Low magnesium levels makes Vitamin D ineffective

Vitamin D can't be metabolized without sufficient magnesium levels. Without magnesium, Vitamin D is not really useful or safe," says study co-author Mohammed S. Razzaque, MBBS, PhD, a professor of pathology at Lake Erie College of Osteopathic Medicine. Razzaque explains that consumption of Vitamin D supplements can increase calcium and phosphate levels even if Vitamin D is deficient. People may suffer from vascular calcification if their magnesium levels aren't high enough to prevent the complication.

Patients with optimum magnesium levels require less Vitamin D supplementation to achieve sufficient Vitamin D levels. Magnesium also reduces osteoporosis, helping to mitigate the risk of bone fracture that can be attributed to low levels of Vitamin D. Deficiency in either of these nutrients is reported to be associated with various disorders, including skeletal deformities, cardiovascular diseases, and metabolic syndrome.

While the recommended daily allowance for magnesium is 420 mg for males and 320 mg for females. Magnesium status is low in people who consume processed foods that are high in refined grains, fat, phosphate, and sugar. Consuming an optimal amount of magnesium may lower the risks of Vitamin D deficiency, and reduce the dependency on Vitamin D supplements.

Magnesium is the fourth most abundant mineral in the human body after calcium, potassium, and sodium. Foods high in magnesium are almonds, bananas, beans, broccoli, brown rice, cashews, egg yolk, fish oil, flaxseed, green vegetables, milk, mushrooms, nuts, oatmeal, pumpkin seeds, sesame seeds, soybeans, sunflower seeds, sweet corn, tofu, and whole grains.
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Links between gut bacteria and obesity

A new Johns Hopkins study of mice with the rodent equivalent of metabolic syndrome has added to evidence that the intestinal microbiome-a "garden" of bacterial, viral and fungal genes plays a substantial role in the development of obesity and insulin resistance in mammals, including humans.

Highlighting the potential to prevent obesity and diabetes by manipulating levels and ratios of gut bacteria, and modifying the chemical and biological pathways for metabolism-activating genes.

Metabolic syndrome, a cluster of conditions including obesity around the waist, high blood sugar and increased blood pressure, is a risk factor for heart disease, stroke and diabetes. While no precise cause for metabolic syndrome is known, previous studies of Toll-like receptor 4 (TLR4), a protein that receives chemical signals to activate inflammation, have suggested that TLR4 may be responsible in part for its development.

TLR4 signaling in different cells and their association with the bacterial environment could result in different effects on the development of metabolic syndrome. To determine whether TLR4 specifically in the intestinal epithelium (layer of cells that line the small and large intestines) would cause the development of metabolic syndrome, the research team ran a series of experiments on normal mice and mice genetically modified to lack TLR4 in their intestinal epithelium.

The researchers fed both groups of mice "standard chow," with 22 percent fat calories, for 21 weeks. Compared to normal mice, those lacking TLR4 showed a series of symptoms consistent with metabolic syndrome, such as significant weight gain, increased body and liver fat, and insulin resistance. The researchers then fed both groups of mice a high-fat diet comprised of 60 percent fat calories for 21 weeks to find out whether diet would affect the development of metabolic syndrome.

The genetically modified mice gained significantly more in weight and had greater body and liver fat than the normal mice. To confirm the role of TLR4 expression in the intestinal epithelium, the researchers genetically modified three more groups of mice: one group expressed TLR4 only in the intestinal epithelium, another group lacked TLR4 in all body cells and the third group lacked TLR4 only in white blood cells.

All groups ate standard chow, and all groups had similar body weight, body and liver fat, and glucose tolerance compared to normal mice. Compared with normal mice, belly and small intestine fat was higher in mice lacking TLR4 only in the intestinal epithelium. This, the researchers say, provides further evidence that deleting TLR4 specifically from the intestinal epithelium is required for developing metabolic syndrome.

To investigate the role the bacterial makeup of the gut had on the mice, they administered antibiotics to the normal and TLR4 intestinal epithelium-deficient mice. Antibiotics significantly reduced the amount of bacteria in the intestinal tract and prevented all symptoms of metabolic syndrome in the mice that lacked TLR4 in their intestinal epitheliums.

This shows that bacterial levels can be manipulated to prevent the development of metabolic syndrome. To further explore the role of intestinal epithelial TLR4 on the development of metabolic syndrome, the research team analyzed fecal samples from the TLR4 intestinal epithelium-deficient and normal mice.

The team found that specific clusters of bacteria that contribute to the development of metabolic syndrome were expressed differently in the deficient mice than in normal mice. They also determined that the bacteria expressed genes that made them "less hungry" and thus less able to digest the nutrients present in the mouse chow. This resulted in a greater abundance of food for the mouse to absorb, which contributed to obesity.

The researchers then analyzed the genes expressed in the lining of the intestinal mucosa-the site at which food absorption occurs in normal and TLR4 intestinal epithelium -deficient mice. Of note, the team determined that important genes in the perixisome proliferator-activated receptor (PPAR) metabolic pathway were significantly suppressed in the deficient mice.

Administering antibiotics prevented the differences in gene regulation between the two groups of mice, as did administering drugs to activate the PPAR signaling pathway. The bacterial sensor TLR4 regulates both host and bacterial genes that play unrecognized roles in energy metabolism leading to the development of metabolic syndrome in
mice.
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Air pollution linked to irregular menstruation

Air breathes in may be causing irregular menstrual cycles. Well documented negative health effects from air pollution exposure include infertility, metabolic syndrome and polycystic ovary syndrome. This study is the first to show that exposure to air pollution among teen girls (ages 14-18) is associated with slightly increased chances of menstrual irregularity and longer time to achieve such regularity in high school and early adulthood.

While air pollution exposures have been linked to cardiovascular and pulmonary disease, this study suggests there may be other systems, such as the reproductive endocrine system, that are affected as well," said corresponding author Shruthi Mahalingaiah, MD, MS, assistant professor of obstetrics and gynecology at Boston University School of Medicine and a physician in obstetrics and gynecology at Boston Medical Center.

The menstrual cycle is responsive to hormonal regulation. Particulate matter air pollution has demonstrated hormonal activity. However, it was not known if air pollution was associated with menstrual cycle regularity, until now. The researchers used health and location data gathered in the Nurses' Health Study 2 plus air pollution exposure metrics from the EPA air quality monitoring system to understand a participants' exposure during a particular time window. They found exposure to air pollution in during high school was correlated with menstrual cycle irregularity.
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Effects of DNA on dieting

Research in animal models with different genetics shows that one diet really doesn't fit all, and what works for some may not be best for others. The researchers used four different groups of animal models to look at how five diets affect health over a six-month period. The genetic differences within each group were almost non-existent, while the genetics between any two of the groups would translate to roughly the same as those of two unrelated people.

The researchers chose the test diets to mirror those eaten by humans-an American-style diet (higher in fat and refined carbohydrates, especially corn) and three that have gotten publicity as being 'healthier': Mediterranean (with wheat and red wine extract), Japanese (with rice and green tea extract) and ketogenic, or Atkins-like (high in fat and protein with very few carbs).

The fifth diet was the control group who ate standard commercial chow.
Although some so-called healthy diets did work well for most individuals, one of the four genetic types did very poorly when eating the Japanese-like diet, for example. The fourth strain, which performed just fine on all of the other diets, did terrible on this diet, with increased fat in the liver and markings of liver damage.

They measured physical signs, especially evidence of metabolic syndrome, which is a collection of signs of obesity-related problems, including high blood pressure and cholesterol, fatty liver and levels of blood sugar. They also studied any behavioral differences, from how much they moved around to how much they ate.

Perhaps as could be expected, both in earlier research and in anecdotal evidence in humans, the animal models tended not to do great on the American-style diet. A couple of the strains became very obese and had signs of metabolic syndrome. Other strains showed fewer negative effects, with one showing few changes except for having somewhat more fat in the liver.

With the Mediterranean diet, there was a mix of effects. Some groups were healthy, while others experienced weight gain, although it was less severe than in the American diet. The results demonstrated that a diet that makes one individual lean and healthy might have the complete opposite effect on another. It depends very much on the genetics of the individual and there isn't one diet that is best for everyone.
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Drinking of alcohol and metabolic factors increase the risk of liver disease

There is an increasing burden of liver disease and liver cancer. The metabolic syndrome and heavy alcohol consumption are associated with increased risks of liver disease, although only a minority of patients with early-stage liver disease (e.g. fatty liver) develop liver failure or liver cancer. Few general population studies have analyzed metabolic predictors of such severe liver complications.

Researchers studied which metabolic factors best predict severe liver complications. Their analysis included people without liver disease who participated in the Finnish population-based Health 2000 Study (2000-2001). The researchers analyzed follow-up data on liver-related hospital admissions, mortality, and liver cancer from national registers.

Some of the participants experienced a severe liver event during follow-up. Factors predictive of liver events were older age, female gender, alcohol use, diabetes, LDL cholesterol, and insulin resistance. Among individuals who consumed higher amounts of alcohol (average alcohol use ?210 g/week for men, ?140 g/week for women), diabetes was the only significant predictor.

Among those who consumed less or no alcohol, older age, alcohol use, smoking, abdominal obesity, LDL cholesterol, and insulin resistance were significant predictors. Alcoholic liver disease ALD and non-alcoholic liver disease NAFLD are considered separate entities, distinguished from each other by an arbitrary threshold of average alcohol intake.

This diagnostic approach assumes that alcohol intake does not affect the course of NAFLD and that the metabolic syndrome is the hallmark of NAFLD is not a factor in ALD. This study reveals that alcohol is a relevant risk factor even when alcohol consumption is within the limits currently used to separate NAFLD from ALD.

Liver disease should perhaps not be considered in terms of mutually exclusive entities of ALD and NAFLD, because in a large number of patients with liver disease, the effect of alcohol is difficult, and sometimes impossible, to separate from the effect of metabolic factors.

 Alcohol use and metabolic factors are taken into account at the same time in order to identify individuals with a high risk for severe liver complications. For a comprehensive liver-risk assessment, lipid abnormalities, abdominal obesity, insulin resistance, diabetes, and alcohol use should all be considered at the same time.
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Foods for healthy heart

Lutein is a xantrophyll-  yellow pigments from the carotenoid family, it is present in brightly coloured vegetables and fruit like yellow and red peppers, kale, carrots, broccoli and spinach. It can reduce risk of cardiovascular disease.

Poor diet increases inflammatory processes in the body. Inflammation is a major factor in many types of coronary artery disease, such as myocardial infarction, lutein has ability to protect tissues from oxidative stress and inflammation.

Regular intake of healthy diet can reduce risk of developing cardiovascular heart disease. High blood concentrations of lutein can reduce coronary heart disease, stroke, and metabolic syndrome.

Lutein is absorbed and stored by the cells of the immune system in the blood.
The higher the level of lutein in the blood, the lower the level of inflammation in the body. Lutein treatment lowers the inflammatory activity of the cells.
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How your brain eat itself

Your brain starts to eat itself if it hasn't had enough sleep, according to a new study. Researchers studied lab mice
and discovered that 'clean-up' cells were more active in their brains when they were sleep-deprived.

The cells act like mini Hoovers in the brain, sweeping up cells as the brain's connections become weak and break apart.

Sleeping for  less than six hours per night is associated with a higher risk of death in people with metabolic syndrome – a combination of diabetes, high blood pressure.

Researchers said the effect was particularly strong in those with elevated blood pressure or poor glucose metabolism.

People with a common cluster of risk factors for heart disease and diabetes were around twice as likely to die of heart disease or stroke as people without the same set of risk factors if they failed to get more than six hours of sleep, according to the study published in the Journal of the American Heart Association.

The researchers randomly selected 1,344 adults with an average age of 49 who agreed to spend one night in a sleep laboratory.

Based on their test results, 39.2 per cent of the participants were found to have at least three of the risk factors, that when clustered together are known as the metabolic syndrome.

Natural cure for high blood pressure

Having high blood pressure increases your risk of having a heart attack or stroke. It can also lead to other problems, like kidney failure, heart failure and blurred vision.

The British Heart Foundation said: “Blood pressure is the pressure of blood running through your arteries. You need a certain amount of pressure in your arteries to keep the blood flowing.”

Experts have revealed a supplement - which is the extract of French Maritime pine bark has been used to normalise blood pressure.

Pycnogenol was investigated in a double-blind, placebo controlled study for patients with borderline hypertension.

The participants were not yet receiving
hypotensive medication. Researchers
have revealed use of Pycnogenol over a period of eight weeks lowered blood systolic blood pressure as compared to placebo.

Experts also found diastolic pressure was found to be lowered as well. Diastolic pressure is the lowest pressure, which occurs between heartbeats when your heart is relaxing.

The innermost layer of our blood vessels are lined with collagen and elastin which help our veins to expand and contract in response to blood flow and keep blood pressure within a normal range.

Pycnogenol, French maritime pine bark extract has been shown in multiple studies to supports the production of collagen and elastin in the body which results in stronger blood vessels.

Pycnogenol improves blood pressure and kidney function in patients with diabetes and metabolic syndrome. The
active ingredients in Pycnogenol can also be extracted from peanut skin, grape seed, and witch hazel bark.