Probiotics: Manipulating Your Internal Ecosystem

The human body is an ecosystem harboring numerous different species living in delicate balance, well-adapted to each other and to their physical environment. The creatures that thrive on our skin and in our noses, mouths, urogenital tracts and guts are microscopic organisms – mainly bacteria, fungi and bacteriophages (viruses carried by bacteria). These organisms comprise the human “microbiome” and perform valuable services for us, breaking down food, making vitamins and other chemical compounds that we absorb, teaching our immune systems how to recognize invaders, and maintaining bowel health. Their genes interact with our genes, up-regulating and down-regulating them as we change our diets.

Research relating the the invisible world of the microbiome to physical states of health and illness is still in its infancy, but has produced interesting data and useful observations about attempts to restore microbiome composition after disruption by illness and antibiotics. Outside this world of esoteric research, entrepreneurs have leapt ahead of the facts, supplying millions of people who wish to better their health with supplements called probiotics, pills containing “living microorganisms, which when administered in adequate amounts, confer health benefits on the host.”

Not a new idea

The idea of manipulating the body’s microorganisms to improve health is not new. In 1908, Nobel prize winner Elie Metchnikoff, the “Father of Immunology,” theorized that the large intestine was a cesspool where putrefaction by bacteria produced autotoxins that aged the body. While some believers advocated removing the colon or administering repeated enemas to cleanse it, Metchnikoff thought that Lactobacilli, bacteria found in the yogurt consumed by long-lived Bulgarians, could battle the putrefactive bacteria, and that consumption of the yogurt, along with other ascetic practices like avoidance of alcohol and intoxicants, would prevent dementia, illness and premature death. Like yogurt, other fermented, bacteria-laden foodstuffs such as kefir and sauerkraut have long been advocated for general good health.

Experimental evidence?

There is tantalizing experimental evidence that the interior microbial world has previously unsuspected ties to overall health. For instance, in germ-free mice, introduction of specific bacteria into the gut will alter energy usage because the bacteria digest incoming food. The mice get fatter on the same amount of food they were fed in the germ-free state because they absorb more of it. Bacteria also produce substances which act like neurotransmitters and communicate with the brain via the gut’s neural network. And they modify the action of their genes to match the types of food we eat, which in turn modifies food absorption and immune system function.

Genetic tools speed modern microbiome research

High speed DNA analysis is the modern tool which drives microbiome research. No longer do scientists struggle with culturing and identifying the multitude of bacterial types that reside in the human body. Based on microbial DNA sequencing of samples from human bodies, we know that we carry over 3.3 million bacterial genes, vastly more than our own 22,000 genes). There is far more diversity between humans in terms of the genetics of the organisms they carry than there is in their genetic profiles – and enough stability in each person’s microbiome to create unique microbial DNA profiles, which can be identified like fingerprints on surfaces people touch. There are even identifiable differences between the fingerprint profiles from an individual’s right and left hands.

Fecal transplants: the ultimate probiotics

The best scientific information about manipulation of the microbiome in the quest for better health comes from the ultimate type of probiotic – the so-called fecal transplant. Transfer of fecal material from one person’s gut to another’s was first tried in the 1950s. In this experiment, a patient suffering severe colitis was spared surgical removal of the colon when restoration of a normal mix of bacteria, as well as everything else in contained in the stool sample used for the transplant, quelled the toxic bacteria eating away his colonic lining. Since that time, fecal transplantation has been 90% successful in treating the severe and often recurrent colitis and diarrhea produced by the bacterium clostridium difficile.

The complex nature of fecal material

Fecal material contains bacteria, viruses, bacteriophages – the viruses that bacteria can transfer among themselves and to the host, other types of microorganisms, and all the chemical products of the metabolic processes of all these living creatures. Each stool donor has a unique microbial profile, as does each fecal transplant recipient. Donor stool is screened for drug resistant and abnormal bacteria, prepared as a slurry and introduced into the colon via colonoscope, or into the stomach or small intestine via a tube. Capsules that resist the acid and enzymatic environment of the upper GI tract also show some promise.

Probiotics: less complex mixtures of living organisms than fecal transplants

Like fecal transplants, probiotics aim to create a healthier balance of bacteria in the gut, but they are capsules containing a few types of freeze-dried bacteria harvested from cultures in labs. When swallowed and exposed to the warmth and moisture of the body’s interior they spring to life. Sold as supplements, probiotics are not subject to FDA quality control.

Probiotics have been studied as treatments for antibiotic-induced diarrhea, allergies, autism, metabolic syndrome, autoimmune ulcerative colitis, Crohn’s, disease, infectious colitis, constipation, traveler’s diarrhea, periodontal disease, and more. The studies are fraught with problems that make most of them inconclusive at best. But as preventives for antibiotic0induced diarrhea and clostridium difficile diarrhea, probiotics may be helpful and are generally not harmful for otherwise healthy people. Theoretically, people with depressed immune systems could contract an infection from one of the organisms included in the product. There has been at least one neonatal death attributed to a contaminated probiotic.

Do the introduced bacteria survive?

A recent, carefully designed study from Israel assessed whether or not probiotic bacteria took up residence in the colon after ingestion. In some people, called persisters, the probiotic bacteria can be found in the recipient, but in others, called resisters, none of the probiotic bacteria survive. The type of bacterial populations already living in the gut make the difference. In addition, another good study demonstrated that probiotic use actually delayed the return of normal bacteria to the colon after a course of antibiotics.

Much work remains in the investigation of the human microbiome and in attempts to improve health by manipulating it. What is clear so far is that each person’s microbiome is unique and that success in understanding and manipulating it will require individualized evaluation. Most probiotic use at this time is a one-size-fits-all approach, done for non-specific reasons. Similar to Metchnikoff’s Bulgarian yogurt.*

*modern science shows that the lactobacillus in the yogurt does not survive the trip through the gut to the colon.

Posted by medical plaintalk

Physician turned medical writer.

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.

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.

Iron: Too Little and Too Much

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

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

Where the body puts iron

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

Iron absorption from food – a tightly regulated process

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

Too Little Iron

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

Who becomes iron deficient?

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

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

Replenishing iron stores

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

Too Much Iron

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

Transfusion-related iron overload

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

Hereditary hemochromatosis

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

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

Posted by medical plaintalk

Physician turned medical writer.

Cholesterol Phobia

Cholesterol research is difficult, esoteric and accessible in journals that seldom make it beyond their target audience – other people doing the same type of work. One theory about the relationship of cholesterol and heart disease has dominated medical practice for over half a century, but there has always been dissension in the ranks of scientists, some of whom labor away in obscurity, slowly building a case that may one day topple the current dogma. I have attempted to make this subject accessible to a non-medical audience because the current paradigms for thinking about heart disease and treating it affect everyone who sees a doctor, listens to the news or reads the popular press – even children, because they eat what their parents believe is healthy for them.
Cholesterol phobia: is the end in sight?

Cholesterol earned a villain’s reputation because it got caught at many criminal scenes where victims succumbed to heart attacks. It was found lurking in the walls of arteries too narrowed by “plaques” to allow blood passage. Even in young healthy men, cholesterol- laden “fatty streaks” were surprise findings at autopsy after accidental or war-related death. Experimentally, fat choked arteries were easy to produce in experimental animals by feeding them food pellets saturated with fat – even olive oil worked. The laboratory work bolstered attempts to show that different populations consuming different amounts of fat had different rates of heart disease. Though both the laboratory and epidemiology studies were fraught with contradictory results, and the dietary cholesterol theory of heart disease was initially rejected by the American Heart Association, the personalities and scientific politics involved eventually catapulted the theory into the lives of all Americans, over 20 million of whom are now on potent drugs to combat the evil substance.

The dietary theory of heart disease

After more than half a century of war on cholesterol, the dietary theory remains just that – a theory – no matter how many commercials remind you that you need to lower your cholesterol. You may be surprised to hear that cholesterol could be absolved of its villainous status, within your lifetime. But don’t expect your doctor to agree, at least not yet. The cholesterol theory has a grip on our culture that is almost religious. The current dogma, advertised everywhere, is simple: there is good cholesterol, labeled HDL, and bad cholesterol, labeled LDL and anyone who cares a whit about his health will do whatever it takes to get those numbers in line with the current recommendations of the American Heart Association –eat a low fat diet, exercise, and take the right drugs.

Inconvenient facts

Inconvenient facts have always dogged the theory. Cholesterol levels plummet in seizure patients treated with high fat, no carbohydrate diets. Heart attacks occur despite normal cholesterol levels. Low fat diets raise cholesterol levels -President Eisenhower was one of the most famous examples. And buried in the literature of the last half century are many clues pointing a blaming finger away from cholesterol and toward the complex lipoproteins that ferry it around the body. As more and more questions are raised about the efficacy and dangers of drugs that reduce cholesterol, more attention may turn to these lipoproteins. After all, like cholesterol, they have been part of the statistic most closely associated with heart disease – the LDL (low-density lipoprotein) cholesterol.

What are lipoproteins?

Total cholesterol measures cholesterol attached to lipoproteins. Lipoproteins are combinations of phospholipids (fats that dissolve in water) and specialized proteins that fit like keys into receptors on cells. Lipoproteins function like cargo ships, carrying fats to cells for fuel, to fat tissue for storage, and back to the liver for reprocessing when demanded. More or less cholesterol crowds aboard each boat depending on the number of boats available. The size of the fleet, in turn, depends on the amount of triglycerides (another type of fat), awaiting shipment – not on the amount of cholesterol.

Triglycerides rule

Triglycerides and cholesterol are very different fats. Triglycerides provide the fatty acids that fuel most cells and are stored in fat tissue for later energy demands. Cholesterol yields no energy at all. It is a building block, used in the construction of all cell membranes and in the making of hormones and bile. Not all cholesterol comes from fat in the diet. The brain makes its own, and the liver and skin make whatever the body needs – raising production whenever dietary intake is low. Cholesterol and triglycerides attached to lipoproteins are like citizens of two different countries travelling together on one of the country’s boats. That country that builds the boats belongs to the triglycerides. The more triglycerides present in the body, the more lipoproteins in the fleet.

The varying density of lipoproteins

Lipoproteins fully loaded with cholesterol and triglycerides are fluffy and buoyant (fat floats) and called very low density lipoproteins, VLDL for short. They dock at cells in need of fuel or cholesterol, unload some cargo, lose some buoyancy, and become a little denser. Eventually they become low-density lipoproteins (LDL) and , with no energy or building material left to give up, they return to the liver for recycling. Another particle type called high-density lipoprotein (HDL) is even less buoyant – and less well understood. In contrast to cholesterol bound to LDL and VLDL, the cholesterol carried by HDL particles, like the cholesterol carried away from the intestines by chylomicrons (very large lipoproteins) does not contribute to the storage of fat in any tissues so is not associated with plaque formation in arteries. Normal to high levels of HDL cholesterol are associated with lower risk of heart disease.

What do the anti-cholesterol drugs do?

The widely prescribed statin drugs block the body’s ability to make cholesterol, which makes less cholesterol available to be loaded on to the lipoprotein boats. But boat making proceeds apace because it is driven by the amount of triglyceride awaiting transport- and the triglycerides, remember, come from dietary carbohydrates. Lowering cholesterol manufacture does not lower lipoprotein production – the lipoprotein boats will simply carry less cholesterol per lipoprotein particle, making each particle smaller and denser. Will this magically keep cholesterol out of artery walls? Not a good bet. Lipoprotein research labs have identified seven different particle types within the LDL fraction of total cholesterol. Heart risk appears to be correlated with the smallest and densest sub-fraction – the kind carrying the least amount of fat per molecule. (The anti-cholesterol drugs do have an independent anti-inflammatory effect which may be the way they diminish risk of a cardiac event in people with heart disease.)

Take-away message

So how does this complicated information change your life? Triglycerides, the stimulus for VLDL and LDL production, are a product of carbohydrate processing – especially of sugars and refined grains. Lowering VLDL production and hence LDL production requires lowering dietary carbohydrates – not fat, not cholesterol. Blood cholesterol isn’t even a good marker for total body cholesterol, which includes cholesterol squirreled away in artery walls. Cholesterol in arteries behaves much like cholesterol stored in fat tissue. It is responsive to the entire array of interconnected feedback loops involving not only fats, but carbohydrates and insulin and all the other hormones. It is time to respect its complexity and quit expecting that coaxing the body to make less cholesterol by taking drugs to block its production, or by eliminating it from the diet will end the scourge of heart disease.

Posted by medical plaintalk

Physician turned medical writer.

Partners: Fiber and Bile

Everyone knows you need fiber in your diet. Everyone knows fiber comes from plant foods. And everyone knows that fiber helps move food through the system – just like a lot fiber in grass and hay help move a horse’s food through its unusually long and tortuous bowel. Fiber in the human diet helps package waste in softer, bulkier bowel movements, and a high fiber diet reduces constipation, which in turn reduces the risk of hemorrhoids, diverticulitis and even colon cancer.

More than a laxative

What is not obvious is just how a diet high in fiber lowers cholesterol levels and improves the other cardiovascular risk factors associated with the metabolic syndrome (obesity, high blood pressure and diabetes). How can the indigestible component of food, which releases no energy and is not absorbed into the body, affect metabolism? And how does moving food through the body with greater ease and efficiency alter body chemistry? The answers are interesting and worth knowing, since they provide impetus for even the unconstipated to pay attention to fiber intake.

What is fiber?

By definition, fiber is the indigestible component of food. Both cooking and chewing break fiber-rich food down in size, but fiber is impervious to stomach acid and digestive enzymes. The stiff portions of the plants – the parts that that give them shape and cover– are carbohydrates called cellulose and lignins. Since this type of fiber doesn’t even dissolve in water, it is called “insoluble fiber.” Insoluble fiber is what most people think of when they read about the virtues of a high fiber diet. It is like the horse’s hay and grass.

The softer plant parts provide a different kind of fiber which does dissolve in water and is therefore “soluble.” Soluble fiber is made up of carbohydrates called pectins, mucilages and gums. Because it attracts water, soluble fiber helps ease the passage of food by making it softer and bulkier. So far, then, this kind of fiber seems like nothing more than a softer version of insoluble fiber. But along with water, soluble fiber attracts bile, making soluble fiber much more than a passive factor in the transit of food. The bile connection is the key component in the role of dietary fiber in cholesterol metabolism.

What is Bile?

Bile is a solution of chemical compounds called bile salts that act like detergents in breaking down fat and making it ready for absorption from the intestine. Using cholesterol as the main building block, the liver makes about 4 cups of bile a day, storing it in the gall bladder until food arrives in the stomach. The gall bladder then squirts bile into the small intestine. Without bile we could not absorb necessary fats and fat-soluble vitamins. The liver also uses bile as a shipment device for the fat soluble debris and toxins it filters from the bloodstream, especially the breakdown products of hemoglobin. Bile is the trash hauling contractor for the liver.

Elimination or recycling?

Bile breaks down once it has completed its digestive work. Its pieces get absorbed in the last part of the small intestine and carried back to the liver via the blood – or it escapes the body via the waste in the colon (bile imparts the color to bowel movements). Like the oil in your car, which accumulates dirt and get sluggish, bile that is re-circulated concentrates more and more fat-soluble waste. Escaping bile takes the waste along with it. And the less bile returned to the liver for recycling, the more cholesterol the liver has to use in the bile manufacturing process – making less cholesterol available for clogging up arteries.

In the small intestine, soluble fiber also sops up other carbohydrates, slowing their digestion and the absorption of sugar into the blood stream. This function appears to improve insulin sensitivity, making soluble fiber beneficial to people who have type 2 diabetes. Slowing carbohydrate absorption indirectly improves fat metabolism as well.

Soluble fiber and the colonic environment

Once soluble fiber reaches the colon, it begins another phase of its work. The colon, unlike the sterile small intestine, contains numerous bacteria. Bacteria need to eat, and they take whatever they can from the food passing through. Soluble fiber, for bacteria, is eminently digestible. They chew it up and produce short-chain fatty acids, creating an environment favorable for the absorption of minerals like calcium and iron. Some researchers think the acid environment helps slow cancer development.

Getting enough fiber

Is it hard to get enough fiber in your diet? Yes. Not because it is not available, but because we opt for easy food – easy to get, easy to prepare, and easy to eat. On average adult Americans get about half the 25-35 grams of fiber a day that they need, and children only about 20%. Constipation is a cardinal sign of a fiber poor diet. Bowel movements that are hard and dry, with frequency of less than once every three days, and the regular need to strain to evacuate the bowels are all signs of constipation. Constipation is also made worse by inactivity. Other results of a fiber deficient diet are less visible and occur over the long term: development of outpouchings of the colon wall called diverticuli, inflammatory changes in the colon lining, cancerous changes in colon cells, and the possible contributions to the metabolic syndrome and heart disease.

The best sources of insoluble fiber are the plant foods with tough structures: vegetables and whole grains. Soluble fiber comes in the form of oat bran, fruits, nuts, beans, and peas. The most useful fiber shopping rules are to stay as far as possible from manufactured foods and to choose liberally from the fresh produce section of the grocery store. Fiber supplements? Studies of their metabolic effects are contradictory, but supplements such as psyllium, guar gum and pectin appear to do no harm. If they produce satisfactory results in terms of easing bowel symptoms, they are probably helpful.

Posted by medical plaintalk

Physician turned medical writer.

When Diets Fail: Bariatric Surgery

“A Roux-en-Y gastric bypass is the strangest operation I have ever participated in… (It) removes no disease, repairs no defect or injury. It is an operation that is intended to control a person’s will and to manipulate a person’s innards so that he will not overeat again.” Dr. Atwul Gawande, Complications, 2002.

Human evolution occurred in a world of varying food supply. The body’s ability to store some fat insured survival when food was scarce. For most of us now there are no lean times when a few extra pounds disappear, so getting rid of them means voluntarily diminishing food intake to amounts less than we require for normal activity. This is easy if we haven’t strayed more than 10-20lb over normal weight. Above this level, gains and losses tend to become cyclical – weight that comes off reappears easily, and tends to increase with each round of dieting. When obesity becomes “morbid” – in the neighborhood of about 100 excess pounds – weight loss by conventional means is all but impossible.

A surgical way to restrict calories

So far, bariatric (from Greek words bari:heavy weight, iatr: physician, ic: pertaining to) surgery has provided the only long-term solution to morbid obesity, by restricting the amount of food entering the stomach and by altering the route the food takes through the small intestine. Patients who undergo bariatric surgery often see immediate results. Pounds finally melt away and, surprisingly, so do many previous food compulsions. Many patients maintain losses of 60-65% of their excess weight for many years. Most interesting is a profound effect on diabetes that appears before any significant weight disappears. This rapid reversal of impaired glucose control that the surgery triggers has opened a whole new frontier of research. But weight loss surgery is a drastic measure, and no one knows the results of living 30 to 50 years with this type of intestinal re-routing.

Early attempts

Beginning in the 1950s, pioneers in bariatric surgery, doctors and patients alike, learned from early negative experiences. The first approach, stapling the stomach to reduce its size, made patients lose weight, but long term results were poor. Tiny stomach pouches stretched, staple lines broke down and patients were able to eat their way back to obesity. The next approach blocked absorption of food by rerouting its path from the stomach to distant portion of the small intestine, bypassing the upper small intestine where much nutrient absorption normally occurs. Early procedures bypassed too much small intestine and caused malnutrition, foul smelling diarrhea and a very unpleasant set of symptoms called the dumping syndrome (cramps, nausea, faintness and diarrhea). Refinements of technique resulted in fewer symptoms, though patients require supplementary vitamins and minerals, and some dumping symptoms still occur.

Modern Procedures

Today, gastric “banding” with an adjustable silicone noose placed around the upper stomach and a procedure called vertical gastric banding are the least invasive and most reversible of the commonly done bariatric procedures. They are also the least effective in terms of amount, speed and persistence of weight loss. The best operation for treating obesity is the Roux-en -Y procedure, the type of surgery most commonly meant when the term gastric bypass is used.

Understanding the Roux-en-Y

Under normal circumstances, food travels from the mouth, through the esophagus and into the stomach, which is about the size of two fists. There, it sloshes around for about 20 minutes before passing through a valve to the first part of the small intestine (the duodenum), where it mixes with bile and pancreatic enzymes. After Roux-en-Y surgery, incoming food finds only a tiny pouch of stomach, 5% of its original size, opening directly into the second part of the intestine (the jejunum). Surgical rerouting has separated 95% of the stomach and the the entire length of the duodenum from the food stream and plugged the end of the duodenum back into the system farther down the jejunum. The small amount of food tolerated by the tiny stomach bypasses several feet of small intestine before it meets up with bile and digestive enzymes.

After Surgery

Under the best circumstances, weight loss following Roux en Y surgery is prompt and long-lasting. Initially patients can eat only an ounce or 2 at a time. They must schedule meals and plan content carefully in order to meet their protein and fluid needs and to avoid constipation. Over time they can begin to eat a little more at one sitting. Most patients lose 35-40% of their bodyweight over 12-15 months, and maintain that for at least 15 years. Diabetes is cured in over 80-95% of patients. Hypertension, sleep apnea, acid reflux, arthritis, infertility, stress incontinence, fatty liver, and leg infections also disappear or are significantly improved.

Candidates for Surgery
Given all of these positive results, why not offer this type of surgery to less than morbidly obese patients who struggle to lose weight? Currently weight loss surgery is limited to patients with BMIs (Body Mass Index) of 40, or 35 if the patient already suffers from obesity related diseases like hypertension or diabetes. BMI is a calculation of weight divided by height squared, with measurements expressed in kilograms and meters. A BMI of 30 qualifies a patient as obese; 19-24.9 corresponds to appropriate weight. Statistical analysis of risks and benefits of bariatric surgery set the acceptable range for surgery. Surgical candidates must also undergo extensive medical tests and psychiatric analysis, and have made serious attempts to lose weight. They must understand that gastric bypass is drastic and usually permanent, that complications can be bad, and that success is not guaranteed. Some patients manage to regain all their weight and then some.

Oversight

Bariatric surgery is regulated by American Society of Metabolic and Bariatric Surgery, which sets professional standards for hospitals and surgeons, establishes centers of excellence, and promotes research and data collection about the procedures. In 2007, surgeons performed over 200,000 surgeries for obesity, up from around 16,000 in 1992. Advances in laparoscopic surgery have made recovery faster and less uncomfortable. The best surgical mortality rates are 1% and peri-operative complication rates 10% – acceptable numbers given the worse risks of morbid obesity.

Complications and Long Term Results

Possible complications of bariatric surgery include blood clots travelling to the lungs, heart attack, respiratory compromise, suture line leaks, hernias, ulcers, GI bleeding, bowel obstruction, and gallstones. Calcium iron and some vitamins are not well absorbed and they require life-long monitoring and supplementation. All bariatric surgeons emphasize that long term success depends on patient cooperation with major eating and lifestyle changes forever. This is especially important when the choice of procedure involves only change in stomach size, as is the case with the gastric banding procedures.

Clues about metabolism and diabetes

Sheer calorie restriction accounts for some of the success of all types of bariatric surgery. When the surgery also bypasses a segment of small intestine, more is at work than meets the eye. The rapid disappearance of diabetes before significant weight loss occurs and the remarkable loss of previous cravings are clues to unappreciated biochemical and hormonal complexity of the intestines. The surgical assault on obesity appears to have much to teach us about energy metabolism and diabetes. One day, hopefully, such strange surgery will be unnecessary.

Resources:
American Society of Metabolic and Bariatric Surgery (http://www.asmbs.org/): Access to readable, professional information regarding bariatric surgery.
http://www.obesityhelp.com/: Support group website for patients contemplating surgery or looking for related information

Posted by medical plaintalk

Physician turned medical writer.

The Obesity Epidemic: Blame it on Science Too

When I was a child I thought my grandfather and Jackie Gleason were two of the fattest men in the world. Last year I happened on a rerun of The Honeymooners and was taken aback by Mr. Gleason’s modest girth. And an old movie of my grandfather shows, at most, a size 40 waist – practically svelte these days. What’s happened to us? We’ve become accustomed to widespread obesity in men, women and children. Is this one of the prices we pay for our market-driven, entertainment-loving culture? Look at all the factors conspiring to load the scales: escalating inactivity, a vast snack and soft drink industry, supersizing, frenetic lives, fast food restaurants, the demise of the family-centered, home-cooked meal and its replacement with eating anywhere and everywhere, all the time. There is blame aplenty to go around, but this is a medical column, so we’ll stick to the role of science. Why pick on the medical science? Because we need to know how the expert advice we rely on plays out over time and if well-intentioned advances lead us astray.
Taking fat out of the diet
In the 1950s, medical researchers took on the epidemic of heart disease that had begun around 1900. Fatty streaks in the aortas of young soldiers dead in the Korean War made pathologists think that heart disease actually began early in life. They created an animal model for study, feeding rabbits cholesterol dissolved in vegetable oil instead of lettuce and carrots. When fat showed up in the rabbit arteries, the dietary theory of heart disease came to life. Some scientists quibbled, claiming that the problem was more complex, that other dietary factors like sugar might be equally to blame, but they lost the debate. Dietary cholesterol became the enemy, and over the next half-century the public learned to view the egg as a toxic substance, despite its near perfect protein and yolk full of valuable vitamins.

Along came the observation that Mediterranean populations had little heart disease compared to Americans. They also walked more, ate regular meals in family settings, didn’t snack, doused all but breakfast in olive oil, and scoffed at tasteless, pre-packaged food. But what we saw was lots of pasta, with not an ounce of cholesterol in it. Pasta was the ideal candidate to replace fat. We embraced the carbohydrate age, and turned a blind eye to the fact that, for years, we had managed to turn cattle fat by feeding them carbohydrates.

The national waistline ballooned, but can we at least say that the dietary agenda paid off in terms of heart disease? The answer is murky, because there were other, simultaneous prongs of attack: a fruitful campaign against tobacco use; drug treatment of high blood pressure; drugs that keep the body from absorbing or making cholesterol and drugs that calm the heart. Galloping technological advances allowed doctors to ream out plugged coronary arteries, prop them open with metal struts, or bypass them altogether. Nevertheless, cardiovascular disease remains our leading cause of death and the total number of patients with the disease has increased. Only the death rate from heart attacks has fallen and that statistic is attributable to the interventions and drugs and declines in smoking. The effect of the officially sanctioned diet on the epidemiology of heart disease, if any, is hard to discern. Now we face even more cardiovascular disease as epidemic abdominal obesity brings with it more diabetes, high blood pressure, and inhibition of physical activity.

A contribution from chemistry: artificial sweeteners

Science contributes to the obesity epidemic in other, more subtle ways. Through chemistry, we possess the magic of intense sweetness without a caloric price. An enormous rise in artificial sweetener use parallels the obesity epidemic. Well, is that a surprise? Everyone’s trying to lose weight. But what if, in addition to failing to stem the tide of weight gain, non-nutritive sweeteners are contributing to it? A few studies raise this unsettling possibility, and no study shows any significant effect of these chemicals on the process of weight loss, unless they are used in conjunction with a disciplined program of eating and exercise.

How could something with no caloric value contribute to obesity? Perhaps by raising levels of insulin, hormone which promotes fat storage. At least one artificial sugar (Xylitol) stimulates enough insulin release in dogs (who ate the stuff accidentally) to cause profound hypoglycemia and death. Do “non-nutritive” sweeteners cause release of insulin in people as well? This hasn’t been studied well. Artificial sweeteners were developed for Type I diabetics, who lack insulin altogether, so there wasn’t any point in measuring the hormone. But there is an insulin burst from the pancreas within thirty seconds of sweetness arriving in the mouth (the cephalic insulin response), and most people who use non-nutritive sweeteners do make insulin, which efficiently converts any extra calories in the meal accompanying the drink to fat. Some studies do suggest that insulin levels are higher in regular artificial sweetener users than non-users.

Tipping the scales while fixing the mood?

Chemistry also gives us the drugs that make people happy – or at least less unhappy. Over the last 30 years, antidepressant use for life’s inevitable miseries has skyrocketed. We are engaged in the very new practice of using these drugs in children. One side effect, perhaps more common than advertised, is difficulty withdrawing from the drugs. Another is weight gain. Some depression requires drugs, and antidepressants or antipsychotic agents don’t always cause weight gain. But the drugs are in such widespread use that you probably know someone who has packed on 20 pounds in the course of a divorce or other life stress that prompted antidepressant use and someone else who accepts the weight gains because they can’t stop the drugs.

Will science solve the obesity epidemic?

Should we look to medical science or to the mega-million dollar diet industry to reverse our big obesity problem? To the development of new surgical procedures, more appetite suppressing drugs, sterner diet and exercise prescriptions, or new versions of deprivation diets (which rarely lead to permanent weight loss)? I think not. And who knows what unexpected consequences might come along for the ride. For a significant statistical improvement in the obesity problem, the answers will have to come from all of us and from our choices about how we act and what we value – from the culture, not from science. For too long we have treated food as an enemy, taking the joy and taste out of eating, without much to show for our efforts. Heart disease is still the number one killer, obesity is epidemic, and diabetes is hot on its heels. Extra weight comes off for good in the same slow, sneaky way it crept on – a few hundred calories a day out of balance with caloric needs. That’s just one dessert, or a beverage or two. Or a brisk walk instead of an hour of television. Every day we make the choices that determine our energy balance – elevator or stairs? TV or a walk? Coke or water? Vote for the guy who wants to put PE back in school or the one who doesn’t care? Yes, extra weight takes a very long time to lose, but next year will come around before you know it, no matter what you do. The choices will have added up, one way or the other. Every choice counts. In an epidemic, every person counts.

Posted by medical plaintalk

Physician turned medical writer.

Common Sense Eating

My acerbic Irish grandmother would take a look at our modern obsessions with nutrition, light up a Camel, and ask what good comes of all the worrying. She’d have a point. After fifty years of expert advice on diet, what do we have? The fattest society on earth, an epidemic of diabetes, and the first generation that will not meet, let alone exceed, the life expectancy of their parents.

We live in bodies exquisitely suited to life forty-thousand years ago. The sweetest things on the planet were some sparse berries. The only drink was water. No one fattened up wild game with corn. Getting food required considerable expenditure of energy, and who would waste energy chasing more food than they needed? But just in case extra food came along, the body was equipped with a highly efficient means of squirreling away the excess as fat, to cover inevitable times of short supply. Lights went out when the sun went down, and everyone rested up for the next day’s pursuit of food.

These old-fashioned bodies are now awash in too much food that is too easy to obtain, and in manufactured food full of unnatural, but edible chemicals. We are also awash in advice, calorie counts, carbohydrate grams and recommended daily allowances. Looking at the results, our grandparents might guess that the average man is more in need of common sense than tables, charts, diets and recommended daily allowances. So here are some common sense suggestions about how to navigate the modern world of food.

Shop the perimeter of the grocery store

Everything your body needs is out there. Don’t skip any of the departments, spend the most time and money on fruits and vegetables, go for color, avoid sugar, and remember that there are vitamin and micronutrients in dairy products, meats and fish that are scarce elsewhere. Egg whites are one of nature’s best proteins. The closer food is to its actual source, and the less the processing, the better its nutritional value.

In the middle aisles, stick to a list

There is nothing in this part of the store that you need for survival, but there are cooking essentials like olive oil and spices, convenient staples like canned tuna and tomatoes, and whole-grain, high fiber cereals. Look for packages with the fewest ingredients. Remember – “natural flavors” often come from manufacturing plants on the New Jersey turnpike, soy protein is a very unnatural derivative of the manufacture of soybean oil, vegetable oils that go rancid are not good for you, and oils derived by cold pressing are closer to their original sources than those that are refined like petroleum.

Opt for fresh food over manufactured food whenever possible

The addition of high fructose corn syrup and preservatives to almost every packaged food gives us cheap, long-lasting and attractive products, but think of these foods as emergency rations. If you built your home with poor materials and filled your car with unsuitable fuel, they might hold up for awhile, but over time they would suffer premature failure. Fresh and frozen foods that haven’t strayed too far from their original sources are the materials and fuel your body is built to handle.

Think regular meals with smaller amounts and balanced composition

We are designed to need a balanced mixture of food every 4-6 hours (while awake). Your hand is a rough guide to amount and mix of food for each meal. You need protein, carbohydrate and fat and you don’t need to read labels to know if you are getting them all. Protein comes from living things that were able to move around on their own, and necessary fat comes along with protein. Beans are the only exception and their protein comes by virtue of bacteria which transport nitrogen into the roots of bean plants and which do move around. Carbohydrates come from stationary living things. The carbohydrate portion of a meal should cover the palm of the hand. The protein component fits in the area from the base of the thumb to the big central crease. The fat that you need comes along with your protein source, in the olive or coconut oil needed for cooking, and in any milk you drink.For perspective on old fashioned eating, consider a sample meal in a California museum that is a replica of a hotel of the Gold Rush era. Dinner consists of a hard roll, an apple, and a few clams and some leafy greens floating in a thin broth – fuel enough for the people who did the hard labor of building this country.

Make the time to prepare food and eat in a nice setting, with good conversation

Get back to the way your body is designed to eat, the way people have eaten for thousands of years, and you’ll save time by being healthier and more energetic and not having to read diet articles. And lighten up – a small amount of ice cream or pie or chocolate now and then is fine. Amount is the key.

Choose water

If you are thirsty, you need water. If you want liquid to help wash down food, pick water. If you want water to taste like something else, choose a liquid that lacks high fructose corn syrup and has some nutritional value: fresh, pulpy juices with their vitamins and fiber, or milk, with its protein, minerals and vitamins. Coffee and tea? Fine. No one has ever been able to pin much bad on either one, in moderation. Ditto for wine, in even more moderation.

Avoid fake food

Artificial sweeteners – a real boon for diabetics – are unnecessary chemicals for everyone else. There is no evidence that artificial sweeteners promote weight loss. They may even lead to weight gain. Not worth it for the mere 12 calories in a teaspoon of sugar. And margarine? Even ants won’t eat that (but they do like butter).

We are where we are after over half a century of harping on fat and cholesterol. Common sense tells us they can’t be the only problems. Common sense is what we need – along with a diet, sleep and physical activity suitable for life 40,000 years ago.

Posted by medical plaintalk

Physician turned medical writer.

Gout and Girth: A Sweet Relationship?

At Hampton Court, one of King Henry VIII’s sixteenth century palaces outside London, tour guides regale visitors with tales of Henry’s obesity and the miseries he suffered during flare-ups of gout – exquisitely painful episodes of arthritis that come from the buildup of uric acid crystals in joints. Gout was known as “the king’s disease,” because it afflicted wealthy people who could afford the meats and sea foods that trigger uric acid crystal formation. The guides also point out the “confectionary,” a corner room near the kitchen wing, and describe the sugar-rotted royal teeth produced by the then scarce sweetener. The guides do not link Henry’s gout to the royal sweets, but perhaps they should. Sugar is composed of equal parts glucose and fructose, and scientists are now beginning to link increased fructose intake not only to obesity and type II diabetes, but also to increased uric acid in the blood – a risk factor for gout.

What is uric acid

Some uric acid in the blood is normal, because every cell in the body makes uric acid out of purines, chemical compounds that come from the regular breakdown of DNA and RNA as cells recycle themselves. Purines also come from many foods, but are particularly concentrated in red meat, organ meats like liver, many fish and shellfish, and yeasty beverages like beer and red wine. Uric acid in the blood is not bad – it serves as a powerful antioxidant. However, in some genetically susceptible people, uric acid levels become too high because they make too much, or because their kidneys don’t excrete enough into the urine.

When uric acid crystallizes

Abnormally high uric acid levels in the blood, a condition called hyperuricemia, can be present for 10-20 years without any symptoms. But just as minerals crystallize out of water in caves and form stalagmites and stalactites, uric acid can crystallize out of fluids in the body, forming microscopic deposits in tissues, especially kidneys, joints, tendon sheaths and skin. The painful part comes with the inflammation that ensues when the body attempts to eliminate the crystals. The classic case of gout, also known as podagra, begins suddenly with exquisitely painful, bright red swelling in the joint space between the foot and the big toe. Symptoms last from days to weeks.

The swelling comes from inflammatory fluid in the joint space. Diagnosis of gout depends on withdrawing some of this fluid through a needle and examining it under a microscope, where the uric acid crystals show up as pointy spicules which bend light waves in an identifiable way. Fluid withdrawal can also relieve some of the pain, but the mainstays of treatment during acute attacks are anti-inflammatory drugs such as Indocin, ice and or heat, and plenty of water. Prevention of attacks depends on efforts to lower uric acid levels, by diet, weight loss and use of medications that block uric acid production or increase its elimination in the urine.

Fructose is a building block for uric acid

For centuries, dietary advice about gout has revolved around foods high in protein. But as numbers of gout cases climbed steadily over the last forty years and average uric acid levels in people without gout also increased, a correlation with increased sugar consumption began to emerge. Scientists are now studying the relationship of sugar intake to uric acid and gout and also attempting to tie uric acid to hypertension, obesity and heart disease.

Sugar consumption was once rare to non-existent. Table sugar, a mixture of the two simple sugars sucrose and fructose, came only from sugar cane, which originally grew only tropical regions. Sugar’s spread around the world followed trade routes, and accelerated markedly after the discovery of the beet as a sugar source in the 18^th C. But the most dramatic rise in sugar consumption followed the invention of high fructose corn syrup (HFCS) in the 1970s. From work done so far, it appears that sugar’s fructose is a bigger culprit than its glucose in aggravating the metabolic syndrome (obesity, high blood pressure, heart disease and diabetes). And the metabolism of fructose actually produces uric acid.

When the glucose/fructose mix of sugar enters the body, glucose is transported directly into cells for use, but fructose requires processing. This requires energy, provided by ATP (adenosine triphosphate), and ATP breakdown produces uric acid. Eating fructose regularly also makes fructose easier to metabolize because it “induces,” or makes the body produce specific enzymes required to break it down. For someone prone to overproducing uric acid, or someone whose kidneys excrete it inefficiently, a diet chronically high in fructose may not only provide the building blocks for uric acid, but also speed its production.

Cutting fructose may help – and will do no harm

Cutting purine-rich foods down in a diet helps many susceptible people remain gout free. There is no data yet on the effectiveness of limiting fructose intake on gout or hyperuricemia, but such a diet can do no harm. Limiting fructose sources to whole fruits would dramatically lower total fructose intake for most people. Fructose is the major sugar in fruits, but it is combined with fiber and vital nutrients and present in much lesser quantities than in sugar-sweetened beverages, soft drinks, baked goods and many processed foods. Even ketchup contains HFCS.

When dietary modification is not enough to keep people gout free, drugs that block uric acid production or increase its elimination help. Ideally, uric acid levels should be in the range of 3-6 mg/dl. Diet is important not only for those who have suffered acute gout attacks, but also for those who have high uric acid levels without any symptoms. Hyperuricemia warrants a good look at the amount of dietary fructose.

Henry VIII’s confectionary was a clue to the relationship of girth to gout. As uric acid research progresses, blood tests for uric acid will probably become routine, because high levels often precede the development of high blood pressure and Type II diabetes, even in people not susceptible to gout.

Other Gout Facts

Many diuretics in common use raise uric acid levels and can trigger gout, especially the thiazide group.

Gout attacks commonly follow trauma or surgery because tissue breakdown produces purines.

Cancer treatments may also raise uric acid levels as tumor cells break down.

Uric acid levels increase in women after menopause and women rarely suffer from gout before then.

Uric acid levels in men rise at the time of puberty.

Posted by medical plaintalk

Physician turned medical writer.

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