“All substances are poisons: it is the dose that determines whether they act as a poison or a remedy”
We live in a toxic world, and most people would agree we have no one to blame but ourselves. After all, as far back as 1981 more than 100,000 industrial chemicals were already registered with the European Inventory of Existing Commercial Chemical Substances. (1) And, with industry busily churning out 150 to 200 new chemicals every year – usually after conducting only the most rudimentary pre-market toxicity testing – it’s easy to understand why our planet is awash in potentially harmful substances.
However, while humankind has done more than all other species combined to defile the only habitable orb within spitting distance, it must be acknowledged that Earth has always been a challenging place to live. Long before Homo sapiens was so much as a cipher on the celestial drawing board, single-celled organisms drifting about in Earth’s primordial environs were contending with deadly gases, noxious chemicals, and hazardous radiation. These simple organisms couldn’t flee from such threats or modify their surroundings to ameliorate them, so they had to develop the metabolic machinery to deal with them.
Take ultraviolet light, for instance. Early in Earth’s history, when the atmosphere was still relatively thin, UV light represented a major deterrent to a cell’s survival and successful reproduction. Some experts believe that microorganisms living in the upper layers of Earth’s ancient seas, where UV light was most intense, used cholecalciferol (vitamin D3) to shield their delicate DNA from the pernicious effects of the sun’s rays. In an elegant example of evolutionary adaptation, early microbes acquired the means to exploit the very entity that could injure their chromosomes – UVB light – to synthesize cholecalciferol. Later, with the arrival of multicellular organisms, vitamin D3 became important in intra- and intercellular signaling. Still later, vitamin D3 assumed additional roles in calcium metabolism, skeletal maintenance and immunity. (2) The metabolic pathway used to manufacture cholecalciferol has persisted through billions of years of evolution.
Oxidation, an inevitable consequence of living in Earth’s atmosphere, is another force that can wreak havoc on a cell’s chromosomes, as well as it enzymes, structural proteins, and other vital components. Unfettered oxidation causes derangements in most biological processes and ultimately leads to cellular death. Paradoxically, oxidation is also the process cells employ for catabolizing carbohydrates, fats, and amino acids to produce adenosine triphosphate (ATP), which is the principal source of energy required by all living cells. Furthermore, oxidation is a necessary step in the neutralization of many toxic substances, as well as the synthesis or activation of a variety of useful ones. Hence, in order to survive a cell must be able to capitalize on the oxidative processes that are beneficial while simultaneously harnessing those that are inherently harmful. As is the case with cholecalciferol synthesis, the metabolic machinery needed to channel the power of oxidation has survived for eons and is strikingly similar in all living organisms. According to the ruminations of the evolutionary biologists, about 3.5 billion years ago an assortment of molecules called cytochromes first appeared in primitive life forms, most likely in prokaryotic bacteria. (3) Cytochromes are a diverse group of proteins that share a common central feature: an iron-containing heme group that allows them to transfer electrons from one molecule to another. Since electron transfer is crucial to the process of oxidation (as well as its inverse operation, reduction), cytochromes have been recruited to perform a multitude of metabolic tasks through the ages. The fundamental importance of cytochromes is reflected in their persistence through millennia of evolution and their presence in all species lines. Cytochrome c, the key to oxidative phosphorylation and ATP production in all aerobic cells, is found in the most primitive as well as the most advanced organisms. Likewise, the cytochrome P450 system (CYP450) is a family of metabolic enzymes found throughout the biosphere; CYP450 enzymes drive the oxidation and hydroxylation reactions that can either detoxify harmful substances or initiate the synthesis of compounds that are critical to life.
Most cells in the human body are endowed with a full contingent of cytochromes, in addition to the genes needed to regenerate these indispensable enzymes. (Red blood cells, which shed their nuclei and organelles during maturation, are the exception; the few cytochrome-like molecules found in red blood cells cannot be renewed and must last for the lifetime of the cell.) Cytochromes are usually closely associated with cellular membranes, which provide an architectural framework that allows a given group of cytochromes to function more efficiently. Cytochrome c – the cytochrome involved in energy production – is primarily located along the inner membranes of mitochondria. (Mitochondria are intracellular organelles where the lion’s share of a cell’s energy is produced.) The CYP450 enzymes, which participate in the metabolism of the astonishing array of substances that enter our bodies each day, are typically linked to a cell’s endoplasmic reticulum, Golgi apparatus and similar structures. Liver cells, which are subjected to higher toxic exposures than other cells, are particularly rich in CYP450 enzymes.
Nearly every foreign substance – whatever we eat, drink, inhale, or absorb through our skin – is a potential substrate for the CYP450 system. Without this protective array of enzymes, our cells would quickly succumb to the direct and indirect effects of the myriad chemicals we encounter as we proceed through life. Indeed, the mere act of consuming a meal (even one composed entirely of organic foods) would overwhelm our cells with an unmanageable burden of toxins. The beauty of the CYP450 system rests in its ability to detoxify such a wide variety of compounds, including many that are novel to our environment (i.e., industrial chemicals, drugs, etc.). Unfortunately, cytochromes cannot protect us from every potential threat. Many natural and manmade toxins are not effectively neutralized by cytochromes, and some compounds – certain drugs and insecticides, for example – can actually become more poisonous when they are metabolized by cytochromes. Still other toxins exert their deleterious effects by altering the activity of one or more cytochromes: cyanide kills by interfering with cytochrome c’s electron-transferring capability, thereby halting oxidative phosphorylation and terminating all cellular energy production.
Although living organisms (including people) have a surprising capacity for detoxifying whatever we throw at them, that capacity cannot be infinite. The mechanisms cells rely on to protect themselves (and us) from toxic influences evolved in more pristine circumstances. While there is obviously some room for accommodation within these systems, we may be reaching the limits of their ability to adapt. We are unquestionably witnessing some of the effects of our inveterate irresponsibility: scientists point to manmade toxins as an underlying cause for extinctions of non-human species and for increasingly prevalent health problems among human populations. It isn’t clear how long we can continue on our current course until we overtax our already burdened planet. Despite the strident claims of those who advocate for a larger human presence in the only home we’ll ever know, it would be prudent to preserve and protect what we have.
1. Chemicals in the European Environment: Low Doses, High Stakes? The EEA and UNEP Annual Message 2 on the State of Europe’s Environment (October 1998)
2. Carlberg C. Genome-wide (over)view on the actions of vitamin D. Front Physiol. 2014;5:167
3. Deng J, Carbone I, Dean RA. The evolutionary history of cytochrome P450 genes in four filamentous Ascomycetes. BMC Evol Biol. 2007 Feb 26;7:30
“Pedal edema” is a term physicians use to describe swelling caused by the accumulation of fluid in one or both feet. While it is generally acknowledged that excess salt consumption can lead to fluid retention (which in turn may trigger foot swelling) pedal edema has many potential causes, and not all of them respond to salt restriction.
Edema, which can develop in nearly any organ or body region, results from an imbalance in the opposing mechanical and chemical forces that normally keep fluids inside your blood vessels. Much like water traveling through a porous soaker hose, the liquid coursing through your arteries and veins tends to get pushed into the surrounding tissues by hydrostatic pressure within the vessels. Usually, this fluid is drawn back into your circulation by reverse osmotic pressure – a sort of “chemical sponge” – generated by the relatively higher concentration of proteins and electrolytes within the capillaries, where hydrostatic pressures are low. Fortunately, the back-and-forth exchange of fluids, nutrients, gases and electrolytes occurs at an unconscious level; it’s only when this finely tuned mechanism fails that we become aware of our own fluid dynamics.
Simply stated, if the hydrostatic pressure that pushes liquid out of your vessels exceeds the osmotic pressure that pulls it back in, the fluid starts loitering in your tissues, where it eventually becomes noticeable as swelling. In many cases, the feet are the first body parts affected by edema, because they’re located where the hydrostatic pressures are highest. (After all, water follows gravity when it is given the opportunity.)
Most women who have been through a pregnancy are familiar with pedal edema, which is nearly universal during the last trimester. The pedal edema associated with pregnancy is believed to stem from several factors: increased blood volume, compression of the veins that return blood from the legs to the heart, and hormonal changes that increase capillary permeability (leakiness). Although many doctors still tell pregnant women to cut back on salt to relieve foot swelling, elevation of the lower extremities, daily walking (which pumps blood from the legs) and compression stockings are likely to be more useful than salt restriction. Following delivery, the pedal edema associated with pregnancy typically resolves.
There are other times when pedal edema is a transient, benign condition. Individuals who take long trips or who sit for prolonged periods often discover a bit of swelling in their feet and lower legs when they finally slip their shoes and socks off at the end of the day. This edema, which results from pooling of tissue fluid in dependent body parts, usually disappears following a short walk or elevation of the legs. When you’re forced to sit for prolonged periods, periodically standing and walking – or intermittently performing some toe raises if you can’t leave your seat – will help prevent this type of edema from developing in the first place.
While the pedal edema associated with pregnancy or prolonged sitting is usually self-limiting, persistent or recurrent foot swelling warrants a visit to a healthcare provider, as it could signal a serious underlying condition. In medical disorders where pedal edema occurs, diuretics (“water pills”) are routinely prescribed. Removal of excess fluid from the circulation not only alleviates the edema; it usually improves other symptoms associated with the underlying problem, as well. And, since excess sodium in the bloodstream and tissues encourages fluid retention, patients suffering from “fluid overload” are typically advised to restrict their salt intake.
For example, congestive heart failure, which is characterized by a reduction in the heart’s ability to push blood through the body, is frequently accompanied by pedal edema. When the blood returning to a weak heart has to “wait in line” before being pumped back out to the body, it gets temporarily stored in places where the hydrostatic pressures are lowest or the blood vessels are leakiest: the feet and lungs, usually. Excess tissue fluid in these body parts causes pedal edema and – as the air sacs in the lungs fill with fluid – shortness of breath. Removal of excess fluid with diuretics not only reduces pedal edema in patients with congestive heart failure; it often improves their breathing. And, because congestive heart failure paradoxically increases
sodium retention, salt restriction is also a part of the therapeutic regimen for patients with this condition.
Other causes of bilateral pedal edema (swelling in both feet) include liver failure, kidney disease, venous insufficiency (often heralded by varicose veins) and certain medications (nonsteroidal anti-inflammatory drugs, calcium channel blockers and corticosteroids, for example). Diuretics may be indicated for these disorders, just as they are for congestive heart failure.
Unilateral pedal edema – swelling that occurs in only one foot or leg – is often caused by blockage of the venous return in the involved extremity. Venous insufficiency – typically a benign but chronic problem – can cause unilateral pedal edema that comes and goes. Sudden onset of unilateral foot or leg swelling could be caused by a blood clot in the veins of the leg. This condition, called deep vein thrombosis (DVT), can be life-threatening; immediate medical evaluation is warranted.
Diuretics are not indicated for treating venous insufficiency or DVT. Compression hose, weight control, avoidance of prolonged standing or sitting and daily walks are usually helpful for people with venous insufficiency; surgery may be indicated for severe cases. For patients with DVT, anticoagulants (“blood thinners”) are used to prevent the clot from extending up the leg or fragmenting to the lungs; hospitalization may be recommended when DVT is associated with signs or symptoms of clot fragmentation, such as shortness of breath, anxiety, rapid heartbeat or low blood pressure.
People who take prescription diuretics for pedal edema often question whether they can use herbal diuretics instead. Advocates of herbal diuretics argue – justifiably – that these preparations contain vitamins, minerals and other nutrients that aren’t found in prescription drugs. Unfortunately, herbal diuretics may not be potent enough to remove the volumes of fluid needed to successfully treat serious medical disorders, such as heart failure or end-stage liver disease. Therefore, while an herbal diuretic such as dandelion
, parsley or juniper might be useful for benign, self-limiting edema, people with medical conditions should always check with their physicians before supplanting their prescription diuretics with herbal ones. Pregnant women, too, should consult their midwife or doctor before using any herbal diuretic. While many herbal diuretics, such as dandelion or parsley, are generally considered safe when consumed as foods during pregnancy, not enough is known about these agents to ensure their safety at the higher dosages needed to increase urine flow. And some herbal diuretics, such as juniper, have been linked to miscarriages, premature labor or fetal damage.
The National Cancer Institute estimates there will be nearly 230,000 new cases of lung cancer in the United States in 2013, and approximately 160,000 Americans will die from this disease. While smoking accounts for the vast majority of lung cancers, 10 to 15 percent of all lung cancer deaths are related to factors other than smoking. According to a 2009 review in Clinical Cancer Research
, lung cancer in “never smokers” may be attributable to a variety of causes. Unfortunately, the risks imposed by most of these entities are not easily quantified, nor are there many clear-cut measures for dealing with them. Radon Is the Second Leading Cause of Lung Cancer
Second only to tobacco smoke as a cause of lung cancer, radon is responsible for approximately 20,000 deaths each year in the U.S. Radon is a colorless, tasteless, odorless gas that emanates from decaying uranium in geological formations around the world. In outdoor environments radon is present in concentrations too low to cause health problems. However, when this radioactive gas concentrates in closed spaces – basements, homes and workplaces – it can be inhaled in amounts that damage your cells’ genetic machinery and trigger tumor development.
A never smoker’s risk for radon-induced lung cancer is directly related to the level of exposure. On average, being exposed to radon increases your background risk for lung cancer by 10 to 20 percent. The only way to know if you are getting more than your share of radon is to place detectors in places where you spend a significant amount of time. High radon concentrations can be mitigated with specialized venting techniques. Secondhand Smoke Is an Important Risk Factor
Dozens of studies and multiple expert reviews have confirmed that secondhand smoke causes lung cancer, and the Environmental Protection Agency has classified secondhand smoke as a known human carcinogen. A 2004 analysis in the International Journal of Cancer
estimated that nonsmoking spouses of smokers have a 23 percent excess risk for developing lung cancer, meaning they are 23 percent more likely to get lung cancer than the nonsmoking spouses of nonsmokers. (If you are the nonsmoking spouse of a smoker and you are also exposed to radon, your excess risk jumps to 30 to 45 percent.) According to the American Lung Association, approximately 3,400 nonsmokers die from lung cancer every year solely as a result of exposure to secondhand smoke. Occupational Exposures Are In the Running
A number of agents – beryllium, coal dust, pesticides, paint fumes, asbestos, silica dust, chromium, arsenic and many others – have been implicated in lung cancers arising from occupational exposures. For people who have never smoked, research shows a consistent link between lung cancer and occupational exposure to asbestos, silica and arsenic. For other agents the data is less consistent. The specific risks due to any one agent are difficult to assess, as many people are exposed to more than one hazardous substance, both in and out of the workplace. In addition, most studies linking lung cancer to occupational exposures have included smokers, whose risk for lung cancer may be greatly magnified by exposure to certain agents.
For example, a smoker who is not exposed to asbestos is 13 times more likely to develop lung cancer than a never smoker. If a smoker is also exposed to asbestos, the risk for lung cancer jumps to at least 50 times that of a nonsmoker. As If That Wasn’t Enough…
Some studies have suggested an increased risk for lung cancer in never smokers who are exposed to high levels of air pollution. Other studies, however, do not support this association. Similarly, a link between lung cancer and diet or certain infections – human papillomavirus and HIV, for example – has not been firmly established in nonsmokers, although such associations have been found in smokers. While chronic lung diseases, such as tuberculosis, asthma and chronic obstructive pulmonary disease, have been linked to lung cancer in smokers, only asthma has been associated with increased rates of lung cancer in never smokers.
Finally, recent research suggests your genetic makeup may be the final determinant of whether you develop lung cancer in a given situation. A 2012 review in Human Molecular Genetics
demonstrated associations between several common genetic mutations and an increased risk for lung cancer. This supports what many people already know intuitively: since most smokers never develop lung cancer, genetics must be a potent force in determining an individual’s risk. Eventually, genetic testing may be used for identifying people at risk for lung cancer so they can begin screening – with low-dose chest CT, for example – at a time when diagnosis of lung cancer could make a difference in their long-term prognosis. Sources
- National Cancer Institute: Lung Cancer
- Clinical Cancer Research: Lung Cancer in Never Smokers: Clinical Epidemiology and Environmental Risk Factors
- International Journal of Cancer: Secondhand Smoke Exposure in Adulthood and Risk of Lung Cancer among Never Smokers: A Pooled Analysis of Two Large Studies
- American Lung Association: Lung Cancer Fact Sheet
- Human Molecular Genetics: Influence of Common Genetic Variation on Lung Cancer Risk: Meta-Analysis of 14,900 Cases and 29,485 Controls
Endometriosis, a gynecological disorder characterized by areas of endometrial tissue growing outside the uterus, affects up to 15 percent of reproductive-age women and at least one-third of infertile women.
The endometrium is a layer of renewable tissue that lines your uterus. During each menstrual cycle, this layer thickens in response to hormonal stimulation as it prepares for implantation of a fertilized egg. If fertilization does not occur, the endometrium is shed and the cycle begins again. Just like the endometrium within your uterine cavity, endometrial implants in other areas of the body cycle in response to monthly hormonal fluctuations. As endometrial implants thicken, bleed, and shrink again, they can trigger inflammation and pain.
Your ovaries, fallopian tubes and the cul-de-sac behind your uterus are the most common sites for endometrial implants to occur, but they can appear nearly anywhere in a woman’s body. Endometriosis can scar surrounding tissues and disrupt the function of nearby organs. Chronic pelvic, abdominal, back and thigh pain, irregular periods, pain during intercourse and infertility are common in women who have endometriosis.
The number of endometrial implants in your pelvis, abdomen or other body regions does not necessarily correlate with the severity of your symptoms. Some women with extensive endometriosis have minimal discomfort, while others with very few implants suffer from severe, intractable pain and infertility. Medical Treatment for Endometriosis
Women who are diagnosed with endometriosis may find their therapeutic options limited. Conventional treatments for this condition include drugs that suppress ovarian function and reduce endometrial growth (oral or injectable contraceptives, hormone-secreting IUDs [Mirena], Danazol, or Lupron), ablative surgery to remove individual endometrial implants and reduce scarring and, in severe or stubborn cases, hysterectomy. Pain control with nonsteroidal anti-inflammatory drugs (ibuprofen, naproxen, sulindac, nabumetone, etc.), acetaminophen (Tylenol) or narcotic painkillers is usually of mild to moderate benefit.
Recent studies suggest that endometriosis may be driven by autoimmunity in a significant percentage of women. This discovery may one day lead to new therapies aimed at modulating the immune response in a select group of patients. However, since it isn’t yet clear whether endometriosis is the cause or the effect of immune hyperactivity, and since immunomodulation carries its own burden of side effects, it may be some time before these treatments are available.
Given the paucity of effective treatment modalities – and acknowledging that the most effective treatments can temporarily or permanently impair fertility – it’s little wonder many women simply opt for the best pain medication they can find and hope for the best. Alternative Therapies for Endometriosis
Alternative and complementary remedies for endometriosis are aimed at alleviating pain, reducing the influence of hormones on endometrial implants and balancing your immune system. In general, alternative therapies are less effective than conventional medical treatment for reducing pain, and none has been shown to improve fertility. Phytoestrogens
A great deal of controversy surrounds the use and effectiveness of plant-based estrogens, particularly in women who have a history of breast, ovarian, or uterine cancer. However, some evidence indicates that phytoestrogens exert a selective effect on estrogen receptors and may even be of benefit in patients with estrogen-dependent cancers.
Phytoestrogens, which are plant-based compounds that resemble estrogen, bind to estrogen receptors in the human body. However, phytoestrogens aren’t as potent as the estrogens your body produces. Therefore, in situations where less estrogen stimulation is desirable – endometriosis, for example – phytoestrogens may reduce your symptoms by occupying estrogen receptors and preventing your own estrogen from exerting its full effects. Conversely, when your own estrogen levels are low (e.g., menopause), phytoestrogens bind to receptors that would not otherwise be occupied and exert a weak estrogenic effect.
Sources of phytoestrogens include (in no particular order):
- Soy or tofu
- Burdock root
- Dried beans
- Sweet potatoes
- Red clover
- Mung beans
- Alfalfa sprouts
- Wild yam
Estradiol is the most potent form of estrogen in your body. Conversion of estradiol to weaker forms, such as estriol, occurs naturally in your liver. Like phytoestrogens, estriol binds to estrogen receptors but exerts a weaker effect than estradiol.
Indole-3-carbinol, a compound found in cruciferous vegetables like broccoli, cauliflower and cabbage, hastens the conversion of estradiol to estriol. Thus, a diet that is high in indoles – or an indole supplement – may reduce the symptoms of endometriosis. As an added benefit, indoles appear to decrease your risk for certain malignancies, such as colon cancer. Controlling Inflammation
Inflammation is the driving force behind the pain and scarring that characterize endometriosis. Interrupting the inflammatory process requires a multi-factorial approach that includes proper diet, sufficient rest, stress reduction and anti-inflammatory herbs.
Some key measures to consider:
- Avoid refined or processed foods; limit sugar, alcohol and caffeine.
- Eat foods that are rich in alpha- and gamma-linolenic acids, which help regulate the levels of inflammatory prostaglandins in your body. These healthy fatty acids can be found in evening primrose oil, black currant seed oil, flaxseed oil, and borage oil.
- Maintain an adequate intake of antioxidant vitamins C (500 – 1000 mg daily) and E (400 – 800 IU daily) through diet or supplementation.
Consider these anti-inflammatory herbs:
Other Important Measures
- Devil’s claw
- White willow bark
- Licorice root
Women who exercise several hours weekly appear to have a lower risk for developing endometriosis, and their symptoms are less severe if they already have it. This may be due to lower levels of circulating estrogens in active women.
Cut out non-organic red meat and dairy products, which can be sources of additional estrogen.
Avoid sugars, refined carbohydrates and processed meats, which can aggravate inflammation in your tissues.
Consider using a progesterone cream. Progesterone generally opposes the actions of estrogen, and it may reduce the pain arising from endometrial implants in women with severe disease.
Many women with endometriosis don’t want to submit to surgery – either laparoscopic ablation or hysterectomy – and they prefer to avoid medications that reduce their fertility or cause serious side effects. For these women, alternative approaches to dealing with this troublesome condition are certainly worth a try. Sources
- AR Mounsey, A Wilgus, DC Slawson. Diagnosis and Management of Endometriosis. Am Fam Phys. 2006;74(4):594-600
- R Gajbhiye, et al. Multiple endometrial antigens are targeted in autoimmune endometriosis. Reproductive Biomed Online. 2008;16(6):817-24
- Life Extension Foundation’s Disease Prevention and Treatment, 4th Edition: Endometriosis. Life Extension Media 2003:1245-6
The statements made on this web site have not been evaluated by the United States Food and Drug Administration (FDA) and are not intended to diagnose, treat, cure or prevent disease. All information provided on this web site is for informational purposes only and is not intended as a substitute for advice from your physician or other health care professional. You should not use the information on this web site for diagnosis or treatment of any health problem. Always consult with a healthcare professional before starting any new vitamins, supplements, home remedies, diet, exercise program, or supplications to the gods, before taking any medication, or if you have or suspect you might have a health problem.
A few days ago I ran into an acquaintance who lamented that he couldn’t get his blood sugars under control. He’s a type 2 diabetic who was recently switched to insulin when his usual oral medications stopped working. His doctor wants him to get his hemoglobin A1C below 7, but the intensive insulin therapy required to meet this goal has triggered several episodes of hypoglycemia. When my friend asked his physician what he was supposed to do when he developed hypoglycemic symptoms, the doc told him to just drink a glass of orange juice or eat a candy bar. Not surprisingly, when my friend followed this advice his blood glucose readings skyrocketed, which mandated higher insulin doses, which generated more hypoglycemic episodes, and so on. Within a few days of starting insulin, this poor guy was riding a rollercoaster that is all too familiar to many insulin-dependent diabetics.
I thought my friend might benefit from a simple regimen I learned at some point during my medical career — it’s one of those handy guidelines that found a dusty crevice in my brain where I could find it whenever one of my own patients needed it. It’s called the “Rule of 15.” To help round out this discussion I’ve excerpted the following section from a book I’ve been writing, editing and re-editing for the last two years (this might be the only portion that ever sees the light of day):
“Sooner or later, everyone who takes insulin experiences an episode of hypoglycemia (low blood glucose), and some people — particularly those who strive to keep their glucose levels tightly controlled — have repeated episodes. Obviously, hypoglycemia is more likely to occur if you overestimate your insulin needs or forget to eat after you’ve already taken your insulin. However, even patients who are fairly careful about such things can develop hypoglycemia. In many instances, unanticipated physical activity is the trigger for a hypoglycemic episode: if you exercise longer or more strenuously than you originally intended, your blood glucose can drop precipitously.
The signs and symptoms of hypoglycemia are often subtle at first. You may simply feel fatigued or irritable, or you might have a mild headache. However, as your blood glucose continues to fall, shakiness, sweating, dizziness, nausea, confusion, and disorientation follow; if your hypoglycemia isn’t corrected, unconsciousness, seizures, coma, and even death may ensue.
Because hypoglycemia can develop insidiously and progress rapidly, if you’re taking insulin and you develop any
unusual symptoms, you should check your blood glucose. If you’re new to insulin therapy, you should also check your glucose — at least for a while — around the time your insulin reaches its peak activity (ask your doctor about this). If you’re having hypoglycemic symptoms and your blood glucose is below 70 mg/dL, follow the “Rule of 15”:
- Eat something that contains about 15 grams of carbohydrate (one slice of bread, one-half glass of orange or apple juice, one-half banana, one scoop of ice cream, a small handful of M&Ms, 3 or 4 glucose tablets, etc.).
- Wait 15 minutes and check your glucose again.
- If your reading is still below 70, repeat steps 1 and 2. If your glucose is higher than 70, resume your usual testing schedule. (Keep an eye out for recurrent symptoms, though, particularly if you take a form of insulin with prolonged peak activity, such as NPH.)
- If you can’t get your glucose to rise above 70 and stay there, call your doctor or go to the nearest emergency room or urgent care center.
Diabetics who abruptly change their lifestyles (embarking on a new weight-loss or exercise program, for example) are at particular risk for hypoglycemia. If you alter your caloric intake or your activity level without adjusting your insulin dosage, you could inadvertently drive your glucose down to dangerous levels. Therefore, it’s important to talk to your doctor, dietician, or diabetic educator before
you make any dramatic lifestyle changes.”
To your good health.
Women who drink alcohol during pregnancy place their developing infants at risk for lifelong difficulties. Scientists have characterized a number of overlapping syndromes – collectively known as fetal alcohol spectrum disorders (FASD) – that result from prenatal alcohol exposure: Alcohol-Related Birth Defects (ARBD), Alcohol-Related Neurodevelopmental Disorder (ARND) and Fetal Alcohol Syndrome (FAS). In addition to the medical burdens imposed by fetal alcohol exposure, children with FASD may develop behavioral problems that place them at odds with society. In fact, a 2010 report from the National Center on Addiction and Substance Abuse estimated that 60% percent of FASD children eventually end up in trouble with the law. Behavioral Impacts of FASD
Fetal alcohol spectrum disorders are marked by a wide array of anomalies, including anatomical defects, growth delay, learning disorders and behavioral problems. Poor impulse control, poor school performance, attachment disorders, lack of remorse, poor short-term memory, poor anger-management skills, poor judgment and inability to link actions with consequences are among the cognitive and psychological manifestations of FASD. Not surprisingly, such deficits tend to isolate these children from their families and peers and, ultimately, increase the likelihood they’ll develop aberrant behaviors. Environmental Influences Aggravate Unacceptable Behaviors
In addition to the underlying neurological injury associated with FASD, affected children are frequently subjected to environmental influences that aggravate their behavioral issues. In many cases, parents of FASD children are alcoholics or are otherwise dysfunctional. Inadequate supervision, poor parental modeling, neglect and outright abuse prevent healthy child-parent bonding, create voids in personality development and heighten a sense of isolation. This encourages already vulnerable children to gravitate toward groups that engage in risky or socially unacceptable behaviors, including lawbreaking. FASD Diagnosis Is Often Missed or Delayed
Unfortunately, fetal alcohol spectrum disorders are not always diagnosed at a time when intervention would be useful. In part, this is due to the sometimes subtle neurological injury that stems from prenatal alcohol exposure. Furthermore, diagnosis of FASD may be missed or delayed because physicians don’t have well-defined diagnostic guidelines to aid them in identifying affected children or discriminating among ARBD, ARND and FAS. Failure to identify FASD children early in life only increases the likelihood for aberrant behaviors later on.Recidivism Is High Among FASD Offenders
For a variety of reasons, there are no accurate data regarding the number of FASD-affected individuals in the juvenile or adult criminal justice systems in the United States. (For one thing, it isn’t clear how many undiagnosed people with FASD are among the general population.) A 2004 study performed at Rutgers University estimated there were around 28,000 undiagnosed cases of FASD in U.S. prisons and jails. Given the lifelong nature of FASD and its pervasive effects on behavior, even if these individuals are released from incarceration, the risk for recidivism and re-incarceration is high. Pregnancy and Alcohol Don’t Mix
Alcohol is toxic to developing fetuses. According to the Centers for Disease Control and Prevention, no amount of alcohol is safe during pregnancy, and there is no safe time to drink alcohol if you’re pregnant. Since alcohol can cause fetal injury at any stage of pregnancy and since no one knows how much alcohol it takes to inflict harm, no pregnant woman should drink alcohol. In addition, women who are trying to conceive should stop drinking alcohol, because they could get pregnant and not realize it for several weeks, at which point significant fetal harm may have already been inflicted. Parents who have children they believe may be affected by a fetal alcohol spectrum disorder should share their concerns with their physicians.Sources
1. U.S. Centers for Disease Control and Prevention: Fetal Alcohol Spectrum Disorders
2. U.S. Department of Health and Human Services: Protecting Children in Families Affected by Substance Use Disorders
3. The National Center on Addiction and Substance Abuse at Columbia University: Behind Bars II: Substance Abuse and America’s Prison Population
4. National Center on Birth Defects and Developmental Disabilities: Fetal Alcohol Syndrome: Guidelines for Referral and Diagnosis
Botulism is a rare, potentially fatal illness caused by a bacterial toxin. Clostridium botulinum, the organism that produces this toxin, exists in soils, aquatic sediments and dusts worldwide. Botulinum toxin is most commonly acquired by eating contaminated foods that contain preformed toxin or by swallowing the bacterium’s dormant spores, which then germinate in the intestine and release the toxin. Once botulinum toxin enters your intestine, it is readily absorbed into your bloodstream. Honey and soil are the only two recognized sources of botulinum spores. Botulinum Toxin Blocks Neurotransmitter Release
Scientists have identified 7 distinct botulinum toxins – A through G – which are produced by different strains of C. botulinum or closely related bacteria. Bacteria capable of producing toxin types A and B are found in honey. Once a botulinum toxin enters your bloodstream, it attaches to receptors on your nerve cells and permanently blocks the release of acetylcholine, a neurotransmitter that is necessary for muscle function. The ensuing paralysis, if untreated, leads to respiratory arrest and death. With lethal doses in the sub-1mcg range, botulinum toxins are among the most potent poisons known. Infant Botulism
An April 2002 review in “American Family Physician” reported that approximately 250 cases of infant botulism are diagnosed in the U.S. each year, the majority of them occurring in Utah, Pennsylvania and California. Less than 2 percent of these infants die from their illness, but recovery can be prolonged. Although honey ingestion is a primary risk factor for infant botulism, only about 20 percent of cases report a history of honey consumption.
Infant botulism can be difficult to recognize. The first sign of infant botulism is usually constipation, which can last for several weeks before other signs – weakness, poor feeding or suckling ability, loss of head control, weak cry, poor eye movement, drooping eyelids and breathing difficulties – appear. Specialized tests can usually detect C. botulinum and its toxin in the stool of an afflicted child. Once it is diagnosed, infant botulism is treated with a specific type of intravenous immune globulin. Mechanical ventilation (artificial respiration), tube feeding and physical therapy are usually required. On average, infants remain hospitalized for 6 to 7 weeks. Adult Botulism
Adults usually develop botulism following consumption of food containing preformed botulinum toxin. Improperly canned foods are the most common source of preformed toxin. Recently, several instances of botulism have been linked to consumption of pruno, or “prison wine.” Rarely, adult botulism results from wounds contaminated by C. botulinum. Increasingly, a form of adult intestinal colonization botulism, which is similar to infantile botulism, is being reported in the medical literature. This form of botulism occurs in people with altered intestinal anatomy or physiology, such as patients with colitis or those who have undergone intestinal bypass procedures. Since intestinal colonization botulism stems from ingestion of C. botulinum spores, susceptible individuals could fall ill following consumption of contaminated honey. Adult botulism is treated similarly to infant botulism. Prevention
Infants younger than 1 year are believed to be more susceptible to spore-caused botulism because they don’t possess a full complement of intestinal bacteria to prevent C. botulinum from multiplying. These children should not be fed honey. In homes where honey is frequently used by older family members, environmental surfaces and utensils within a baby’s reach should be cleaned regularly to prevent ingestion of spores. Adults with chronic intestinal diseases or who have undergone bypass procedures may want to avoid honey. Home canners should scrupulously follow food preservation guidelines
, and home-canned foods should be thoroughly inspected and cooked after opening. Sources
1. N Cox, R Hinkle. Infant Botulism
. American Family Physician.
2. Medscape.com: CBRNE – Botulism
3. SS Arnon, et al. Human botulism immune globulin for the treatment of infant botulism
. New England Journal of Medicine.
Wegener’s granulomatosis, also called Wegener’s disease, is an uncommon autoimmune condition that triggers inflammation in the small blood vessels of your body. This inflammation – the result of your immune system attacking your own tissues – leads to the development of granulomas, or nodules, in various organs. As more granulomas form and enlarge, your organs are less able to perform their vital functions. If not treated, Wegener’s disease can be fatal.
Wegener’s can affect nearly any organ in your body, but it most commonly involves the respiratory tract (nose, sinuses, windpipe, and lungs) and the kidneys. The disease affects men and women equally, it can occur at any age (the mean age at onset is 40 years), and it occurs more often in Caucasians than in other ethnic groups. About 1 in 25,000 people are affected by Wegener’s disease.
Since the 1970s, in an effort to develop effective treatments that don’t carry an unacceptable burden of side effects, scientists have earnestly sought a cause for Wegener’s disease. Unfortunately, that cause remains elusive, and the mainstay of therapy for this condition still consists of powerful immunosuppressant drugs that are poorly tolerated by most patients. Signs and Symptoms of Wegener’s Disease
Wegener’s can begin suddenly or it can develop insidiously, taking many years to become manifest. Signs and symptoms – many of which resemble those of other autoimmune conditions – may include:
How is Wegener’s Granulomatosis Diagnosed?
- Loss of appetite
- Weight loss
- Migratory arthritis and joint pain
- Nasal discharge, either purulent (pus) or bloody
- Headache (often due to sinus involvement)
- Ulcerations of the nasal mucous membranes
- Recurrent bacterial infections of the nose and sinuses
- Recurrent ear infections
- Chronic cough, sometimes with bloody sputum
- Skin nodules and ulcerations
- Excessive tearing (due to obstruction of tear ducts)
- Bulging of the eyes (due to development of orbital granulomas)
- Shortness of breath
- Angina and heart attack (due to obstruction of coronary arteries)
- Numbness or abnormal sensations (due to nerve involvement)
- High blood pressure (usually due to kidney involvement)
- Renal insufficiency or kidney failure
Many of the tests used to detect Wegener’s disease are the same ones used to diagnose other autoimmune disorders. Indeed, there is a great deal of “laboratory overlap” among autoimmune disorders:
- Blood tests: Erythrocyte sedimentation rate is often elevated; white blood cell count is commonly high; red blood cell count is often low, sometimes severely so; antineutrophilic cytoplasmic antibodies (ANCA) are often present (specificity for Wegener’s is high with this test, but a positive ANCA screen is not diagnostic).
- When the kidneys are involved, urinalysis may reveal hematuria (blood in the urine), proteinuria (protein in the urine), and casts of red blood cells.
- X-ray studies of lungs or nasal sinuses may reveal typical granulomas.
- Biopsy of an involved organ or tissue is the key to confirming Wegener’s disease. Lung biopsy is the most commonly performed procedure.
Early diagnosis is important, because prompt treatment can induce remission and prevent complications – or even death. Treatment for Wegener’s Granulomatosis
High-dose prednisone and cyclophosphamide are typically the first agents used to treat Wegener’s disease. These drugs effectively suppress immune activity, which reduces inflammation and slows granuloma formation. Unfortunately, this immunosuppressive property also accounts for some of these medications’ side effects, which include opportunistic infections and a heightened risk for certain types of cancer.
Because cyclophosphamide is a particularly toxic drug, it is usually replaced by other medications – methotrexate or azathioprine, for example – once Wegener’s is in remission. Recently, immunomodulators, such as rituximab, and intravenous immunoglobulins have demonstrated their usefulness in treating Wegener’s disease.
Fortunately, most patients with Wegener's disease can begin tapering immunosuppressant medications within two to three years.Source: The Merck Manual of Diagnosis and Therapy, 18th Edition.
Wegener's granulomatosis. Mark H. Beers, MD, Editor-in-Chief. 2006:281-283
Everyone knows that vitamin D builds strong bones and prevents rickets. During the past two decades, scientists have also learned that this important nutrient (which is more like a hormone than a vitamin) plays a major role in regulating immunity. Now, researchers are exploring vitamin D’s potential as a therapeutic agent for managing immune-mediated diseases and treating or preventing cancers. How Vitamin D Works
Autoimmunity and Vitamin D
- Like most of vitamin D’s biological effects, its influence on immune cells is mediated by an intra-nuclear transcription factor known as the vitamin D receptor (VDR), which has been identified in nearly every tissue in the human body. When the active form of vitamin D enters the nucleus of a cell and binds to the VDR, it initiates a cascade of events that culminates in the transcription, or “reading,” of specific genes. (The products of gene transcription are the proteins, enzymes, and hormones that are necessary for life; the genes activated by VDRs modulate a vast array of physiologic functions, many of which haven’t been fully defined.)
- A substantial body of evidence indicates that vitamin D stimulates innate immune responses, which serve as our front line of defense against novel or unfamiliar antigens. However, in most respects, vitamin D’s actions within the immune system are inhibitory. By suppressing specific facets of immune activity and preventing runaway inflammation, vitamin D prevents the inappropriate responses that lead to autoimmunity.
Cancer and Vitamin D
- It’s interesting to note that as latitude increases, so does the prevalence of many autoimmune diseases, including multiple sclerosis, rheumatoid arthritis, and type 1 diabetes. These conditions are more common in temperate and northern regions than in equatorial countries, suggesting a link between lower sunlight exposure (hence, decreased endogenous production of vitamin D) and autoimmunity.
- Some scientists contend that other factors could explain the higher frequency of autoimmune disease in northern climates. However, animal research and human epidemiologic studies demonstrate that vitamin D probably plays a pivotal role in preventing the immune dysfunction that triggers autoimmune tissue damage.
- Cancer cells possess two traits that characterize their unusual and, ultimately, pathologic behavior: rapid growth (proliferation) and poor differentiation (i.e., each successive generation of cancerous cells looks less like its parents). Like most other tissues, many cancers contain vitamin D receptors; through its actions on VDRs, vitamin D promotes cellular differentiation and inhibits proliferation of malignant tumors.
- Epidemiologic studies suggest that vitamin D, in adequate doses, could play an important role in preventing and/or treating cancers of the colon, breast and prostate. Malignant melanomas and certain bone cancers may also respond favorably to high-dose vitamin D. While epidemiologic studies cannot prove that higher vitamin D intake prevents cancer, the evidence is certainly intriguing.
Although it’s pretty clear what dose of vitamin D is required to prevent rickets and other overt signs of deficiency, there’s a great deal of controversy over how much is needed to confer optimal health. In 2010, after reviewing a mounting body of evidence that revealed many people are vitamin D deficient, the Food and Nutrition Board revised its recommendations for vitamin D intake: infants up to one year should receive 400 IU of vitamin daily, adults to age 70 should consume 600 IU daily, and individuals over age 70 need 800 IU of vitamin D each day. A tolerable upper limit – the amount the Food and Nutrition Board considers to be the maximum safe dosage – was established at 4,000 IU daily for adults.
Not surprisingly, many experts believe the Food and Nutrition Board’s guidelines are too conservative. Vitamin D toxicity is very unlikely to occur at daily doses below 10,000 IU, and much higher doses are employed for treating vitamin D deficiency states or managing autoimmune disorders. It’s possible that the Food and Nutrition Board’s tolerable upper limit for vitamin D intake could prove to be the optimal dosage for most people. Sources
- Griffin M, Xing N, Kumar R. Vitamin D and its analogs as regulators of immune activation and antigen presentation. Annu Rev Nutr 2003;23:117-45
- Sutton A, MacDonald P. Vitamin D: more than a “bone-a-fide” hormone. Mol Endocrinol 2003;17(5):777-91
- Guyton K, et al. Vitamin D and vitamin D analogs as cancer chemopreventive agents. Nutr Rev 2003;61(7):227-38
- Hypponen E, et al. Intake of vitamin D and risk of type 1 diabetes: a birth-cohort study. Lancet 2001;358(9292):1500-03
- Munger K, et al. Serum 25-hydroxyvitamin D levels and risk of multiple sclerosis. JAMA 2006;296(23):2832-38
- Merlino L, et al. Vitamin D intake is inversely associated with rheumatoid arthritis: results from the Iowa Women’s Health Study. Arthritis Rheum 2004;50(1):72-77
- McCullough M, et al. Calcium, vitamin D, dairy products, and risk of colorectal cancer in the Cancer Prevention Study II Nutrition Cohort (US). Cancer Causes Control 2003;14(1):1-12
- Feskanich D, et al. Plasma vitamin D metabolite and risk of colorectal cancer in women. Cancer Epidemiol Biomarkers Prev 2004;13(9):1502-08
- Lowe L, et al. Plasma 25-hydroxy vitamin D concentrations, vitamin D receptor genotype and breast cancer risk in a UK Caucasian population. Eur J Cancer 2005;41(8):1164-1169
- Bertone-Johnson E, et al. Plasma 25-hydroxyvitamin D and 1,25-dihydroxyvitamin D and risk of breast cancer. Cancer Epidemiol Biomarkers Prev 2005;14(8):1991-97
- Ahonen M, et al. Prostate cancer risk and prediagnostic serum 25-hydroxyvitamin D levels. (Finland). Cancer Causes Control 2000;11(9):847-852
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