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Copper Deficiency May Underlie Osteoporosis, Anemia and Neurodegenerative Disorders

Despite their obviously different appearances, osteoporosis, anemia, neurodegenerative disorders, cardiovascular disease, and impaired cellular immunity may all be manifestations of chronic copper deficiency, an often-overlooked nutritional problem that is more common than many doctors realize.

Copper plays a key role in myelination of neurons, neutrophil activation, collagen synthesis, hemoglobin formation, and endogenous antioxidant synthesis. “It is a mineral that is greatly under-recognized and under-utilized,” said Ron Grabowski, RD, DC, Professor of Clinical Practice at Texas Chiropractic College, Houston, and Director of Research for the American Chiropractic Association’s Council on Nutrition.

Deficiency can manifest in many different ways including seizures and neurological problems, poor temperature control, connective tissue degeneration, bone mineral loss, pallor, anemia, and poor hair and skin quality. Several recent studies suggest that in addition to the well-recognized neural and hematologic sequelae, copper deficiency also has a role in diabetes and cardiovascular disease.

Copper excess can be problematic too, causing liver damage, neruologic problems, chondroplasia and skeletal abnormalities. But given the way most Americans eat, and the wide use of medications that interfere with copper uptake, deficiency is vastly more common than excess.

Dr. Grabowski contends that many patients diagnosed with iron-deficiency anemia, early-stage multiple sclerosis, and various immunodeficiency disorders actually have unrecognized copper deficiency. Fortunately, this is correctable via supplementation. It may take time, and it requires careful monitoring, but restoring healthy copper levels can greatly improve patients’ health status.

Modest Requirements, Often Unmet

“Our daily need for copper is actually quite modest. For most adults, 1.5–3.0 mg/d is sufficient for good health. That doesn’t sound like much, but more than 30% of people on a typical American diet are not even getting 1 mg per day. Another third of the population is not even reaching the minimum daily allowance (900 mcg),” said Dr. Grabowski.

The primary dietary sources of copper are shellfish (oysters, mussels, clams, lobster, crab, squid) and organ meats (beef liver, kidneys and heart). With a few exceptions like bananas, grapes, tomatoes, avocados and sweet potatoes, most produce lacks copper. Fortunately for vegetarians, nuts (cashews, filberts, macadamias, pecans, almonds, pistachios) and some legumes (peanuts, navy beans, lentils, soy) are good copper sources.

The rising prevalence of copper deficiency is due in part to the fact that many people are simply not eating as many copper-rich foods as they once did. The high prevalence of digestive disorders, and widespread use of drugs and supplements that deplete or interfere with copper are the other major factors.

Easily Absorbed, Easily Blocked

Copper absorption occurs in the upper portion of the small intestine. In people with a healthy digestive tract, it is absorbed very efficiently compared to other minerals. Any disease that affects digestion may interfere with copper absorption or promote copper loss in the lower GI tract. Think about deficiency in anyone with Crohn’s disease, irritable bowel or any other inflammatory GI problem.

Proper copper absorption requires ample stomach acid. Consequently, drugs that block acid secretion impede copper uptake. This includes all proton pump inhibitors and H2 blockers. “In my practice. I see so much copper deficiency and also B12 deficiency in people on these medications,” Dr. Grabowski told Holistic Primary Care.

High fructose consumption increases copper excretion in urine, and also increases demand for superoxide dismutase (SOD), an endogenous antioxidant the formation of which requires copper. “This is a big problem because high-fructose corn syrup is ubiquitous in the American food stream.”

Be aware that whole grains contain phytates that bind copper, zinc and other minerals. This is not to suggest that people shouldn’t eat whole grains, but they shouldn’t take minerals at the same time. “People often do not understand that it matters when and with what they take their supplements. Don’t take them with whole grain breads or brown rice; you won’t get the benefits of the minerals. We need to harmonize supplements with our diets.”

Copper & Zinc: A Dynamic Balance

Much like calcium and magnesium, copper and zinc have a sometimes synergistic, sometimes antagonistic relationship. Both are involved in a host of enzymatic and metabolic reactions. When the balance of zinc and copper is right, these processes proceed well. But, like calcium and magnesium, too much of one diminishes the other. Excesses of either zinc or copper can cause problems.

The first report of a pathologic zinc-induced copper deficiency came out 20 years ago. Mayo Clinic physicians described an individual who took high daily doses of zinc for 10 months. The patient presented with hypochromic-microcytic anemia, leukopenia and neutropenia. When iron failed to resolve the abnormalities, the physicians dug deeper and found extreme copper deficiency, correctable only with intravenous infusion of 10 mg cupric chloride for 5 days (Hoffman HH, 2nd, et al. Gastroenterology. 1988; 94(2): 508–512).

Zinc excess with copper deficiency is common, said Dr. Grabowski. “A zinc to copper ratio of 30:1 will really force people into serious copper deficiency. Some researchers say the problem begins at 10:1. When patients show me their multivitamins and I see 30 mg of zinc to 1 mg of copper, it makes me very, very nervous. The supplements they’re taking to improve their health may actually be inducing a copper deficiency that increases their risk of disease.”

Self-Induced Deficiencies

During the winter cold and flu season, many people unwittingly induce copper deficiency by gobbling zinc lozenges and heavy doses of vitamin C, believing this will enhance immunity and increase antioxidant capacity. But both zinc and vitamin C compete with or interfere with copper absorption. Because copper is essential for production and activation of neutrophils—the first line of defense against pathogens—excess zinc and vitamin C may actually render people more susceptible to the very ailments they’re seeking to avoid.

Two recent papers review the role of copper and other trace minerals in both cellular and humoral immunity. Maggini and colleagues illustrate the vicious cycle occurring when micronutrient deficiencies suppress T-cell mediated and adaptive antibody responses, thus increasing susceptibility to infection, which, in turn, increases micronutrient loss, interferes with metabolism of many nutrients, and reduces nutrient intake (Maggini S, et al. Br J Nutr. 2007; 98(Suppl 1): S29–S35).

In the same journal, Munoz and colleagues point out that careful micronutrient supplementation can boost immune function and reduce infection susceptibility. This is particularly important in the elderly, because vaccinations against respiratory infections are only partially effective (Munoz C, et al. Br J Nutr. 2007; 98(Suppl 1): S24–S28).

Copper is essential for synthesis of one form of superoxide dismutase (SOD), and anything that reduces copper also reduces SOD, diminishing overall antioxidant capacity. People who take high dose vitamin C to boost their antioxidants may be surprised to learn they’re actually inducing the opposite effect. Anything over 1,000 mg of vitamin C per day interferes with copper.

The best way to increase overall antioxidant capacity is by increasing intake of antioxidant rich foods, rather than amplifying one antioxidant vitamin out of the many, said Dr. Grabowski.

Iron, Copper & Anemia

Many doctors reflexively prescribe iron to any patient with signs and symptoms of anemia without actually testing to see if iron is deficient. According to Dr. Grabowski, many cases of alleged iron-deficiency anemia are actually due to copper deficiency. Like iron, copper is involved in hemoglobin formation. Suspect low copper if a patient’s anemia does not resolve with additional iron.

“Copper deficiency can present exactly like iron deficiency and you’ll never know the difference unless you test for it,” he said. There is one other give-away, though: low neutrophil count. Copper is essential for neutrophil production and phagocytic activation. Copper-deficient people show low neutrophil counts, a feature not seen in iron deficiency anemia.

Of course, someone may be deficient in both iron and copper. “Copper has a part to play in iron uptake in the GI tract. If copper is low, iron absorption tends to be low as well.”

In a just-published paper, Cleveland Clinic hematologists show hypocupremia as a cause in 3 cases of cytopenia and bone marrow failure, and suggest it should be added to the differential diagnosis of bone marrow failure syndromes, including myelodysplasia (Haddad AS, et al. Haematologica. 2008; 93(1): 1–5).

This corroborates a 5-case series from Washington University a few months earlier that also points to copper deficiency as a cause of myelodysplasia. In all 5 cases, the problem resolved with copper supplementation (Fong T, et al. Haematologica. 2007; 92(10): 1429–1430).

Copper & CVD

Several recent papers point to lack of copper as a risk factor for cardiovascular disease, but the picture is complex. University of Turin researchers looked at the relationship of dietary copper to a host of metabolic variables in 1,197 individuals. They found clear inverse relationships between copper and diastolic blood pressure, total cholesterol, LDL, blood glucose, uric acid, and total antioxidant status, a clearly high-risk profile. There were linear correlations between copper and both C-reactive protein and nitrotyrosine, a marker of oxidative stress (Bo S, et al. J Nutr. 2008; 138(2): 305–310).

The authors note that, “Marginal copper deficiency is associated with an unfavorable metabolic pattern, but copper supplementation might not be recommended in view of its association with inflammation and markers of oxidative stress.”

In a new review article, Dr. Hamid Aliabadi of the Duke University Department of Neurosurgery notes that, “Dietary copper deficiency has been shown to cause a variety of metabolic changes, including hypercholesterolemia, hypertriglyceridemia, hypertension, and glucose intolerance” (Alibadi H. Med Hypotheses. 2008; epub ahead of print).

At the other end of the spectrum, excess copper and iron may contribute to acute myocardial infarction. Researchers at the University of Sindh, Pakistan studied serum and hair levels of zinc, copper and iron in samples from 130 MI patients and 61 healthy age-matched controls. They found consistently low zinc but high iron and copper in the MI patients, particularly those with second and third MIs, and those who died from MI versus those who survived (Kazi TG, et al. Clin Chim Acta. 2008; 389(1–2): 114–119).

Of Copper & Collagen

When people think about osteoporosis, they immediately think of calcium and vitamin D. Both are important for healthy bone. But copper is just as important, said Dr. Grabowski. It is essential for formation of the collagen component in bone, which is necessary for maintaining bone mineral density (BMD).

“I’ve had people come to me and say that they just had a BMD test done and they were surprised it was low, because they’re taking vitamin D and calcium/magnesium. I’ll do the tests, and yes, vitamin D, calcium and magnesium are fine. But then we look at copper, and it is very low. By supplementing with copper we may be able to improve BMD by improving bone collagen formation.”

As a chiropractor, Dr. Grabowski sees many patients with musculoskeletal injuries. “They’re taking all sorts of things: ibuprofen, Aleve (naproxen), high-dose vitamin C. None of these things will help create new collagen. But copper will.”

Some people take high-dose vitamin C following physical injuries, believing it speeds tissue healing. But because copper is a key factor in collagen and elastin formation, and vitamin C interferes with copper, the excess vitamin may impede rather than facilitate wound healing.

Copper Deficiency & Demyelination: An MS Mimic?

In addition to collagen formation, copper plays a central role in myelin formation. Prolonged deficiency can result in demyelination and neurodegeneration, which shows up as spastic gait, optic nerve inflammation, peripheral neuropathy, and fatigue. In many ways, it is a near-perfect mimic of multiple sclerosis.

According to Dr. Neeraj Kumar, of the Department of Neurology at the Mayo Clinic, Rochester, MN, unrecognized copper deficiency is a common cause of idiopathic myelopathy in adults. “The clinical picture bears striking similarities to the syndrome of subacute combined degeneration associated with vitamin B12 deficiency,” wrote Dr. Kumar, summing up a study of 13 Mayo Clinic patients (Kumar N, et al. Neurology. 2004; 13; 63(1): 33–39).

All had polyneuropathies, with pronounced gait difficulty and sensory ataxia. In addition to measurable copper deficiencies, 7 had high or high-normal zinc. Copper supplements restored circulating levels to normal or near normal in 7 of 12 evaluable patients; parenteral supplementation restored another 3. In all cases, repletion prevented further neurodegeneration; improvement of neurological function was variable.

Copper supplementation fairly easily reverses anemia and neutropenia, but neurologic deficits may be less responsive. “Improvement, when it occurs, is often subjective and preferentially involves sensory symptoms,” he noted (Kumar N. Mayo Clin Proc. 2006 Oct; 81(10): 1371–1384).

An earlier paper by University of Oklahoma neurologists details two cases of myelopathy, neutropenia and anemia linked to copper deficiency and zinc excess (Prodan CI, et al. Neurology. 2002; 12; 59(9): 1453–1456). In both cases, “Hematologic recovery followed copper supplementation, both initially and after relapse off copper therapy, while serum zinc levels remained high and the neurologic abnormalities only stabilized.”

Dr. Grabowski believes many patients diagnosed with MS actually have copper deficiencies. The idea is not so far-fetched. Neurologists have long recognized the value of vitamin B12 for MS, because the vitamin plays a key role in myelination. Most routinely check B12 in patients suspected of having MS. They tend to overlook copper, though it is just as important in myelination.

“It’s not that copper deficiency causes MS. It’s that copper deficiency causes demyelination, which can mimic or be mis-diagnosed as MS,” Dr. Grabowski explained. “We don’t really know if copper deficiency is involved in MS, or if giving copper to MS patients will help. But it is certainly worth thinking about.”

Testing for and Treating Copper Deficiency

Copper supplementation requires careful monitoring. Patients should not try it by themselves, as it is easy to over-do it on copper, thus interfering with zinc.

Dr. Grabowski has found that serum testing for copper is not very reliable. Methods and norms often vary from lab to lab, as was pointed out in a recent study from the University of Ipswitch, UK (Twomey PJ, et al. Int J Clin Pract. 2007; epub ahead of print). Further, serum measurements don’t show the extent to which copper is actually doing its job at the cellular level.

He told Holistic Primary Care that he much prefers the intracellular copper analysis recently introduced by SpectraCell Laboratories (www.Spectracell.com). This test shows copper levels in lymphocytes, and gives a much more accurate picture of how the mineral is taken up and utilized by cells.

Like all of SpectraCell’s tests, the copper assay is based on the fact lymphocytes are the longest-lived cells in circulation, with a typical lifetime of 120 days or more. By way of comparison, neutrophils typically live for several hours to 13 days; platelets have a lifespan of 3–7 days; red blood cells live for 90–100 days. The nutrient content of lymphocytes provides a sort of time-elapsed composite picture of a patient’s nutritional status over the last several months.

SpectraCell incorporates the copper test into its comprehensive Functional Intracellular Assessment (FIA) panel, which gives a broad survey of micronutrients and trace minerals. The FIA enables doctors to detect both deficiencies and excesses of various nutrients, and to track them over time. One can use it to assess the impact of supplementation not only on the target nutrient but on all other nutrients with which it interacts. In the case of minerals, the FIA panel details copper levels as well as iron, zinc, and other trace minerals. So one can see whether increasing copper is changing these others.

“When dealing with copper deficiencies, you need to look very closely at zinc. If I give copper supplements to try and correct a deficiency, I can end up throwing the zinc level way off. I have to test them both periodically,” said Dr. Grabowski. “It’s a balancing act, and one can go back and forth for long periods of time, increasing copper but lowering zinc, then increasing zinc but lowering copper, before one gets it right.”

http://www.holisticprimarycare.net/topics/topics-o-z/vitamins-a-supplements/354-copper-deficiency-may-underlie-osteoporosis-anemia-and-neurodegenerative-disorders

Connie’s comments: White hair may signify lack of copper. You find copper in iron-rich foods.  Up your zinc intake to increase absorption of copper. Add vinegar in salad to up mineral absorption. If you have genetic predisposition to the above, protect you and family with Index Universal Life Insurance with living benefits. Call 408-854-1883

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Peel and pulp of citrus fruits inhibit cancer and good for kidney and heart health

MCP is a derivative of pectin; a soluble dietary fibre found in the peel and pulp of citrus fruits [20], and has inhibitory effects on the progression of several animal models of cancer [24], [30]. MCP is rich in β-galactoside residues and binds to the carbohydrate recognition domain of galectin-3 [22], [23] thereby impairing the lectin’s carbohydrate binding-related functions. Therefore, it could be postulated that if MCP acted only through galectin-3 in FA nephropathy it would not have any effect on intracellular actions including proliferation and apoptosis, while modulating extracellular functions such as inflammation. This proved not the case; MCP treatment reduced tubular proliferation two days following FA administration with no differences in galectin-3 expression.

Most studies have only considered the effects of MCP in relation to galectin-3, but many other pathways could modulate proliferation here, such as MAP kinase activation [31]. One could speculate that an alternative explanation is that it is not just galectin-3 levels but also bioavailability that should be considered. It is possible that similar levels of galectin-3 have less biological effects when MCP is present because its carbohydrate binding roles will be abrogated. This cannot be measured in-vivo at present, but in-vitro studies have shown that both cell migration [24] and agglutination [32] are diminished in the presence of MCP when induced with similar concentrations of galectin-3. The reduced proliferation could also suggest renal recovery is slower in MCP-treated mice or alternatively that MCP may protect the kidney against structural injury. This second explanation is supported by the fact MCP mice have preserved body weight and their kidneys did not exhibit such acute gross swelling as those exposed to FA but maintained on water alone.

MCP decreased renal mRNA and protein levels of galectin-3 at 14 days after FA injection, in concert with significantly improved renal fibrosis as assessed by reduced expression of multiple fibrotic genes. MCP had no effect on galectin-1 and galectin-9, which are also expressed in the kidney [33], [34], suggesting these effects do not result from MCP interactions with other galectins. The direct correlation of less galectin-3 with less renal injury is consistent with studies by Henderson and colleagues [35] wherein mice lacking galectin-3 have less fibrosis and decreased collagen and α-SMA expression seven days after UUO. In contrast, a recent paper reported that fibrosis severity was increased by day 14 post UUO in galectin-3 deficient mice [11]. These observations may not relate directly to our model, however, because the pathology of chronic UUO is very different to FA-induced injury and both of these studies focussed on knock-out mice where both carbohydrate binding-dependent and -independent functions are abrogated.

The growth factor TGF-β plays a key role in the progression of renal fibrosis by promoting myofibroblastic differentiation [36] and galectin-3 has been implicated in this type of differentiation and extracellular matrix production in hepatic stellate cells [37]. MCP reduced TGF-β mRNA here, which may have contributed to reduced myofibroblast formation as evidenced by decreased α-SMA levels. An unexpected finding was the lack of significant differences in collagen III expression with MCP, which contrasts with the other profibrotic factors examined.

A correlation between galectin-3 and collagen I, but not with collagen III, was recently reported by Okamura and colleagues [11]: they noted that lack of galectin-3 led to a relative fall in collagen I but not III over time in UUO. Sharma et al. also observed differential effects of galectin-3 on different collagens [38]: they initially found that galectin-3 was strongly upregulated in an animal model of heart failure, and then infused galectin-3 into the pericardial sac of healthy rats to induce left ventricular dysfunction; this led to a 3-fold increase of collagen I over collagen III. A potential mechanism may be that the collagen I promoter, contains a high number of Sp-1 binding sites [39] through which galectin-3 might act [3] but these are not present for collagen III.

MCP also reduced inflammatory responses at day 14 of FA nephropathy which was accompanied by a loss of galectin-3 positive interstitial cells in the kidney. Galectin-3 is upregulated in several other renal diseases with prominent inflammatory components including systemic lupus erythematosus [40], experimental glomerulonephritis [41] and unilateral ureteral obstruction [11], [35]. An alternative name for galectin-3 is Mac-2 as it is abundantly expressed by subsets of macrophages [42]. Galectin-3 can act in an autocrine or parcrine fashion to induce monocyte migration [43] or alternative macrophage activation [7] and regulate cytokine expression [44]. Therefore, as part of this process is mediated by extracellular actions of galectin-3 [9], we propose that MCP effects on inflammation in FA-nephropathy may in part be mediated by galectin-3.

We also observed a small but highly significant reduction in apoptosis with MCP in the later disease phase. This difference is likely to be biologically important because Coles and colleagues [45] previously demonstrated that small changes in measured apoptosis in the kidney actually reflect larger overall changes in cell death due to apoptotic cells being cleared so quickly. Galectin-3 and MCP have different effects on apoptosis: galectin-3 has a BH1 domain of BCL2 that can protect cells from apoptosis [46], [47] and transfection with the lectin makes T-cells resistant to this type of cell death [48]; MCP, in contrast, promotes apoptosis in angiosarcoma [49] and prostate cancer cell lines [31]. This pro-apoptotic effect of MCP is formulation-dependent, however, because alterations in pH and heat-treatment (as we used here to prepare the MCP) can abrogate these pro-apoptotic effects [50]. We suspect that our observed reduction in apoptosis is not directly related to MCP actions on galectin-3 but simply reflects the reduction in disease severity with the modified pectin leading to less remodelling being required; in this case, decreased early proliferation might generate less ‘unwanted’ cells that need to be deleted by apoptosis later.

In conclusion, our data indicates that MCP is protective in experimental nephropathy through modulation of proliferation, apoptosis, fibrosis and inflammation. However, there are two caveats that need to be considered when interpreting this study. Firstly, it is possible that MCP affects other molecular pathways other than galectin-3 in FA nephropathy which need to be investigated further. Secondly, we need to exert caution when interpreting the effect of MCP on galectin-3 levels as these measurements do not account for the bioavailability of the lectin which may be altered. Nevertheless, this study does identify a new potential therapy for acute kidney injury and further experiments are warranted to examine effects of different doses of MCP, timing of treatment and roles in other renal diseases.

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3072992/

Stroke Risk Factors, take care of your heart and circulatory system

Stroke Risk Factors

Anyone can have a stroke no matter your age, race or gender. But, the chances of having a stroke increase if a person has certain risk factors, or criteria that can cause a stroke. The good news is that up to 80 percent of strokes can be prevented, and the best way to protect yourself and loved ones from stroke is to understand personal risk and how to manage it. Learn interactively about more than 20 leading risk factors for stroke through the interactive risk factor tool.

There are 2 types of risk factors for stroke: controllable and uncontrollable. Controllable risk factors generally fall into two categories: lifestyle risk factors or medical risk factors. Lifestyle risk factors can often be changed, while medical risk factors can usually be treated. Both types can be managed best by working with a doctor, who can prescribe medications and advise on how to adopt a healthy lifestyle. Uncontrollable risk factors include being over age 55, being male, being African American, Hispanic or Asian/Pacific Islander, or having a family history of stroke or transient ischemic attack (TIA).

Controllable Risk Factors:

Uncontrollable Risk Factors:
Controllable Medical Risk Factors Controllable Lifestyle Risk Factors
High Blood Pressure
Atrial Fibrillation
High Cholesterol
Diabetes
Atherosclerosis
Circulation Problems
Tobacco Use and Smoking
Alcohol Use
Physical Inactivity
Obesity

To become more familiar with your personal risk for stroke, National Stroke Association developed an easy-to-use tool called a Stroke Risk Scorecard. The Scorecard provides an idea of a person’s stroke risk. Once the scorecard is completed, discuss the results with a doctor, who will help assess the risk factors and help manage and/or treat any controllable risk factors.

Nutrition: Potassium, Magnesium and calcium, Vitamin B, C, E, A and whole foods. Avoid stress. Take probiotics and digestive enzymes. Do yoga and deep breathing. Avoid extreme weather conditions. Avoid inflammatory substances and foods. Clean air, water and organic foods if possible. Eat more good fat than unhealthy carbs.

Eat less of charred BBQ meat , marinate first

Yes, you can–for starters, the leaner the cut of meat, the better. One type of potentially cancer-causing chemical, polycyclic aromatic hydrocarbons, forms when fat from meat drips into the fire and makes flames flicker up–those flames contain PAHs, which stick to meat if they get near. Less fat means less dripping and lower risk for PAHs.

Still, a second possible carcinogen, heterocyclic amines, can form when any cut of meat is cooked at a high temperature. So consider marinating, which can create a barrier between the hot surface and the meat. And scrub leftover crispy stuff off the grill before each use. All that said, if you eat healthfully in general (grill lots of veggies with those lean burgers!), I wouldn’t worry too much about carcinogens in barbecued meat. Sure, there’s a small risk, but I firmly believe that pleasure factors into a healthy life.

Statin meds tied to cataract by Nicholas B

In one of the largest studies ever done on the subject, researchers have found that taking statins, the widely used cholesterol-lowering drugs, is associated with an increased risk for cataracts. Previous studies had mixed results.

In the latest observational study, published online in JAMA Ophthalmology, scientists retrospectively examined 13,626 statin users and 32,623 nonusers, ages 30 to 85, who were part of a military health care system. The average length of statin use was about two years.

After adjusting for more than three dozen other health and behavioral variables, the scientists found that compared with nonusers, those who took statins had a 9 to 27 percent increased risk for cataracts.

Cataract development may be influenced by statins’ effects on the oxidation process, the researchers say. The cholesterol-inhibiting properties of statins may also interfere with cell regeneration in the eye’s lens, which requires cholesterol to maintain transparency.

“If a patient takes this medication because he is at high risk for heart disease, or already has heart disease, the proven benefit of statins is much greater than the suspected risk of cataracts,” said the senior author, Dr. Ishak Mansi, a professor of medicine at the University of Texas. “But they have side effects, and doctors should not prescribe this medication lightly.”

Weird Facts about Tall and Short People by Lisa Collier Cool

On average, taller people score slightly higher on IQ tests than shorter people, according to a new study published in the journal PLOS Genetics.

If you tower over your neighbors, those findings may add inches to your ego. But don’t let height go to your head! Studies have linked both tallness and shortness to a variety of health risks and benefits.

Genes influence height and intelligence

Using data collected from twins and their parents—totalling nearly 8000 participants—researchers from the University of Colorado Boulder examined links found between elevated height and IQ.

Their findings suggest that two factors may be at play. First, it appears there are genes that influence both IQ and height, notes Matthew Keller, lead author of the study and assistant professor of psychology and neuroscience at the University of Colorado Boulder, in a statement.

“At the same time, it also looks like people who are taller are slightly more likely to choose mates who are smarter and vice versa,” adds Keller. “Such mate choice causes ‘IQ genes’ and ‘tall genes’ to become statistically associated with one another.”

Tallness comes with risks and benefits

Average intelligence isn’t the only thing that grows with height. If you are tall, you may also have a greater chance of:

  • Being bitten by bugs. The Scottish biting midge, a voracious blood-sucking bug, prefers taller and heavier people,found researchersat Rothamsted Research and the University of Aberdeen. Larger people provide larger targets, while producing more heat, moisture, carbon dioxide, and other chemicals that can attract insects.
  • Developing dangerous blood clots. Compared to shorter control groups, taller people are more likely to develop potentially life-threatening blood clots in the deep veins of their legs and other body parts, report researchers in Norway. In particular, the risk is heightened among men and women who are tall and obese.
  • Experiencing cancer. Compared to shorter peers, taller post-menopausal women are at greater risk of cancer, warn researchers in the journal of Cancer Epidemiology, Biomarkers & Prevention. In particular, multiple myeloma, melanoma, and cancers of the thyroid, rectum, kidney, endometrium, colorectum, colon, ovary, and breast are associated with tallness.
  • Earning more money. On the upside, taller men may earn more money on average than shorter men, according to research conducted in Australia. It may be that shorter men experience discrimination in response to their stature, suggest the authors, while taller men may enjoy a boost in social status.

Best Breast Cancer Blogs of 2013

Shortness comes with perks and dangers

Shortness also comes with its share of health benefits and risks. If you are short, you may have higher odds of:

  • Living longer. A recent study of nearly 500 men in Sardinia revealed that shorter fellows were likely to outlive their taller peers by an average of 2 years, based on their height at age 20. In addition, a research review published in Life Sciencesnoted that data compiled from millions of deaths suggests that people of short stature have longer lifespans.
  • Having children. According to researchers from the Netherlands, shorter women tend to have more children than taller ladies. The reasons remain unclear – but lead researcher, Gert Stulp, Ph.D., suspects that shorter women may spend more energy on reproduction. When it comes to men, Stulp found in a separate studythat those of average height appear to have the most children.
  • Developing heart disease. While deep vein blood clots are common among tall folk, the risk of cardiovascular disease in general is greater among short people. In fact, a systematic review of 52 studies found that shorter men and women are approximately 1.5 times more likely to develop symptoms and die from cardiovascular disease than taller people.
  • Having strong character and a sense of humor. John Schwartz, a reporter for The New York Times and author of Short: Walking Tall When You Are Not Tall, believes that many so-called problems associated with shortness have been manufactured or overblown by drug companies that market growth hormones. In an interview with NPR, he credits shortness and its associated stigma with pushing smaller people to work harder, become tougher, and develop a good sense of humor.

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Psychopaths can feel no empathy as shown by their brain tests

Psychopaths are usually described as lacking empathy, and a new study reveals the neurological basis for this dearth of feeling.

When people with psychopathy imagine others experiencing pain, brain regions associated with empathy and concern for others fail to activate or connect with brain areas involved in emotional processing and decision-making, researchers report.

In addition to a lack of remorse, psychopathy is characterized by shallow affect, glibness, manipulation and callousness. The rate of psychopathy is about 23 percent in prisons, compared with about 1 percent in the general population, research shows. [The 9 Most Bizarre Medical Conditions]

To investigate the neurological roots of the disorder, researchers studied 121 inmates at a medium-security prison in the United States. The inmates were divided into highly psychopathic, moderately psychopathic and weakly psychopathic groups on the basis of a widely used diagnostic tool called the Hare Psychopathy Checklist-Revised.

Researchers scanned the brains of the participants while showing them images depicting physical pain, such as a finger getting caught in a door or a toe caught under a heavy object. The participants were told to imagine the accident happening to themselves or to someone else. They were also shown images of neutral ojects, such as a hand on a doorknob.

When the highly psychopathic individuals imagined the accidents happening to themselves, their brains lit up in the anterior insula, the anterior midcingulate cortex, the somatosensory cortex and the right amygdala — all areas involved in empathy. The response was quite pronounced, suggesting psychopathic individuals were sensitive to thoughts of pain.

But when the highly psychopathic inmates imagined the accident happening to others, their brains failed to light up in the regions associated with empathy. In fact, an area involved in pleasure, the ventral striatum, lit up instead. Furthermore, these individuals showed abnormal connectivity between the insula and the ventromedial prefrontal cortex, an area important for empathetic decision-making.

By contrast, the less psychopathic individuals showed more normal brain activation and connectivity in these areas.

The strange patterns of brain activation and connectivity in highly psychopathic individuals suggest they did not experience empathy when imagining the pain of others, and possibly took pleasure in it.

The findings could help inform intervention programs for psychopathy, the researchers say. Having psychopathic people imagine themselves in pain first could be used in cognitive behavior therapies as a way of kick-starting empathy, they wrote in the study detailed today (Sept. 24) in the journal Frontiers in Human Neuroscience.

In fact, past research has shown psychopaths can feel empathy, when explicitly asked to, suggesting this ability to understand another person’s feelings may be repressed rather than missing entirely in psychopathic individuals.

 

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Now hiring recruiters, sales and business builders for financial service firm in the bayarea. Call Connie 408-854-1883 motherhealth@gmail.com or attend 1hr orientation every Tuesdays 7:15pm at 1313 N Milpitas Blvd or every Saturdays 9:45am at 400 Oyster Point Blvd, SSF, Ste 120. Wear formal suit.

Poverty remains high in most US cities from census data by Hope Yen

WASHINGTON (AP) — Even as the economy shows signs of improvement and poverty levels off, new U.S. census data suggests the gains are halting and uneven. Depending on education, race, income and even marriage, not all segments of the population are seeing an economic turnaround.

Poverty is on the rise in single-mother families. More people are falling into the lowest-income group. And after earlier signs of increased mobility, fewer people are moving as homeownership declined for a fifth straight year.

“We’re in a selective recovery,” said William H. Frey, a Brookings Institution demographer who analyzed the numbers.

The annual U.S. survey of socioeconomic indicators covers all of last year, representing the third year of a postrecession rebound.

The figures, released Thursday, also show a slightly faster pace of growth in the foreign-born population, which increased to 40.8 million, or 13 percent of the U.S. Last year’s immigration increase of 440,000 people was a reversal of a 2011 dip in the influx, when many Mexicans already in the U.S. opted to return home.

Many of the newer immigrants are now higher-skilled workers from Asian countries such as China and India. The number of immigrants in the U.S. with less than a high school diploma, who make up the bulk of the total foreign-born population, fell slightly in 2012 to 10.8 million. Immigrants with bachelor’s degrees or higher rose by more than 4 percent to 9.8 million.

In all, 21 states saw declines last year in their Hispanic foreign-born population, led by New Mexico, Illinois and Georgia.

The number of Americans in poverty remained largely unchanged at a record 46.5 million. Single-mother families in poverty increased for the fourth straight year to 4.1 million, or 41.5 percent, coinciding with longer-term trends of declining marriage and out-of-wedlock births. Many of these mothers are low income with low education. The share of married-couple families in poverty remained unchanged at 2.1 million, or 8.7 percent.

By race or ethnicity, a growing proportion of poor children are Hispanic, a record 37 percent of the total. Whites make up 30 percent, blacks 26 percent.

Nearly 2.2 million children were poor in California last year, the most of any state, but the child poverty rate was highest in Mississippi, where more than 1 in 3 children was poor. Nationwide, child poverty stood at 21.8 percent, unchanged from the previous year.

“Stubbornly high child poverty rates in the wake of the Great Recession suggest we have not yet turned the corner three years after its official end,” said Marybeth Mattingly, director of research on vulnerable families at the University of New Hampshire’s Carsey Institute.

The numbers also reflect widening economic inequality, an issue President Barack Obama has pledged would be a top priority of his administration to address. Upward mobility in the U.S. has been hurt by a tight job market and the longer-term disappearance of midskill jobs due to globalization and automation.

The new census data shows that lower-income households are a steadily increasing share of the population, while middle- to higher-income groups shrank or were flat.

In 2012, households earning less than $24,999 made up 24.4 percent of total households, up from 21.7 percent four years earlier. The share of households earning $50,000 to $99,999 slipped from 31.2 percent to 29.9 percent. Top-income households making more than $200,000 dipped less, from 5 percent to 4.6 percent over that period.

The still-weak economy also meant fewer household moves in 2012.

After showing signs of increased migration in 2011, fewer Americans were on the move, many because of few job opportunities or the inability to buy a home.

U.S. migration fell by 0.2 percent in 2012 after edging up the previous year. While the number of longer-distance moves remained steady at 2.3 percent, moves within a county edged lower to 9 percent, particularly among young adults 18-34.

Demographers say that suggests eroding career opportunities and a diminished ability to buy a home. Young adults typically make long-distance moves to seek a new career, while those who make local moves often do so when buying a home.

Homeownership declined for the fifth year in the row to 63.9 percent.

“Many Americans continue to think that a rising tide lifts all boats,” said Sheldon Danziger, a University of Michigan economist. “But the bad news is that given the way economic growth trickles down now, the number of poor and disadvantaged will remain high unless we do more to help those in need.”

With poverty remaining high, food stamp use continued to climb. Roughly 15.8 million, or 13.6 percent of U.S. households, received food stamps, the highest level on record. Just over half of these households, or 52 percent, were below poverty and 44 percent had one or more people with a disability.

By state, Oregon led the nation in food stamp use at 20.1 percent, or 1 in 5, due in part to generous state provisions that expand food stamp eligibility to families. Oregon was followed by more rural or more economically hard-hit states, including Mississippi, Kentucky, Maine, Michigan and Tennessee. Wyoming had the fewest households on food stamps, at 7 percent.

In 45 states and the District of Columbia, poverty rates remained steady at high levels. Mississippi, the poorest state in the nation, was one of just three states posting increases, from 22.6 percent to 24.2 percent. California and New Hampshire were the others.

In Minnesota and Texas, the percentage of people in poverty declined.

Among the 25 largest metropolitan areas, the Washington, D.C., area had the highest median household income in 2012 at $88,233, followed by the San Francisco and Boston metro areas. The Tampa-St. Petersburg metro area had the lowest median house income at $44,402.

The official poverty level is based on a government calculation that includes only income before tax deductions. It excludes noncash government aid such as food stamps. Counting food stamps would have boosted 4 million people, lowering the U.S. poverty rate to 13.7 percent.

Index Universal Life Insurance with Living Benefits, you get the face value without dying and get a higher return

esther pic

  • About every 26 seconds, an American will suffer a coronary event, and about every minute someone will die from one. (American Heart Association, American Stroke Association, Heart Disease and Stroke Statistics, 2008 update)
  • On average, every 40 seconds someone in the United States has a stroke. (American Heart Association, American Stroke Association, Heart Disease and Stroke Statistics, 2008 update)
  • At age 65, the odds are nearly one in two that you will require nursing home services for at least 2.5 years. (Medicare, US Dept. of Health and Human Services, 2007)
  • Fidelity Investments predicts that a 65 year old couple that retires this year will need over $200k to cover medical care cost during their retirement

Living Benefits is a rider in your life insurance so you don’t have to die to use. It covers Terminal Illness, Chronic Illness & Critical Illness, we believe you should get more from a life insurance policy. We think you should have access to benefits you can use, while you are living.

The future is unpredictable… are you and your family prepared?

Critical Illness

Provides you the option of receiving your death benefi t early if a person covered under the policy is critically ill. For purposes of this rider, critical illness is defi ned as a heart attack, stroke, cancer, a major organ transplant, blindness, or having been diagnosed with Lou Gehrig’s disease (ALS) or end stage renal failure.

Chronic Illness

Provides you the option of receiving your death benefi t early if a person covered under the policy is chronically ill. For purposes of this rider, chronic illness means that a doctor has certified that the insured is either unable to perform two of the six daily activities of living without assistance (bathing, continence, dressing, eating, toileting, and transferring) or is cognitively impaired (deterioration or loss in intellectual capacity). Benefits are available after the rider is in force for two years.

If a chronic illness exists and after a 90-day waiting period, you may:

  • Request to accelerate up to 2% of the death benefit each month to use as you wish, or
  • Leave the policy intact for your beneficiary.

This is available at no additional premium and is intended to qualify for favorable tax treatment. This benefi ts may be used for any purpose.

Terminal Illness

Provides you the option of receiving your death benefit early if a person covered under the policy is terminally ill. For purposes of this rider, terminal illness means that a doctor has certified that the insured’s death is expected within two years, one year in CT, VT and PA.

If this situation exists, you may:

  • Request the full acceleration, on a discounted basis, of the policy’s death benefit and use the lump-sum as you wish,
  • Choose to leave a portion of the policy’s death benefit intact for your beneficiary, or
  • Leave the entire policy intact for your beneficiary.

This is available at no additional premium and is intended to qualify for favorable tax treatment. This benefits may be used for any purpose.

——–Calling all college grads, retired, laid off (ages 25 and above)

Now hiring Financial Service pros to help others receive living benefits from their new or current Life Insurance (408-854-1883), get higher returns from their retirement income (8% -13%) and earn residual income while building their retirement nest egg and Plan B to be a business owner with support of a team. Call Connie to find out how to join us all over the USA with assigned field trainers and business coaching 408-854-1883 motherhealth@gmail.com pfaonline.com

Retire early

“I believe that banking institutions are more dangerous to our liberties than standing armies. If the American people ever allow private banks to control the issue of their currency, first by inflation, then by deflation, the banks and corporations that will grow up around [the banks] will deprive the people of all property until their children wake-up homeless on the continent their fathers conquered. The issuing power should be taken from the banks and restored to the people, to whom it properly belongs.” – Thomas Jefferson

Where do we get higher return of our savings?

How can we save more for our retirement?

Are community banks best for business owners and real estate investors?

What is the rule of 72, compounding our money doubles every ? years?

Are economics, finance and business subjects important for our students?

How do we retire early?

Which one is better, business owner working by himself or business owner leveraging people, time and money with full support from a team of people?

Why did Robert Kiyosaki favors network marketing as business of the 21st century?

For answers to the above questions, email motherhealth@gmail.com or call Connie 408-854-1883 or attend our Financial Opportunity Seminar every Tuesdays at 1313 N milpitas Blvd, CA and Saturdays 10am at 400 Oyster Pt Blvd SSF, Ste 120. Wear formal suit.

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Now hiring part time financial service sales, trainers and networkers in the USA. 408-854-1883 motherhealth@gmail.com

Google announces Calico, a new company focused on health , extending quality of life

Google announces Calico, a new company focused on health and well-being

MOUNTAIN VIEW, CA – September 18, 2013 – Google today announced Calico, a new company that will focus on health and well-being, in particular the challenge of aging and associated diseases. Arthur D. Levinson, Chairman and former CEO of Genentech and Chairman of Apple, will be Chief Executive Officer and a founding investor.

Announcing this new investment, Larry Page, Google CEO said: “Illness and aging affect all our families. With some longer term, moonshot thinking around healthcare and biotechnology, I believe we can improve millions of lives. It’s impossible to imagine anyone better than Art—one of the leading scientists, entrepreneurs and CEOs of our generation—to take this new venture forward.” Art said: “I’ve devoted much of my life to science and technology, with the goal of improving human health. Larry’s focus on outsized improvements has inspired me, and I’m tremendously excited about what’s next.”

Art Levinson will remain Chairman of Genentech and a director of Hoffmann-La Roche, as well as Chairman of Apple.

Commenting on Art’s new role, Franz Humer, Chairman of Hoffmann-La Roche, said: “Art’s track record at Genentech has been exemplary, and we see an interesting potential for our companies to work together going forward. We’re delighted he’ll stay on our board.”

Tim Cook, Chief Executive Officer of Apple, said: “For too many of our friends and family, life has been cut short or the quality of their life is too often lacking. Art is one of the crazy ones who thinks it doesn’t have to be this way. There is no one better suited to lead this mission and I am excited to see the results.”

Contact

Leslie Miller
Google Corporate Communications
press@google.com

 

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No hiring part time 1000 financial service sales in the USA, contact Connie 408-854-1883 motherhealth@gmail.com

http://www.pfaonline.com

This Is The New Favorite Pastime Of The Business Elite by Caroline Gregoire

Until the very end of his life, Steve Jobs was an innovator. At the tech leader and Zen Buddhism practitioner’s funeral in October 2011, friends and family received a meaningful parting gift: A wooden box containing a copy of Autobiography of a Yogi, Paramhansa Yogananda’s spiritual memoir, a story of awakening and self-realization.

“That was the message: Actualize yourself,” Salesforce CEO Marc Benioff, who attended the funeral, said recently at the 2013 TechCrunch Disrupt SF conference.

“If you look back at the history of Steve and that early trip to India … He had this incredible realization that his intuition was his greatest gift,” Benioff said. “He needed to look at world from inside out … His message was to look inside yourself and realize yourself.”

More and more business leaders in the tech world and beyond are following Jobs’ lead, tapping into their intuition through meditation, a practice that’s been linked to lower stress levels and boosts in cognitive functioning, creativity, productivity and even empathy.

Here are eight business leaders who say practicing meditation has improved their work and their lives — and sometimes led to game-changing innovation: Marc Benioff, Mark Bertolini, Jeff Weiner, Rick Rubin and many more.

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Now hiring part time financial crisis solution pro and retirement planners, 408-854-1883 ; motherhealth@gmail.com

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