprehensive for all drugs available for the treatment of human disease. However, it is likewise appreciated that Nature is efficient and has organized these thou- sands of receptors into a mere handful of “superfamilies. Recent work by MacKinnon and co-workers has provided groundbreaking structural data on this superfamily. Another, and probably more important, superfamily consists of the highly conserved seven-transmembrane domain G-protein coupled receptors. These receptors are seemingly omnipresent in a diversity of disease states, and are so adaptable that they can detect ligands as big and complex as peptide hormones or as small and subtle as photons of light. Binding of an agonist or antagonist by a receptor is the first step in a long cascade of events leading to the ultimate, macroscopic physiological effect of the drug or endoge- nous substance. A more complex chain of events takes place in the vast majority of receptors—those utilizing chemical signaling, such as the G-protein coupled receptors, for transmembrane chemical signaling. The general scheme of transmembrane chemical signaling begins with the arrival of an extracellular first messenger—a neurotransmitter, hormone, or another endogenous substance, or an exogenous ligand such as a drug or bacterial toxin. The receptor– ligand interaction takes place outside the cell, and in most instances the ligand does not enter the cytoplasm. There are, however, some exceptions, as discussed in the previous section on receptor internalization. Generally, the signal delivered by the ligand is con- veyed to the cell interior by the receptor–ligand complex, which interacts with a trans- ducer. The receptor–ligand–transducer ternary complex then interacts with an amplifier, usually an enzyme, which produces a substance that activates an internal effector (usually a phosphorylase kinase); the effector kinase then phosphorylates—and thereby activates or deactivates—a site-specific enzyme that regulates the final cellular response. Membrane receptors that operate through adenylate cyclase can do so either by activat- ing the amplifier (see below) or by inhibiting it. These protein transducers—either stimulatory (G ) or inhibitorys (G )—become activated in the binding process. Presumably, the G protein is then reconstituted from the three subunits in the inactive form, ready for the next binding cycle with an occupied receptor. It must be kept in mind that the recep- tors, the G proteins, and the cyclase interact in a mobile system by collision coupling, and thus a large diversity of receptors can activate the same population of G proteins and cyclase. This ubiquitous enzyme then phosphorylates and acti- vates enzymes with functions specific to different cells and organs.
In countries where it is not recognized trusted isoptin 120mg, it may be difficult to persuade a doctor to assist you in the monitoring that is needed to safely use it discount isoptin 40 mg line. Natural Diabetes Cure: Lower Blood sugar 20% in Two Weeks Moringa Leaf Moringa is an herb that has been used in Africa as a nutritional supplement to treat and prevent malnourishment. There have been studies done, in which the leaf powder lowered blood sugar after administration. If you search online for Moringa in association with diabetes, the references are plentiful, but many of them are produced by herbal supplement companies, so their reliability is suspect. This is a supplement I had never heard of until doing some research through articles on diabetes. The references to diabetes in association with it are direct, not abstract, but they range from outright claims of studies, to "suspected" references. And while the herb is listed in many sources as being safe, no studies have been done to validate that claim. It is high in a wide range of nutrients and trace elements, so the affects are varied. Use it with caution, keep your doctor informed, and monitor your sugars carefully. Green Tea Green tea has been heralded in the last few years as the latest miracle herb. In fact, it is not that, it is not the only herb with the benefits that it provides, and it has a nasty backlash that other options do not have. Because several cultures use tea as a recreational drink, and indeed, part of the very fabric of their lives, it is promoted wholesale as a safe and healthy drink. No one will criticize it, because it is much more lucrative (as it always has been), to promote the drink as something people should have more of, not less. It is long associated with social status, and for centuries, tea and money were so closely entwined that tea had its own value equivalent to currency. We still have associations in society regarding tea that have nothing to do with the drink itself. Green tea is high in antioxidants of a particular type, and as such, it is recommended for a wide variety of purposes. Stimulants have their own set of risks, and while they can temporarily convey a sense of energy, they do not in fact speed up the metabolism - rather, you get a temporary boost, then a drop. It is also addictive, partly due to the caffeine in it, but also due to other substances. This means that over time, like coffee, the stimulant effect wears off, and you need it just to function, and no longer gain anything from it. It is potentially dangerous to pregnant or breastfeeding mothers - it can cause uterine contractions, and it does carry over to the baby through breastfeeding. Of special note is that it should not ever be used by those who are on chemotherapy, because it can increase or decrease the effectiveness of those medications, leading to an increased risk of reoccurrence, or potential toxicity from the drugs. Considering that a balanced diet, combined with intelligent supplementation with your choice of a wide range of other foods or supplements could do the same thing as green tea, it is not something that is worth getting addicted to, in my opinion. Red Rooibos tea, mangosteen or acai fruit, or any other high antioxidant food or supplement would be a far better bet, with fewer potential side effects. Grapeseed Extract Grapeseed extract is a bit harder to find than some other supplements, and may be fairly expensive through some sources. It is high in components that have an anti-oxidant effect, and is considered one of the best sources of the elements it contains. It has been shown in studies to support healthy collagen and elastin, which are important to tissue health. It improves the usage of vitamin C in your body, and is considered to help offset the affects of aging. There are preliminary suggestions that grapeseed extract may be helpful for varicose veins, heart disease, and diabetes, but I cannot find evidence to support those claims. It is also reasonable to suppose that it might be beneficial in slowing pancreatic deterioration in certain circumstances. This is a supplement which I intend to try, but since I am currently adding several others to my diet, one at a time, it will be several weeks before I am able to do so. It is important to point out that this is an herbal compound, not a single nutrient supplement, so it has multiple nutrients. It may affect more than just one system, and may have stronger negative affects as well, so proceed with caution if you choose to use it. Grapeseed extract is sometimes used as a natural preservative in natural or organic cosmetic products. It is an herb which also has other affects on the body, so it certainly is not appropriate for everyone, diabetic or not. In herbal lore though, warnings about it dropping blood sugar levels are given to people who are not diabetic also, so the evidence that it does do that is fairly conclusive. The reason warnings exist against use by diabetics is that it can cause severe hypoglycemia. I could find no instructions anywhere on appropriate dosage, when to take it, or what to expect if you did. This is an herb which I feel might be helpful for me to test, but only if I am sure that I am not pregnant at the time. The information available seems to suggest that it would need to be taken on a meal-by-meal basis. But whether it would need to be taken before the meal, with the meal, or just after the meal is unclear. It is theorized that it causes the body to either use insulin more efficiently, or to release more insulin. Very low initial doses, and close monitoring (testing at 1 hour, 1 1/2 hour, and 2 hours postprandial instead of just at 2 hours) would be required until a predictable result could be determined, as well as being prepared with emergency glucose if required. Even at that, there may be significant risk if you have problems with hypoglycemia at any point. The one other common warning with Goldenseal is that it is thought to be a blood thinner, so people with clotting disorders should avoid its use, or consult a physician about it. Exotic Herbs There are a range of herbs from all over the world which have had preliminary and mostly informal testing done for diabetes control. I have not tried any of them because they all have significant risks, dosages must be carefully controlled to avoid toxicity in many of them, and quality of available supplements is not consistent.
In thisﬁnal sec- tion effective isoptin 120 mg, that informationisapplied to the use of antiarrhythmic drugs in the treatmentofspeciﬁccardiac arrhythmias discount isoptin 240 mg on-line. Chapter 10 reviews some basic principles that should be kept in mind whenusing an- tiarrhythmic drugs. On the basisofthegenerally limited efﬁcacyofantiarrhythmic drugsaswell as their inherent propensity to cause serious problems, the ﬁrst principle should be completely self-evident;namely, one should avoid using antiarrhythmic drugs whenever possible. Thus, when one has decided to prescribe an antiarrhythmic drug, the ﬁnal step before actually writing the order should be to ask, “Does this patient really need this drug? Before prescribing an antiarrhythmic drug, the physician should be certain that the arrhythmia meets one of these two conditions. The second basic principle istokeep the goal of treatment clearly in mind and to tailor the aggressiveness of one’s therapyaccordingly. If one is treating an arrhythmiatoprevent death or permanent in- jury, for instance, a relatively aggressive approach may be appropri- ate and necessary. In theory, if the object istospare life and limb, one should err on the side of efﬁcacy, perhaps willingly accepting the risk of certain drug toxicities. Inpractice, however, as we will see in Chapters 11 and 12, there are relatively fewinstances today where oneought to rely primarily on antiarrhythmic drugs to treat arrhythmias that threaten life and limb. In these cases, one generally shoulduse a stepwise strategy, beginning with milder, less risky forms of treatment, and carefully reassessing the risk-to-beneﬁt ratio before each potential escalation of therapy. All too oftenphysicians pursue the treatment of relatively insigniﬁcant arrhythmias with Ninja-like intensity, an error that can result in unnecessary injury or death. The ﬁnal basic principle of using antiarrhythmic drugs is that, if one feels compelled to expose a patient to the risk of the drugs, one should also feel compelled to take every reasonable precaution to reduce the risks. For instance, given the almost universal risk of proarrhythmia, one should oftenconsider placing patients on a cardiacmonitor while antiarrhythmic drugs are being initiated be- cause, although proarrhythmia can occuranytime during the course of treatment, a signiﬁcant proportion of these events occur during the ﬁrst 3 or 4days of drug usage. The accompanying tables summarize the factors that should be consideredinchoosing antiarrhythmic drugs for patients with and withoutsigniﬁcant underlying cardiacdisease. Pro- cainamide, for instance, shouldnot be usedinpatients with systemic lupus erythematosus; quinidine shouldnot be usedinpatients with chronic colitis;patients with severe lung disease (in whommild drug-inducedpulmonary toxicity goes a long way) ideally shouldnot receive amiodarone;patients with a history of heart failure should not receive drugs with negative inotropic effects. Beyond these obvious individual considerations, the presenceor absenceofunderlying heart disease is the most important variable in choosing an antiarrhythmic drug,because heart disease predisposes patients to reentrant circuits and, therefore, to proarrhythmia. Amiodarone rises in rank because of its relatively low risk of producing proarrhythmia. Sotalol and dofetilide carry a moderate risk of torsades de pointes for all patients. Amiodarone carries a substantial risk of signiﬁcantend-organ toxicity for all patients, thoughonly a rela- tively small risk of proarrhythmia. The drug of choice in treating both atrial and ventricular tach- yarrhythmias dependson the presence or absenceofunderlying cardiacdisease. For ventricular arrhythmias, the primary con- siderationinpatients without underlying heart disease (i. As soon as one moves beyond these two classes of drugs, onebeginsaccepting asubstantial risk of proarrhythmia or other signiﬁcant toxicity. On the other hand, for patients with underlying heart disease who require therapy for ven- tricular arrhythmias, efﬁcacy(which here includes avoiding proar- rhythmia) is often the primary consideration. Thus, amiodarone is often the ﬁrst drug considereddespite its potential for causing long-term end-organ toxicity. To summarize, whenit comes to using antiarrhythmic drugs, there are no pretty choices. If this is not possible, one must proceedwith the goals of treatment clearly in mind and take every precaution to avoid producing more problems than are caused by the arrhythmias being treated. Such maneuvers include Valsalva, carotid massage, ocular massage, and dunking one’s face in ice water. Antitachycardia pacing techniques are also highly effective in termi- nating supraventricular arrhythmias, butsincesomany less invasive options are available, pacing is rarely usedunless an atrial pacemaker is already in place. Prior to the 1990s, pharmacologic therapy was the only viable option for most patients. Given that choice, many patients quite reasonably opted for no therapy at all and accepted the fact that they would have to make periodic pilgrimages to emergency rooms to terminate acute episodes. With thistechnique, critical components of the reentrant path- ways responsible for a patient’s arrhythmia can be mappedinthe electrophysiology catheterization laboratory and cauterized (usually with radiofrequencyenergy) directly through the electrophysiology catheter. Therefore, treatmentaimed at maintain- ing sinus rhythmis inherently difﬁcult and relatively risky. Often, it is more appropriate to accepta“lesser” therapeutic goal—that is, to allow the underlying arrhythmiatopersist while controlling the ventricular rate. The treat- ment of these arrhythmias, therefore, should include a systematic search for a primary cause. Arrhythmias caused by systemic processes (electrolyte distur- bances, hyperthyroidism, pulmonary disease, and use of alcohol or stimulant drugs) often improve or disappear once the systemic pro- cess isaddressed. Arrhythmias associatedwith underlying heart dis- ease, on the other hand, oftenpersist evenwhen therapy of heart disease isoptimized. Consequences Atrial ﬁbrillation and atrial ﬂutter have three major consequences that must be takeninto considerationwhenplanning therapy: loss of the atrial kick, the rapid heart rate itself, and the risk of throm- boembolism (Table 11. Loss of atrial kick The function of atrial contractionis to boost diastolic pressure within the ventricles just before ventricular systole begins. The atrial kick isvitally important in patients whose ventri- cles are noncompliant(i. Thus, patients with poor ventricular compliance de- velop severe symptomsalmost immediately if atrial ﬁbrillation oc- curs; atrial kick isvital in these patients. On the other hand, patients with dilatedcardiomyopathies have enlarged, “baggy” ventricles that are signiﬁcantly more compliant thannormal. These patients tend to have relatively little change in their baselinesymptoms with the onset of atrial ﬁbrillation,and they often Treatmentofsupraventricular tachyarrhythmias 143 are unable to perceive any difference, at least acutely, between sinus rhythm and atrial ﬁbrillation. Patients with normal ventricular compliancetend to experience intermediate symptoms with the onset of atrial ﬁbrillation. These patients canusually pinpoint the timeofonset of atrial ﬁbrillation,but in most cases, theirsymp- toms are limited to palpitationsand a mild-to-moderate sensation of breathlessness. The transient decrease in stroke volume resulting from the loss of the atrial kick is partially compensated by an increase in sympathetic tone, which di- rectly increases the heart rate and frequently also causes a sensation of anxiety. Thus, it is not unusual for a patient with acute atrial ﬁbrillation or atrial ﬂutter to present with very rapid heart rates and to experience extreme palpitations.