the-psoriasis-treatment

When I was in high school, one of my best friends was a long-distance runner and a dancer. After only a few months of training, I knew something was wrong. She changed her diet to one of protein and almost no other calories. She was obsessed with exercise leading to a loss of many of her friends. Later on she lost a lot of weight and, to me, instead of becoming healthier she appeared to look pretty unhealthy. What I didn't know then was that my friend may have suffered from the "female athlete triad". It is a three-part syndrome that affects the health and performance of female athletes and includes osteoporosis, disordered eating and menstrual disorders. Each of these are inter-related and inter-play. Together they can cause serious illness or death. Writing in a review in British Medical Journal, Dr. Karen Birch explains that the syndrome can be caused by pressures psychological and physiological associated with a sports requirements to perform optimally, which can l

Growth hormone, also known as human growth hormone, seems to be implicated in a number of metabolic conditions associated with aging, and, more generally, poor health. In adults, growth hormone deficiency is associated with: decreased calcium retention and osteoporosis, loss of muscle mass, increased fat deposition, decreased protein synthesis, and immunodeficiency. In children, growth hormone deficiency is associated with stunted growth. Levels of growth hormones decline with age, and their decrease is believed to contribute to the aging process. Abdominal obesity is associated with low levels of growth hormone, and is also associated with the onset of the metabolic syndrome , a precursor of diabetes and cardiovascular disease. While there are many treatments in the market that include exogenous administration of growth hormones (e.g., through injection), there are several natural ways in which growth hormone levels can be increased. These natural ways can often lead to more effective

I would like to comment on a recent  article comparing the Atkins, Ornish and South Beach diets (Miller et al., 2009; full reference at the end of this posting), which has been causing quite a lot of commotion among bloggers recently. Especially low carb. bloggers. An excellent post by Michael Eades clarifies a number of issues with the study, including what one could argue is the study's main flaw. Apparently the study compared a half-hearted Atkins diet, with probably equally half-hearted Ornish and  South   Beach  diets. I refer to the study's Atkins diet as half-hearted because it seems to rely on a daily consumption of between 120 and 180 grams of carbohydrates. This is unlikely to lead to ketosis, the cornerstone of the Atkins diet, where the body uses ketone bodies (made from dietary as well as body fat) as a source of energy. As I see it, the main findings of the study were that the participants in the half-hearted Atkins diet, after a period of 4 weeks on the diet,

My thoughts after reading "A Review of Family Meal Influence on Adolescents' Dietary Intake" by Sarah Woodruff and Rhona Hanning: It's pretty easy to imagine why having dinner with one's family would instill positive nutritional habits. Even the word family exudes in its meaning what goes further to credit an environment of caring and, above all, nurturing. When mother and father are at the table, they are naturally given to see to it that their children are eating well. At the same time, they must also set the right example. Thus, it's clear why the authors of the article found that the studies reviewed found that those adolescents who ate with their families had a higher intake dairy, fruits and vegetables. I would further suggest that family influence comes with wisdom as to healthy eating pattens. For example, when grandma or grandpa or mom or dad make a meal, they themselves are passing on food traidtions that may have well sustained generations with bet

The hypothesis that blood cholesterol levels are positively correlated with heart disease (the lipid hypothesis) dates back to Rudolph Virchow in the mid-1800s. One famous study that supported this hypothesis was Ancel Keys's Seven Countries Study, conducted between the 1950s and 1970s. This study eventually served as the foundation on which much of the advice that we receive today from doctors is based, even though several other studies have been published since that provide little support for the lipid hypothesis. The graph below (source: canibaisereis.com , with many thanks to O Primitivo) shows the results of one study, involving many more countries than Key's Seven Countries Study, that actually suggests a NEGATIVE linear correlation between total cholesterol and cardiovascular disease. Now, most relationships in nature are nonlinear, with quite a few following a pattern that looks like a U-curve (plain or inverted); sometimes called a J-curve pattern. The graph below (sou

Alanine aminotransferase (ALT) is an enzyme that is concentrated in the hepatocytes. When the liver is injured or affected by disease, the enzyme is released into the bloodstream. When jaundice occurs, for example, elevated ALT levels can distinguish a liver injury or disease instead of red blood cell hemolysis. The test is performed on a patient by collecting 7-10 mL of blood in a red-top tube, then sending it to a lab for analysis. If a patient does have liver dysfunction, then the clinician should note that bleeding times may be longer. Significantly elevated ALT levels may indicate hepatits, hepatitis necrosis or hepatits ischemia. Moderately increased levels may indicate cirrhosis, cholestatis, a hepatic tumor, a hepatotoxic drug, obstructive jaundice, severe burns or trauma to striated muscle. Drugs that may elevate ALT levels include acetaminophens, clofibrate, codeine, salicylates, tetracyclines among many others. ALT levels may also increase to a lesser extent due to myositis

An abnormal lipid profile is a consistent indicator of atherosclerosis and cardiovascular disease (CHD). Blood lipids include total cholesterol, LDL-C, HDL-C and triglycerides. Because each of these factors are ultimately affected by diet, it serves to reason to recommend dietary strategies to help lower total cholesterol and LDL-C, increase HDL-C and reduce triglyceride levels. ATP III uses the term therapeutic lifestyle changes (TLC) for recommendations that can help to improve abnormal lipid profiles and reduce risk of CHD. TLC makes recommendations for saturated fat (less than 7% of total calories), polyunsaturated fat (up to 10% of total calories), monounsaturated fat (up to 20% of total calories), total fat (25-35% of total calories, fiber (20-30g/d), protein (approx. 15% of total calories), and cholesterol (less than 200 mg/d). The total calories recommendation, in addition, is based on a balance of energy intake and expenditure to maintain a healthy weight (1). Because it is of

I have three children, one boy, 13 and two girls, 10 and 11. As far as I’m concerned prevention of atherosclerosis should begin as early as possible. That means yesterday. However, I understand that there exists some uncertainty of exactly what age to begin prevention. It has to do partly with juvenile fatty streaks. What may appear unimaginable is that the occurrence of juvenile fatty streaks somehow may have an importance in child development. Most North American children develop fatty streaks in their aortas by age 3 and in coronary arteries along with macrophage foam cells by age 10 (1); by the time children are reaching puberty, they may already have developed fatty streak lesions. Fatty streaks are nothing new. As offered by McGill et al, our hominin forebears likely developed them as do current non-human Old and New World primates even when living in natural habitats. Studies of other mammals reveal that many of them also develop fatty streaks. From an evolutionary perspective,

A few years ago I went to the doctor for a routine appointment, and I was told that my LDL cholesterol was elevated. I was in my early 40s. My lipid profile was the following - LDL: 156, HDL: 38, triglycerides: 188. The LDL was calculated. I was weighing about 210 lbs, which was too high for my height (5 ft 8 in). My blood pressure was low, as it has always been - systolic: 109, diastolic: 68. My doctor gave me the standard advice in these cases: exercise, lose weight, and, most importantly, reduce your intake of saturated fat . I was also told that I would probably have to take statins, as my high LDL likely had something to do with my genetic makeup. Again, this is quite standard, and we see it all over the place, particularly in commercials for statins. I told my doctor that I would do some research on the topic, which I am going to save for other posts. Let me get to the point, by telling you what my lipid profile is today - LDL: 123, HDL: 66 , triglycerides: 46 . Again, the LDL va

Normally, measuring insulin directly is more accurate with diabetics. But C-peptide levels more accurately reflect islet cell function in situations of insulinomas as well as cases of diabetics taking exogenous insulin (for treatment or secretly). C-peptide, short for "connecting peptide" is the protein connecting beta/alpha chains of proinsulin. The chains are separated when proinsulin becomes insulin and C-peptide. C-peptide ends up in equal amounts to insulin in the portal vein, lasts longer than insulin so can be found more readily in peripheral circulation, and correlates with insulin levels. Summarized from Pagana, K.D., Pagana, T.J. Mostby's Manual of Diagnostic and Laboratory Tests, 3rd ed. Mosby Elsvier, 2006, p. 197.

Measuring blood glucose periodically is critical for staying off the blood sugar rollercoaster. But how can a clinician be sure a patient hasn't gotten on board the rollercoaster? This is when glyosylated hemoglobin comes into the picture. What happens is that when a person is diabetic and doesn't adequately control blood glucose, her or his blood glucose becomes elevated. The hyperglycemia that results begins to affect certain proteins in the blood as well as hemoglobin. Blood glucose bonds to the hemoglobin and it becomes "glycosylated". The glycosylation mainly happens to hemoglobin A (HbA, the major form of hemoglobin, and it's pretty much irreversible. After a few weeks, the amount of glycosylated hemoglobin will decline, but only if blood sugar is controlled. If it's not controlled, then a physician can order a glycosylated HbAIC test, or AIC test. A person without diabetes should have about 4-8% HbAIC and the American Diabetes recommends diabetics to st

John and Susan are both prone to being overweight. They are concerned that their infant son, Steven will also have weight problems. They are referred to you when Steven is 5 months old. Steven's growth data are as follows Age Weight Length Birth 8lb 20inches 1 week 8lb 1oz 20 inches 1 month ll lb. 21.5 inches 2 month 12lb 8oz 23 inches 3 month 14lb 8oz 23.5 inches 4 month 16lb 25.5 inches 5 month 18lb 26.5 inches Steven breast feeds six times daily for about 20-25 minutes at each feeding. He is not presently receiving any other sources of nourishment. Answer the following questions for John and Susan: Their pediatrician told them that Steven's weight is above average. Is he gaining too much weight? When charted, Steven’s birth weight and weight gain for the next two months is at about the 50th percentile (1 p. 566). His weight gain afterward appears to be higher than average and he is at the 90th percentile by 5 months (1 p. 566). Steven’s birth length for four months is at abo

The gut’s immune system is ultimately responsible for maintaining a healthy gut free of infection or infestation. It must accomplish this task while at the same time being unresponsive to food and helpful bacteria (1). Gastrointestinal inflammation etiology is largely infection such as via parasite. However, modern lifestyles have increasingly been harassed by new chronic inflammatory diseases such as Crohn’s or ulcerative colitis (1). These are associated mainly with genetic mutations or adaptive immunity affecting immune system recognition as well as by epithelial permeability (1). Stool tests indicating gastrointestinal inflammation include those for fecal proteins such as eosinophil protein-X (EPX), fecal calprotectin (FC) and fecal myeloperoxidase (MPO): FC is a calcium-binding protein found in large amounts in neutrophils and macrophages, which rush into the lumen at onset of inflammation (2-4). FC is considered more sensitive than endoscopy, for example, for evaluating inflammat

Nutritional and energy needs for a child differs profoundly from that of an adult because of a child's continual growth and development. A child is in greater need of nutrient-dense foods--although not to the extent as infants--and requires more energy for basal metabolic rate, physical activity and thermic effect of food. Energy needs are highest during rapid growth and expansion of lean mass. Each individual child is best understood by first dividing stages of child growth and development into two periods: a preschool period and a school-age period: During the pre-school period, from 2-6 years of age, the child grows more slowly in comparison to infancy. A toddler will quadruple birth weight in a full year or so. The brain of the toddler also grows more slowly than as was expected as an infant so head circumference will only increase by a couple of centimeters. A toddler's weight increase can range from 2.5 kg per year for ages 2 and 3 to 2 kg per year for ages 4 and 5. She o

Protein status is assessed by evaluating both somatic and visceral protein status. Somatic protein status is a measure of the protein in skeletal muscle while visceral protein status is a measure of all other proteins (organs, viscera, serum, blood cells, white blood cells). Evaluation of somatic protein status can generally be performed using muscle circumference or mid-arm muscle area. However, because no single indicator is completely accurate biochemical measures can help better provide perspective for somatic protein status. Creatinine serves as a useful measure because creatinine is produced in the skeletal muscle. The more skeletal muscle a person has, the more creatinine will be excreted. A 24-hour urinary creatinine excretion test is easily tested in the laboratory. The measure can then be compared to standards based on stature and body weight. The 24-hour urinary creatinine excretion can also be compared to reference values from the creatinine-height index (CHI). The CHI is a

The infant, despite whether healthy term or high-risk, will require energy for BMR, thermic effect of food, physical activity, maintenance, growth and for energy lost in feces and urine. There is also energy needed just to maintain body temperature until the early extrauterine period passes. The newborn requires approximately 108 kcal/kg for about six months followed by 98 kcal/kg for the next six. The high-risk newborn will have the same energy requirements, but Calorie needs will differ in whether or not the infant is enterally fed or parenterally fed. The enterally fed infant needs a greater amount of Calories, at 120/kg, than the healthy infant due to specific dynamic action and cold stress. The parentally fed will need fewer amount of Calories, at about 80-90 kcal/kg, than the healthy infant because of the infant won't use as many calories for activity, cold stress, specific dynamic action or stool losses. Caloric needs for both enterally and parenterally fed high-risk infants

One interesting detail I came across while researching teratogens is that a protein-deficient diet may enhance the effects of xenobiotics in general. For example, dietary protein deficiency along with exposure to inorganic arsenic through injection in mice was found to increase risk of birth defects, possibly because of lack of methyl donors for arsenic methylation (1). Also, high-dose caffeine teratogenicity is increased when in combination with protein deficiency (2). Other xenobiotics such as tobacco carcinogens, anticonvulsants and sedatives appear to be teratogenic depending on the status of the cytochrome P450 system of the fetus (1). The effect may or may not be related to protein deficiency. The toxicity is thought to occur due to lack of anitoxidative enzymes such as GSH peroxidase and GSH reductase, which would increased endogenous oxidative stress and cumulative damage (3). Reference List 1. Lammon CA, Hood RD. Effects of protein deficient diets on the developmental toxi

I was shocked to learn that FDA in 1980 had determined that caffeine in amounts exceeding 300 mg could potentially be teratogenic (1). Teratogens are agents that cause fetal malformations or birth defects. Good thing caffeine does not harm the fetus when taken in smaller amounts, despite evidence in rats to the contrary (1-2). However, after digging deeper, I found that the researchers did find that caffeine potentiated teratogenic effect of smoking and alcohol (2). The mechanism appears to be through inducing materno-fetal vasoconstrictions that lead to ischemia (2). If caffeine potentiates effects of other teratogens in amounts less than 300 mg, I imagine it's still wise of pregnant women to avoid caffeine altogether during pregnancy just in case they are exposed to teratogens of some kind and are unaware of it. Reference List 1. Mitchell MK. Nutrition Across The Life Span. Long Grove, IL: Waveland Press, 2003. 2. Nehlig A, Debry G. Potential teratogenic and neurodevelopmenta

Cannabis sativa’s psychoactive tetrahydrocannabinol (THC) has not been established as a human teratogen (1), but there is a history of teratogenic effects linked to use by expectant mothers (2). The perinatal exposure is thought to interfere with neurodevelopment and affect neurobehavorial outcomes (1-2). Although the teratogenicity of marijuana is not as catastrophic as other illicit drugs such as cocaine, it’s harm can still lead to problems such as disturbed sleep and attention deficit disorder (2-3). Worth noting is that when cocaine exposure is accompanied by marijuana, the neurological effects can be pronounced (3). There is also indication that maternal marijuana use may increase risk of acute myeloid leukemia, however, more recent research has not been able to confirm this relationship (4). Reference List 1. Kozer E, Koren G. Effects of prenatal exposure to marijuana. Can Fam Physician 2001;47:263-4. 2. Reece AS. Chronic toxicology of cannabis. Clin Toxicol (Phila) 2009;47

Nutritional needs soar when you have a multiple pregnancy. According to Barbara Luke from University of Miami, the mother has a “greater nutritional drain” on her body. Because of quicker glycogen depletion that might slow fetal growth rate, Luke suggests a diabetic regimen with caloric ratio of 40% carbs, 20% protein, and 40% fat. In addition, she suggests supplementation with iron, calcium, magnesium and selenium for preventing “complications and improvement of postnatal health”. Reference List Luke B. Nutrition and multiple gestation. Semin Perinatol 2005;29:349-54.

Eggs, considered a nutritional powerhouse, is an excellent food to recommend to these women during pregnancy. According to Niva Shapira of Tel-Aviv University in Israel, eggs can provide various nutrients, vitamins and minerals that are also found in human milk and that support peak brain development (1). If those eggs are also produced in such a way as to contain high levels of DHA, then they become even more supportive to the young one’s brain (2). Reference List 1. Shapira N. Modified egg as a nutritional supplement during peak brain development: a new target for fortification. Nutr Health 2009;20:107-18. 2. Carlson SE. Docosahexaenoic acid supplementation in pregnancy and lactation. Am J Clin Nutr 2009;89:678S-84S.

On July 17, 2008, a study was published (1) that I believe should change how nutritionists and dietitians would look at the current Dietary Guide for Americans, the Food Guide Pyramid and the whole concept of a “heart-healthy” low-fat diet as recommended by the American Heart Association. The paradigm-shift study was a 2-year intervention trial in The New England Journal of Medicine in which weight loss was compared among moderately obese subjects who were assigned to either a restricted-calorie Mediterranean diet, a non-restricted calorie low-carbohydrate, or a typical restricted-calorie low-fat diet (1). What did they find? Surprising results. All the subjects lost weight, but were greater in both the low-carbohydrate group (despite nonrestricted calories) and the Mediterranean-diet group (1). The lipid profiles, more surprisingly, improved in the Mediterranean-diet group and most in the low-carbohydrate group (1). Best LDL cholesterol levels were found among the Mediterranean-diet g

Once the “war on cancer” was declared in 1971 by Congress, researchers have sought to defeat it (1), but after losses of many knights in shining armor, a newfound respect has come around for this dragon of a disease (1). In the 1990s and 2000s, however, a new sense of hope had come about. “End cancer by the year 2015” was the message shared in 2003 by Andrew C. von Eschenbach, MD, director of the National Cancer Institute (NCI). And although he’s had many critics saying it couldn’t be done, others joined him in saying it could. Just two years afterward, in 2005, NCI modified it’s lofty goal to a softer “alleviate pain, suffering and death associated with cancer” (2). The change meant a new direction of “controlling” but not “curing” the disease . The same year, 2005, one Eschenbach supporter put forward a plan for a victory (3). His name was Mikhail V Blagosklonny, MD, PhD, and his approach was by combining strategies that target cancerous cells directly while protecting normal cells i

I just read a citizen's petition to FDA by Gail Elbek calling for the removal of soy because of antinutrients (trypsin inhibitors and phytates) and endocrine disruptors. Gave me a bit of a laugh, but I expect it will scare a lot of unwitting people. The outrageous claims Ms. Elbek makes are not grounded in any science. Soy phytotoxicity is going to “kill our children”? Please. I’m not about to throw out my soy milk, tofu and soy sauce. What’s next? Spinach. Spinach contains a lot of phytates. Many raw foods like raw soybeans contain all sorts of anti-nutrients, but that’s why we dehull, cook, or ferment these raw foods. Most anti-nutrients are eliminated just by the processing. There is a point to be made about high amounts of concentrated phytoestrogens (soy isoflavones) in a few dietary supplements, which are often marketed to women as natural hormonal therapy. These are basically drugs of which we don’t know enough about. The research is still out on whether or not they’re benef

Boron's ability to induce sex hormone levels give it a role preventing chronic disease. For example, adequate dietary boron may potentially reduce risk of lung cancer (1). The effects also explain why boron supplementation may support bone density guarding against osteoporosis (2). However, caution should be exercised before supplementation with boron. Greater estrogen levels due to boron supplementation may potentially increase risk of breast cancer (1;2). Thus, boron should not be taken by women with high risk of breast cancer or who've had breast cancer. Reference List 1. http://www.pccnaturalmarkets.com/health/2813008/ 2. http://www.osteopenia3.com/Boron-Osteoporosis.html

Nickel is a known carcinogen. When in the diet in toxic amounts it contributes to oxidative stress, just as mercury and cadmium do, by reducing glutathione thereby interfering with cell membrane integrity and increasing lipid peroxidation (1). The oxidative damage, like from free iron or copper, can cause DNA damage (2). Reference List 1. Valko M, Morris H, Cronin MT. Metals, toxicity and oxidative stress. Curr Med Chem 2005;12:1161-208. 2. Tkeshelashvili LK, Reid TM, McBride TJ, Loeb LA. Nickel induces a signature mutation for oxygen free radical damage. Cancer Research; 53, 4172-4174, September 15, 1993.

As one travels around the world, especially in developing countries, the state of oral health stands out as an issue that needs attention. Fluoride treatment of drinking water can be an important step in improving oral health (1), but some populations may find it's not necessary because they may already be consuming adequate or even too much fluoride daily. Careful review of fluoride exposure must be evaluated region by region before deciding to treat local water with fluoride (2). According to the World Health Organization (WHO), flouride intake can vary depending fluoride already in water, on diet and other variables such as local pollution (2). Areas of greater volcanic activity, for example, tend have highest concentrations of fluoride in groundwater (2). The act of tea drinking can provide significant amounts of fluoride (1). In parts of China where high-fluoride coal is burned, the ash that pollutes crops may be providing fluoride (2). And in Tanzania, the use of contaminated

A young electrician with a painful gouty arthritis in 2005 became the first case observed of occupational exposure of toxic amounts of molybdenum (1). Molybdenum is an activator of xanthine oxidase, which oxidizes xanthine producing uric acid (2). Too much produced hyperuricemia (1). The electrician can be thankful that his doctors found the cause of the gout because of previous men afflicted with gout by having consumed 10 to 15 mg of molybdenum daily (3;4). Tolerable uptake limits are set at 2 mg (2). Reference List 1. Selden AI, Berg NP, Soderbergh A, Bergstrom BE. Occupational molybdenum exposure and a gouty electrician. Occup Med (Lond) 2005;55:145-8.2. Gropper SS, Smith JL, Groff JL. Advanced Nutrition and Human Metabolism. Belmont, CA: Thomson Wadsworth, 2009.3. http://lpi.oregonstate.edu/infocenter/minerals/molybdenum/ 4. http://www.crnusa.org/safetypdfs/027CRNSafetyMolybdenum.pdf

Toxicity of manganese is more common than its deficiency (1), which unfortunately cause damage to the brain. Manganese appears to cause neurogeneration by activating microglia and causing them to release neurotoxins such as reactive oxygen and nitrogen species, which produce oxidative damage (2). The neurotoxins are also thought to possibly alter influence of neurotransmitters such as dopamine or gamma-aminobutyric acid (GABA) (1). According to a studies on non-human primates exposed to high doses of manganese, the mineral can lead to deficits in working memory performance and even induce an increase of beta-amyloid production linking manganese to Alzheimer's disease (3;4). Reference List 1. Anderson JG, Fordahl SC, Cooney PT, Weaver TL, Colyer CL, Erikson KM. Manganese exposure alters extracellular GABA, GABA receptor and transporter protein and mRNA levels in the developing rat brain. Neurotoxicology 2008;29:1044-53. 2. Zhang P, Wong TA, Lokuta KM, Turner DE, Vujisic K, Liu B.

The biochemical mechanism by which metals are mutagenic is by their effects on DNA. The main pathway shared by iron, copper, chromium, vanadium and cobalt is by redox-cycling reactions and mercury, cadmium and nickel by depleting glutathione and bonding to sulfihydryl groups (1). Free iron, in particular, can cause oxidative damage on DNA that can cause cancer in the spleen (2). Arsenic, in particular binds directly to critical thiols producing DNA damage (1). Cadmium interferes with and inhibits DNA repair (3;4). Reference List 1. Valko M, Morris H, Cronin MT. Metals, toxicity and oxidative stress. Curr Med Chem 2005;12:1161-208. 2. Wu X, Kannan S, Ramanujam VM, Khan MF. Iron release and oxidative DNA damage in splenic toxicity of aniline. J Toxicol Environ Health A 2005;68:657-66. 3. Slebos RJ, Li M, Evjen AN, Coffa J, Shyr Y, Yarbrough WG. Mutagenic effect of cadmium on tetranucleotide repeats in human cells. Mutat Res 2006;602:92-9. 4. Giaginis C, Gatzidou E, Theocharis S. DNA

Calcium (Ca) and magnesium (Mg) are non-heavy metals with the same valence charge that are both critical for physiologic function, yet overlap each other in their mechanisms. For example, they both use the same transport systems in kidney competing with each other for absorption. They also oppose one another in blood coagulation, smooth muscle contraction and PTH release. The relationship between Ca and Mg is important as it promotes a balance in given biological systems for proper function of the body. Deficiency either mineral could result in an improper balance leading to problems.

Vanadyl ions can act in an insulin-like manner in the body. Thus, when taken orally they may potentiate insulin’s effects, which can potentially improve situations of type 2 diabetes (1). Bioavailability of vanadyl compounds, however, can depend on whether of organic or inorganic nature (2). The organic bis-ligand oxovanadium appear to be far more bioavailable and efficacious than inorganic vanadyl sulfate (2). According to a couple of trials performed earlier this year in Canada, the organic version taken in doses of 10-90mg has no adverse effects (2). Further, it was found to help reduce fasting blood glucose levels and improves glucose tolerance (2). Reference List 1. Conconi MT, DeCarlo E, Vigolo S et al. Effects of some vanadyl coordination compounds on the in vitro insulin release from rat pancreatic islets. Horm Metab Res 2003;35:402-6. 2. Thompson KH, Lichter J, LeBel C, Scaife MC, McNeill JH, Orvig C. Vanadium treatment of type 2 diabetes: a view to the future. J Inorg Bioc

As Gropper, Smitth and Groff tell it, arsenic "conjures an image of toxicity" unlike any other ultratrace mineral (1), but there are good things that come of arsenic and its story is worth discussion. Without arsenic, DNA synthesis couldn't happen. This is because arsenic is needed for normal metabolism. Specifically, the mineral is required for forming and using methyl groups to S-adenosylmethionine (SAM) (1). SAM is used for methylation to form DNA compounds (1). Arsenic, in fact, may have once been part of DNA itself. The mineral is very similar to phosphorus, which is currently the backbone of nucleic acids. Because this is is so it has been suggested that arsenic may have served as an alternate element early on, although not possible in modern biochemistry (3). According to scientists Felisa Wolfe-Simon, Paul Davies and Ariel Anbar, there may even be possibility that organisms may still be using arsenic in their DNA today, but simply not yet found (3). Reference List

Estrogen appears to directly influence bone turnover. Its mechanism is byacting on estrogen receptors in bone cells (1). The hormone influencesvitamin D metabolism by increasing conversion of 25-hydroxyvitamin D(25OHD) to 1,25-(0H)2D as it does in birds (2). The increase of 1,25-(0H)2D then enhances calcium absorption in the bones(2). Estrogen, thereby, contributes to bone density by slowing down boneloss and its absence can lead to lower bone density and predispose forosteoporosis (1;2). This biochemistry supports evidence that already exists that estrogenreplacement therapy (ERT) combined with adequate calcium and vitamin Dintake as well as exercise may help prevent osteoporosis (3;4). Despite the effects, however, I have the same opinion about using long-term estrogen replacement therapy (ERT) in postmenopausal women for osteoporosis as I do about estrogen for reducing risk of cardiovascular disease in postmenopausal women. While there are benefits outlined suggesting that future re

Because of chromium’s known ability to potentiate action of insulin, an adequate chromium status is important especially for people with diabetes, insulin resistance and hypoglycemia to maintain glycemic control (1;2). According to an evaluation of 15 randomized clinical trials, amounts of about 200 mcg per day appear to improve use of glucose (3). In addition, a placebo-controlled trial of 180 Chinese patients found that doses at 200 mcg and as high as 1,000 mcg of chromium taken per day lowered blood glucose levels by 15-19% (3). Dose may depend on form of chromium since one form may be more bioavailable than another. Chromium picolinate appears to be the most bioavailable and, thus, the most potent (3). The amount of chromium taken, however, should not exceed 1,000 mcg per day due to potential toxicity (1). Chromium picolinate, in addition, should not be taken in amounts over 600 mcg because of association with renal failure and hepatic dysfunction (1). Reference List 1. Groppe

Advertisements that suggest chromium picolinate may help consumers lose fat or gain muscle mass are largely overstated. A double-blind, randomized, placebo-controlled 12-week trial in 2001 found that chromium picolinate offered moderately obese women participating in an exercise program no significant changes to body composition, resting metabolic rate, plasma glucose, serum insulin, plasma glucagon, serum C-peptide or serum lipid concentrations (1). The 2001 study’s results supported at least three previous studies of which had also shown that chromium picolinate had been ineffective in changing body composition in obese women, in military personnel and in weight-lifting football players (2-4). A 12-week randomized, placebo-controlled trial in 2008 combined chromium picolinate with conjugated linoleic acid and evaluated effects on body composition changes of young, overweight women for 12 weeks (5).; still, no significant changes were found (5). Lastly, because of chromium’s known eff

Prostate cancer has been associated with low serum selenium concentration. To investigate the mechanisms by which selenium affects gene expression prostate tissue, researchers set out to measure activity of glutathione peroxidase in men with relatively high serum selenium concentration (1). The researchers measured serum selenium concentration in 98 men using atomic absorption spectrometry. Afterward, 12 men were selected for having the highest serum selenium concentration and another 12 were identified as having the lowest serum selenium concentration. Fresh prostate tissue samples were taken of the selected men to measure selenium concentration and glutathione peroxidase activity. The study, which was published in July 2007, reported a positive correlation found between a higher serum selenium concentration and a prostate tissue concentration. However, there was no significant increase of glutathione peroxidase activity associated with the higher concentration of selenium concentrati

Summary: Complementary preventive therapy for Alzheimer’s disease should include DHA for its biochemical implications, especially in apoE4-genotype obese-diabetic patients. DHA mechanisms involve reducing adiposity and secretions, improving insulin sensitivity, guarding against oxidative stress, and guarding against beta-amyloid plaque, neurofibrillary tangles and advanced glycation end-products. Background: Urgent Call for Alzheimer’s Disease Preventive Therapies Foresight warns that the present epidemic of obesity and diabetes in the United States of America will lead to future medical epidemics and among them will be Alzheimer’s disease (AD), the most common neurodegenerative disease seen in aging. AD is seriously debilitating and at present time has no cure. Current treatments are limited to cholinesterase inhibitors to improve function of signaling pathways in memory, but are not intended to prevent or slow further brain damage. Preventive strategies are currently being studied to