Tuesday, September 30, 2014

Olive oil may revive a failing heart


A potent ingredient in olive oil may hold the key to beating heart failure, a new research suggests.
Oleate, a common dietary fat found in olive oil, restored proper metabolism of fuel in heart cells in an animal model of heart failure, researchers have found.

Heart failure is not the same as having a heart attack — it is a chronic disease state where the heart becomes enlarged, or hypertrophic, in response to chronic high blood pressure which requires it to work harder to pump blood.

As the heart walls grow thick, the volume of blood pumped out diminishes and can no longer supply the body with enough nutrients.

Failing hearts are also unable to properly process or store the fats they use for fuel, which are contained within tiny droplets called lipid bodies in heart muscle cells.

The inability to use fats, the heart's primary fuel source, causes the muscle to become starved for energy.

Fats failing hearts manage to break down into toxic intermediary by-products that further contribute to heart disease, researchers said.

The researchers at University of Illinois at Chicago College of Medicine looked at how healthy and failing hearts beating in rats reacted to being supplied with either oleate or palmitate, a fat associated with the Western diet and found in dairy products, animal fats and palm oil.

When the researchers perfused failing rat hearts with oleate, "we saw an immediate improvement in how the hearts contracted and pumped blood," said E Douglas Lewandowski, director of the UIC Center for Cardiovascular Research and senior and corresponding author on the study.

Lewandowski and colleagues tracked the location of fat molecules in the cells of the diseased hearts by tagging them with a nonradioactive heavy isotope of carbon, which is detected using magnetic resonance spectroscopy.

This technology allows researchers to watch biochemical reactions, like metabolism, as they occur in real-time in functioning organs.

Using this technique, Lewandowski noticed that the metabolism of fats within the cardiac cells of these hearts became normalised.

In contrast, when the researchers perfused the diseased hearts with palmitate, fat metabolism was imbalanced, and cells struggled to access fuel.

There was also a rise in toxic fatty byproducts — another consequence of dysregulated or impaired fat metabolism.

In addition to balancing fat metabolism and reducing toxic fat metabolites in hypertrophic hearts, Lewandowski said, oleate also increased the activation of several genes for enzymes that
metabolise fat.

"This gives more proof to the idea that consuming healthy fats like oleate can have a significantly positive effect on cardiac health," Lewandowski said.

The findings were published in the journal Circulation.



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38-year-old heart mystery explained


Scientists have explained a 38-year-old mystery of how the function of a key cardiac protein changes in heart failure.

Heart disease is the number-one killer in the developed world. The end stage of heart disease is heart failure, in which the heart cannot pump enough blood to satisfy the body's needs, researchers said.
The molecular structure of the heart muscle changes as heart failure progresses, though scientists cannot always agree on what changes are good or bad.

One change that occurs is an increase in "calcium sensitivity".

Calcium ions are pumped in and out of the muscle cell with each heartbeat, turning contractions on and off. When the calcium sensitivity increases, contractility increases, but at a price: the relaxation of the heart becomes slower.

Both phases of cardiac function are important: impaired contraction leads to systolic heart failure, while impaired relaxation leads to diastolic heart failure. Both types of heart failure are similar in terms of overall prevalence, symptoms and mortality.

Since 1976 medical researchers have known that the heart regulates its calcium sensitivity by phosphorylating (adding negative phosphate groups) to a key cardiac protein called troponin I.
The troponin complex is made up of three proteins, C, I, and T, which trigger muscle contraction in response to calcium.

In heart failure, the phosphate groups are removed from troponin I, but it wasn't known how this caused an increase in calcium sensitivity.

Peter Hwang, an assistant professor in the Department of Medicine, working with professor Brian Sykes in the Department of Biochemistry at the University of Alberta, studied the troponin complex with nuclear magnetic resonance (NMR) spectroscopy, a powerful method that uses superconducting magnets to probe atomic level structure.

They observed that unphosphorylated troponin I binds to troponin C to keep it in an optimal orientation for triggering contraction.

The (N-terminal) region of troponin I that interacts with troponin C is very positively charged, while troponin C is very negatively charged, so adding negative phosphate groups to troponin I disrupts the interaction and releases troponin C so that it becomes less efficient at triggering contraction.

"Scientists believed that the dephosphorylation of troponin I seen in heart failure somehow caused the troponin complex to become less functional," said Hwang, lead author in the study.

"Actually, the change brings it into the optimal alignment to trigger contraction. The heart has other mechanisms of regulating calcium sensitivity that probably also act by stabilising or disrupting this arrangement," Hwang said.


The study was published in the journal PNAS.




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Monday, September 29, 2014

What We Don't Know About Heart Disease Can Kill Us

Heart disease is the number one killer of people worldwide, so you'd think that we'd be up to speed on the risks. Evidently not, based on a poll of people in the United Kingdom.

Are you smarter than a Brit when it comes to risk factors? Take our quickie quiz and find out:
So are you smarter than a Brit? Here's how the 2,000 people polled by the British Heart Foundation fared:
  • Ninety percent wrongly believe that high blood pressure comes with symptoms. Alas, no.

  • One-third of people don't realize that smoking doubles the risk of having a stroke or heart attack.

  • Half of Brits said there's no link between diabetes and heart disease. In fact, people with diabetes are twice as likely to develop heart disease, and often at a younger age.

  • And maybe you don't want to worry, but cardiovascular disease is much more likely to kill you than cancer, HIV or Ebola. Heart attacks and stroke are the number one and number two causes of death, according to the World Health Organization, accounting for 14 million deaths each year.
We Americans may be a bit more up to speed than our colleagues across the pond, according to surveys by the American Heart Association. A 2013 poll found that 23 percent of Americans consider themselves at risk for heart disease, and 14 percent think it's the greatest health problem facing Americans, behind obesity and cancer.

Even better, the vast majority of people know they should be exercising more, lowering blood pressure, reducing cholesterol levels and dropping the cigarettes to reduce their risk.

Still, 43 percent of Americans think their heart health is ideal, according to the heart association poll, even though 8 percent of those folks have been diagnosed with a heart condition, and two-thirds have at least one health issue that puts them at risk.

And even though we know how to reduce risk, we aren't stepping up our efforts to have a healthy heart.


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Scientists discover early signs of pancreatic cancer

  Scientists have discovered the early signs of pancreatic cancer that show the symptoms for the disease.

Scientists at Dana-Farber Cancer Institute, of the Massachusetts Institute of Technology (MIT), US, identified that an upsurge in certain amino acids that occurs before the disease is diagnosed, is a sign of the early development of the disease.

Although the increase wasn't large enough to be the basis of a new test for early detection of the disease, the findings would help researchers understand better how pancreatic cancer affected the rest of the body, particularly how it could trigger the sometimes deadly muscle-wasting disease known as cachexia.

The researchers utilised blood samples collected years earlier from 1,500 people participating in large health-tracking studies. They analysed the samples for more than 100 different metabolites, substances produced by the metabolic process, and compared the results from participants  who had gone on to develop pancreatic cancer and those who had not.

Brian Wolpin, co-senior author of the new study said they found that the higher levels of branched chain amino acids were present in people who went on to develop pancreatic cancer compared to those who did not develop the disease.

The amount of time that would elapse before those individuals were diagnosed with pancreatic cancer ranged from two to 25 years, although the highest risk was several years before diagnosis, the researchers found. Wolpin added that it helped them to hypothesise that the increase in branched chain amino acids was due to the presence of an early pancreatic tumor.

The researchers found the increase was due to a breakdown of muscle tissue, which caused branched amino acids to be released into the bloodstream. The process was similar to what occurs in patients with cancer cachexia.

The study is due to be published in the journal Nature Medicine.


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Magnesium and its effect on Diabetics, Cardivascular Health, Osteoporosis etc

 Magnesium, an abundant mineral in the body, is naturally present in many foods, added to other food products, available as a dietary supplement, and present in some medicines (such as antacids and laxatives). Magnesium is a cofactor in more than 300 enzyme systems that regulate diverse biochemical reactions in the body, including protein synthesis, muscle and nerve function, blood glucose control, and blood pressure regulation . Magnesium is required for energy production, oxidative phosphorylation, and glycolysis. It contributes to the structural development of bone and is required for the synthesis of DNA, RNA, and the antioxidant glutathione. Magnesium also plays a role in the active transport of calcium and potassium ions across cell membranes, a process that is important to nerve impulse conduction, muscle contraction, and normal heart rhythm .

An adult body contains approximately 25 g magnesium, with 50% to 60% present in the bones and most of the rest in soft tissues . Less than 1% of total magnesium is in blood serum, and these levels are kept under tight control. Normal serum magnesium concentrations range between 0.75 and 0.95 millimoles (mmol)/L . Hypomagnesemia is defined as a serum magnesium level less than 0.75 mmol/L. Magnesium homeostasis is largely controlled by the kidney, which typically excretes about 120 mg magnesium into the urine each day. Urinary excretion is reduced when magnesium status is low .

 Assessing magnesium status is difficult because most magnesium is inside cells or in bone. The most commonly used and readily available method for assessing magnesium status is measurement of serum magnesium concentration, even though serum levels have little correlation with total body magnesium levels or concentrations in specific tissues . Other methods for assessing magnesium status include measuring magnesium concentrations in erythrocytes, saliva, and urine; measuring ionized magnesium concentrations in blood, plasma, or serum; and conducting a magnesium-loading (or "tolerance") test. No single method is considered satisfactory. Some experts  but not others consider the tolerance test (in which urinary magnesium is measured after parenteral infusion of a dose of magnesium) to be the best method to assess magnesium status in adults. To comprehensively evaluate magnesium status, both laboratory tests and a clinical assessment might be required .

Magnesium and Health

Habitually low intakes of magnesium induce changes in biochemical pathways that can increase the risk of illness over time. This section focuses on four diseases and disorders in which magnesium might be involved: hypertension and cardiovascular disease, type 2 diabetes, osteoporosis, and migraine headaches.

Hypertension and cardiovascular disease

Hypertension is a major risk factor for heart disease and stroke. Studies to date, however, have found that magnesium supplementation lowers blood pressure, at best, to only a small extent. A meta-analysis of 12 clinical trials found that magnesium supplementation for 8–26 weeks in 545 hypertensive participants resulted in only a small reduction (2.2 mmHg) in diastolic blood pressure . The dose of magnesium ranged from approximately 243 to 973 mg/day. The authors of another meta-analysis of 22 studies with 1,173 normotensive and hypertensive adults concluded that magnesium supplementation for 3–24 weeks decreased systolic blood pressure by 3–4 mmHg and diastolic blood pressure by 2–3 mmHg. The effects were somewhat larger when supplemental magnesium intakes of the participants in the nine crossover-design trials exceeded 370 mg/day. A diet containing more magnesium because of added fruits and vegetables, more low-fat or non-fat dairy products, and less fat overall was shown to lower systolic and diastolic blood pressure by an average of 5.5 and 3.0 mmHg, respectively . However, this Dietary Approaches to Stop Hypertension (DASH) diet also increases intakes of other nutrients, such as potassium and calcium, that are associated with reductions in blood pressure, so any independent contribution of magnesium cannot be determined.

Several prospective studies have examined associations between magnesium intakes and heart disease. The Atherosclerosis Risk in Communities study assessed heart disease risk factors and levels of serum magnesium in a cohort of 14,232 white and African-American men and women aged 45 to 64 years at baseline. Over an average of 12 years of follow-up, individuals in the highest quartile of the normal physiologic range of serum magnesium (at least 0.88 mmol/L) had a 38% reduced risk of sudden cardiac death compared with individuals in the lowest quartile (0.75 mmol/L or less). However, dietary magnesium intakes had no association with risk of sudden cardiac death. Another prospective study tracked 88,375 female nurses in the United States to determine whether serum magnesium levels measured early in the study and magnesium intakes from food and supplements assessed every 2 to 4 years were associated with sudden cardiac death over 26 years of follow-up . Women in the highest compared with the lowest quartile of ingested and plasma magnesium concentrations had a 34% and 77% lower risk of sudden cardiac death, respectively. Another prospective population study of 7,664 adults aged 20 to 75 years in the Netherlands who did not have cardiovascular disease found that low urinary magnesium excretion levels (a marker for low dietary magnesium intake) were associated with a higher risk of ischemic heart disease over a median follow-up period of 10.5 years. Plasma magnesium concentrations were not associated with risk of ischemic heart disease . A systematic review and meta-analysis of prospective studies found that higher serum levels of magnesium were significantly associated with a lower risk of cardiovascular disease, and higher dietary magnesium intakes (up to approximately 250 mg/day) were associated with a significantly lower risk of ischemic heart disease caused by a reduced blood supply to the heart muscle .

Higher magnesium intakes might reduce the risk of stroke. In a meta-analysis of 7 prospective trials with a total of 241,378 participants, an additional 100 mg/day magnesium in the diet was associated with an 8% decreased risk of total stroke, especially ischemic rather than hemorrhagic stroke . One limitation of such observational studies, however, is the possibility of confounding with other nutrients or dietary components that could also affect the risk of stroke.

A large, well-designed clinical trial is needed to better understand the contributions of magnesium from food and dietary supplements to heart health and the primary prevention of cardiovascular disease .

Type 2 diabetes

Diets with higher amounts of magnesium are associated with a significantly lower risk of diabetes, possibly because of the important role of magnesium in glucose metabolism . Hypomagnesemia might worsen insulin resistance, a condition that often precedes diabetes, or it might be a consequence of insulin resistance . Diabetes leads to increased urinary losses of magnesium, and the subsequent magnesium inadequacy might impair insulin secretion and action, thereby worsening diabetes control .

Most investigations of magnesium intake and risk of type 2 diabetes have been prospective cohort studies. A meta-analysis of 7 of these studies, which included 286,668 patients and 10,912 cases of diabetes over 6 to 17 years of follow-up, found that a 100 mg/day increase in total magnesium intake decreased the risk of diabetes by a statistically significant 15% . Another meta-analysis of 8 prospective cohort studies that followed 271,869 men and women over 4 to 18 years found a significant inverse association between magnesium intake from food and risk of type 2 diabetes; the relative risk reduction was 23% when the highest to lowest intakes were compared .

A 2011 meta-analysis of prospective cohort studies of the association between magnesium intake and risk of type 2 diabetes included 13 studies with a total of 536,318 participants and 24,516 cases of diabetes . The mean length of follow-up ranged from 4 to 20 years. Investigators found an inverse association between magnesium intake and risk of type 2 diabetes in a dose-responsive fashion, but this association achieved statistical significance only in overweight (body mass index [BMI] 25 or higher) but not normal-weight individuals (BMI less than 25). Again, a limitation of these observational studies is the possibility of confounding with other dietary components or lifestyle or environmental variables that are correlated with magnesium intake.

Only a few small, short-term clinical trials have examined the potential effects of supplemental magnesium on control of type 2 diabetes and the results are conflicting . For example, 128 patients with poorly controlled diabetes in a Brazilian clinical trial received a placebo or a supplement containing either 500 mg/day or 1,000 mg/day magnesium oxide (providing 300 or 600 mg elemental magnesium, respectively) . After 30 days of supplementation, plasma, cellular, and urine magnesium levels increased in participants receiving the larger dose of the supplement, and their glycemic control improved. In another small trial in Mexico, participants with type 2 diabetes and hypomagnesemia who received a liquid supplement of magnesium chloride (providing 300 mg/day elemental magnesium) for 16 weeks showed significant reductions in fasting glucose and glycosylated hemoglobin concentrations compared with participants receiving a placebo, and their serum magnesium levels became normal . In contrast, neither a supplement of magnesium aspartate (providing 369 mg/day elemental magnesium) nor a placebo taken for 3 months had any effect on glycemic control in 50 patients with type 2 diabetes who were taking insulin .

The American Diabetes Association states that there is insufficient evidence to support the routine use of magnesium to improve glycemic control in people with diabetes . It further notes that there is no clear scientific evidence that vitamin and mineral supplementation benefits people with diabetes who do not have underlying nutritional deficiencies.

Osteoporosis

Magnesium is involved in bone formation and influences the activities of osteoblasts and osteoclasts . Magnesium also affects the concentrations of both parathyroid hormone and the active form of vitamin D, which are major regulators of bone homeostasis. Several population-based studies have found positive associations between magnesium intake and bone mineral density in both men and women . Other research has found that women with osteoporosis have lower serum magnesium levels than women with osteopenia and those who do not have osteoporosis or osteopenia . These and other findings indicate that magnesium deficiency might be a risk factor for osteoporosis .
Although limited in number, studies suggest that increasing magnesium intakes from food or supplements might increase bone mineral density in postmenopausal and elderly women . For example, one short-term study found that 290 mg/day elemental magnesium (as magnesium citrate) for 30 days in 20 postmenopausal women with osteoporosis suppressed bone turnover compared with placebo, suggesting that bone loss decreased .

Diets that provide recommended levels of magnesium enhance bone health, but further research is needed to elucidate the role of magnesium in the prevention and management of osteoporosis.

Migraine headaches

Magnesium deficiency is related to factors that promote headaches, including neurotransmitter release and vasoconstriction . People who experience migraine headaches have lower levels of serum and tissue magnesium than those who do not.

However, research on the use of magnesium supplements to prevent or reduce symptoms of migraine headaches is limited. Three of four small, short-term, placebo-controlled trials found modest reductions in the frequency of migraines in patients given up to 600 mg/day magnesium . The authors of a review on migraine prophylaxis suggested that taking 300 mg magnesium twice a day, either alone or in combination with medication, can prevent migraines .

In their evidence-based guideline update, the American Academy of Neurology and the American Headache Society concluded that magnesium therapy is "probably effective" for migraine prevention. Because the typical dose of magnesium used for migraine prevention exceeds the UL, this treatment should be used only under the direction and supervision of a healthcare provider.

Health Risks from Excessive Magnesium

Too much magnesium from food does not pose a health risk in healthy individuals because the kidneys eliminate excess amounts in the urine . However, high doses of magnesium from dietary supplements or medications often result in diarrhea that can be accompanied by nausea and abdominal cramping . Forms of magnesium most commonly reported to cause diarrhea include magnesium carbonate, chloride, gluconate, and oxide. The diarrhea and laxative effects of magnesium salts are due to the osmotic activity of unabsorbed salts in the intestine and colon and the stimulation of gastric motility .

Very large doses of magnesium-containing laxatives and antacids (typically providing more than 5,000 mg/day magnesium) have been associated with magnesium toxicity , including fatal hypermagnesemia in a 28-month-old boy  and an elderly man . Symptoms of magnesium toxicity, which usually develop after serum concentrations exceed 1.74–2.61 mmol/L, can include hypotension, nausea, vomiting, facial flushing, retention of urine, ileus, depression, and lethargy before progressing to muscle weakness, difficulty breathing, extreme hypotension, irregular heartbeat, and cardiac arrest . The risk of magnesium toxicity increases with impaired renal function or kidney failure because the ability to remove excess magnesium is reduced or lost .


Magnesium Deficiency

Symptomatic magnesium deficiency due to low dietary intake in otherwise-healthy people is uncommon because the kidneys limit urinary excretion of this mineral . However, habitually low intakes or excessive losses of magnesium due to certain health conditions, chronic alcoholism, and/or the use of certain medications can lead to magnesium deficiency.

Early signs of magnesium deficiency include loss of appetite, nausea, vomiting, fatigue, and weakness. As magnesium deficiency worsens, numbness, tingling, muscle contractions and cramps, seizures, personality changes, abnormal heart rhythms, and coronary spasms can occur . Severe magnesium deficiency can result in hypocalcemia or hypokalemia (low serum calcium or potassium levels, respectively) because mineral homeostasis is disrupted .

 Selected Food Sources of Magnesium

foods Milligrams
(mg) per
serving
Percent
DV*
Almonds, dry roasted, 1 ounce8020
Spinach, boiled, ½ cup7820
Cashews, dry roasted, 1 ounce7419
Peanuts, oil roasted, ¼ cup6316
Cereal, shredded wheat, 2 large biscuits6115
Soymilk, plain or vanilla, 1 cup6115
Black beans, cooked, ½ cup6015
Edamame, shelled, cooked, ½ cup5013
Peanut butter, smooth, 2 tablespoons4912
Bread, whole wheat, 2 slices4612
Avocado, cubed, 1 cup4411
Potato, baked with skin, 3.5 ounces4311
Rice, brown, cooked, ½ cup4211
Yogurt, plain, low fat, 8 ounces4211
Breakfast cereals, fortified with 10% of the DV for magnesium4010
Oatmeal, instant, 1 packet369
Kidney beans, canned, ½ cup359
Banana, 1 medium328
Salmon, Atlantic, farmed, cooked, 3 ounces267
Milk, 1 cup24–276–7
Halibut, cooked, 3 ounces246
Raisins, ½ cup236
Chicken breast, roasted, 3 ounces226
Beef, ground, 90% lean, pan broiled, 3 ounces205
Broccoli, chopped and cooked, ½ cup123
Rice, white, cooked, ½ cup103
Apple, 1 medium92
Carrot, raw, 1 medium72
*DV = Daily Value. The DV for magnesium is 400 mg for adults and children aged 4 and older. Foods providing 20% or more of the DV are considered to be high sources of a nutrient.

 Recommended Dietary Allowances (RDAs) for Magnesium

Age Male Female Pregnancy Lactation
Birth to 6 months30 mg*30 mg*  
7–12 months75 mg*75 mg*  
1–3 years80 mg80 mg  
4–8 years130 mg130 mg  
9–13 years240 mg240 mg  
14–18 years410 mg360 mg400 mg360 mg
19–30 years400 mg310 mg350 mg310 mg
31–50 years420 mg320 mg360 mg320 mg
51+ years420 mg320 mg  
*Adequate Intake (AI)
 ps- note that there are risks by taking excessive of magnesium, so kindly consult your doctor before taking any steps.

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