Hospice: Not a Place

In her 1972 testimony before Congress, Dr. Elizabeth Kubler-Ross, author of the 1969 best-selling book On Death and Dying, stated that “We live in a very particular death-denying society. We isolate both the dying and the old, and it serves a purpose. They are reminders of our own mortality.” What she wanted was recognition on the part of the government that families could be helped more with home care and visiting nurses at the end of a loved one’s life than with institutional and aggressive medical care. Her testimony was a description of a philosophy of medical care known in England as hospice – a medieval word for the traveler’s hostels run by monks in the Alps.

The hospice movement begins in the USA

The hospice movement in the US had begun in the 1960s when the nursing school dean at Yale University invited Dame Cicely Saunders, the mother of the hospice movement in England, to teach for several months. Hospice growth was stuttering over the next few decades, with growing pains coming not only from wrangling over Congressional allocations of money, but also from the process of trying to identify the suitability of patients for hospice care. The requirement for a prediction that a patient entering hospice care would live less than 6 months proved extremely difficult, particularly when the patients did not have cancer.

Misconceptions

Initially, hospice care was viewed negatively by many as either giving up on life or as a form of euthanasia or doctor-assisted suicide. It is none of these. Hospice is a shift away from attempting to cure medical problems and toward care of the whole patient by a multidisciplinary team with the patient and family at the center. From demonstration hospice projects launched in 1979 to the current care of more than 1.65 million Americans a year, the philosophy of caring rather than curing has proven itself good. In 2007, a paper in the Journal of Pain and Symptom Management reported that patients who had hospice care lived slightly longer than similarly ill patients who were treated conventionally. This surprising conclusion was followed two years later by a New England Journal of Medicine report that patients with non-small cell lung cancer may live longer with hospice care than with other therapies.

Shifting the focus

Hospice is medical care, but care with an aim different from the curative focus of conventional medical care. There is no fighting imagery used in hospice – no war on the cancer, no battle to be bravely fought. The care in hospice is palliative, emphasizing comfort and acceptance, with the meeting of physical needs in an environment as close to home as possible. The patient and family are the unit of care, and the team consists of the patient’s doctor, a hospice doctor, nurses, nurses’ aides, social workers, physical therapists, spiritual counselors, bereavement counselors and volunteers. The focus of patient care is pain and symptom control, as well as emotional and spiritual support for all involved.

The process

Hospice care begins with a doctor’s referral when a patient and his family realize they are ready to turn away from the aggressive attempts to cure a problem which will eventually result in death. The Medicare Guidelines for entering a hospice program require that a patient have a terminal illness with less than six months to live. (Medicare is the payment source for most hospice care). But that six-month prognosis should not be confused with length of care in hospice – care is provided for however long it is necessary. Over 12% of hospice patients live past the initial 6 months of care.

The team

Once a hospice referral is made, a team member, usually a nurse, begins an assessment of physical and emotional needs and crafts a team to meet those needs. Hospice provides the home equipment, medications and support for family as they learn to provide physical care. Volunteers help with respite care to allow family members time to themselves. Social workers evaluate economic needs and pastoral care members address spiritual and emotional needs. Short term hospitalizations are arranged if necessary for symptom control. While most hospice care takes place in the home, similar teams operate in institutions like hospitals, nursing homes and fee-standing hospice facilities, depending upon the availability and competence of family members.

A longer period of comfort

Sadly, over a third of hospice enrollees live less than a week. The time to begin thinking about hospice care is early in the course of a potentially lethal illness since preparation may help a patient live a longer period of a terminal illness in more physical and emotional comfort.

It is helpful to have time to see what hospice organizations are available locally, to check certifications, and to talk with people who provide hospice services. The National Hospice and Palliative Care Association is an invaluable source of information.* Hospitals are committed to helping arrange hospice care and a direct appeal to the hospital’s hospice coordinator is possible if the patient’s doctor does not make a referral. If a patient is not ready for hospice care, but is also unwilling to continue aggressive curative attempts, palliative care is also available – care aimed at comfort and symptom control alone rather than cure. An example is quitting or refusing chemotherapy for cancers which respond poorly.

Finances

Hospice care is paid for by most insurance policies in the US (but not in other countries) and under the Medicare Hospice benefit. Medicaid is also a payer. Surveys report that 94% of families feel their experience with hospice care was very good or excellent. The US Department of Health and Human Services is now behind expanding the availability of hospice care because it “holds enormous potential benefits for those nearing the end of life…” So as medicine moves into the brave new age of genetics, with new, individualized treatments for cancer, and more and more procedures to rewire, replumb and reconstruct the body, hospice care also moves forward, bringing the elderly and the dying out of isolation and educating the people who love them about the universal and necessary process of dying.

*https://nhpco.org

Posted by medical plaintalk

Physician turned medical writer.

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.

Posted by medical plaintalk

Physician turned medical writer.

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.

Posted by medical plaintalk

Physician turned medical writer.

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.

Posted by medical plaintalk

Physician turned medical writer.

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

Posted by medical plaintalk

Physician turned medical writer.

Polar Moods

Bipolar disorder, previously called manic-depressive disease, is a not a new diagnosis. But it is one being made with increasing frequency, particularly in children and young adults. In psychiatry diagnoses are legion, but they all fall into one of three categories: disorders of mood, thinking, or personality. Bipolar disorder is a problem in the sphere of mood, described in the 1880s by Emil Kraepelin, the German psychiatrist whose Compendium der Psychiatre was the world’s first systematic classification of mental disorders. At the time, psychiatrists recognized separate illnesses called mania and melancholia, but Kraepelin was the first to see that some patients cycled between these opposite poles of mood. Over time, the term cyclical insanity gave way to manic-depressive disease, and finally to bipolar disorder, type I or type II (the milder variety). Melancholia is now called unipolar depression and mania is no longer a diagnosis but rather a behavioral symptom in all kinds of psychiatric disorders.

Normal ups and downs in mood

Everyone has ups and downs in mood. Mood involves both subjective feelings and outward behaviors. It is clear from “normal” mood swings that both internal and external factors influence ups and downs. Many of those factors, such as sleep, stress, physical activity, diet, and abuse of alcohol, nicotine and drugs, also affect general health.

The definition of mood disorder

Normal ranges of mood vary greatly from person to person, so the psychiatric definition of “mood disorder” rests on the degree to which disrupted behavior interferes with carrying out the normal activities necessary for functioning at a given stage of life. Clearly abnormal symptoms like hallucinations, which define the thinking disorder schizophrenia, may also appear in bipolar type I. New genetic work suggests that mood and thinking disorders are not as separate as our classification systems try to make them, so it is not surprising that symptoms at times overlap.

The down side of the mood spectrum

Depression, the low side of the mood spectrum, robs a person of interest and joy in his activities. He has little energy, sleeps more than usual, or may be unable to sleep through the night, waking up anxiously at two or three AM. He may gain or lose weight. He tends to ruminate, repetitively chewing over negative thoughts. Sadness permeates his world. Of course these same symptoms can be completely appropriate responses to terrible life events that cause profound grief. A depressed mood becomes abnormal when it occurs or persists unrelated to circumstances, blocks the activities necessary for normal life, and/or includes persistent thoughts of death or suicide.

The up side

At the other end of the mood spectrum, mania, the mind speeds up. Thoughts are rapid, distractibility is high, speech is pressured, and ideas become grandiose. Sleep isn’t necessary. The manic person engages in risky behaviors and feels invincible. He undertakes grand schemes, spends money with abandon, and becomes obsessed with projects or ideas. When the exuberant moods are still under some control (hypomania), they can be very productive. The afflicted individual seems lively and charismatic, the life of the party. But when mania spirals out of control it can become life threatening. As mentioned above, mania not confined to bipolar disorder. It is a symptom that can happen in mood, thinking and personality disorders.

Bipolar: more down than up

Most patients with true bipolar disorder spend far more time on its depressive side, experiencing few manic phases. In fact, it is now felt that many cases unipolar depression, with no history at all of hypomanic or manic episodes, actually represent bipolar mood disorders, making diagnosis tricky. Correct diagnosis is important. In unipolar depression, the response to conventional antidepressant therapy takes weeks, but in bipolar depression, the same drugs can tip the patient into a manic state quickly. It is possible that the reported cases of suicide shortly after antidepressants are started may be related to this phenomenon.

The danger of wrong diagnosis

In our current medical and economic climate, the threshold for using antidepressants is very low. Frequently the drugs are prescribed by non-psychiatrists, without concurrent talk or behavioral therapy, and without adequate follow-up. So it is imperative for patients who are given antidepressants to understand that a rapid response, within days to a week, and feelings of agitation or irritability might mean that the diagnosis of unipolar depression is wrong. For bipolar patients, the drug of choice is a mood stabilizer, which calms manic states and can prevent return of depression.

Stabilizing the mood

The most effective mood stabilizer is lithium. Lithium is a simple chemical element in the same family of elements as sodium, potassium, calcium and magnesium, rather than a complicated molecule like other psychoactive drugs. Its mechanism of action remains elusive, though it is thought that it makes the neurochemical transmitter norepinephrine less available and less effective in the brain. Lithium must be monitored carefully, with urine levels performed regularly. Toxic side effects include diarrhea, tremors, thirst, weight gain, drowsiness, and impairment of kidney and thyroid function.
If lithium is ineffective or poorly tolerated, drugs normally used for treatment of seizures may work as mood stabilizers. One, valproate, is particularly effective for people who also have substance abuse problems, a not uncommon occurrence. Antidepressants may also be necessary at some point, but not without concurrent use of mood stabilizers. Bipolar disorder is a lifelong problem that requires careful monitoring, variable amounts of drug therapy, and simultaneous counseling aimed at development of cognitive skills and habits that help blunt the effects of mood swings on behavior.

Are we creating more lifelong psychiatric problems with drug treatment?

Some psychiatrists feel that the widespread use of antidepressants and other mood altering drugs to treat poor behavior or reactions to life’s inevitable problems changes brains enough to change the way true psychiatric problems now evolve. These days, we have increasing numbers of bipolar diagnoses. Compared to past decades, bipolar patients now cycle more rapidly between highs and lows. While the increasing frequency of bipolar disorder diagnosis may represent increasing labeling of behavioral problems, we also must consider the disturbing possibility that temporary alteration of brain activity with drugs is leading to long term psychological and behavioral changes. Readers who are interested in more extensive discussion might want to read Anatomy of an Epidemic: Magic Bullets, Psychiatric Drugs, and the Astonishing Rise of Mental Illness in America by Robert Whitaker, Broadway; (August 2, 2011).

Posted by medical plaintalk

Physician turned medical writer.

More On Shingles

Readers wanting to know more about some topics pose very good questions. My original magazine column about immunization to prevent shingles (September 2011) generated enough reader mail to warrant another column sharing some of the answers.

Recognizing recurrent shingles episodes:

One reader had suffered through an eruption of ophthalmic shingles, which involves the nerve that carries sensation from the eye, including the cornea, from the skin around the eye, and also from the forehead. The reader wanted to know “What are the signs and symptoms for a re-occurrence of the zoster virus in the eye so I would know what to look for if I am getting an attack?” As in other areas of the body, symptoms that come before the rash erupts in the eye and the face are sensory – tingling, burning, itching and pain. Warning sensations in ophthalmic shingles might also include irritating dryness and a sense something lodged in the eye. Our reader understood that taking an antiviral drug early in the course of an eruption might lessen the likelihood of scarring of the cornea, so paying attention to early symptoms has therapeutic consequences. If an abnormal sensation persists for several hours without explanation or response to simple measures like rinsing the eye out, then the symptom is worth bringing to the attention of the doctor. That said, the use of antiviral drugs early in the course of a shingles outbreak does not prevent the eruption from progressing, but it may shorten the duration and lessen its intensity. When the surface of the eye is involved, anything that can be done to prevent corneal scarring is of some value.

Drugs that make the virus awaken

The same reader also wanted to know what drugs might predispose her to another eruption, and how to avoid them. The drugs that put people at most risk for a herpes zoster outbreak are the ones that suppress the function of immune cells in the body. The most common offenders belong to the steroid class on anti-inflammatory drugs, and have names like prednisone, dexamethasone, decadron, and prednisolone. They are used to treat conditions like multiple sclerosis and lupus and rheumatoid arthritis and when used for periods longer than a week, they begin to impair immune response. Sometimes they are part of a chemotherapy regimen for cancer. Other chemotherapy drugs and radiation also impair immune cell function, so shingles eruptions are not surprising in patients undergoing cancer treatment. Paradoxically, steroids are part of the treatment for shingles – but they are used for only a short time, to decrease inflammation.

Vaccine questions

Another reader wrote:” My husband never had Chicken Pox and yet he did have a severe case of shingles and he was in his 40’s when they occurred. At that time we were told the opposite of the article…we were told he got shingles because he had never had Chicken Pox. This was over 20 years ago so perhaps research has changed that. Does the fact he had shingles mean he cannot get the vaccine?” There are many people whose childhood chicken pox was so mild that they have no memory of the disease. Blood testing will show whether or not there is any trace of immunity to the virus in people who think they did not have the disease. An adult who contracts chicken pox for the first time has a rash that involves much more of his body than the shingles rash does. He is also extremely sick, much more so than a child with the disease. So if an adult develops what is a typical shingles rash, it is considered proof that he has had chicken pox in the past.

You probably did have chicken pox

Age 40 is on the young side for shingles, but there are many idiosyncrasies in the immune system, with some people have worse immune “memory” for specific viruses than others do. Having had a shingles eruption does not prevent this reader’s husband from getting the vaccine, and given that it is now over 20 years since the last time the virus stimulated his immune system, immunization might be a very good idea. Guidelines for vaccine administration also do not exclude people who think they did not have chicken pox as a child, even though, in theory, a vaccine made from a live, weakened virus could cause a full blown case of chicken pox in a chicken pox virgin (more on different vaccine constructions below). It is estimated that 99% of people in the US have had chickenpox, whether or not they are aware of it.

Being refused the vaccine

Getting an immunization proved difficult for another reader. He went to his county health department seeking a shingles immunization, but he was turned down because he has non-Hodgkin’s lymphoma, a form of lymphatic system cancer. While his disease is in remission and his blood work indicates good immune cell function, there is a theoretical risk that the vaccine, which contains a live, weakened version of the virus, will reactivate the line of white cells that caused his lymphoma. Many people face this type of risk-balancing problem in choosing whether or not to get a vaccine, and each individual case requires weighing risks versus benefits. In some cases, for example someone with AIDS who has good white blood cell tests and is not sick, the patient’s doctor may advise getting the vaccine because the risk of the effect of a shingles outbreak is greater than the risk that the virus in the vaccine will cause trouble. In the case of people with history of cancers that arise directly from immune system cells, however, no one wants to take a chance of triggering cells to become cancerous by the introduction of a live virus in the form of a vaccine. In addition, no one wants to introduce an infection that the immune system cannot control. These problems are the reason that researchers have pushed to develop a new vaccine, just becoming widely available in in 2017-18, which does not contain any live virus.

The old and the new vaccines

Lastly, several readers inquired about the frequency of the zoster vaccination. Immunizing for shingles is relatively new, and recommendations may change, but right now, Zostavax, the old vaccine, is recommended for all people over age 60, as a one time shot. Zostavax cuts the rate of shingles by 51% and the development of post-herpetic shingles pain by 65%. The new vaccine, Shingrix, is recommended beginning at age fifty and in tests improves these prevention rates to 98% and 85% respectively. Shingrix requires two separate doses. The effectiveness of the vaccines does wane over time, and there is more experience with the old one. Currently there are not any guidelines about repeat administration, but there are no contraindications to getting the new vaccine for people who have already had the old one.

Where to get immunized

Immunizations are available at pharmacies, grocery stores, county health offices, and walk in clinics and all of these facilities have guidelines which will exclude some people. Anyone excluded by general criteria should review the reason with a doctor who cares for the problem that caused the exclusion.

Posted by medical plaintalk

Physician turned medical writer.

Shingles:Chicken Pox Re-Awakened

Chicken pox is a common and usually mild childhood disease caused by the varicella virus. The same virus is also the cause of a very painful skin rash known as shingles in adults. These two very different illnesses demonstrate the two missions of all viruses – to reproduce themselves and to stay alive. Reproduction keeps the varicella virus spreading from child to child. Hibernation keeps it alive in adults, giving it another chance to reproduce. While chicken pox is usually a mild disease, shingles is painful and at times disabling.

Vaccinations

Since 1995, vaccination against the varicella virus has been very successful in reducing the number of childhood chicken pox cases. In 2005, a vaccine designed to boost adult immunity cut the number of cases of shingles in adults in half and a vaccine about to be introduced now, in 2017, promises much better protection against shingles for older adults, especially for older adults. Both chicken pox and shingles vaccines mark significant progress against the varicella virus, which infects 95% of unvaccinated people.

Who gets shingles

Shingles typically afflicts older people or in people with weakened immune systems. In them, the long-sleeping varicella virus has suddenly awakened, erupting in an intensely itchy, blistered rash known confined to one patch of skin, usually on the trunk, but sometimes on the head or extremities. Doctors call shingles herpes zoster, which sometimes causes confusion with the common cold sore, caused by the herpes simplex virus. Both herpes simplex and varicella viruses are members of a larger family of “alphaherpes” viruses, with similar abilities to live in peace inside the body and revive periodically.

Why name it shingles?

Shingles is a more descriptive name than herpes zoster. When fully developed and severe, the shingles rash has a rough, red, pebbled surface formed by multiple blisters packed in tight formation, often rectangular in shape. Like a roof shingle, the patch of virus- laden blisters can look like it has been laid on top of the skin. The distribution of this adult eruption of the varicella virus is very different from the random and widespread distribution of blisters in chicken pox. The difference between rashes caused by exactly the same virus is a visual lesson in the way the varicella virus infects, reproduces, goes into hiding and reemerges.

The initial infection: chicken pox

The varicella virus enters the body through the nose or mouth. It is picked up by immune cells in the lymphatic fluid and then makes its way through the rest of the body in a trip that takes 7-10 days. Since the immune system doesn’t see the virus as much of a threat, there are often no symptoms of any illness in this period. But once the virus reaches the skin, real battle begins. Troops of immune cells produce small red dots on the skin, then red bumps and finally blisters which rupture and release new viral particles to the air. Mission number one, reproduction is accomplished.

The virus goes into hiding

Mission number two, staying alive, is more complicated. While varicella viruses spread easily from ruptured blisters or via coughing and sneezing, once the viruses dry out, they die. Dried, crusted rashes are no longer contagious. But underneath the skin, some viruses begin another journey. They travel up long thin nerve fibers that carry sensory information from the skin to the spinal cord. Their first stop is the nerve cell bodies that sit in little clumps of tissue called ganglia, just outside the spinal cord. Here, for reasons that are unknown, the viruses are allowed to integrate their genetic material into the nucleus of the cells, alongside the DNA and RNA responsible for normal protein production.

Re-awakening

For years, varicella viruses demand nothing of their host nerve cells. Then in later life, or sooner in people who have suppressed immune systems from diseases like AIDS or treatment of diseases like cancer, the varicella virus may suddenly commandeer the protein-making machinery in the ganglionic nerve cell. It makes multiple copies of itself, sending them back out to the skin along the same nerves by which they entered the ganglia. The rash that appears affects only the part of the skin innervated by those nerves. The sensory nerves are arranged in “stripes” around the trunk and down the limbs, and the rash looks like a portion of that stripe.

Why the re-awakened virus causes so much pain

Pain is a central feature of shingles because the immune system attacks the virus for a second time. This time, the attack starts in the ganglia where the virus has emerged from hiding. When the immune battle against the virus begins, the nerve cells report the action to the brain, even before a skin rash appears. The unwitting patient begins to feel sharp and shooting pains, as well as numbness, tingling and itching sensations in the skin as long as two or three days before a rash appears. Occasionally fever, headache and back pain appear. Sometimes pain remains even after the rash resolves, a distressing condition called post-herpetic neuralgia, which is often difficult to manage.

Other complications

Pain is not the only complication of shingles. Permanent damage may result from re-emergence of the virus in a sensory distribution that involves organs other than skin. Rashes that involve the eye can cause scarring the cornea, and those that involve the ear sometimes cause permanent deafness. Shingles cannot be transmitted, but if someone who has never had chicken pox or been vaccinated against it comes in contact with blister fluid from the shingles rash, they will get chicken pox. Adult chicken pox is a far worse illness than the pediatric version.

Immunity

Immunity to the chicken pox virus diminishes with age, and shingles rarely appears before the late 50s. About one in every three people who’ve had chicken pox will get shingles; the risk of a second episode is also about one in three and higher if pain persists more than 30-60 days. Recurrences rarely happen more than twice, indicating that the reawakened virus stimulates renewed immunity.

Avoiding the often disabling pain of an acute shingles episode and diminishing the risk of post-herpetic neuralgia are both good reasons to consider adult immunization against the chicken pox virus. Not only does the adult vaccine cut the risk of getting shingles in half, it makes cases that do occur significantly less severe. The large study that yielded these results also turned up no vaccine safety issues. When you next think about getting a flu shot, give some consideration to prevention of shingles too.

Posted by medical plaintalk

Physician turned medical writer.

Consciousness Unplugged*

Turn on the bedside lamp. Arrange the pillows. Settle in with a book in progress and open to last night’s marked page. Recognize nothing. Memory for those parts read as sleep stole over you never formed.

Go back a page or two…ahh! Here is something familiar. Start there. All is smooth for a page or two. Then the pace slows. The distance between words and meaning lengthens and a struggle to understand begins. Time slows and suddenly the still visible words no longer symbolize anything. This second, or fraction of a second, marks the border of an elusive state in which the self stands apart, still awake and aware, but disconnected from the machinery it normally uses. Catching the sensation, without slipping into the oblivion of sleep, is like being suspended in time and separated from all the meanings automatically assigned to what is seen, heard and felt in the real world – yet the world is still here.

Sleep steamrolls the elusive state almost instantly, but, while it lasts, it is a fascinating sense of “being,” poised between two worlds. One is the world of the bedroom, the light, the book, the sheets, and the surrounding walls. The other is a world detached from the meanings of all those familiar, objective things. I suspect, but do not know for sure, that this thin little membrane between wakefulness and sleep is the target area of people who are skilled in meditation and of contemplatives who seek a spiritual connection between themselves and something outside nature.

Imagine being able to hang in the in-between place, without succumbing to the all-powerful tide of sleep, yet to be detached from the cold, hard world of the surrounding room and also aware that you are still you. Reports from skilled seekers of enlightenment, from faithful meditation practitioners and from some of the great religious traditions of wisdom suggest that exploration of consciousness unplugged from its routine state might be rewarding. And for some reason, physical health benefits like lower blood pressure and more even moods come back from that place.

There is real appeal, too, in personal experience that lends credence to the idea that there is more to each of us than $5.00 worth of raw materials – that some part of us rises above the chemistry. My Stroke of Insight, Jill Bolte Taylor’s first person description of her expansive trip through her own brain while in the middle of a stroke, rocketed around the internet not because of its neuroanatomy and physiology, but because it added to the hope that the human creature is more than an animal. The hope that the nagging sense of otherness, the need to be good and to do good things, the ability to imagine, the drive to create art and music, and the love of symmetry and beauty reflect more than random biologic events culled out of DNA by the drive to survive.

When I was a child I tried to hold myself poised in another early phase of sleep – the one in which vivid imagery parades across the inner screen – in my case it was always from left to right. The images were always complex, detailed and colorful –unrelated by any story line, and not necessarily imagery form any of my real-life experiences. Elephants decked out in magnificent jeweled saddles and the like. The trick was to not pay them too much attention, or I would be back up in wakefulness, but also to pay them just enough that I would not fall into the sleep pit.

Adulthood put an end to the drifting mode of getting into sleep. Busy days and chronic sleep deprivation made cliffs out of the previously gentle slopes surrounding the sleep pit. No more lollygagging into unconsciousness. But I suspect those childhood experiences were the beginning of my unshakeable sense that the watcher of these fascinating states of consciousness, as well of dreams, is the deepest part of the self – a part that can be unplugged from the $5.00 body. The partial unplugging that precedes sleep is fun. The complete unplugging that comes at the end of life? I suppose it depends on what you believe. Is there something else? Is there nothing else? No way to know for sure. But I would not like to experience a persistent, conscious sense of self in a void. That might be hell.

*this was not written for an Elks Magazine Healthline column.

Posted by medical plaintalk

Physician turned medical writer.

Genetics in Medicine: A Game of Odds

Each of us begins life as a single cell. The chromosomes within, formed out of long chains of DNA called genes, carry all the information necessary for the formation of a human being. The entire complement of DNA, including long segments that have no known function, must replicate itself billions of times over the course of development of the baby and the life of the individual who emerges from the womb. If there were never any errors in the original DNA, if there were never any errors in replication of DNA, and if genes did not turn on and off in response to environmental factors, aging would not occur and human misery would be confined to infectious diseases and trauma. Now that the human genome has been decoded, can we look forward to a disease free world and to extension of the seemingly fixed lifespan of 110-120 years? Not likely, but the focus on the genetic contribution to disease will change medicine, for better and for worse, in the years to come.

Visible genetics: the family history

Doctors have always taken a family history as part of the initial evaluation of a patient. Physical features, health and ailments that run in families are visible genetic information. Height and body shape, nose shape, bunions, baldness, premature white hair all “run in” families. So do a variety of illnesses. Family history tells the story of genes that have expressed themselves already. Laboratory analysis of an individual’s genes attempts to predict what may happen in the future.

Laboratory genetics

In a few rare illnesses such as cystic fibrosis, sickle cell disease, and some devastating neurological degenerative disorders resulting from errors in very small parts of the genetic code, the genetic information is clear cut – the individual has an abnormal gene, and they have or will eventually show signs of the disease. These diseases, along with problems of chromosome breakage or duplication such as Downs syndrome, are the object of prenatal screening tests. For the most part, however, genetic results are statistics – the odds that a problem will eventually appear. Potentially damaging treatments applied to healthy people, based only on future odds, is the “for worse” change that may come with the addition of genetic information in the practice of everyday medicine.

The problems with statistical medicine

Statistical predictions apply to large numbers of people, not to individuals. Not all people who have a gene associated with Alzheimer’s dementia will get the disease, but since more people born with that particular gene will develop Alzheimer’s than those born without it, the gene is said to increase the risk for the Alzheimer’s disease. The prediction of a strongly hereditary trait – one associated with an 85% likelihood that some kind of illness or cancer will appear by a given age – gives the impression that the illness is almost inevitable for every member of the family. But from the standpoint of an individual within the family, the risk is always 50%. Either they will or will not be affected.

The importance of treatment availability when disease risk is high

What does knowing that there is an increased risk of suffering a given disease do for you? If there is a treatment that prevents the evolution of the disease, and it has no adverse effects, then it would be reasonable to gamble on undergoing treatment based on worry that the disease will appear, rather than waiting to see if one is in the lucky percentage that escapes. Women who undergo removal of their breasts and or ovaries because they have a genetic trait that greatly increases risk for cancer in these organs have made this judgment. (They also must accept the minuscule risk that breast or ovarian cancer can still occur even after surgical removal of the organs.)

In the case of the devastating brain degeneration known as Huntington’s disease (HD), people usually know they are at risk because one parent has developed the characteristic dementia and movement disorder in midlife. Because of the so called dominant inheritance pattern of HD, half of the offspring of the parent, statistically, will also be affected. But no one knows which children carry the gene unless testing is done. Now available and definitive, the genetic test for this disease is a double-edged sword. Life is normal for the carriers of the gene until middle age. The knowledge of what is coming might convince the bearer of the gene not to reproduce, but also make living a full and happy life seem out of reach.

The role of genetics in common diseases

What about the prediction of increased susceptibility to more common diseases, such as heart disease and some cancers? This aspect of genetic testing may help people with their motivation to lose weight, exercise, eat well and get their routine colonoscopies. Genetic analysis of cancers that have already developed is already proving helpful in the design of specific treatments for specific tumors. All tumors of lung or liver or brain are not alike and “one size fits all” treatments, the only type available in the past, will give way to individualized plans and drugs. An individual’s responses to drugs for conditions such as high blood pressure and heart disease, including both desired and to adverse effects, is also based on genetic makeup. Personalized treatments are already increasing for these problems.

Genetics and aging

Genetic studies are also teasing out at least some of the pathways involved in aging. Will advances someday lead to immortality? Very unlikely, and a bad social idea anyway. But understanding the way the genes gradually fail in their the mission of cellular repair may well lead to better old age. The key will be to use the knowledge early in life. So far it looks like preventing the errors in DNA replication that contribute to the diseases of old age depends on the same old things that your grandmother might have advised – eating modest amounts real food, preferably from fresh sources in all food groups, avoiding sugar and other refined carbohydrates, drinking little alcohol, avoiding sunburn, keeping in motion, sleeping enough, and most importantly, avoiding the biggest DNA error trigger of all – cigarette smoke. Of equal importance is recognizing that no matter how much we know and try to prevent, life will eventually wind down. Living one’s individual allotment well and fully is as important as avoiding cancer – and may actually help genes replicate correctly.

(For readers especially interested in how the genetic code works, Francis Collins’s The Language of Life, and Matt Ridley’s Genome: The Autobiography of a Species in 23 Chapters are good starting points.)

Posted by medical plaintalk

Physician turned medical writer.

No more posts.