Ketosis v.s. Ketoacidosis: Insulin makes the Difference

Ketosis is a word which you may have seen recently in print and online media, usually in material about a very low carbohydrate diet in which most calories come from fat and protein. One recent headline alluded to a plan by the Pentagon to increase military fitness by imposing the “keto diet” on some of its soldiers. But you might also have the impression that there is some controversy around the diet, and that ketosis, whatever it is, might not be good for you. After all, it is very similar to that word ketoacidosis which is associated with poorly controlled diabetes, the problem that put your friend’s daughter in the hospital ICU for a week. In fact, both ketosis and ketoacidosis refer to physiologic body states that occur when come chemicals called ketones are produced from normal metabolic processes that produce energy from the body’s own fat. The circumstances surrounding ketone production determine whether ketones cause ketoacidosis (bad) or ketosis (not so bad but maybe not so good over a long period of time).

How your body produces energy

Most of the time you are utilizing at least some fat to create energy and producing ketones in small amounts as the fats are metabolized. At the same time, the bulk of your energy is derived from the carbohydrates you eat, all of which, even the “healthy” grains, vegetables and fruits, become a simple sugar called glucose in the process of digestion. That is correct – for the most part, you burn sugar to produce energy. Under normal circumstances, with sufficient food and regular eating schedules, some glucose is burned immediately by all parts of the body for energy production. Any remaining glucose gets shuttled off to the liver and muscles to be clumped into long chains called glycogen and stored for use between meals. These reserves last for about 24 hours at which point your metabolism switches over to fat burning, and to breaking down a little protein, mainly from muscle, to supply the liver with building blocks for making more glucose.

The brain has special needs

At this point, you must eat again or rely on free fatty acids from the triglycerides stored in your body fat. The brain, however cannot burn free fatty acids. But it can burn some of the ketones, called ketone bodies, that come from the breakdown of triglycerides. By about three days of starvation, the brain is a ketone burning organ, supplemented by a little glucose constructed in the liver from amino acids given up by proteins.  The body is in a state of ketosis, with excess ketones exhaled, giving the breath a fruity odor, and released in the urine, turning a dipstick stick test positive.

Acidity makes the difference

Ketosis is not ketoacidosis. Ketoacidosis appears when the acidity rises in all the body’s tissues while it is in a state of ketosis. Acidity is measured as pH, and a fall in the body’s pH signals rising acidity. Outside a narrow range of pH, the body’s metabolic workings begin to fail.  Rising acidity produces symptoms like rapid breathing, nausea, vomiting, abdominal pain, low blood pressure, mental impairment, lethargy, heart arrhythmias and ultimately, if uncorrected, death. In otherwise healthy people, diets that promote ketosis by restricting carbohydrates do not appreciably change the body’s pH, despite the acid nature of ketones and other breakdown products of triglycerides. What keeps severe acidity and its dire consequences at bay?  In short, insulin, the central hormone of metabolism.

Insulin keeps the brakes on fat burning

Insulin is secreted by the pancreas in response to eating carbohydrates. In fact insulin is such a reponsive hormone that a burst appears from the pancreas in response to anything sweet in the mouth (the so called cephalic insulin response that prepares the gut to receive expected incoming carbohydrate, even when the sweetness is artificial and no carbs arrive in the stomach).  In addition to its role escorting glucose into cells for energy production, insulin keeps the brakes on fat burning. When insulin circulates at normal or high levels in response to carbohydrate ingestion, triglycerides remain locked in fat cells, unavailable for energy production. As night falls and eating ceases, the liver and muscles break down their glycogen to glucose to keep the supply up. When this supply dwindles, insulin levels fall, unleashing fat burning. Free fatty acids and ketones appear in the blood, but in a controlled manner, unless insulin disappears altogether. Then the brakes come off fat burning, fatty acids and ketones flood the system, and their acidity begins to drop the body’s pH.

Ketoacidosis comes from insulin’s diappearance in type 1 diabetes

Type 1 diabetics are the most at risk for ketoacidosis because immune attacks against the insulin producing cells in their pancreases severely diminish or obliterate insulin production. Their blood sugar levels  rise because sugar cannot get into cells. Fat burning comes to the rescue for energy production, and, with little or no interference from insulin, free fatty acids and ketones pour out into the blood. In new Type 1 diabetics, before treatment with insulin, major weight loss is very common – as is presentation to an emergency room in a state of profound ketoacidosis, requiring intensive medical care. Once patients are stabilized, urinary ketones are a useful guide for adjusting insulin dose– their appearance means more insulin is needed.

Type 2 diabetes is a different problem

Type 2 diabetics have a different problem, called insulin resistance. Their cells do not allow insulin to bring glucose in from the blood.  In an attempt to compensate, their pancreases make more insulin. Blood glucose levels rise, but at the same time high levels of insulin block fat breakdown, preventing the release of large amounts of potentially acidifying fuels, and diminishing the risk of ketoacidosis. But if a crisis such as trauma, infection, or surgery occurs, sugar levels can rise to extraordinary levels in Type 2 diabetics, causing huge amounts of water to be lost in urination as the body passes the sugar out through the kidneys. Severe dehydration and electrolyte abnormalities make this condition, called hyperosmolar hyperglycemia, a crisis requiring intensive care, even without acidosis. When insulin production begins to fail in Type 2 diabetics, ketoacidosis does occur and type 2 diabetics account for 20-30% of ketoacidosis cases in hospitals. One class of Type 2 diabetes drugs, the SGLT2 inhibitors known as gliflozins, has been reported to trigger ketoacidosis.

The caveat about ketosis as a dietary strategy

There is some concern, from epidemiological research, that when a very low carbohydrate diet is continued over the long term, chronic ketosis may trigger insulin resistance, the underlying problem in type 2 diabetes. Insulin resistance is not well understood, but it is associated with a cascade of health problems associated with metabolic problems.  If chronic ketosis does somehow trigger insulin resistance,  the enthusiasm for deliberately inducing ketosis to lose weight and improve fitness will wane. The word ketosis will fade back into the scientific world.

Morning Foot Pain: Plantar Fasciitis

 

“.as we know, there are known knowns; there are things we know we know. We also know there are known unknowns; that is to say we know there are some things we do not know. But there are also unknown unknowns—the ones we don’t know we don’t know.”  Donald Rumsfeld former US Secretary of Defense

 

In medicine, what we “know” changes regularly as long as curiosity keeps opening doors.  For many decades, the complaint of pain in the bottom of the foot, just in front of the heel bone and always worse with the first few steps of the morning or after prolonged periods of inactivity, fell into the “known known” category. Doctors and physical therapists confidently made diagnoses of plantar fasciitis, certain there was inflammation in the plantar fascia, the band of tough fibrous tissue that spans the bottom of the foot. The condition was common, especially in runners, in people who spend a lot of time standing on hard surfaces and in post-menopausal women.  Most of the time it resolved but there were enough prolonged and vexing cases that did not get better with anti-inflammatory medications and rest that some practitioners began to suspect that plantar fasciitis was a “known unknown” – maybe the cause was not so simple as the inflammation that they postulated. After all, no one had actually looked at the troublesome tissue under a microscope before.

 Plantar fascia gets an inspection

In 2003, a Philadelphia podiatrist and pathologist, Harvey Lemont, took microscopic samples of the plantar fascia from patients undergoing surgical release of their presumably inflamed connective tissue. In all 50 samples he found no evidence of inflammation. But the tissue was not normal. The collagen structure was disorganized and degenerated, as if it had been deprived of sufficient blood flow. Some samples contained crystals from prior cortisone injections, common treatment for plantar fasciitis, but by 2000 known to carry significant risk of causing the plantar fascia to separate from the heel bone. Degeneration of plantar fascial structure,  a previously unknown unknown, was discovered, and that prompted a change in the name  plantar fasciitis to plantar fasciosis, a term which indicates chronic structural disruption but not inflammation.

Lack of inflammation prompts new thinking

Lack of inflammation in Dr. Lemont’s pathologic examinations explained the failure of conventional treatment many cases of plantar fasciitis. And his work raised significant questions about the cause of the problem. Why does the plantar fascia begin to degenerate? What exactly hurts? Is it the bone where the connective tissue attaches? Is it the connective tissue itself? Study of the feet of non-shoe wearing cultures in which our most common foot problems are practically non-existent, and more attention to foot, leg and gait biomechanics began to yield some different ideas, not only about the heel pain syndrome, but about bunions and hammertoes.

Are shoes the problem?

When we are babies and young children, our feet are widest at the tips of the toes. By the time we wear conventional shoes for decades, with shallow, narrow and tapered toe boxes and elevated heels (even running shoes have a 1-1.5” heel elevation), the big toe begins to curve toward its mates, which begin to curl under. The muscle that normally pulls the big toe away from the other toes is pulled inward and weakens because of inactivity. What does this have to do with the plantar fascia? The big toe muscle runs from heel to toe on the foot’s inside edge, right over the artery near the heel that supplies blood to the plantar fascia. Pulling it inward narrows the artery and decreases blood flow to the plantar fascia. It is possible that morning heel pain is ischemic pain, from lack of sufficient blood flow while the foot is dropped down during sleep.  Gradual Improvement in the pain with walking may reflect better blood flow with activity, but over time insufficient blood flow takes a toll on the integrity of the tissue in the plantar fascia, adding pain from stressed attachment to the heel bone.

Wimpy foot muscles

For many years people with plantar fasciitis were told they had collapsed arches and flat feet. Or high arches and no flexibility. Or that they pronated – walking on the inside of their feet. Or supinated, walking on the outside of their feet. The treatment was external support with rigid orthotics. But feet are very individual in their structure, and there is little solid evidence that arch height causes problems. Much more evidence implicates weakness at the ends of the arch – the toes and the heels, which bear the weight of the body and are supported by muscles in the feet and in the lower legs.

A shift in treatment plans

Treatment of the heel pain syndrome is shifting to restoration of strength and flexibility in the foot. The plantar fascia functions as a windlass, a pulley that adds to the arch strength when the foot lifts at the heel and bends at the big toe joint to propel the body forward. The goal of therapy is not to stretch that windlass, but to realign the big toe and strengthen the not only the foot muscles that flex the toes and the sole, but also the muscles of the lower leg, the knee and the hip.  The toes are coaxed to flatten out and spread by stretching the top of the foot and the front of the ankle and wearing toe spacers. (Useful resource below.)

In the acute phase of plantar heel pain, some external support of the foot under the arch often helps, as does a boot that keeps the foot from dropping down in bed at night. But these aids are temporary while the work of regaining foot strength and flexibility gets under way. It can be difficult to transition from elevated heels to flat shoes, and that process is almost like training for a new physical activity – short bouts at first, gradually increasing over time.

Improvement takes patience, persistence and consistency. All footwear needs to change to shoes with wide, deep toes boxes, flexible soles at the forefoot, and no elevation between heel and toe. Perhaps we will find more unknown unknowns and a way to combine healthy feet with fashionable shoes, but at the moment, the known knowns suggest that changing fashion norms to align them with natural foot function is more likely to be successful.

 

Resources:

https://naturalfootgear.com

Foot Conditions

Sleep Debt: The Hidden Costs

Everyone has a sleep bank. Each night your accounts get credited with 7-8 hours of the physical and mental benefits of sleep and each day the accounts pay out those benefits in the form of emotional, intellectual and physical energy. Just like in any bank account, withdrawals can’t exceed deposits without incurring debt. Sleep debt, though, is easy to ignore because physical activity keeps alertness high. As long as you move around instead of reading or watching TV, you won’t nod off and you can keep thinking that 5 or 6 hours of sleep a night meets your needs. But covering the debt with activity is like keeping a bank balance out of the red by borrowing money and paying interest. Sleep debt exacts a toll on the body that goes beyond depressed mood, irritability and lack of ability to concentrate and learn, not to mention the potential for causing motor vehicle accidents.

The biological clock

As sleep debt mounts, the body’s biologic clock goes awry. This clock, located deep in the brain, controls circadian rhythms – regular ups and downs in behavior, body temperature, appetite, hormone production, alerting mechanisms, and the urge to sleep. When the clock malfunctions chronically, the results show up in the form of weight gain, high blood pressure, diabetes and diminished immunity to infection.

Setting the clock

Regular periods of darkness are required to set the brain’s internal clock to keep the body in synch with the 24-hour day set by the sun. Sleep researchers have shown that, when living in a research setting where there are no external clues about time of day or night, subjects’ internal clocks actually work on a 25-hour cycle. Normal peaks of sleepiness and alertness work themselves into the wrong time of the  24-hour day and night outside the sleep lab, producing weeks of daytime sleepiness and nighttime insomnia in the research subjects. Over time, the peaks cycle back into synchrony with day and night producing several weeks of normal daytime alertness and nighttime sleepiness.

Laboratory settings may exaggerate these patterns, but most people know that during some weeks they simply perform better during the day and sleep better at night  than during other weeks, indicating that in the modern, artificially lit world, the 24-hour day is more like a 24-25 hour day as far as the body’s natural rhythms are concerned. This clock drift is very sometimes very evident. Cyclical insomnia and daytime sleepiness are in common in blind people, in people at very high latitudes where the summer sun circles the sky for almost 24 hours, and in shift workers who are up all night in brightly lit environments. These problems, while distressing, respond to maintaining regular sleeping schedules and closing out all light during sleep periods, which resets the clock.

Why the clock matters

The internal clock is easily disrupted by one or two day episodes of sleep deprivation that people experience for reasons as varied as extra work loads, exams, brief periods of emotional upheaval, or any of the other myriad problems that keep people awake, but studies have repeatedly demonstrated that a few days of “catching up” on sleep restore the body to normal rhythms, contributing to a widely held impression that sleep deprivation, while responsible for serious accidents, doesn’t cause real health problems.
However, bigger problems do come from disturbing circadian rhythms more chronically. In recent years research attention has shifted from short term sleep deprivation to the chronic, partial sleep deprivation that is so common in our modern society, where nodding off during monotonous and sedentary activities like reading or watching TV are almost expected. Many people think they need no more than 5-7 hours of sleep at night, but while a few truly short sleepers exist, most people require around 8 hours of sleep each night to achieve maximal alertness throughout the day. Chronically shortchanging sleep by even an hour a day changes the timing and levels of multiple hormones, causing other metabolic changes and weakening the immune system.

Lack of sleep wreaks havoc on hormones

One of the first hormonal changes produced by chronic short sleep involves cortisol, the stress hormone produced by the adrenal gland. Normally cortisol levels decline during late evening hours, but without enough sleep, production continues unabated, Cortisol then begins to contribute to immune stress and to insulin resistance, which leads to diabetes and fat deposition. A second contributor to insulin resistance is a change in growth hormone secretion from one large burst during sleep to two, smaller bursts before and after sleep. A third change comes from failure of the pituitary gland to produce its normal night-time rise in thyroid stimulating hormone, the stimulus for the thyroid gland to produce more thyroid hormone. All of these changes are consistent with the fact that as little as one week of 4 hour sleeping nights can convert healthy young people to a pre-diabetic state. Observational studies do show higher rates of diabetes in chronically sleep-deprived women.

Lack of sleep and obesity

If these hormone changes are not enough to convince a short sleeper to turn out the lights earlier, studies on the appetite influencing hormones leptin and ghrelin, produced by fat tissue and the stomach respectively, might help. Leptin, which signals when to stop eating, diminishes markedly after 6 days of four- hour sleeping nights, despite no change in caloric intake. Ghrelin, which stimulates appetite, particularly for high carbohydrate foods, goes up when sleep is short.

Sleep debt is all around you

    All of these hormonal factors are significant in society where people lead overscheduled lives in stimulating, loud and bright environments without regard to natural day and night. We do not need sleep studies to tell us that we are in an age of significant sleep debt – just count the number of people, including children, asleep on planes and buses, over books and newspapers, and on couches in front of TVs. If you fall asleep regularly under these circumstances, you are in chronic sleep debt. Given the increase in obesity and diabetes over the last few decades, sleep is another potential therapeutic avenue – a fruitful and inexpensive area of health over which we have considerable control.

Managing the sleep budget: factors under your control

Environmental
1. Take the television out of the bedroom.
2.Darken the room completely, or wear a comfortable, opaque eye mask.
3. If noise is a problem were soft ear plugs.
4. Keep the temperature low at night and invest in a comfortable mattress that does not move.

Behavioral
1. Keep the biologic clock in sync with the sun by getting outside regularly.
2. Get regular exercise like walking, but avoid exercise in the last 3-4 hours before bedtime.
3. Keep naps short – 45 minutes or so – and confined to early afternoon hours.
4. Avoid heavy meals and alcohol in the last 4 hours before sleep.
5. Aim for the same bedtime every night, well before midnight, and develop a quiet bedtime ritual

Internal factors
1. Empty your bladder right before getting in bed.
2. Seek medical treatment for heartburn if causes frequent awakening. Ditto for urination.
3. Evaluation for sleep apnea is a must for someone who snores and suffers from daytime sleepiness.
4. Treatment of arthritis with exercise, physical therapy and medications, if necessary.
5. Try to get weight down to normal: sleep apnea, heartburn, and arthritis pain all benefit

The Latest on Charley Horse: How Muscle Cramps Work

No one knows for certain how “charley horse” became a name for muscle cramps.  Baseball lore from the late 1800s links the term to a player named Joe Quest, who may or may not have compared his cramp-prone teammates to an old, stiff-legged white horse named Charley who pulled heavy loads in his father’s machine shop in New Castle PA. The first newspaper story using the term charley horse in the context of players who pulled up with thigh cramps was allegedly the Chicago Tribune, during Quest’s 1879-1882 stint with the Chicago White Stockings. The first retrievable story using the term, in the Boston Globe in 1886, referred to the Tribune story as the origin of the name. By that time, Quest was with the Philadelphia Athletics and at the end of his career, but the off-hand description he may or may not have coined has become a household word, spread far beyond the world of baseball.

What is a muscle cramp?

Muscle cramps of are involuntary, intense and painful contractions which harden the muscle and last seconds to minutes. Aching pain and even chemical indications of muscle damage may persist much longer.  Electrical recording of muscle activity during cramping and between bouts of cramping indicates that the baseline or normal amount of electrical activation of the muscle is increased – maybe a measurable correlate of the feeling that a muscle is “about to cramp.”

Theories about cramps

Long-held theories have blamed muscle cramps on dehydration, electrolyte losses from sweating, extreme environmental conditions of heat and cold, or inherited problems of energy production. In addition, cramps happen more in people taking some medications some medications such as cholesterol lowering drugs and diuretics. While these factors may play supporting roles, they do not explain the mechanism of cramping. Nor do they explain why stretching, as well as folklore-based remedies like the Amish combination of vinegar, ginger and garlic, or consumption of pickle juice, mustard or hot peppers help cramps. Newer, “neural” theories about the mechanism of cramping, which implicate feedback loops between muscle and the spinal cord, might account not only for exercise related cramps but also for and the kind that grab hold of a leg as you roll over in bed.  And they might explain the seeming success of peculiar remedies. To understand the neuromuscular feedback loops we must diverge briefly into a little muscle anatomy and physiology.

How your muscles move things

When you decide to lift this magazine, your brain sends a message to motor nerve cells in the spinal cord, the alpha motor neurons, which then fire signals down nerves to the biceps muscle and to all the other muscles are involved in the task, telling some to contract and others to relax.   That is the simple part. The complex part, which goes on in the background at all times, is the feedback from two types of specialized muscle receptors which act much like strain gauges used in civil engineering to detect forces deforming land and buildings.

Strain gauges in every muscle: moderators of muscle tone

One type of muscle receptor strain guage is a muscle spindle. It calculates stretching forces in the belly of a muscle. The other is a Golgi tendon organ, which calculates the stretch in the tendon, the fibrous end of the muscle that attaches to bone.  Muscle spindles send messages to the spinal cord motor cells to fire up and contract the muscle when the muscle lengthens too much. Golgi organs send the opposite message to prevent the tendon from becoming too tight as the muscle contracts. All of this occurs rapidly and constantly, in a balance that keeps your muscles at the right degree of tone for all your movements.

In 1997, researchers suggested that unbalanced feedback from these little muscle strain gauges was the primary cause of cramping.  In fatigued muscle, at least in animal studies, the spindles were more active than normal, and the Golgi tendons less active.  The net result caused alpha motor neurons to fire up the muscle fibers than they usually do. Passive stretching of the muscles, which stretches tendons, woke the Golgi receptors back up, prompting them to send more cease and desist orders to the motor neurons. The cause of cramping thus appeared to be too much spindle input.

Regulation from above

Motor neuron feedback loops also receive input via pathways that originate higher in the nervous system. Swallowing liquids with striking tastes stimulates sensory cells in these spinal pathways, sending messages up to the brain and down through the spinal cord. Cramp researchers speculate that stimulation of these pathways tamps down some of the incoming messages from the muscle spindles, providing an explanation for the efficacy of some old-fashioned cramp remedies.

The well-known tendency of baseball players to suffer cramps might also bolster the neuromuscular feedback theory.  Baseball players wait to explode into motion from crouches, get up from slides to race back to safety after failed base stealing attempts, and stop, start and reverse direction abruptly.  It is easy to imagine some Golgi tendon organs and muscle spindles lulled into altering their feedback and then lagging in adjusting to the abrupt new actions.

Cramps in bed

But what about the cramps that are not associated with the fatigue of exercise? Shortening of the muscle in certain positions, such as lying in bed, may set them up for the same imbalance in input from the stretch receptors. The increasing frequency of cramp problems with age could be a result of general loss of strength and flexibility in muscles that are not used as much as in the past.  The ideal input from muscle stretch receptors occurs in the rested muscle which has maintained its youthful length and flexibility.

Practical application of the latest theory

Practical application of the neuromuscular feedback theory of cramping applies not only to charley horses, but also to musculoskeletal injury prevention in general.  Maintenance of flexibility and balance of strength in opposing muscle groups such as the quadriceps and the hamstrings keeps the spindles and Golgi tendon organs in balance, and muscles which are less stiff and prone to cramping allow movement with less discomfort as life moves on. Such maintenance requires regular work, especially if you want to avoid some of the creeping stiffness of old age.

Note: the muscle receptors and their connections  may well play roles or even be the culprits in some mysterious muscle disorders that are associated with cramping or decreased muscle tone. Muscle research is a blossoming field in this new age of genetic research. All muscles bear the stamp of their genetic makeup in their differing structural proteins. Some people have big bulky muscles, some long slender ones; some have more fast twitch fibers that make them speedy, others more slow twitch fibers that endure for marathons.  And some people are relatively inflexible, others loose and prone to twisting ankles. You get what you get from the usual complement of both parental versions of DNA, in the nucleus of the cells. (But if you want to complain about your speed, blame your mother- she provided all the DNA in the mitochondria which power the cells.)

Fatigue: Gentle Messenger…and Tyrant

As Supreme Court Justice Potter Stewart famously said, when confronted with a decision about what constituted pornography, the definition is hard, but “I know what it is when I see it.” An all-encompassing definition of fatigue is similarly difficult, but everyone knows what fatigue feels like. The profound lassitude that signals an oncoming flu is a gluey, mesmerizing state of mind and body that renders one incapable of remembering ever feeling good, of imagining ever feeling energetic again, or of conceiving of a desire to participate in any physical, social or mental activity beyond crawling beneath the bedcovers.  

The perception of energy failure

 Where there is life, there is fatigue. All plants and animals run on energy produced in little chemical factories (mitochondria) in every cell. The ultimate source of biologic energy is the sun’s nuclear energy, converted to usable form by plants and transferred to animals as food. The more complex the living thing, the more obvious the need for periods of rest and recovery to replenish energy. When the demand energy use outpaces the time needed for recovery, or when normal function is derailed by illness, drugs or toxins, fatigue is the name we give to what we feel, mentally and physically. To the research scientist, fatigue is a by-product of numerous little proteins (cytokines) produced by the immune system to protect us from outside invaders and internal disorders like cancer. How these proteins create the feeling of fatigue is a mystery, but there is admirable logic in a system that commandeers a patient’s energy, drive and ambition and sends him packing off to bed while an internal battle rages.  

Voluntary fatigue

Less admirable is our ability to override the biology that produces tiredness, and to become passive, cranky and sleep-deprived. In fact, most complaints of fatigue reflect the deliberate choice to ignore the symptom and would and yield to simple lifestyle changes – if one were willing and able to sleep more, lose weight, eat regular, well-balanced meals, exercise enough, manage time wisely, avoid smoking, excess alcohol, and junk food, and engage in satisfying work. In our culture these are tall orders, and a background level of fatigue is often accepted as normal. 

Evaluation of fatigue 

New, unexpected and persistent tiredness, however, may signal underlying illness or environmental stress and warrants a serious evaluation, with clear communication about exactly what fatigue means to the patient. First, a description of the patient’s normal “background energy” is important. Some people are full of energy from the day they are born. Others are inveterate couch potatoes, happy to sit and watch life go by. The feeling of fatigue that prompts one to see a doctor is, by definition, different from the patient’s normal state, but the doctor sees only a snapshot in time. Patients and families should never be shy about volunteering information about what life used to be like. 

Defining the symptom

Next, the language used by patients to describe fatigue needs to be clear. “I’m tired” sometimes means “I’m weak,” and “I’m weak” sometimes means “I’m tired,” but in the jargon of medicine, weakness means loss of muscle strength. Provided that they exert full effort, tired people can generate normal muscle power upon request, but people with strokes or nerve and muscle diseases cannot. Separating weakness from fatigue is the doctor’s first job – otherwise he may head off on the wrong diagnostic road. Description of the activities affected by tiredness and/or weakness, and characterization of changes fatigue brings to daily life are crucial to the process of diagnosis.   

Finding the source

Once a doctor understands the way fatigue affects life for a patient, he moves on to a “review of systems” – a top to bottom list of questions ranging over all the body’s organs, looking for clues to the presence of heart, kidney or liver disease, diabetes, cancer, sleep apnea, restless leg syndrome, insomnia, degenerative neurologic diseases like Parkinson’s, autoimmune illnesses like lupus or MS, chronic infections, eating disorders and problems of the thyroid, adrenal and pituitary glands. A good doctor will then delve into the lifestyle and life events surrounding the appearance of fatigue. Tiredness is a complex, high level symptom that may also originate in the mind – it is one of the cardinal symptoms of depression. 

Is it the drugs

Next comes a careful inventory of all medicines in use, prescription and non-prescription. New fatigue symptoms may parallel the addition of new drugs (even antibiotics can cause fatigue). An inventory of potential toxins and hazards in the environment may turn up a faulty furnace producing carbon monoxide or exposure to toxins such as volatile hydrocarbons that can damage the part of the brain called the cerebellum – a major player in energy balance. 

Following the clues

 Following a good, inquisitive medical history, a complete physical exam (the kind that requires undressing) may turn up other clues that suggest the need for more than “routine” tests. Fatigue is messenger bringing information about conditions ranging from minor to mortal. When not readily explained, fatigue warrants the best of our medical tools to ferret out the source of trouble. The first step though, is still a careful history and physical examination. Without these, advanced medical technological evaluation of fatigue is little better than a fishing expedition sent to sea with no information about where the fish hang out. 

                                                    The Chronic Fatigue Syndrome

Definition:

Profound, life-altering fatigue lasting more than 6 months.

May follow a viral infection, but no test abnormalities persist along with the fatigue.

Physical and mental activities both worsen symptoms.

Variety of accompanying symptoms: weakness, muscle and skeletal aches and pains, impaired memory, lack of drive, poor sleep.

Diagnosis:

No specific tests, other than exclusion of other illnesses that produce these symptoms, among others. CFS is a “diagnosis of exclusion.”

Conditions to be excluded:

Chronic infections, mononucleosis, autoimmune disorders (lupus, M.S.), hypothyroidism, low adrenal function, sleep apnea, cancer (particularly pancreatic), obesity, eating disorders, drug and alcohol abuse, major psychiatric disturbances: schizophrenia, depression. 

                          A Balanced Life

Humpty Dumpty sat on a wall,


Humpty Dumpty had a great fall. 


All the king’s horses, 
and all the king’s men,

Couldn’t put Humpty together again.

No one ever said why Humpty fell off the wall. If he’d managed to stay up there, he would have been OK. That’s the way it is with older people with thin bones. Osteoporosis doesn’t make people fall but it makes them break when they do. The real question is why they fall.

Why do older people fall down?
Falling is a risk of age because balance, strength, flexibility and speed decline over time. Even if you have no problems with balance it is worth understanding how balance works – how you maintain an upright posture and adjust to changes in the terrain under your feet, and how you manage to catch yourself and not fall as your foot slips on an icy path. The good news is that “use it or lose it” applies to balance, strength, flexibility and speed. You have some say in their preservation.

The systems that create balance

Your sense of balance comes from the integration of messages from muscles and joints, eyes and ears. Try experimenting and you’ll feel how these sensations contribute to balance. First, stand on one leg. Then try doing it with your eyes closed. Then try doing it after spinning around in a circle, and disturbing the fluid in the inner ear. With each maneuver, you subtract some of the sensory input to your brain and make it harder to control the muscle strength and tone needed to keep you upright. Fortunately, we don’t have to “think” about the actions that keep us balanced. They happen automatically.

What happens when the balance systems go awry?

When some part of the entire balance system goes awry, you feel “dizzy” or “lightheaded” or “off” or “tipsy.” The doctor who hears your complaint will ask you questions related to all the components of the balance system, and to all the medical conditions that can disrupt your eyes and ears, your peripheral nerves, your spinal cord, or your brain. He or she may order hearing tests or brain scans, blood tests or electroencephalograms. Patience, careful observation of symptoms, and systematic ruling out of problems is the best approach.

Vertigo

A sense of spinning dizziness, called vertigo, makes balance almost impossible. Vertigo is most frequently the result of an inner ear problem Three semicircular canals deep in each ear lie at right angles to each other and are filled with fluid that moves when you move your head. The fluid stimulates nerves that add information to the balance system. Viruses can affect the ear and produce profound vertigo with even tiny head movements. Some tumors of the nerve to the ear (acoustic neuromas) affect balance and hearing. A benign condition called Meniere’s disease causes episodes of hearing loss and vertigo. Though acute ear problems are sometimes at fault, very often dizziness that comes from the ears is a result of disuse of the inner ear canals. Ears that are unaccustomed to change in position because body movement has become limited and slow no longer cope well with rolling over in bed or turning the head quickly, and such routine activities can make the room spin. This is called benign positional vertigo and the treatment consists of exercises of the head and neck to re-accustom the semicircular canals to movement.

Muscle and joint receptors keep track of the body in three dimensions

Tiny receptors in the muscles and the joints perceive gravitational stress and muscle tension and movement. These receptors tell the brain where the body is and how much muscle tension is needed to hold you up and to move the way you intend to move. Balance suffers when nerves don’t function properly (neuropathies) because of diabetes, kidney disease, vitamin deficiencies, medications, exposure to toxic substances, or a variety of esoteric blood and autoimmune diseases. Balance also suffers when pain messages from joints and muscles override the compensatory adjustments that have to be made quickly to avert a fall.  Arthritic diseases of the spine, spinal tumors, or diseases that affect the peripheral nerves can disrupt the pathways in the spinal cord that carry the messages from the nerves to the brain.

Vision: an important component of the balance system

Visual input contributes a lot to the brain’s interpretation of the world and to where the body is in three dimensional space. Darkness, by removing visual clues, sometimes uncovers balance troubles before they are apparent in good light. Of course, people who have never had vision have developed balance systems that function perfectly well without visual input and sighted people who lose vision eventually adapt their balance to its lack.
Brain: coordinating the input and determining the output

The brain takes incoming sensory information and converts it to a sense of where the body is in space. It also sends messages back down the spinal cord and out over the motor nerves to the muscles to stimulate them to contract and relax in just the amounts necessary the body where you want it. Interference with these finely tuned functions can cause feelings of dizziness and imbalance that are harder to describe than the vertigo caused by ear problems. These sensations are termed central imbalance and can come from strokes, side effects from medicines, or a fall in blood pressure on standing up too rapidly. Less common causes are a variety of degenerative diseases, like Parkinson’s disease, and cerebellar degeneration.

Keep you balance and you won’t have to retrieve it later

Even if you are young, practicing balance activities that challenge you and maintaining muscle strength, quickness and range of motion are useful habits that serve you well in youth as well as in older age. If you do slip, you will have the best balance possible and the strength required to get your feet back underneath you. Choices abound that give you opportunities to stimulate your balance circuits. Put your pants and socks on while standing. While you brush your teeth! where you can grab onto something if necessary, practice one-footed standing with eyes open, then closed. Do regular head rolling exercises, gently and slowly at first, to get those semicircular canals used to some movement or take dance lessons and get back to spinning movements. Make yourself move briskly at all times to keep speed in your repertoire. Squat completely and rise as often as possible when only bending is required. Try one-footed squats. Use the stairs instead of elevators. Balance on your toes, and on your heels. Walk an imaginary tightrope, frontward and backward. And if you still ride a bike or ski or dance or skate or run, keep it up. Unlike Humpty Dumpy, you’ll have a better chance of staying up on the wall.

Muscle: Designed for Action

“Use it or lose it.”  Jimmy Connors

When the weather turns cold, black bears retreat to their dens. During their period of winter sleep, they occasionally rouse themselves and shiver to raise their body temperatures, but for the most part, they engage in little physical activity. In the spring, the bears emerge from their dens, having lost a lot of body fat, but only a little muscular bulk. They are fit enough to begin the season’s hunt for food. A human emerging from an equivalent period of bed rest, however,  would be in terrible shape, in need of a wheelchair to make it to the grocery store because his muscle mass would have declined nearly 80 percent. He would face a long and arduous period of rehabilitation to regain the muscular strength and bulk he lost due to inactivity. 

Human muscle isn’t bear muscle

The difference between the muscle of humans and that of hibernating mammals lies in the genetic makeup of each type of muscle. Human muscle is programmed for almost continuous activity. During times when it is not called into action to contract or resist the force of gravity, it heeds some mysterious signal to begin closing up shop. In medical terms , it begins to atrophy. Anyone who has ever broken a leg or had surgery that required the immobilization of a limb remembersWhen the weather turns cold, black bears retreat to their dens. During their period of winter sleep, they occasionally rouse themselves and shiver to raise their body temperatures, but for the most part, they engage in little physical activity. In the spring, the bears emerge from their dens, having lost a lot of body fat, but only a little muscular bulk. They are fit enough to begin the season’s hunt for food. A human emerging from an equivalent period of bed rest, however,  would be in terrible shape and would be in need of a wheelchair to make it to the grocery store because his muscle mass would have declined nearly 80 percent. He would face a long and arduous period of rehabilitation to regain the muscular strength and bulk he lost due to inactivity.

The difference between the muscle of humans and that of hibernating mammals lies in the genetic makeup of each type of muscle. Human muscle is programmed for almost continuous activity. During times when it is not called into action to contract or to resist the force of gravity , it heeds some mysterious signal to begin closing up shop. In medical terms , it begins to atrophy. Anyone who has ever broken a leg or had surgery that required the immobilization of a limb remembers the sad, shrunken state of the muscles in the limb that emerged after weeks in a cast. The bone has healed but the muscles atrophied. 
.How does muscle shrink?

Atrophy occurs because, in response to inactivity, the normal balance of protein recycling in muscle cells shifts in favor of breaking protein down rather than building it up. During this process, tiny protein-based fibers called myofibrils, the contracting and relaxing elements in all muscles, begin to shrink and disappear. Unless muscles are called into action, atrophy continues and, within two weeks, the loss of muscle mass is visibly apparent.

Other triggers for muscle atrophy

Muscles also shrink in response to some serious illnesses. In these cases, the triggers that set atrophy in motion are things other than inactivity. One trigger  is a substance called tumor necrosis factor, which the body produces in response to some cancers and infections and which contributes to dramatic loss of weight in cancer patients. Another trigger is loss of nerve supply to muscle cells such as happens when the controlling motor nerve cells in the spinal cord die in diseases like polio and amyotrophic lateral sclerosis (also known as Lou Gehrig’s disease) or when nerves that run from those cells to the muscles are severed by trauma or damaged by diseases or toxins (examples are diabetes and lead exposure). Old age, with its lower testosterone levels, gradually robs muscle of some of its bulk. But no matter what the trigger is, once atrophy is set in motion the result is the same. Muscle shrinks. It becomes weak, fatigues easily, and consumes less energy. The body’s metabolism slows down, sensitivity to insulin declines, and fat accumulation becomes easier.

Atrophy conserves energy

Energy demand is the key to understanding muscle atrophy. All living things conserve energy whenever possible. This bedrock survival principle applies not only to the visible animal world , where animals do little but rest when they are not eating or seeking food, but also to the microscopic world of cellular physiology. Those cells that do not get used get put to rest. Muscle is a heavy consumer of the body’s limited energy resources and it has a mysterious ability to measure the time since it has been called upon to work. Once inactivity has exceeded a few days, muscle cells begin to shrink as a means of conserving the body’s precious energy stores. In a gravity-free environment like the International Space Station, for example, astronauts’ muscles atrophy because the work of moving bones is greatly reduced outside the earth’s gravitational field. Weightlessness is rest for muscles. Astronauts use stationary bikes and other exercise equipment in an attempt to counteract muscle atrophy, but these measures do not make up for the normal and continuous activity of resisting gravity.

Muscle loss with age

Muscle atrophy can also occur more subtly over the course of a lifetime and the patterns of muscle loss are related to lifestyles in different cultures. The human foot,  for instance, has more than twenty muscles that control the motion of its intricate, bony structure. In non-shoe wearing cultures around the world, people have remarkably strong and flexible feet because they demand much of the muscles in them. In some of these cultures, people use their feet to grasp the surfaces of trees as they climb in search of things like coconuts. Activities like these, in addition to the lack of the kind of general support that shoes provide, help keep the muscles in their feet strong. Conversely, people in shoe wearing cultures with smooth walking surfaces demand much less of their foot muscles.Not only do their feet lack strength and flexibility, but they frequently develop bony abnormalities like bunions, overlapping toes and hammer toes. The same principles apply to the muscles of the legs and hips. In cultures where people squat instead of sitting in chairs, the ability to squat and rise is retained better than it is in populations where squatting is not required in the daily routine of life. 

Retrieving muscle

Muscle is very forgiving and will respond to resumed calls for action, even in people in their eighties. When they begin to use their muscles in more demanding and repetitive activities, muscle cells once again begin to make more proteins than they break down. Muscle fibers increase in size and tensile strength. As health returns in someone who has been weakened by a debilitating illness, increasing activity improves strength. Following nerve damage, muscle may recover if the nerve supply is re-established, al­though this recovery is usually limited if a long period of time has elapsed between nerve damage and repair of nerve supply. For instance, if muscle has become weak from pressure on spinal nerves and surgical decompression has been delayed, muscle strength may not fully return. Passive electrical stimula­tion of muscles which have no nerve supply helps prevent atrophy but is never as effective as active use in restoring muscle strength.

Maintaining muscle

The lessons to be learned from muscle atrophy are that humans are designed for motion and that healthy muscle is integral to a healthy overall metabolism. Hence the constant refrain from doctors and health writers that exercise is necessary to prevent chronic illnesses like obesity, diabetes, and coronary artery disease. But how much movement is necessary to keep muscles healthy and prevent atrophy? The easiest way to answer this question is to picture the world in which early humans evolved. There were no cars, no chairs, and no grocery stores. Life involved hunting and gathering, squatting around camp­ fires, climbing trees, running from predators and after prey. In such a world, no groups of muscles were neglected. In the modern world, it takes more effort-such as learning Pilates or yoga-to make sure that the muscles of the shoulders, hips, and torso are used regularly. Still, it is easy to find daily opportunities to squat and rise, to walk without shoes, run a few steps, and add a little bounce and speed to  stair climbing.  If you need to sit for prolonged periods of time, be certain to take frequent breaks and stand up and move around. Mindfulness and willfulness about physical activity are keys to healthy muscles in the modern world. Unlike black bears, humans are programmed for short, regular intervals of rest, not for long months of hibernation. Nature will wait only a few days before moving on with her overriding goal of conserving energy. Use it or lose it is her rule. •

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