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Hemoglobin F consists of two alpha and two gamma chains sildigra 120 mg line erectile dysfunction statistics by age, while Hgb A buy sildigra 100 mg otc zocor impotence, the major constituent of adult hemoglobin, consists of two alpha and two beta chains. The oxygen-hemoglobin dissociation curves for adult (curve a) and fetal (curve b) hemoglobins are shown in Figure 4-13. Fetal hemoglobin has a higher affinity for oxygen so that the curve for fetal hemoglobin is shifted to the left. At any given oxygen tension (pO2) fetal hemoglobin is more highly saturated with oxygen, and thus can carry a greater volume of oxygen than can adult hemoglobin. In this figure, fetal hemoglobin would carry 18 ml O2/100 ml at a pO2 Of 40 torr, whereas adult hemoglobin would only carry 14 ml O2/100 ml at the same pO2. The higher affinity of fetal hemoglobin for oxygen is important in the fetal environment, because oxygen exchange occurs in the placenta at a lower pO2 than it does in the adult lung, so that having a “stickier” hemoglobin aids in oxygen exchange. This advantage only exists at the low pO2s associated with the fetal environment, however. At a normal post-natal pO2 of 100 (Figure 4-13), adult and fetal hemoglobin are both 100% saturated and carry the same amount of oxygen per ml. In fact, this can be deleterious to the sick newborn, since fetal hemoglobin binds oxygen more avidly and thus oxygen is less readily dissociated from fetal hemoglobin to peripheral tissues. It is controversial whether this disadvantage of fetal hemoglobin in the post-natal state is of clinical importance. It is likely not significant to the normal newborn but could hinder tissue oxygen delivery to the tissues in the newborn with severe respiratory or cardiac disease. Because some of this oxygen is contained in water vapor, when breathing room air, the alveolar pO2 is normally about 105 torr. Since pulmonary venous blood does not completely equilibrate with alveolar pO2 when passing through the lungs, pulmonary venous pO2 (and thus also systemic arterial pO2) is about 95 torr, corresponding to a hemoglobin saturation of 95-97%. In the body tissues, oxygen is extracted, and systemic venous pO2 decreases to approximately 40 torr (hemoglobin saturation of approximately 70%). There are two components of oxygen in the blood: dissolved oxygen and hemoglobin-bound oxygen. Dissolved oxygen is a linear function of the partial pressure of oxygen (pO2) whereas hemoglobin-bound oxygen is determined by the oxygen-hemoglobin dissociation curve (see above). The course of the fetal circulation is schematically illustrated in Figures 1-1, 1-2 and 1-5. We will examine the anatomy and physiology of the fetal circulation, and review the incredible changes which occur in the perinatal transitional period (Figure 2-1) eventually leading to the adult circulation (Figure 2-2). Several structures which play an important role in the fetal circulation, including the placenta, umbilical cord (including the umbilical arteries and umbilical vein), ductus venosus, foremen ovale, and ductus arteriosus. The only means of communication between the fetus and the outside world is the placenta. The placenta is embryologically derived from both maternal and fetal tissue, and the blood supply of the two components normally remains separate. However, the placenta is not as efficient an oxygen delivery organ as are the lungs, so that the maximum volume of oxygen that can be exchanged is limited by the venous pO2 of placental blood. The umbilical arteries are branches from the fetal iliac Fetal Circulation & Congenital Heart Disease - Daniel Bernstein, M. When the umbilical vein enters the abdomen, it courses in a cephalad direction on the underside of the anterior abdominal wall. Where the inferior vena cava enters the right atrium there is a flap of tissue known as the Eustachian valve. This valve helps direct inferior vena caval blood flow preferentially across the foramen ovale. The foramen ovale is a flap valve (shaped somewhat like a windsock) in the interatrial septum. Because the pulmonary circulation is vasoconstricted during fetal life, the lungs receive only a small percentage of fetal right ventricular output, which preferentially flows through the ductus arteriosus to the lower resistance lower body circulation and to the placenta (because of its high vascular cross-sectional area, the placenta is a very low resistance vascular bed). As we shall see later, the fetal left ventricle ejects mainly into the ascending aorta and the fetal right ventricle into the descending aorta, essentially as two separate or parallel circulations. The area of the aortic arch between the head and neck vessels and the ductus arteriosus (called the aortic isthmus) carries only approximately 10% of fetal cardiac output. Experiments in fetal lambs show that division of this part of the aortic arch does not significantly affect the “parallel” fetal circulation. In the fetus, because there are communications between the pulmonary and systemic circulations at several levels (great arteries via the ductus, atria via the foremen ovale) the fetal pulmonary and systemic blood flows are not exactly equal, with the right ventricle transiting slightly higher volumes of blood flow. There are also important differences in fetal intracardiac pressures, oxygen saturations and vascular resistances in comparison to the newborn or to the adult. Figure 1-2 shows the intracardiac and intravascular pressures in the late-gestation fetus. The ductus arteriosus is a large communication between the pulmonary artery and the descending aorta, thus pressure in the pulmonary artery and aorta are approximately equal although resistance in the pulmonary circulation is much higher than in the fetal descending aorta, resulting in blood flowing right to left across the ductus arteriosus. Fetal right and left ventricular pressures are also equal because they are both coupled to the systemic circulation. Systemic arterial pressures in the fetus are lower than adult values, whereas fetal pulmonary arterial pressures are higher than those in the adult. Although the maternal systemic arterial pO2 is about 95 torr, the pO2 of the maternal venous side of the placenta is only about 40 torr. Furthermore, the pO2 of fetal blood does not equilibrate totally with the pO2 of maternal blood during passage through the vasculature of the placenta. Due to the higher oxygen binding affinity of fetal hemoglobin, this low pO2 corresponds to an oxygen saturation of about 70%, which is still quite low compared with the normal post- natal systemic oxygen saturation (Figure 1-2. Umbilical venous blood has the highest oxygen saturation in the fetus (70%), having just returned from the placenta (Figure 1-2). This stream of oxygenated blood is then preferentially shunted across the foremen ovale, further increasing the oxygen saturation of the blood entering the left atrium. Blood from the left atrium enters the left ventricle, and from there is delivered mostly to the upper body, brain and (via the coronary arteries) to the myocardium itself. From the right ventricle, blood is pumped via the pulmonary artery across the ductus arteriosus to the descending aorta and primarily supplies the lower body and placenta. A small portion of right ventricular blood (approximately 7%) flows from the pulmonary arteries directly into the lungs. The fetal circulation is essentially a parallel rather than a series one: the right ventricle pumps blood predominantly to the lower body; the left ventricle predominantly to the upper body. Figure 2-3 shows the actual volumes of Fetal Circulation & Congenital Heart Disease - Daniel Bernstein, M. Compare these volumes with the volumes of blood passing through the heart post- natally (Figure 2-4). This degree of right ventricular dominance is less pronounced in the human, mainly because of the much large brain size in the human requiring larger volumes of ascending aortic (and thus left ventricular blood flow). The volumes of blood ml/min/kg that flow through ejected by each ventricle and various chambers and vessels in returning to each atria are similar the late-gestation fetus. About 2/3 of the descending aorta flow goes to the placenta, whereas the rest goes to the fetal lower body. Certainly, heart rate does vary in the fetus, but there is controversy about how important are changes in stroke volume.

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Ingeneral 100 mg sildigra erectile dysfunction treatment chandigarh, reverse use dependence isadetriment to the effec- tiveness of antiarrhythmic drugs sildigra 120 mg on line erectile dysfunction pump canada. Because these drugs are intended to treat tachyarrhythmias, it is generally not a usefulthing for them to lose efficacy at faster heart rates. Furthermore, because drugs dis- playing reverse use dependence produce greater potassium-channel blockade at slower heart rates, these drugs are more likely to pro- duce torsades de pointes at these slower (i. A potentially very troublesome problem,however, is that rare cases of early neu- tropenia(within 6 weeks of initiation) have been reported, which, at thistime, appears to reverse when the drug is stopped. Several clinical trials with azimilide have beenconducted to date testing the drug in the treatmentofsupraventricular arrhythmias, and several additional trials are ongoing. Interestingly, azimilide is also being evaluated for the treatment of ventricular arrhythmias. Newdrugsaimed at ventricular arrhyth- mias have become a rarity in recent years, since the widespread adoption of the implantable defibrillator and the recognition that antiarrhythmic drugs (aside from amiodarone) often increase mor- tality in patients with underlying heart disease. While it is probably disappointing to the manufacturers of azim- ilide that this drug did not reduce mortality whenused as primary prophylaxis in high-risk patients, it is noteworthy that (unlike vir- tually every other antiarrhythmic agentexceptamiodarone) it did not increase mortality in these patients. An additional trial isongoing to examine the utility of azimilide in reducing recurrentventricular tachyarrhythmias in patients with implantable defibrillators. Hav- ing an effective agenttouse in this clinical situation, in addition to amiodarone, would be quite helpful. Dronedarone If one were to ask electrophysiologists to describe the ideal antiar- rhythmic drug, most wouldprobably describe a drug that was as effective as amiodaronebut without its incredible array of toxici- ties. Indeed,an“amiodarone without the side effects”isvirtually the Holy Grailofantiarrhythmic drugs. Dronedarone(developed by Sanofi-Aventis, also the developer of amiodarone) isaderiva- tive of amiodaroneand is held by sometopotentially be that Holy Grail. The major difference is that dronedaronelacks the iodine atoms that are a major feature of amiodarone. The iodine in amiodarone is al- most certainly responsible for its thyroid toxicity, so it isagood bet that dronedarone will not cause similar thyroid-related side effects. Furthermore, the lackofiodine in dronedarone makes the drug sig- nificantly less lipophilic than amiodarone, and much of the organ toxicity of amiodarone isspeculated to be duetoits affinity for fat. In over 1200 pa- tients presenting with atrial fibrillation or atrial flutter, dronedarone proved significantly more effective thanplacebo in preventing recur- rence of the atrial arrhythmias. Additionally, dronedaroneappears to be useful in controlling the ventricular response in patients with chronic atrial fibrillationwhen therapy with digitalis, beta blockers, and calcium blockers has failed. Often,such patients are referred for atrioventricular nodal ablation and placementofapermanent pace- maker. A pharmacologic solution to rate control in these patients would obviously be an attractive alternative to ablating the patient into a state of permanent complete heart block. Head-to-head trials will be necessary to prove anyexceptional antiarrhythmic efficacy. Inclinical trials to date, none of the thyroid,lung,orhepatic toxicity so prominent with amiodarone has been seen. Furthermore, neither torsades de pointes nor other formsofproarrhythmia have been seen. Overall, whether or not dronedarone proves to be the Holy Grail thus far it does appear to be a very promising addition to the arsenal of antiarrhythmic drugs. In the atria, it blocks at least oneofthechannels responsible for phase 4depolarization,an effect that tendstoproduce bradycardia. The bradycardic effectoftedisamil, in fact, led to its initially being evaluated as an antianginal agent. An early clinical trial with tedisamil showed that it effectively con- verted atrial fibrillation of recentonset whengivenintravenously. Because of a relatively high incidenceofapparent proar- rhythmia, the clinical programwith tedisamil has been temporarily suspended. While the manufacturer hopes to develop tedisamilas both anintravenousagent for acute conversion of atrial fibrillation and an oral agent for maintaining sinus rhythm, the status of the drug at this writing isquestionable. Not surprisingly, therefore, it has been asserted that serotonin can induce atrial tachyarrhythmias. Piboserod, which blocks serotonin receptors in the atria, isbeing evaluated as a drug that might suppress atrial fibrillation. Piboserodis also being evalu- atedinthe treatment of heart failure and irritable bowel syndrome. Arandomized, placebo-controlled trial of azimilide using heart rate variability for risk stratification. This chapter con- siders in detail three varieties of adverse events that are common to manyantiarrhythmic drugs:proarrhythmia, drug–drug interactions, and drug–device interactions. Proarrhythmia It may seemparadoxical that drugs designed to suppress cardiac arrhythmias may insteadworsen them or evenproduce arrhyth- mias that did not initially exist. Proarrhythmiabeginstomake sense, however, when one considers that most arrhythmias ultimately are caused by some change in the cardiac actionpotential and that most antiarrhythmic drugs work by causing changes in the car- diac actionpotential. We always hope that the changes in the ac- tionpotential produced by an antiarrhythmic drug will make ar- rhythmias less likely to occur. However, whenever we choose to use these drugs, we must accept the possibility that the opposite might happen. At least four categories of drug-inducedproarrhythmia can be seen: bradyarrhythmias, worsening of reentry, torsades de pointes, and arrhythmias resulting fromworsening hemodynamics. Because subsidiary pacemakers distal to the Hisbundle are unreliable whendistal heart blockoccurs, antiar- rhythmic drugs should be usedwith particular care in patients with known or suspecteddistal conducting systemdisease. Ingeneral, the treatmentofdrug-induced bradyarrhythmias isto discontinue the offending agentand use temporary or permanent pacemakers as necessary to maintain adequate heart rate. By changing the conduction velocity, refractoriness, or both in various parts of the reentrant circuit, Common adverse events with antiarrhythmic drugs 119 A (a) A (b) A (c) Figure 9. To review, consider a patient who has an occult reentrant circuit whose electrophysiologic properties do not support a reentrant arrhythmia. Giving the patient mexiletine, a drug that reduces actionpotential duration, may preferentially reduce the re- fractory period of one pathway, giving this circuit the characteristics shown in Figure 9. Asimilar scenario can be developed for a pa- tient with the circuit shown in Figure 9. Unfortunately, whenever an antiarrhythmic drug is given to a patient with a potential reentrant circuit, the drug may render an arrhythmia less likely to occurorit may render an arrhythmia more likely to occur. Thissad truth followsbecause the mechanism that produces an antiarrhythmic effect(namely, the alteration of con- duction velocity and refractory periods) is the very same mechanism that produces a proarrhythmic effect. Exacerbation of reentranttachycardias can occur whether one is treating supraventricular or ventricular arrhythmias. Clinically, this form of proarrhythmia is manifested by an increase in the frequencyorduration of a reentrant arrhythmia. If the arrhythmiabeing exacerbatedisventricular tachycardia, the clinical manifestation of proarrhythmia may be suddendeath. Treating any drug-related exacerbation of a reentrant arrhythmia requires the recognition that the “new” arrhythmia is caused by a Common adverse events with antiarrhythmic drugs 121 drug.

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It is synthesized from phenylglycine purchase sildigra 120 mg bisoprolol causes erectile dysfunction, which is partially reduced by lithium in liquid ammonia buy cheap sildigra 100 mg on line impotence exercises, which forms 1,4-cyclohexadienylglycine (32. Like all of the other drugs described above, it acts as a bactericide by disrupting the process of restoring the membranes of bacteria. Second-generation cephalosporins Second-generation cephalosporins (cefuroxime, cefamandole, cefonicid, ceforanide) are char- acterized by more expressed activity with respect to Gram-negative bacteria in comparison 32. They have high beta-lactam resistance, although they do not have a noticeable effect on enterococci, Pseudomonas aeruginosa. In addition, drugs belonging to the second-generation cephalosporins are cefoxithin, synthesized from cefamicin C, cefotetan, a semisynthetic derivative of organomycin G, and also cefaclor. Their unique chemical feature is the presence of an additional methoxy group in position C7 of the aminocephalosporanic acid frag- ment, and the unique chemical feature of cefaclor, the absence of a substituted group at posi- tion C3 of the aminocephalosporanic acid fragment is also characteristic of all cephalosporins. Finally, removal of the benzhydryl protection using trifluo- roacetic acid gives the desired cefuroxime (32. Antibiotics Another simpler way of the synthesis of cefuroxime is by direct acylation of 7-amino- 3-aminocarbonyloxymethyl-3-cefem-4-carboxylic acid (32. It is highly active with respect to Gram-negative microorgan- isms (intestinal and hemophilial bacilli, salmonella, shigella, enterobacteria, and gonococci). It is also active with respect to Gram-positive microorganisms (staphylococci, streptococci). It is inactive with respect to various types of Pseudomonas, most strains of enterococci, many strains of Enterobacter cloacae, methylcillin-resistant staphylococci, and L. It is used for bacterial infections caused by microorganisms that are sensitive to the drug. These may be abdominal and gynecological infections, sepsis, meningitis, endocarditis, infec- tions of the urinary and respiratory tracts, bones, joints, skin, and soft tissues. It is widely used for pneumonia as well as bacterial meningitis in children, and for post-operational infectious complications. Protecting free amino group in 7-aminocephalosporanic acid by formylation with formic acid in the presence of acetic anhydride produces 7-formamidocephalosporanic acid (32. The acetoxy group of this compound is replaced by a reaction with 1-methyl- 1,2,3,4-tetrazol-5-thiol, after which the N-formyl protection is removed by hydrochloric acid, giving 7-amino-3-(1-methyl-1,2,3,4-tetrazol-5-yl)-thiomethyl-3-cefem-4-carboxylic acid (32. Reacting this with a mixed anhydride synthesized from mandelic acid and phosgene gives the desired cefamandole (32. It is synthesized by a method analogous to that of the synthesis of cefamandole [120–123]. It is also synthesized by methods analogous to the synthesis of cefamandole [124–128]. Cefoxitin and cefotetan, which are cephamicins and differ from other cephalosporins principally in the presence of a methoxy group at position 7 of the cephalosporanic sys- tem, which significantly increases their resistibility with respect to beta-lactamases, belong to the second-generation cephalosporins. In one of the examples of the synthesis of cefox- itin starting from cefamicin C, the free amino group is initially protected via tosylation, and the product in the form of a well-crystallizing dicyclohexylamine salt is isolated (32. Next, the carbonyl group at position 2 of the cephalosporanic system is ester- ified using methylchloromethyl ether. When reacted with nitrous acid, the product is diazotized, giving the diphenyl methyl ester of 7-diazocephalosporanic acid (32. A subsequent reaction of the resulting compound with triethylammonium azide in dichloromethane and then with bromine azide gives the diphenyl methyl ester of 7-bromo-7-azidocephalosporanic acid (32. Treating this with methanol in the presence of silver borofluoride results in the replacement of the bromine atom, giving the diphenylmethyl ester of 7-methoxy-7-azidocephalosporanic acid (32. Acylation of this compound with 2-(2-thienyl)acetylchloride gives the ben- zhydryl ester of 7-methoxy-7-[2-(2-thienyl)-acetamido]cephalosporanic acid (32. The resulting product is then hydrolyzed by the enzyme Citrusi acetylesterase to the potassium salt of 3-hydroxymethyl-7-methoxy-7-[2-(2-thienyl)acetamido]-3-cefem- 4-carboxylic acid (32. Antibiotics is accomplished not with 2-(2-thienyl)acetylchloride, but with bromoacetyl bromide. This drug is synthesized from the most accessible antibiotic of this series, cefalotin (32. Reacting this with potassium ethyl xantogenate replaces the acetoxy group in the third position of the cephalosporin sys- tem, giving the corresponding S-derivative (32. Upon reducing this compound using zinc in formic acid, the product is desulfurized, giving the 4-nitrobenzyl ester of 3-exo-methylen-7-(2-thienylacetamido)-cefem-4-carboxylic acid (32. The exo- methylene group is oxidized by ozone and the resulting dicarbonyl derivative tautomerizes to the enol form (32. Then, the hydroxyl group is replaced with a chlorine atom upon reaction with thionyl chloride, giving the 4-nitroben- zyl ester of 3-chloro-7-(2-thienylacetamido)-3-cefem-4-carboxylic acid (32. The resulting product undergoes deacylation upon reaction with a mixture of pyridine with phosphorous pentachloride in isobutanol, forming the hydrochloride of 4-nitrobenzyl ester of 7-amino-3-chloro-3-cefem-4-carboxylic acid (32. This is acylated with an N-protected derivative of phenylglycine, (N-tert-butoxycarbonyl)-D-α-phenylglycine in the presence of N-ethoxycarbonyl-2-ethoxy-1,2-dihydroquinoline in tetrahydrofuran, giving 32. The tert-butoxycarbonyl protection in this molecule is removed by heating in acetonitrile in the presence of p-toluenesulfonic acid. Finally, upon hydrogen reduction using zinc and hydrochloric acid in dimethylformamide, the 4-nitrobenzyl pro- tecting group is removed from the resulting tosylate (32. Synonyms of this drug are panoral, alfatil, dista- clor, panecef, ceklor, and others. Third-generation cephalosporins The third generation of cephalosporins (cefotaxim, ceftizoxime, ceftriaxone, ceftazidime, cefoperazone, and moxalactam) differs in their high antimicrobial activity against enter- obacter, including those resistant to other antibiotics. They are relatively more resistant to hydrolysis by beta-lactamases, and they have the broadest spectrum of Gram-negative activ- ity. At the same time, they exhibit moderate activity with respect to staphylococci, and are used in polyresistant Gram-negative infections for treating bacterial meningitis and gonorrhea. Antibiotics a dihydrooxazine ring in place of the dihydrothiazine ring common in all other cephalosporins. Thus, it is not a cephalosporin, a cefamicin, or penicillin; however, in terms of the pharmacological action, it is a compound related to the three antibiotics listed above and is classified as a third-generation cephalosporin. From a chemical point of view, the thing that unifies them is that practically are all derivatives of 7-aminocephalosporanic acid that are acylated at the amino group of 2-(2-amino-4-thiazolyl)-2-methoxyiminoacetic acid. In terms of the pharmacological action of third-generation cephalosporins, they generally differ one from another in their pharmacokinetic unique features, as well as in a few differences with respect to their relationship with P. The ethyl ester of 2-(2- amino-4-thiazolyl)-2-methoxyminoacetic acid necessary for this synthesis, as well as for the synthesis of a number of other antibiotics of the cephalosporin series, is synthesized from ace- toacetic ester. Nitrosation of acetoacetic ester with nitrous acid gives isonitrosoacetoacetic ester (32. O-Methylation of the hydroxyl group of obtained product with dimethylsul- fate in the presence of potassium carbonate gives ethyl 2-(methoxyimino)acetoacetate (32. Brominating the resulting product with bromine in methylene chloride in the pres- ence of p-toluenesulfonic acid gives 4-bromo-2-methoxyiminoacetoacetic ester (32. Reacting this with thiourea according to the classic scheme of preparing of thiazoles from α- bromocarbonyl compounds and thioamides gives the ethyl ester of 2-(2-amino-4-thiazolyl)-2- methoxyiminoacetic acid (32.

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This could cause you to run low in cortisol and other hormones order genuine sildigra on-line impotence yeast infection, as described in chapter 10 120 mg sildigra erectile dysfunction treatment photos. That’s easy: it hasn’t gotten the same research attention as the others, likely because there is no financial incentive for pharmaceutical manufacturers. Despite all my medical training, I knew nothing about it until I took an advanced hormonal seminar with a European endocrinologist. Indeed, pregnenolone is largely unknown in the United States, although that’s beginning to change. The Solution Stress is your response to change, such as external or internal factors that knock us out of homeostasis. Negative stressors, especially the emotional type, lead to excess glucocorticoids. A common pattern in women after age thirty-five is to have low cortisol during the day and high cortisol at night, which may make it hard to fall asleep and/or stay asleep. Although The Gottfried Protocol solutions below are separated into algorithms for high and low cortisol, remember that balancing cortisol is related to stress reduction. So whether your cortisol is high or low, always start with the lifestyle changes that you can make to mitigate stress in your life, both real and perceived. Here’s a recap of the aim of The Gottfried Protocol: • Start with lifestyle redesign: optimize nutrition, exercise, and mental retraining. No need for testing or consulting with a practitioner before beginning these strategies. Testing may also be helpful to identify and fix efficiently your missing vitamins, minerals, and amino acids (the building blocks of protein). Part A: The Gottfried Protocol for High Cortisol Although it may be appealing to treat excess stress with sugar and coffee, I consider these “fake” energy boosts that ultimately undermine your hormonal progress. My preference is that we make the necessary tweaks so that you wake up each morning feeling restored, and coffee is not necessary. Start with Step 1 and the interventions that are easiest to integrate into your life, since you’ll be more likely to sustain habits that fit into your day. Of course, talk to your doctor about what supplements and dosages might be best for you. Excess stress also can cause you to excrete magnesium, a mineral key to calcium absorption. If you are suffering with five or more symptoms of low cortisol, and your low progesterone is confirmed through testing with your doctor, I recommend taking all of them. If you are suffering from fewer than three symptoms, and are a minimalist who wants to see how few supplements it takes to optimize your adrenal function, I recommend starting first with lifestyle adjustments. If you need more adrenal healing after four to six weeks, move on to the B vitamins. In what may be the most popular study ever performed on cortisol, dark chocolate (40 grams per day for two weeks) lowered urine cortisol levels. But take the results with a grain of salt (perhaps combined with the square of chocolate)—the study was sponsored by Nestlé. Alcohol raises cortisol, and the effect persists for twenty-four hours in men—probably longer for women. Caffeine, the world’s most popular psychoactive substance, directly induces the adrenocortical cells to produce more cortisol, as well as more epinephrine, norepinephrine, and insulin. Advocates of coffee point to the studies of the antioxidant benefits and longevity. If you suffer from insomnia, anxiety, or bruxism, which is clenching or grinding your teeth at night, I suggest you wean yourself off caffeine. What is the smallest dose of caffeine that supports your productivity yet doesn’t undermine your health? Massage of the pressure receptors in and under the skin stimulates vagal activity, which is one reason massages are so relaxing. One study compared people who had a single forty-five-minute session of either Swedish “light” massage or deep tissue massage. The deep-tissue massage lowered cortisol and raised oxytocin, the hormone of affiliation and bonding. A pilot study of traditional acupuncture, three times a week for twelve weeks, versus sham or no acupuncture, showed a decrease in hot flashes and night sweats, lower twenty-four-hour urinary-cortisol levels, and improved quality of life in menopausal women. Another way of observing yourself, if you need more external accountability, is to purchase a gizmo called an emWave HeartMath. Briefly, HeartMath methodology is based on the fact that the time between each beat of your heart varies according to emotional arousal, heart-rate variability. Loss of variability is a sign of inner emotional stress and waning adaptive suppleness, as well as of heart disease. If a patient rolls her eyes at my prescription of yoga or meditation, I whip out my emWave, which is smaller than a smartphone. While this has been documented in healthy men, but not women, forgiveness training has been shown to lower stress and anger. If you think it sounds fringy, consider that stroking of the clitoris was once used as therapy for women with hysteria, though the more sanitized term was “medical massage. Within sixty seconds of orgasm, oxytocin, the hormone of love and bonding, floods your system. Oxytocin lowers cortisol, and women are designed, physiologically and neurologically, to generate far more oxytocin than men. Direct your anxiety toward your health: use your concerns about your high cortisol and elevated blood pressure to motivate you to stay positive and appreciate what you do have, not what you lack. Pantethine (B5) appears to reduce the hypersecretion of cortisol in humans under high stress. Shown to lower cortisol in surgical patients and children in stressful situations, vitamin C is a safe supplement to add to your regimen. Vitamin C at a dose of 1,500 mg per day has been shown to lower postrace blood cortisol in ultramarathoners. This supplement is an extract from the membrane of a cell, a portion called the phospholipid component, and has been shown to reduce cortisol levels when taken in pill form. Men and women who took 4,000 mg (4 grams) of fish oil a day for six weeks lowered morning cortisol to healthier levels and increased lean body mass. A component of green tea, the amino acid L-theanine is thought to reduce stress without causing sedation. Another amino acid that serves as a precursor to important neurotransmitters that can be depleted by stress, such as norepinephrine and dopamine, L-tyrosine has been shown in a randomized trial to improve response to stress. Another study showed that in men and women, supplementation with L- tyrosine improved working memory in a multitasking environment and prevented rise of cortisol. I just go-go-go all day, then I feel overwhelmed and stressed, as though I’m not doing enough. At the beginning of the teleseries, on a scale of 1 to 10 (10 means you feel like a superhero), she rated her energy as 2/6/4/3, or 2 when she awakens in the morning; 6 at lunch; 4 at dinner; 3 before going to bed.