The Fibrillating Heart

Fibrillation is a word used to describe rapid, uncoordinated, wormlike wriggling of muscle fibers. Heart muscle fibrillation is the most common cause of cardiac “arrest.” Many people have seen devices called cardiac defibrillators and heard campaigns urging education in their use. Some people have even seen people rescued from imminent death by the electrical shock of a defibrillator. But many people also know friends and family members who have a heart condition called atrial fibrillation – one with which they live normally. Why is fibrillation sometimes lethal and sometimes simply a chronic heart condition? The answer lies in the heart’s muscular and electrical anatomy.

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An electrically driven pump

The heart is a pump made from muscle and driven by an electrical system. Normal heart muscle contraction begins with electrical activity in the atria, the two upper chambers of the heart. There, the  “sinus node,” the body’s inborn pacemaker, begins generating a rhythmical electrical signal three to four weeks after the human egg is fertilized. An orderly wave of electrical activity and muscular contraction spreads through the atria to the lower chambers, the left and right ventricles. The muscle contraction pushes blood from atria through valves into the two ventricles below. The wave of contraction in the ventricles pushes blood from the right ventricle into the lungs and from the left ventricle out to the body. You feel each contraction of the ventricles as your pulse. Once the heart has emptied, it relaxes and blood passively accumulates in the atria, coming from throughout the body through big veins in the abdomen and the neck. After fraction of a second, the sinus node fires again and the pump goes into another round of action.

When the sinus node is no longer in charge

When atrial muscle fibrillates and the contraction of the atria no longer follows an orderly path, the atria no longer squeeze and push blood – but  most of the atrial blood still falls through the valves into the ventricles. Some decline in exercise capacity might result from incomplete emptying of the atria, but life goes on.  The disordered electrical activity from the atria often stimulates much too rapid, but still well-ordered activation of the ventricles and pulse rates as high as 170-200. When this happens the ventricles don’t have enough time to fill with blood between contractions, making symptoms worse and rate controlling drugs necessary. More on this later.

Ventricular fibrillation – an intolerable situation

When ventricular muscle fibrillates and there is no longer any coordinated pumping action to push blood out to the lungs and the body. Consciousness promptly fails, and the victim loses muscle tone. Technically the heart has not stopped, but its pumping action has. While there is still electrical activity, as there is in fibrillating muscle, an external shock can restore orderly heart muscle activity, which is why defibrillators work.

The origins of fibrillating heart muscle

Why does heart muscle fibrillate? The reasons are many and varied, but all are related to the fact that the primitive cells that formed the heart all possessed the ability to produce spontaneous electrical activity. Some of these, by virtue of their location in the developing heart, became the dominant pacemakers and conductors of electrical current. In the aging adult, changes in the heart’s structure wrought by both age and disease disturb the tidiness of the electrical conduction system, particularly in the thin walled, expandable atria. Some of the original electrical excitability of muscle returns and disordered patterns of muscle contraction result.

Who Fibrillates

Atrial fibrillation (AF) is a relatively common problem. It is age related, and more common in men than women. Underlying problems with coronary arteries, with heart valves, with high blood pressure, congestive heart failure and diabetes seem to trigger it. Transient atrial fibrillation is common after heart surgery, particularly valve surgery. It is also associated with binge drinking and stimulant use, and with use of prescription strength non-steroidal anti-inflammatory drugs (no study has been done yet to see if the same association is present in users of over-the-counter NSAIDS). AF is more common in people with long histories of high level endurance exercise (Nordic skiers), possibly because years of high volume demand on the heart stretch its muscular and electrical architecture. Hyperthyroidism can trigger AF and people with sleep apnea or lung diseases may develop it. Lone atrial fibrillation is the name applied when no risk factors are present. In these cases, abnormal electrical activity appears to originate near the pulmonary veins.

Ventricular fibrillation is almost always the result of underlying scarring in the heart, from prior heart attacks, from heart infections, or from deprivation of blood flow to the ventricular muscle during an acute heart attack. Other causes include congenital heart disease which affects electrical conduction pathways, cocaine and methamphetamine use and severe electrolyte imbalances such as seen in anorexia nervosa.

What does fibrillation feel like?

Atrial fibrillation may occur in brief episodes before it becomes a chronic heart rhythm. The cardinal symptom is an irregular pulse. Some beats are stronger than others. Sometimes the pulse is very rapid as well as irregular. While the normal, orderly electrical activity of the heart responds to physical demands via some complex physiology, the fibrillating atria do not allow that to happen and the predictable increase in pulse demanded by exercise such as climbing stairs can’t be met. In people who have fibrillating atria, shortness of breath with exertion is a common first symptom. An electrocardiogram shows a characteristic abnormal electrical activation pattern.

Symptoms of ventricular fibrillation are immediate and devastating – consciousness is lost within 30 seconds or less. Brain cells begin to die in 4 minutes. Ventricular fibrillation can be preceded by a very high pulse rate called ventricular tachycardia, often accompanied by lightheadedness and shortness of breath, or by premature or “ectopic” heartbeats which cause a sensation of skipped heart beats followed by very strong beats. They warrant medical attention.

Diagnosis and treatment of atrial fibrillation

Diagnosis of atrial fibrillation is important because not only for relief of symptoms, but also for preventing strokes. A fibrillating atrium is often dilated, with blood flow inside slow and sludgy. Clots may form in the nooks and crannies of the atrial chambers, later to be dislodged and sent upstream to the brain. It is estimated that 20-25% of strokes are caused by AF and sometimes a stroke is the symptom which brings the heart problem to attention. Because AF can be intermittent, it may not show up on one EKG. A monitor which can be worn for several days at home may be required to pick up episodes.

Shocking treatments: cardioversion and radio frequency ablation

A fibrillating atrium can be shocked back into a normal contraction pattern, in a controlled laboratory situation. This treatment is called cardioversion and is usually accompanied by drugs to prevent recurrence of fibrillation, and also drugs to control rate of ventricular contraction should atrial fibrillation recur. Surgical procedures using radio frequency ablation of sites of overactive electrical activity on the surface of the heart can be very successful in terminating AF and in preventing its recurrence, especially in cases of lone AF.

Preventing strokes

Blood thinners are necessary, temporarily, for patients being cardioverted or undergoing ablation surgery, to make certain that no clot is present in the heart at the time of conversion of the heart rhythm. Once it is clear that normal rhythms are holding, anticoagulants may be stopped. In chronic AF patients, however, blood thinners are always necessary.

Prevention

A variety of cardiac drugs, called anti-arrhythmics, are prescribed prevent abnormal heart rhythms in people who are at risk for ventricular fibrillation, usually people who have known heart disease. They are the same as or similar to similar the drugs used to keep the heart rate from becoming too fast in people who already have AF.  careful control of other medical problems like diabetes is important. recognition and treatment of AF early may help prevent the development of chronic atrial fibrillation.

The biggest controllable risk factor: alcohol

While doctors know that excessive alcohol use is one of the leading risk factors for atrial fibrillation and realize that most patients underreport their alcohol consumption, they often do not emphasize the value of drastically cutting alcohol consumption once atrial fibrillation has occurred. Some of the other risk factors for atrial fibrillation, like aging, are beyond control, but alcohol consumption requires lifting the glass to the lips and swallowing. That is a choice and one well worth avoiding when the heart muscle has protested.

Breaking the Tobacco Smoking Habit

 

We are now 100 years into an epidemic of avoidable, tobacco-induced health problems and over 50 years into the attempt to stop it, with more knowledge accumulating every year about the toll tobacco smoking takes on every part of the human body. Each year, smoking costs US society $130-170,000,000 in medical care, $150,000,000 in lost productivity and 400,000 lives lost prematurely. Over 160 million people live with serious, smoking related illnesses. Still, 20% of adults smoke regularly, and young people continue to join their ranks. If you never picked up the habit, be glad. If you have picked it up and managed to kick it, congratulations. You are part of a slow public health success story, and, by understanding the smoking habit, you may be able to help someone else quit.

The evolution of cigarettes

Tobacco was the first crop sold for profit by the American colonists, who introduced Europeans to pipe-smoking and tobacco chewing in the 1600s. However, the smoking habit did not begin in earnest until the invention of a cigarette rolling machine in 1883. By the 1940s smokers in the United States lit up 300 billion cigarettes per year and during WWII, soldiers’ ration kits included cigarettes. By the 1950s, 44% of US adults smoked regularly. Psychiatry texts in the 1960s urged doctors to light up with their patients and, by then, cigarette consumption topped 500 billion per year. Older adults today recall being raised in smoke-filled houses, driven around (without seatbelts) in smoke-filled cars, and sent to the corner store to buy cigarettes for their elders.

Recognition of the problem

Though the 1964 Surgeon General’s report confirmed what many people by then knew – that tobacco was bad for health, wrinkled skin prematurely and caused lung cancer, other lung problems and vascular disease  – cigarette consumption rates continued to climb well into the 1980s. But then decades of educational, political, legal and economic pressures on smokers began to work. By 2012, public places were largely free of tobacco smoke, ex-smokers outnumbered active smokers, and cigarette consumption rates had fallen back to the 1940’s levels. Anti-smoking advocates are rightly proud of their efforts, but the credit must also go, in great measure, to the individuals who did battle with the smoking habit and succeeded. Breaking the smoking habit is difficult, often requiring many attempts and relapses before the goal is achieved.

Nicotine is addictive

Smoking becomes a habit because tobacco contains nicotine, which changes the chemistry of the brain in a way that makes the tobacco user uncomfortable when the nicotine level falls. Tobacco companies have exploited the addictive qualities of nicotine by manufacturing their products to diminish negative physical effects and enhance addictive ones. Menthol soothes the smoke-irritated throat. Nicotine is added in just the right dose – not enough to provoke toxic symptoms like nausea, vomiting dizziness and diarrhea, but just enough to ensure the desire for more.

In addition to physical addiction, smokers develop psychological addiction, a learned desire or craving for smoking that arises from the association of smoking’s pleasure with certain situations such as social gatherings, meals, stressful or anxiety provoking circumstances or boredom. Sophisticated advertising techniques add to the social cachet of smoking and subtly enhance these psychological cravings. The combination of physical and psychological addiction means a two-pronged attack is often necessary to help a smoker who wants to quit.

Two-part attack on a two-part addiction

    Physical addiction to any substance produces withdrawal symptoms when the substance is no longer available to the body. In the case of tobacco, irritability, anxiety, insomnia, abdominal cramps and depression occur within hours of smoking cessation. These symptoms peak and begin to diminish within several days and will stop in a predictable period of time – about 2-4 weeks – after the last does of nicotine.

    Since nicotine can be delivered to the brain without the many carcinogenic chemicals in cigarette smoke, nicotine replacement therapy (NRT) is helpful to someone who is trying to stop a smoking habit, allowing time to deal with the psycho Nicotine is available in non-prescription gums, lozenges and skin patches. Nicotine inhalers and nasal sprays require a prescription. Eventually, though, the physical withdrawal symptoms will have to be suffered when the ex-smoker decides to give up the nicotine.

    E-cigarettes also deliver smoke-free nicotine, by vaporizing it in water. They are highly engineered products containing plastics, ceramics and metals and their long term risks are as yet unknown. Unlike the other nicotine delivery systems, e-cigarettes involve regular smoking behaviors and cannot be expected to help diminish the psychological cravings involved in the habit. 

    Psychological cravings that prompt smoking are often far longer lasting than physical withdrawal symptoms – and more responsible for relapse. In most studies of smoking cessation, behavioral therapy is key to long term cessation. Such intervention can take many forms, including one-on-one counseling, supportive group therapy and even online group participation. Many online resources are available to help smokers cope with this aspect of tobacco addiction. (see list below).

Two drugs are also commonly prescribed to help smokers quit. One, varenicline (Chantrix), attaches itself to nicotine receptors partially stimulating them and relieving withdrawal symptoms and at the same time blocking a sense of reward from inhaled nicotine. Another drug, Bupropion (Wellbutrin), is an antidepressant. These drugs improve smoking cessation rates slightly, and are more effective if used in conjunction with NRT. Both, however, are associated with some troublesome reports of behavioral changes, now noted in black box warnings on their packaging.

The cold turkey method- just as effective 

While public health measures have contributed significantly to decreasing smoking rates, breaking the smoking habit remains an individual project and the single most effective measure a smoker can take to improve health. One curious smoking cessation statistic confirms what many doctors have long observed – that cold-turkey quitting is as effective as any of the assisted methods. It appears that the whole-hearted decision to stop, once made without any reservations, could be the most important factor in long term success. This method has no unwanted side effects or risks and does not require withdrawal of nicotine replacements once the psychological smoking habit is tamed. Non-smokers can play a large role in aiding people whom they care about to make this final decision.

Resources for Smokers Who Want to Quit
http://smokefree.gov/
http://www.cdc.gov/tobacco/quit_smoking/how_to_quit/
http://www.lung.org/stop-smoking/how-to-quit/
http://www.nlm.nih.gov/medlineplus/quittingsmoking.html

Why We Cry..and How We Make the Tears

 

 

“It is such a secret place, the land of tears.” The Little Prince, Antoine de Saint-Exupery

Do animals cry? Probably not. Indian gamekeepers told Charles Darwin stories of elephants that shed tears of sadness, and dog lovers have tales of canine tears, but the emotional tears of humans are unparalleled in the animal kingdom.

We are always making tears

All land dwelling animals, including people, make tears constantly. Eyes are windows on the world, and baseline tears are constant window washers. The window pane is the cornea, a thin panel of collagen, containing very few cells, no blood vessels, and more nerves per square inch than any other part of the body. These nerves signal alarm and summon an army of reflexive tears in response to a speck of dust, a cold wind, or a whiff of an onion. Reflexive tears, which are just a lot of baseline tears, wash out intruders and fill in dry patches on the cornea, keeping it clear and moist to focus light entering the eye. Emotional tears appear in humans during infancy, but not immediately. The crying that infants first do to signal their needs is much like the crying of little chimpanzees – tearless. Emotional tears come later, just like talking. Both are outward expressions of the lives of our minds, and they take a while to learn.

What tears are made of

Tears are much more than little beads of salt water running down your face. They are a three layer sandwich. The oil-containing molecules in the outer layer tighten up the surface of the watery middle layer to keep it from spilling over eyelid and sliding off the surface it protects. The oil floats on the watery middle layer and smooths its surface, optimizing the passage of light through to the eye’s interior. The third part of the sandwich, inside and closest to the eye, is the mucinous layer, kind of a gluey protein that helps tears stick to the eyeball. The mucinous proteins capture and kill biologic intruders like bacteria and viruses, and soak up some of the watery layer to help transfer nutrients, oxygen and moisture to the cornea. Both the oil and mucin slow evaporation of tears as blinking spreads them over the eye.

Evaporation and drainage

Dry spots appear on the cornea after just fifteen non-blinking seconds – easy to do while concentrating or daydreaming. Even with blinking, tears evaporate, or they drain out from the eye into the nose via two tiny lacrimal ducts on the upper and lower eyelids near the nose. If these ducts become scarred or blocked by infection, tears overflow. Six to 10% of babies are born with tear ducts not yet open, but 95% of these will open by age one without any attempt at surgical repair. Conversely, one way of treating dry eyes is to block these ducts with small plastic pellets.

Dry eyes

Too few tears, tears with abnormal composition, and decreased blinking cause dry eyes that itch, sting, burn, get red, and cause blurred vision. Dry eyes are an increasing problem in our air-conditioned, airline-traveling, contact lens-wearing, Lasiked, medicated and aging society. The list of drugs that dry eyes includes many commonly prescribed classes: decongestants, antidepressants, antihypertensives, antihistamines, beta-blockers, hormones, diuretics, ulcer medications, acne drugs, and oral contraceptives. Other causes of dry eyes are infections and immune diseases like rheumatoid arthritis and Sjogren’s syndrome as well as  radiation and radioactive iodine treatment can also damage the tear producing cells. All of these conditions damage the tear producing cells  – the machinery for tear production. 

Remedies for dry eyes 

Treatment of dry eyes is always aimed at removing offending problems and increasing lubrication. The usual tactics include artificial tears, wind protection, air humidification, cessation of unnecessary medications, and treatment of underlying diseases and infections. Excessive tearing often means allergies, or blocked lacrimal ducts leading to poor drainage of baseline tears into the nose.

 

The tear producing machinery

The medical conditions mentioned above shut down tear production and cause pain and swelling in the lacrimal gland, a spongy little structure tucked up under the upper outer corner of the eyelid. The lacrimal gland is the tear producing factory, aided by the oil-producing Meibomiam glands near the eyelashes, and a cluster of mucin-producing cells in the eyelid lining.

The controls for the machinery

When the lacrimal glands get a call for more tears, either reflexive or emotional, the messages come through the autonomic nervous system, which oversees the automatic functions of the body. Reflexive tears spring from messages sent from the eye and nose. Emotional tears come from messages sent by the limbic system, the deepest and oldest part of the brain, the part that conjures up feelings.

What are emotional tears?

What are emotional tears? Are they just more voluminous baseline tears? Or does emotional crying rid us of “humors of the brain,” as Hippocrates thought? In Roman times, mourners used small glass vials called lachrymators to collect their tears for burial with the one for whom they cried. In today’s laboratory, emotional tears are almost as hard to come by as research money to investigate them. Some dedicated men such as Professor William H. Frey II (Dept. of Pharmaceutics at the U. Of Minnesota) have learned enough to suggest that tears of grief rid the body of some of the products of stress, supporting the claim that crying makes people feel better. Compared to reflexive tears, emotional tears contain up to 25% more proteins, of classes related to stress. Why? No one knows – yet. Emotional tears are still a land of mystery, part of the unique expression of inner life that separates the human animal from the others.

 

Thin Bones

Osteoporosis is an equal opportunity disease. Everyone is at some risk for age- related thinning of the bones. Prevention is the best treatment, and understanding how osteoporosis happens is the key to prevention.

Bone is alive

Bone may resemble concrete, but it is vibrant, living tissue that is perpetually under reconstruction. From the time of birth, when bones are composed mostly of soft, pliable cartilage, they shape and reshape themselves. Cells called osteoblasts appear in the cartilage and begin to lay down a protein matrix, spinning it into flexible tendrils like fine rope. A mixture of minerals, mostly calcium and phosphorus, hardens the matrix, creating the blend of strength and flexibility needed for the forces the skeleton has to bear. Throughout life the bones restore, remodel and repair themselves in response to the stresses of life on a planet governed by gravity.

Bones are storage depots for calcium

The bones also store calcium for the rest of the body and respond to its constant demands for the mineral. Cells called osteoclasts break bone down to free calcium for use elsewhere, and to remodel bone where changes are needed. So there is a constant interplay of bone construction and bone destruction throughout life, with the material of you skeleton renewing itself completely every ten years or so.

Bones build, remodel and breakdown

In youth, bone construction goes full blast. Once maturity hits, the process evens out. In older age, breakdown begins to exceed construction. Just another sign of inevitable decline? Yes, but don’t give up hope. You control some things that influence how fast bone loss occurs, and science is making strides to help.

You are the general contractor

You are in charge of the building material that your bones use. A healthy balance of food, including protein, fat, calcium and Vitamin D makes healthy, well-mineralized bones. You need 1200 milligrams of calcium a day, the amount in about three glasses of milk, and 400 IU of Vitamin D, which is made in the skin when it is exposed to sunlight (10-15 minutes of sun on hands arms and face, or back, twice a week). Vitamin D deficiency is common in the elderly because of indoor lifestyles, and in northern climates. Many foods are fortified with Vitamin D, and cod liver oil and fish are excellent natural sources.

Childhood habits matter

The bone density that you achieve in youth is important because it is the starting point for the gradual losses that come later. Maximal bone density for life is achieved in the early twenties The generations of children that have opted for pop over milk are at a disadvantage, arriving at adulthood with less calcium than past generations have.  and pediatricians are already seeing more children with fractures than in the past. The cost of neglecting childhood nutrition is bound to rise as time passes.

Gravity and exercise matter

You are also in charge of the activity that stimulates bone formation. When you are upright and fighting gravity, the osteoblasts lay down more bone matrix where it is needed to bear weight, particularly in the pelvis, lower spine and hip. But as soon as the stresses diminish, the osteoclasts start their breakdown work. Just a few days of bed rest sets them in motion. Astronauts in the space lab, under minimal gravity, lose as much bone in a month as a post- menopausal woman loses in a year. Even the impaired movement of a bone under a cast causes localized osteoporosis.

The more you exercise against gravity – as in walking, running, doing yoga or calisthenics, or weight lifting – the more you will call osteoblasts into action. Sit out life, and your osteoclasts will dominate.

Who does osteoporosis affect?

Youth compensates for deficits in diet and activity, but as growth-related hormones fall with age, the cost comes due.  Genetic makeup counts too. Women lose more bone than men, smaller-framed people more than larger-framed people, and Caucasians,and Asians more than dark-skinned people. Smokers and heavy drinkers are also at higher risk for osteoporosis, as are people who are confined to bed or taking steroid medications.

The cost of thin bones

Thin bones break and fractures are costly, about $10 billion for the 1.5 million fractures a year in the USA. Spinal fractures, the most common breaks, are very painful and cause spinal deformity and loss of height. Of all the people who fracture hips, 50% are permanently disabled, and twenty percent are dead within a year, from the consequences of immobility. This mortality rate is even greater in men, who are 20% of the 44 million people who have or are at risk for osteoporosis.

Prevention of  osteoporosis and fractures

The best treatment for osteoporosis is prevention, starting in childhood. Prevention means solid diet and habitual weight bearing exercise throughout life, and, as the risk of falling increases, exercises to maintain speed and balance. Canes, walkers, hip protectors (padded garments worn over the hips), and attention to the living environment (clear walkways, even surfaces, handrails, etc.) are forms of external prevention.

The role – and the problems – of pharmacologic attempts at prevention

Doctors often recommend bone density tests and sometimes they prescribe drugs to slow the loss of bone. At menopause, bone loss accelerates, and estrogen supplements for a few years have been common practice. Newer drugs such as Evista mimic estrogen’s effects on bone alone and may be safer than the older hormone supplements, which are associated with increased risks of strokes and some cancers, especially when used for many years. The biphosphanates, like Fosamax, slow the work of the osteoclasts by attaching to bone to block breakdown. But they bond to the bone and cannot be released. Some unusual and serious side effects such as sudden, unprovoked leg bone fractures and death of jaw bone after dental procedures. Fortunately these have been fairly rare occurrences.   Calcium and Vitamin D supplements improve bone-building supplies, but calcium absorption is not as good from pills as it is from whole foods, and sunlight exposure produces much more Vitamin D than pills can provide. More severe osteoporosis warrants more unusual treatments like shots of calcium-regulating hormones.

You job

Your skeleton will outlast you. Your job is to do your best to make sure it supports you while you are here, and to pass the word to the younger generations who are still building their bones.

Iron: Too Little and Too Much

Poison is in everything, and no thing is without poison. The dosage makes it either a poison or a remedy.
Paracelsus. Swiss-German physician (1493-1541)

 

Iron is present in abundant quantities in the earth’s core and crust, in the sun, the stars and meteorites – and inside all living things. In humans, iron carries oxygen to all the body’s cells, carries carbon dioxide back to the lungs, enables many chemical reactions related to energy production, and binds oxygen inside for use in muscle cells. It is a vital nutrient – a substance that must be part of the diet, but also one which the body cannot excrete except by losing blood and skin cells. Both too little iron and too much iron present us with problems.

Where the body puts iron

Iron is absorbed from food in the upper part of the small intestine. Specialized proteins
carry it in the blood and store it in the liver and other organs. Ten percent of total body
iron is attached to myoglobin in muscles, 25 percent is stored in the liver and in specialized cells throughout the body, and the major portion, 65 percent, is bound to hemoglobin inside red blood cells. Hemoglobin-bound iron is constantly recycled as old red blood cells are destroyed and new ones are made.

Iron absorption from food – a tightly regulated process

Iron must be bound to proteins or it excites free radical damage in cells. When all of the protein binding sites for hemoglobin in the body are filled, the liver sends a signal to the small intestine to decrease the amount of iron taken in from food. This regulation of iron absorption is a very sensitive and tightly regulated process in which a message is sent to the intestines conveying how much iron is already in the body. That amount determines how much or how little iron is absorbed from food. This feedback loop is necessary because, beyond minor blood loss and regular shedding of skin and bowel cells, the body has no way to get rid of extra iron. Most health problems related to iron come from too little iron in the diet, from too much iron, delivered intravenously in the form of blood transfusions, or from genetic defects in the feedback loop that tells the intestines how much iron to take in.

Too Little Iron

Deficiency of iron in the body causes weakness, fatigue, and shortness of breath because of inability to carry enough oxygen in the blood and failure to produce required energy. Skin and nail beds are pale because mature red blood cell production is limited (iron deficiency anemia). Dizziness and fainting upon standing up can occur.
Iron deficiency comes about because dietary iron is insufficient to make up normal losses of iron through menstrual blood loss , or abnormal losses that might occur chronically, such as from an unsuspected stomach inflammation, an intestinal tumor or abnormally heavy menstrual bleeding.

Who becomes iron deficient?

Dietary iron deficiency is very common, especially in people who restrict calories, avoid meat or have poor diets.  Women of childbearing age, children and the elderly of both sexes are the most at risk. Dietary deficiency can also be aggravated by increased need for iron, as in pregnancy and childhood growth. While many foods contain iron, it is better absorbed from animal sources like beef, chicken liver, fish and mollusks than from plant based sources like spinach and beans. Iron absorption also requires an acid environment, which acid relieving drugs block.

Iron deficiency in post-menopausal women or in men of any age group always raises suspicion of low grade, unsuspected blood loss, which usually comes from the gastrointestinal tract. Causes are gastritis (often from use of anti-inflammatory drugs), ulcers, colitis, diverticulitis, tumors and rare vascular malformations are all causes. Black, tarry and metallic smelling stool is often a clue.

Replenishing iron stores

Treatment of iron deficiency requires improving diet and finding and correcting sources of blood loss. Iron is  better absorbed by the stomach from food than it is from pills. Red meat is the best source.  But iron supplements are necessary when iron deficiency has caused symptoms. Several different versions of iron supplements may have to be tried – ferrous sulfate is the most commonly prescribed, but can be hard on the stomach. Ferrous gluconate may cause less nausea and stomach upset. Ferrous fumarate contains more iron per pill. The addition of Vitamin C to the diet  helps absorption of iron supplements and iron can also be delivered by injection if dietary methods and oral suuplements fail.

Too Much Iron

Iron overload is called hemochromatosis and its symptoms come from damage to the cells in which iron is stored once the normal iron binding proteins can hold no more.  The damage is very slow and cumulative and the liver and the heart bear the brunt.  Testicles and thyroid gland are also storage sites. Skin storage may cause the patient to look inappropriately tanned, but weakness, lassitude, weight loss, shortness of with breath and abdominal pain typically bring the patient to the doctor.   

Transfusion-related iron overload

Hemochromatosis  can be caused by repetitive transfusions of blood. Transfusion related hemochromatosis afflicts patients with bone marrow diseases such as  myelofibrosis and multiple myeloma. Repeated transfusions are the treatment for severe anemia in these patients and each unit of packed red blood cells delivers enough iron for six months. Iron overload begins to develop quickly.

Hereditary hemochromatosis

Hemochromatosis can also be caused by a genetic problem in which too much iron is absorbed. This hereditary version of hemochromatosis occurs in about 5 in 1000 people in the US. Caucasians are more susceptible than other races. While men and women are affected equally, men typically develop symptoms in their 30s or 40s, a decade or two earlier than women, because women are able to shed iron on a monthly basis until menopause.

Hemochromatosis is treated by regular bleeding, performed in the same way that blood donations are collected. But bleeding is not suitable treatment for patients whose severe anemia is the problem that forces them to receive repeated blood transfusions. The only option for them is chelation of the iron with drugs that bind iron in the blood and carry it out of the body, a difficult and time consuming process, but one that lengthens survival time. A new oral drug may soon make the process easier. At this time in medical history though, using iron as a remedy is easier than treating iron as a poison.

Chronic Fatigue Syndrome Gets Renamed

Imagine the way you felt the last time you had the flu. You were flattened, devoid of all energy. Staying upright to get dressed was more than you could handle. You slept – and slept – and slept – and still experienced none of the normal refreshment that a good night’s sleep provides. A fog descended on your mind and fuzzed up memory, destroyed drive and made your head ache. You could not concentrate on simple mental tasks like reading. Though you were doing nothing physical, your muscles ached. Then it all went away and you forgot about it.

But now imagine that it didn’t go away. The same misery persists and dramatically alters your life. You cannot work. You move from bed to couch and back to bed. You go to doctor after doctor and they find nothing wrong. Routine blood tests, X-ray and scan results are normal. Someone prescribes an antidepressant, confirming the suspicions of family, friends, and some doctors that your debilitating physical symptoms are “all in your head.” Eventually, you find your way to a doctor who makes a diagnosis. You have CFS which stands for chronic fatigue syndrome, and which, as of early 2015, has been renamed system exertion intolerance disease or, in our acronym-laden age, CFS/SEID.

A long history, with different names

CFS/SEID has probably been around for more than 200 years, making its appearance in the medical literature as “neurasthenia,” a term applied to patients who were lacking in physical, emotional and cognitive energy without any discernible disease to account for their malaise, without any improvement over time and without any progression that brought them to a worsened state. They were mostly ladies, whose frail constitutions prevented them from exerting themselves and who mysteriously took to their beds for weeks at a time.

The Yuppie flu

British doctors in the 1950s christened the symptom complex myalgic (painful muscles) encephalitis (inflammation of the brain), even though there was no evidence for inflammation to account for the headaches, difficulty concentrating and memory problems patients experienced. In the US in the 1980s, the syndrome was dubbed the Yuppie Flu because it seemed to follow viral infections like infectious mononucleosis and occurred in cities where young urban professionals (“yuppies”) congregated. When reported from other settings as well, the name was changed to chronic fatigue syndrome.

No apparent cause, but a real illness

Because no single infectious, hormonal or immunologic cause for CFS emerged from many attempts to identify its cause, because it was impossible to measure the subjective complaints constituting the syndrome, and because some improvements occurred when antidepressants were prescribed, CFS was, for decades, viewed as a psychological disorder. But this view became more and more untenable as it became clear that the illness hit people who had no history of depression or inability to cope with life. Many CFS patients continued to be very productive, learning how to manage their lives within the limitations of their fatigue and mental fog. Laura Hillenbrand, author of Seabiscuit and Unbroken is one outstanding example. Though no cause has yet been identified for the illness, the name change from chronic fatigue syndrome to systemic exertion intolerance disease signals that the illness is one rooted not in psychology but in an, as yet, unidentified physical cause.

Epidemiology and diagnostic criteria

It is estimated that there are about 1 million patients with CFS/ SEID in the US at any given time. There is no evidence that its incidence is increasing, but it is quite possible that some cases are hidden on among the legions of people who have been diagnosed only with depression. CFS/SEID is more common in women than in men. Sometimes it follows directly upon an acute flu-like illness, but at other times appears out of nowhere. The diagnostic criteria at this time include 6 months of unexplained, life-altering fatigue and orthostatic intolerance, which means the inability to stand for more than very short periods. Four of eight other symptoms are also required and these include disturbances in memory and concentration, persistent sore throat, tender lymph nodes, muscle pain, joint pain, headache, disturbed sleep patterns, and malaise following even minimal exertion. Additional symptoms may include increased sensitivity to tastes, odors, temperature and noise.

A relapsing illness

A small minority of CFS/SEID patients get completely better and never suffer a relapse. The majority suffer relapses for prolonged periods of time, perhaps the rest of their lives. Relapses are triggered by infections, surgery, temperature extremes and stressful events. Another minority are severely affected from the beginning of their illness and require support in the activities of daily living for the rest of their lives. Deterioration, though, is unusual and suggests the diagnosis of CFS is wrong and further attempts to find the correct diagnosis are indicated.

Problems in mitochondrial energy production?

While there is no identifiable single cause for CFS/SEID, poor energy production seems to be at the root of the many symptoms in this illness, which has focused some researchers’ attention on mitochondria – the powerhouses of all cells in the body. Mitochondria must continuously recycle the molecules they use to produce energy and there is some indication that this process is impaired in people with CFS/SEID. Perhaps this is why experience has taught many CFS/SEID patients to pace their lives, always allowing significant time for recovery from exertion.

Boosting energy production

In addition to pacing life to allow recovery time, lifestyle alterations that seem to help CFS/SEID patients minimize relapses also happen to be useful in maximizing mitochondrial function. These include avoidance of drugs and environmental toxins, avoidance of processed foods with high carbohydrate and sugar concentrations, addition of whole foods containing plenty of antioxidants and high quality protein, correction of hormonal problems, especially of the thyroid gland, and decreasing chronic inflammation associated with obesity and allergies. Gradual and graded programs of exercise, outdoors with some sun exposure help prevent the loss of muscle associated with inactivity and improve Vitamin D levels, with positive effects on immune function. Continued research will most likely show that CFS/SEID has many causes, all of which result in impaired mitochondrial function.

Lyme Disease: A Whodunit Tale

Some medical advances begin with old-fashioned detective work. Lyme disease, which was unknown in this country prior to 1975 is a good example.  That fall, two mothers from Old Lyme, Connecticut convinced the state Department of Public Health and Yale University to explore a mysterious outbreak of cases of inflammatory arthritis among the town’s children, because they were unsatisfied with the explanations they had been given for the cause. The investigation that winter centered on thirty-nine children and twelve adults from Old Lyme, all of whom had developed painful swelling of one or more joints between June and September.

Clues in clinical histories

Although blood tests and physical exams of the affected people had not previously revealed any known cause for the painful, swollen joints, investigators noted that there were striking similarities in the patients’ histories. Especially notable was a peculiar spreading rash that appeared about a month prior to the development of the arthritis and resembled an archer’s bull’s eye target. The affected people also lived close to one another, all in heavily wooded areas. The researchers concluded that the area where the cases clustered and the time of year in which they occurred were both crucial clues to the mystery. They believed that the illness could be an unknown type of infection but would have to await the next disease “season” for confirmation of this theory.

More clues in old European medical literature

In the meantime, investigators began combing through European medical literature, where they discovered similar descriptions of rashes going back to 1909. Over time, the Europeans had named the skin lesion erythema migrans and associated it with an illness that was similar to the one being reported in Connecticut, although without the arthritis. Some European reports mentioned tick bites in conjunction with the rashes, as well as successful treatment with antibiotics. Back in Connecticut, the next summer produced thirty more cases of what was by then being called “Lyme arthritis,” which investigators now believed was some kind of infection transmitted during outdoor activity.

Figuring out the tick relationship

The next pieces of evidence came from field studies of ticks. The distribution of a particular type of tick called Ixodes scapularis (variously known as the blacklegged tick, deer tick, or bear tick) near Old Lyme matched the distribution of local arthritis cases. Tick autopsies conducted in New York on Shelter Island, another hot spot for this mystery arthritis, showed that most of the ticks carried a spiral-shaped bacterium called Borrelia burgdorferi. Blood tests on affected individuals for antibodies to this organism tied it to the clinical cases of arthritis. Over the next two decades, the explosion of the deer population carrying the tick made the disease more common and widely known.As knowledge about and experience with the new disease accumulated, Lyme arthritis was renamed Lyme disease.

Early  Lyme disease symptoms

Lyme disease symptoms include an early stage of fatigue, muscle and joint pains, swollen glands, and headaches and fever that begin days to weeks after the infected tick bite. These symptoms represent the immune system’s response to the bacterial invasion. If a bull’s eye rash at the site of a former tick bite is present, diagnosis is easy. If not, diagnosis depends on a clear history of a tick bite and on the development of antibodies to the organism, which usually occurs later than the first few weeks of the illness.

Later symptoms

Left untreated, some, but not all infected patients develop symptoms within the next few weeks to months after the infected tick bite. Symptoms include arthritis, nerve pains, facial nerve paralysis, heart palpitations, shortness of breath, and chest pains. An even less common late phase that can occur up to two years after an infected tick bite might include migrating joint pains, muscle aches, abnormal muscle movements, weakness, heart arrhythmias, and cognitive complaints such as memory problems. These symptoms are not well understood and may represent a combination of the body’s ongoing fight against persistent bacteria and an autoimmune response that they trigger.

Treatment

Treatment of Lyme disease with oral antibiotics, either doxycycline or amoxicillin, is usually curative. If an infected tick is attached for more than thirty-six hours (the least amount of time it takes for transmission of the infection) and was encountered in an area where more than 20 percent of the deer tick population carries Borrelia burgdorferi, most patients are given a prophylactic one-time dose of doxycycline. Otherwise, treatment with antibiotics for two to four weeks begins as soon as the diagnosis of Lyme disease is made. The earlier the treatment, the faster the disease responds and symptoms subside. Late-phase treatment of neurological, cardiac, or arthritic symptoms may require intravenous delivery of antibiotics over longer periods. Although rare cases of persistent symptoms after treatment exist, no study has yet shown enough benefit from very long-term antibiotic use to justify the potential adverse effects of such a treatment.

Prevention of tick bites

Prevention of Lyme disease is the best way to deal with the illness, and there are things you can do to protect yourself. In the states where most cases occur (the New England states and New York, New Jersey, Maryland, Virginia, Wisconsin, and Minnesota), be aware that ticks tend to cling to high grasses and shrubbery in areas where deer roam. By hiking in the center of paths, away from tall grasses and shrubs, and wearing protective clothing, such as long sleeves and pants, you can reduce the chances of a tick bite. Shirt tails should be kept tucked in at the waist, sleeves should be kept closed at the wrists, and pants cuffs should be kept tucked into socks at the ankles. Additionally, spraying with insect repellent containing 20 to 30 percent DEET can help.

Self-examination is very important after potential tick exposure

The type of tick that transmits Lyme disease is Ixodes scapularis. It may be either a six-legged, immature tick nymph the size of a poppy seed or the slightly larger, eight-legged mature tick. Both forms excrete an anesthetic in their saliva that prevents you from feeling their bite, so close examination of your body is necessary after potential exposure. Bathe within two hours of coming inside and do a full body exam, with the aid of a mirror, paying close attention to areas covered with hair. Inspect all gear, clothing, and pets for ticks, and tumble clothing in a dryer at high heat to kill any hidden ticks.

Tick removal

Should you find an attached tick on your body, to remove it place the tip of a clean, fine-tipped tweezer as close to the skin as possible and pull gently, in a straight line. Dispose of all ticks in a toilet or drown them in alcohol and then seal them in a plastic bag for disposal. Clean bites with alcohol or iodine. Because the transmission of an infection from a tick to a human requires thirty-six to forty-eight hours of attachment, ridding yourself of ticks in the first twenty-four hours is effective prevention. Longer attachments that occur in high-risk parts of the country merit a single dose of doxycycline within seventy-two hours of a bite. Otherwise, be alert for symptoms or a rash, and seek treatment as soon as possible if they occur.  (See blow for a link to an interesting tick removal tool.*)

Research continues

The detective work surrounding the unraveling of the Lyme disease mystery continues today in the laboratory. Now researchers tend to focus on the rare people who, despite receiving adequate antibiotic treatment after contracting Lyme disease, experience persistent, unexplained, or recurring symptoms. These people remain almost as much of a mystery to researchers today as the initial thirty-nine children and twelve adult with arthritis were to researchers in the mid-1970s.

 

*Tick removal tool

https://www.thegrommet.com/tickease?utm_campaign=20180626&utm_content=49931&utm_medium=email&utm_source=CC&trk_msg=77TUPK4NDPL4R992MUGHP52NOS&trk_contact=4ACPOO38FT83AKKO084SUBGRPC&trk_sid=ICRD996NV2C3PQ9D216CFKVDLG

 

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