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

The Life of a Kidney Stone

Under the right conditions, water and minerals combine to create crystals and stones. Towering stone formations called stalactites and stalagmites grow in caves where water drips though mineral-laden rock roofs.  In the human body, crystals and stones can form in urine, which is a combination of water, minerals and other waste products filtered out of the blood by the kidneys.  If the balance between water and mineral concentrations in the urine tips in the wrong direction, or if the urine becomes too acidic, crystals may form from minerals and coalesce into kidney stones. The physical consequences depend on the size and location of the stones.

Location matters

Stones can form anywhere in the kidney’s “collecting system,” which begins with the calyx, a hollow chamber emerging from the middle of the organ. Urine made by each of your two kidneys fills its calyx and then passes into a long, narrow tube called the ureter. Each ureter connects its kidney high in the back of the abdomen, one on the right side of the spine and the other on the left,  to the bladder located , deep in the center of the pelvis below. The bladder is a reservoir where urine is stored until it is released from the body. Symptoms of kidney stones depend on their size and location in the collecting system and on the presence or absence of other problems such as infection.

When confined to the kidney’s calyx, the most common stones, made of calcium, are small and cause no symptoms. But the calyx is also the site where large, branched stones called staghorn calculi can grow and fill the hollow structure, clinging to the kidney tissue and damaging it even to the point of kidney failure. Staghorn calculi are associated with recurrent urinary tract infections caused by bacteria that that cause precipitation of magnesium along with calcium.  Staghorn stones are often found as a result of the patient developing fever, back pain and cloudy painful urination – all symptoms of kidney infection. These elaborately branched stones may encase bacteria and grow to huge size before producing symptoms such as blood in the urine, unless a small portion breaks off and passes into the ureter.

The worst pain: when a stone stretches the ureter

A kidney stone may pass from the calyx and through the ureter unnoticed, but if it stretches and irritates the narrow tube as it moves along the resulting pain is intense and colicky, waxing and waning in spasms – and often described the worst pain someone has ever experienced.  Ureter pain is felt in the back, between the ribcage and pelvis, or sometimes in the groin or in the testicle. Sometimes fever and bloody urine accompany the pain. Once the stone passes out of the ureter to the bladder, pain disappears.

Bladder gravel

In the bladder, the stone may remain or pass out through the urethra with urination, causing pain with or without bleeding. When stones accumulate in the bladder they are something like gravel, irritating the lining and precipitating frequent need to urinate, burning urination, bloody urine and low pelvic pain. They may also lower the threshold for bladder infections as bacteria cling to the stones, triggering more stone formation and more symptoms. In medieval times, when clothing was changed infrequently and bathing was a yearly event, bladder infections and stones were so frequent and caused such miserable symptoms that people called stonecutters traveled England’s countryside and cities, peddling the ability to remove bladder stones via an incision between the rectum and the urethra.  There are even reports of people performing the procedure on themselves.

Who gets kidney stones?

Kidney stones are more common in men that women and tend to run in families. Obesity, chronic bladder or kidney infections, inflammatory bowel disease or a history of gastric bypass, surgery, and prior history of stone formation are all risk factors, as are some rare forms of kidney disease and even rarer parathyroid gland tumors. Doctors don’t know exactly why people form stones, but dehydration is almost always a factor in their appearance. When water intake is low the kidney responds by making urine very concentrated and deep yellow. Concentrated urine contributes to the conditions that promote kidney stone formation. Morning urine is much more concentrated than daytime urine because most people do not drink water during the night. Deliberate lack of drinking water during the day in order to avoid the need for bathroom use makes some people such as surgeons and airline pilots particularly prone to kidney stones. People who live in very dry climates or who lose a lot of water through perspiration may have very concentrated urine without realizing that they are chronically dehydrated.

Diet may play a role

Another factor correlated with kidney stone formation is a high protein diet, which increases urine acidity, promoting crystallization of calcium.  High salt diets aggravate the tendency to form stones because as the kidney gets rid of excess sodium, it also pulls calcium into the urine. Curiously, while calcium supplement use may produce kidney stones, calcium from food sources does is not a problem. Rarely, uric acid stones occur in people who have the genetic tendency to gout, or who are taking diuretic hormones.

Treatment

Treatment of kidney stones, like their symptoms, depends on stone size and location. Often, a period of pain control and hydration is often enough to get the patient through the acute problem. If not, the stone can be retrieved from the bladder through a cystoscope passed in through the urethra. A ureter can also be dilated through the scope to remove a stone stuck there. Another technique, called lithotripsy, employs ultrasonic waves applied externally to bombard and shatter stones, rendering them small enough to pass out of the body.

Followup

Beyond the acute phase of treatment, patients who have passed stones need evaluation for conditions like gout, urinary tract infection, and problems with calcium metabolism. Analysis of the stone’s composition can help, especially if it is not the common calcium type. Staghorn stones require more aggressive measures, possibly including open surgical removal.

Anyone who has suffered through the life of a kidney stone needs to be vigilant about drinking water, enough to keep urine very light in color at all times. Weight loss if appropriate, decreasing dietary salt and protein from animal sources, and avoiding calcium and Vitamin D supplements are all helpful in prevention of further stones. Sunlight is a safer source of Vitamin D in those at risk for kidney stones.

 

 

A Slip of Memory: Transient Global Amnesia

Search the internet for drugs that cause memory problems and you will immediately become familiar with a fascinating syndrome called transient global amnesia (TGA). A website at the top of the list of results opens with these words: My personal introduction to the incredible world of transient global amnesia (TGA) occurred six weeks after Lipitor was started during my annual astronaut physical at Johnson Space Center.  TGA is not listed as an adverse effect associated with cholesterol lowering drugs, but with 12 million Americans now consuming these products, recognition of this peculiar syndrome by patients and doctors becomes important.  Beyond the tightly controlled world of pre-market drug approval studies, unexpected symptoms need to be noted.

Transient global amnesia is a short–lived problem, over in less than 24 hours. It involves all aspects of new memory formation. Nothing gets recorded during the event and the sufferer fails to remember anything from the event after it is over. To appreciate the disconcerting nature of the syndrome, imagine suddenly losing your ability to put any information into your memory. In addition, you lose access to a few hours or days or even years of past memory, but not to information about yourself. You look around but cannot identify why you are where you are. Depending on how much access to the past you’ve lost, your current situation might be totally unknown to you. With great urgency you question the people around you. “What am I doing here?” How did we get here?” What’s going on?” Someone answers and for about 30 seconds you can hold on to the information. But your ability to put that information into memory has gone offline. You forget that you just asked the question. You ask again, and again, and again, with obvious anxiety. All your other mental capacities work. You can speak, read, write – even drive and problem solve. Except for your anxiety, you are the same person as always. Then the confusion ebbs. You start to encode information again. Your past gradually returns, in chronological order. Once again you are tethered to time and place, but you will not ever remember what went on while you were cut loose and for a little while you might complain of a little headache.

The first descriptions of this odd set of symptoms appeared in an obscure medical journal in 1956. More cases came to light, and by the early 1990s there were a few epidemiological studies that suggested that TGA occurs in about 10/100,000 people, or as many as 25-32/100,00 in the peak age group of 50-80. Far from being a harbinger of impending stroke or evidence of seizures, these episodes seemed to have no correlation with any problems other than a history of migraine and left no problems in their wake. They recurred in somewhere between 5 and 25% of the cases, with one patient having over a dozen recurrences. No definite cause has ever been found, though many physicians have associated them with immediately preceding, physically or emotionally strenuous events.

Very rarely, underlying brain problems like tumors involving the deep middle and frontal areas, where memory formation takes place, turn up in TGA cases, but careful examination of these cases inevitably reveals some deviation from the typical clinical symptoms, or some type of abnormality on neurological examination. TGA research studies, using sophisticated scanning and EEG techniques, suggest that there is decreased activity in areas of the brain involved in memory formation, but give no clue about the mechanisms involved.

In 1990, criteria for diagnosis of the syndrome were published (listed below), and when a diagnosis of TGA strictly adheres to these criteria, it is almost always safe to predict that there is no underlying neurologic or vascular problem. Nevertheless, when a patient appears in an emergency room with TGA symptoms, good practice still requires a CT or MRI scan and an EEG at some point to rule out the remote possibility of an underlying tumor, hemorrhage or seizure disorder.

Reports like those of Dr. Duane Graveline, the astronaut/physician author, are considered anecdotal and not of the same value as information gleaned from statistical analysis of controlled studies .  The cholesterol lowering drugs are in widespread use and considered very safe by most physicians. However, there have been cases of muscle and nerve problems, as well as cases of decline in cognitive function attributable to the drugs, possibly mediated by damage to mitochondria, the power houses of all cells in the body. Since the drugs are viewed as valuable additions to the battle against heart disease and are likely to be used over long periods by increasing numbers of people, it is important to understand and catalogue their unintended consequences.  Once drugs reach large populations outside medical studies, more problems emerge, sometimes beginning as odd, single cases.  In the meantime Dr. Graveline has died after a progressive illness which resembled Lou Gehrig’s Disease (progressive loss of muscular strength and bulk). His memory, however, remained good.

Diagnostic Criteria for Transient Global Amnesia

  1. A witness must be present to describe what happened.
  2. The patient must be unable to form new memories of any kind (anterograde amnesia).
  3. The patient must have full knowledge of his identity and an unclouded state of consciousness.
  4. All other mental functions are normal, including speech.
  5. There are no other neurological symptoms or signs.
  6. There are no signs of a seizure.
  7. There is no history of seizures within the last 2 years, or of recent head injury.
  8. The patient is back to normal within 24 hours.

 

 

 

Sleep Apnea

In ancient Greek, pneuma meant the breath of life and apnea meant the cessation of that breath. Pneuma in modern medicine is only a fragment of many words related to breathing but apnea has made the transition from the ancient lexicon unchanged.  It means no breathing. Sleep apnea is a condition in which breathing halts over and over during sleep, sometimes hundreds of times a night. The resulting disruption of sleep and respiratory physiology triggers chronic health problems like high blood pressure, cardiovascular disease and strokes. Other negative results are psychosocial and accidental, stemming from chronic daytime sleepiness. Motor vehicle accidents are but one example.

My first exposure to someone with sleep apnea was during childhood, in my grandparents’ house, where visiting grandchildren were divvied up among the adult rooms for sleeping.  My grandmother was a Camel smoker who read the New Jersey tabloids late into the night. I knew she was finally asleep when her snoring began, at first softly with a regular cadence, and then gradually increasing in volume and depth, building to a crescendo that would suddenly end…in silence. I tried holding my breath as long as she held hers, but seldom made it to the point when she would suddenly snort, inhale in a ragged fashion and then settle back into the snoring rhythm, building up to another period of no breathing. I gave up worrying about whether or not she would restart, because she always did. I wondered why my grandfather, a Lucky Strike smoker snoring away in an adjoining bedroom, breathed steadily, never stopping like she did.

The upper airway is the problem

While smoking can cause snoring, my grandmother stopped breathing intermittently because her upper airway was anatomically different from my grandfather’s and it became obstructed when the muscle relaxation caused by sleep made her throat go slack. In 1965, upper airway obstruction was finally discovered to be the cause of the marked daytime sleepiness that often affected obese people, whose airways collapsed under the excess neck fat when they lay down and fell asleep. Charles Dickens made this kind of  hypersomnolence famous in the 1800s by  his creation of the character Joe the Fat Boy in The Pickwick Papers.

Sleep research begins

The discovery of the cause of daytime sleepiness in obese people happened to coincide with the development of interest in and funding for research into sleep disorders. The first sleep lab was begun at Stanford University in 1964. Prior to that time not much was known about normal sleep, let alone disordered sleep.  By the 1970s the hundreds of awakenings interrupting the sleep of people with upper airway obstruction had been demonstrated. Sleep cycles were continuously disrupted in these patients, and sleep apnea was on its way to being tagged as a common disorder with serious consequences in terms of morbidity and mortality.

Risk factors

Who suffers from sleep apnea? According to one estimate, approximately one quarter of people between 30 and 70. Despite the increased awareness of sleep apnea in the last few decades, experts also estimate that 70-80% of people who suffer from the condition remain undiagnosed. Men are about four times more likely than women to be affected. Obesity is the largest risk factor because increasing body fat encroaches on the upper airways. Smoking irritates sensitive tissues, making them swell and further narrowing the throat. In some people, the jaw shape and position are anatomical culprits. Sleeping medicines and alcohol consumption can also alter breathing patterns in sleep and contribute to sleep apnea.

Snoring is the first symptom

Not every snorer will develop sleep apnea, but snoring is the first phase of the condition. When the snoring becomes associated with breathing cessation, problems begin.  Apnea causes an immediate fall in blood oxygen and a rise in carbon dioxide. Rising carbon dioxide triggers the respiratory drive center in the brain. The sleeper wakens in order to breathe, though he may not be aware of it.  Multiple awakenings interfere with normal cycling through progressively deeper stages of sleep back up into lighter stages of dreaming sleep, cycles that are necessary for mental and physical health.  Over time, lack of normal sleep cycles takes significant physical and mental tolls. Levels of inflammatory markers and hormones associated with stress rise; the vascular changes that lead to heart disease speed up; heart rhythms become erratic; blood pressure goes up and stroke risk rises.  Profound daytime sleepiness results in attention deficits, errors of omission, motor vehicle accidents, mood disorders and memory problems.

Other clues

Might you suffer from sleep apnea? If people complain about your snoring, if you awaken with headaches and feeling unrested, if you are lacking in energy though not ill and if you cannot stay awake once you are not physically up and about – for instance when you sit down to read or watch TV, you might want to talk to your doctor about the possibility of sleep apnea, especially if you are also overweight.

Diagnosis

The definitive diagnostic test for sleep apnea is an overnight stay in a sleep lab, where polysomnography – multiple measures of physiologic function including electroencephalography or brain wave testing are monitored while the subject is sleeping. Treatment will depend on the severity of the findings. How many awakenings occur per hour? Are there associated heart rhythm or brain wave abnormalities during the apnea?

Treatment works

In mild cases, lifestyle treatments such as weight loss, cessation of smoking, alcohol and sleeping pills, and avoidance of sleeping on the back are all that will be advised. In other cases, the addition of a mask and device that pumps continuous positive air pressure (CPAP) into the upper airway is necessary. CPAP treatment is very effective, and improvements occur rapidly. Less commonly, mouthpieces to alter jaw position, or surgery to increase airway space are advised.

I never noticed daytime sleepiness in my grandmother.  She weighed no more than 100 pounds and was an Irish whirlwind of housekeeping activity. Until she developed an autoimmune disease in her 70s, she was, to all appearances, healthy, despite the ever present cigarettes. Sleep apnea is a medical condition on a continuum, dependent not on just the upper airway obstruction component but on other aspects of the sufferer’s health. As with all physical problems, differences in disease severity reflect differences in the whole people in which the problems occur.

Floaters

Eventually, everyone sees floaters- the dark wavy lines or spots or cobwebby filaments that drift lazily through the visual field of one eye or the other. Quick eye movements up, down or sideways will clear them from your line of sight, but slowly, because floaters move through a jelly like substance in the center of the eyeball. Like the ghosts wandering around Harry Potter’s Hogwarts School, ocular floaters are most often harmless annoyances. And like so many of life’s problems, they are an accompaniment of aging, particularly in people who are nearsighted (those who require glasses to see clearly at distances).

Blame aging
Aging produces changes in collagen, the structural protein that gives form to much of the body. As a result, we develop skin wrinkles, stiff tendons, unpliable heart valves and brittle cartilage, to name just a few obvious accompaniments of living to old age. Few people know that there is collagen in the middle of the eye, which is filled with a glob of jelly-like material called the vitreous humor. Most descriptions of the vitreous humor conjure up a picture of a clear, colorless ball of Jell-O that fills the posterior chamber of the eye (the space between the lens behind the pupil and the retina lining the interior of the eyeball). The vitreous keeps the eyeball from collapsing and helps hold the retina in place.

Vitreous humor – a complex structure

But appearances are deceiving. Though the transparent, jelly-like glob is composed of 99% water, it is also a delicately complex structure in which collagen plays an important  structural role. Like skin, the vitreous ages. Along with the years come the floaters.
You are born with the vitreous humor in place. Should it be removed, by surgery or trauma, you will not grow another. This is in contrast to the aqueous humor, a clear liquid that fills the space between the cornea that protects the eye and the colored part called the iris (called the anterior chamber of the eye – see diagram). The aqueous humor is manufactured by the ciliary body, a muscular structure that gives rise to the iris. From its manufacture point just behind the iris, the fluid circulates through the pupil, fills the space behind the cornea, and exits via a channel  formed by the junction of the iris and the cornea. This evenly balanced system of fluid manufacture, circulation and exit controls the pressure within the whole eye. No such recycling system exists for the vitreous humor – as in Las Vegas, what happens in the vitreous humor stays in the vitreous humor.

eye anatomy

What happens without recycling?

The  collagen structure within the vitreous humor is an airy honey-comb of interconnected collagen fibrils – microscopic fibers cross-linked and held apart by chemical and electrostatic forces. The network is loosely attached at some points to the retina that lines the inside of the back of the eyeball. The spaces in the honeycomb contain a solution of many minerals and polysaccharide molecules (chains of sugars) dissolved in water. The collagen network is, in part, held open by the pressure of the watery solution. With age, the system has mini-collapses of collagen fibrils, resulting in some clumping of the collagen networks. Floaters are the result. Occasional macrophages (white blood cells that clean up debris) float about, but they are a lonely workforce.

When are floaters more than a nuisance?

A sudden increase in the number of floaters, accompanied by transient light flashes, is sometimes indicative of a segment of the vitreous pulling away from an attachment point on the retina. This condition is known as a posterior vitreous detachment. By itself, a posterior detachment is not a serious problem, but occasionally the point of shrinkage also pulls the retina away from the vascular layer underneath it. Now you have a retinal detachment, and your vision either develops a blind spot or the sensation of a curtain pulled over part of the visual field. Such symptoms require immediate ophthalmologic evaluation and treatment to prevent further detachment of the retina.

Treatment

There is no special treatment for floaters but at times, floaters are troublesome enough for an ophthalmologist to attempt to remove the vitreous humor entirely. The surgery is very difficult and fraught with hazards such as retinal detachment or damage resulting in partial blindness.  Called a vitrectomy, it is a procedure done more often  for other reasons such as  eye trauma. After vitrectomy, the vitreous has to be replaced to maintain the shape of the eye. Research by physicists and bioengineers on suitable replacement substances has been the biggest source of information about the physical nature of the vitreous humor and the origin of the near universal phenomenon of floaters. However, to date the replacement is still done with saline, which is then naturally replaced by the same fluid that fills the anterior chamber.

Natural history of floaters 

What happens once you begin to notice floaters? They come and they go – eventually sinking out of view. The process is very slow because there is no circulation pattern in the vitreous humor and the body has not assigned a vigorous cleanup crew to the problem. Because of this slowness, and because the vitreous passively absorbs substances from the bloodstream via the blood vessels in the retinal layer, coroners sometimes use the vitreous humor to search for toxic substances like drugs at autopsy. Chemical traces remain there after they have disappeared from other body fluids; and. the vitreous humor also retains its integrity longer than other parts of the body.

Plato’s cave

As for “seeing” floaters? You are not actually looking at the clumps of collagen. Just as in Plato’s story about people in a cave interpreting shadows created by firelight as reality, you see only the shadows of floaters cast on the retina by light coming through the pupil. For this reason, floaters are clearest when you are looking at a bright background such as snow or water. Even when you see floaters with your eyes closed, light is passing through the thin eyelid and into the pupil, the only opening in an otherwise light proof box. Who knew these little annoyances could illustrate a philosophy lesson?

 

 

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