Vitamins and Minerals: micronutrients

Micronutrients are the vitamins and minerals found in food that nourish your body and help to keep you healthy.

According to the U.S. Department of Agriculture (USDA), adult Americans do not typically get enough of the following nutrients:
• Calcium
• Potassium
• Fiber
• Magnesium
• Vitamins A, C and E
Try to incorporate more of these nutrients in your daily diet. Keep in mind that it's best to consume a variety of foods, instead of just taking a multivitamin, to make sure that your body is able to absorb the micronutrients properly.

Read More »»

Exercise Benefits part2

Exercise Health Benefit 7: A hedge against colon cancer
Colon cancer is one of the leading causes of cancer death in men. Approximately 80% of cases of this disease could be prevented. A healthier diet (with more fiber and whole grains) is part of the prescription. But exercise turns out to be just as important as diet. Studies have shown that physical activity may reduce colon cancer risk by as much as 30 to 40%.
Exercise Health Benefit 8: Strong bones
Another unwelcome effect of aging is thinning bones, which can lead to a greater risk of fractures. In a study that followed 3,262 men from their 40s to their 60s, strenuous physical activity dramatically lowered the risk of hip fractures.
Exercise Health Benefit 9: Weight loss
A lifetime of regular physical activity — even activities as simple as walking half an hour most days — can help keep that belly from bulging over your belt. 3500 calories in one pound.
Exercise Health Benefit 10: A longer life
Add it all up and an active life also means a longer and healthier life. In a 2004 study researchers followed 15,853 men aged 30 to 59. Over a 20 year period, men who engaged in physically active leisure activities — jogging, skiing, swimming, playing ball, or doing serious gardening — were up to 21% less likely to develop cardiovascular disease or to die of any cause during the study period.
How much exercise do you need to reap these health benefits?
The answer to how much exercise you need depends partly on what you’re after. Burning about 1,000 extra calories a week in activities is likely to extend your life. Walking half an hour most days of the week is all you need to significantly lower your risk of colon cancer and diabetes. But the more physical activities you can weave into your daily life, the healthier you’ll be. Most studies of physical activity show a strong dose-response rate, the more you do, the more you benefit.

Read More »»

Exercise Benefits

Exercise Health Benefit 1: Lower cholesterol
As most men get older, cholesterol numbers begin to move in the wrong direction. Levels of so-called bad cholesterol — low-density lipoprotein (LDL) — gradually increase. Levels of good cholesterol, called high-density lipoprotein (HDL), tend to fall. Unfortunately, that combination of high LDL and low HDL is one of the leading risk factors for heart disease. Excess cholesterol accumulates on the inner lining of blood vessels, leading to arthrosclerosis and heart attacks. The best way to keep LDL cholesterol levels down is to eat a diet low in saturated fat (the kind found in meat and high-fat dairy products.) The single best way to boost good HDL cholesterol? Exercise. Limit cholesterol in diet to 300 mg/day.
Exercise Health Benefit 2: Lower triglycerides
Triglycerides are a form of fat found in the blood. Rising triglyceride levels are associated with increased risk of heart disease.
Exercise Health Benefit 3: Lower risk of high blood pressure
As blood pressure climbs, the risk of heart disease and stroke accelerates. Unfortunately, blood pressure levels typically climb as men get older.
Exercise Health Benefit 4: Reduced inflammation
Regular exercise has been shown to reduce levels of C-reactive protein, a measure of inflammation. That matters because cholesterol-laden plaques on the lining of arteries are most likely to break off and cause heart attacks when they become inflamed.
Exercise Health Benefit 5: Better blood vessels
To respond to changing demands for oxygen, blood vessels must be flexible enough to widen and narrow. Smoking, cholesterol build-up, and just plain aging tend to stiffen vessels, increasing heart attack risk. A growing number of studies show that exercise training helps maintain the ability of blood vessels to open and constrict in response to changing physical demands.
Exercise Health Benefit 6: Lower risk of diabetes
Adult onset diabetes — fueled mostly by too much body fat — is one of the biggest health worries on the horizon. Staying active can help you keep the weight off. But research shows that even for people who are overweight or obese, exercise reduces the risk of diabetes. The Diabetes Prevention Program found that an exercise and weight loss program lowered the risk of type 2 diabetes by a whopping 58% over a three-year period. And the volunteers in that program weren’t running marathons. In fact, the exercise they were doing was the equivalent of burning only an additional 593 calories of energy — about the equivalent of walking around six miles a week for most men.

Read More »»

Injuries

The leading cause of fatal accidents among men is motor vehicle crashes, according to the CDC. To reduce your risk of a deadly crash:
Wear your seat belt.
Follow the speed limit.
Don't drive under the influence of alcohol or any other substances.
Don't drive while sleepy.
Falls and poisoning are other leading causes of fatal accidents. Take common-sense precautions, such as using chemical products only in ventilated areas, using non-slip mats in the bathtub and placing carbon monoxide detectors near the bedrooms in your home.

Read More »»

Cancer

Lung cancer is the leading cause of cancer deaths among men — mostly due to cigarette smoking, according to the American Cancer Society. Lung cancer is followed by prostate cancer and colorectal cancer. To decrease the risk of cancer:
Don't smoke or use other tobacco products. Avoid exposure to secondhand smoke.
Include physical activity in your daily routine.
Eat a healthy diet rich in fruits and vegetables, and avoid high-fat foods.
Limit your sun exposure. When you're outdoors, use sunscreen.
If you choose to drink alcohol, do so only in moderation.
Consult your doctor for regular cancer screenings.

Read More »»

Heart disease

Eat a healthy diet rich in vegetables, fruits, whole grains, fiber and fish. Cut back on foods high in saturated fat and sodium.
If you have high cholesterol or high blood pressure, follow your doctor's treatment recommendations.
Include physical activity in your daily routine.
Don't smoke or use other tobacco products. Avoid exposure to secondhand smoke.
Maintain a healthy weight.
If you choose to drink alcohol, do so only in moderation. Too much alcohol can raise blood pressure.
If you have diabetes, keep your blood sugar under control.
Manage stress.

Read More »»

Big picture strategies for healthy eating

Eat enough calories but not too many. Maintain a balance between your calorie intake and calorie expenditure—that is, don't eat more food than your body uses. The average recommended daily allowance is 2,000 calories, but this depends on your age, sex, height, weight, and physical activity.
Eat a wide variety of foods. Healthy eating is an opportunity to expand your range of choices by trying foods—especially vegetables, whole grains, or fruits—that you don't normally eat.

Keep portions moderate, especially high-calorie foods. In recent years serving sizes have ballooned, particularly in restaurants. Choose a starter instead of an entrée, split a dish with a friend, and don’t order supersized anything.

Eat plenty of fruits, vegetables, grains, and legumes—foods high in complex carbohydrates, fiber, vitamins, and minerals, low in fat, and free of cholesterol. Try to get fresh, local produce

Drink more water. Our bodies are about 75% water. It is a vital part of a healthy diet. Water helps flush our systems, especially the kidneys and bladder, of waste products and toxins. A majority of Americans go through life dehydrated.

Limit sugary foods, salt, and refined-grain products. Sugar is added to a vast array of foods. In a year, just one daily 12-ounce can of soda (160 calories) can increase your weight by 16 pounds. See suggestions below for limiting salt and substituting whole grains for refined grains.

Don’t be the food police. You can enjoy your favorite sweets and fried foods in moderation, as long as they are an occasional part of your overall healthy diet. Food is a great source of pleasure, and pleasure is good for the heart – even if those French fries aren’t!

Get moving. A healthy diet improves your energy and feelings of well-being while reducing your risk of many diseases. Adding regular physical activity and exercise will make any healthy eating plan work even better.

One step at a time. Establishing new food habits is much easier if you focus on and take action on one food group or food fact at a time

Read More »»

H1N1-influenza as Lazarus: Genomic resurrection from the tomb of an unknown

The 1918–1919 pandemic of H1N1 virus influenza was the greatest acute plague of the 20th century. Incurring over 20 million human fatalities, however, was not a good strategy for sustaining the evolutionary fitness of the virus, because it is no longer extant; whereas, say, measles and chickenpox remain with us with no evidence of remarkable genetic change, although this may become more evident if they were to face total or near eradication through vaccination programs. The folly of flu virulence remains our chagrin, because the threat always looms over us that this family of viruses, endemic in birds, again may generate human-lethal gene reassortments. We had valid scares about that contingency with the appearance of H5N1 variant flu in Hong Kong just 3 years ago. Influenza can be regarded as a zoonosis prevalent in birds, many of them world travelers, with occasional outbreaks in humans and other animals mainly rooted in nature's own experiments in genetic engineering. Special importance is attached to reassortments between bird- and human-adapted strains most likely to occur in habitats with close contact between birds, e.g., ducks, humans, and swine (as a mixing reservoir; ref.
1). For these reasons, high urgency attaches to efforts to resurrect genetic information about the singularities of H1N1–1918. The intact virus is nowhere to be found, but genomic fragments can still be detected sensitively and diagnosed. Exemplifying the latest technical advances in the use of DNA amplification, reverse-transcriptase–PCR (RT-PCR), Jeffery Taubenberger and his associates at the Armed Forces Institute of Pathology initiated the tour de force of recovering sequences of flu from paraffin-embedded pathological specimens preserved since 1918 in the AFIP collections
(2). These sources then were augmented by samples from frozen remains of an Inuit woman who succumbed to the flu in 1918 and was buried in permafrost at Brevig Mission on the Seward Peninsula of Alaska's western coast, not far from the Bering Strait. This nameless woman has left an indelible mark on world medical history
(3). Now, as reported in this issue, the AFIP team has joined forces with teams from the U.S. Department of Agriculture and the Peter Palese/Adolfo García-Sastre groups at Mt. Sinai Medical School in a further quest for the RNA sequences of H1N1–1918 that might account for its historic human virulence
(4).

The flu genome comprises about 13,500 bases of single-stranded RNA, disposed in eight segments varying from approximately 900 to 2,341 each. This genome is only a few millionths of the complexity of the human genome, but it is organized with great efficiency, lacks “junk R/DNA,” and encodes for a short dozen of identified gene products (Fig. 1). Many strains of flu have been sequenced fully; this feat will be achieved for H1N1–1918 with arduous labor, because the RNA, although frozen, is fragmented into snippets no larger than approximately 120 bases each. The practical way now available is to devise probes by using segments from extant flu strains, guessing at possible homologous strings, or synthesizing probes with calculated degeneracy. Until a complete genomic sequence is achieved, and it is hard to see how that will be authenticated, it is possible even that H1N1–1918 contains extraneous inserted sequences quite foreign to the canonical flu strains. Very reasonably, initial efforts focus on flu genes already identified in viruses recovered from recent outbreaks in humans, birds, swine, and other animals.
Previous work has focused on two well studied gene products: hemagglutinin (HA) and neuraminidase (NA), which dominate the surface specificities of the virus and underlie most of its taxonomy (e.g., H1N1 refers to type 1 hemagglutinin, type 1 neuraminidase). These gene products are also the chief determinants of specificity in vaccine prophylaxis for flu strains circulating at any given time. HA variation can account for fluctuations of virulence and host specificity of extant flu viruses. However, nothing remarkable was seen in the HA or the NA of H1N1–1918. The next gene to be scrutinized now is NS1 (nonstructural protein 1), which the Palese/García-Sastre groups have fingered recently as an interferon antagonist and as gene essential for flu virulence in a mouse model. A reasonable conjecture was that the hypervirulence of H1N1–1918 might be lodged in its NS1, and this might be revealed in reinsertions of the 1918-NS1 segment into mouse-adapted flu strains. This challenging construct was generated in the laboratory—one hastens to footnote, under BL-3+ conditions, and under the USDA's stern regulatory scrutiny—and tested in mice. The unexpected and perhaps disappointing result was the mitigation not enhancement of virulence in this species. The incapacitation of the NS1-virulence function in the mouse was ascribed to interaction with its host factors; the other variable would be other elements of the genome of the mouse-adapted flu strain. NS1 singularity for the human virulence of H1N1–1918 is neither falsified nor corroborated by these findings.

There still remain a handful of gene candidates, including the polymerases essential for the replication of the virus. This label does not preclude any of them from also functioning in networks and pathways that are expressed as virulence. It should caution us about the nominalist fallacy to recall that the δ crystallin of the bird's lens does double duty as argininosuccinate lyase, an enzyme in the urea cycle.

In principle, the NS1 hypothesis (and its alternatives) might be tested by using similar gene constructs based on flu viruses adapted to other animal species, including primates, and challenging the corresponding hosts. Negative results would be as inconclusive as those with the mouse. Positive results, namely the association of hypervirulence with a gene sequence borrowed from N1H1–1918, would be a great advance in medical science and would offer constructive models for the development of prophylactic and therapeutic measures. They would also induce great alarm about the potential hazards to human health, if humans were also susceptible, and the virus might escape. Any such experiments should be done with strains for which current vaccines are disseminated widely and have proven effectiveness.

To conduct such experiments with human-adapted strains and challenge to human subjects as the probative step, is well nigh unthinkable. But nature is under no such restraint! The current results are a caution to look closely at the involvement of NS1 (as well as HA and NA) variation in natural outbreaks in many species and to look out for their reassortment into human strains. In addition, it might be well to undertake a special search for close homologues to 1918-NS1 in viruses circulating in avian and other species, in which they may appear to be benign in their current hosts (as in the present mouse experiments). That would be nature's inverse of the current report.

The publication by Basler et al. (4) will attract great admiration for its technical finesse and will serve as an example of the fruits from convergence of natural history, field exploration, clinical insight, and sophisticated molecular wizardry. It also will awaken anxieties about the obvious opportunities for abuse. The really fateful step was taken with the very first cultivation of pathogenic bacteria and viruses a century ago—perhaps most importantly with the discovery of the concepts of germs and communicable diseases. The notion of using ever more sophisticated technology for intentionally constructing or reconstructing ever more pathogenic variants lends further weight to that anxiety. The great debate of the mid-1970s led to sensible measures for the regulation of recombinant DNA research. There has been increasing understanding that some of nature's pathogens deserve equal or greater respect. We should be sure that we continue to devote as much reasoned ingenuity to the design of safeguards and to informed and transparent third-party scrutiny of potential hazards as we do generally to the authentication of scientific claims. We cannot afford to forego the deepest research into the plagues that beset humankind. Nor can we afford to blunder into mistakes that will do primary injury to bystanders and incur incommensurate social sanctions.

My deepest anxieties pertain to the smoldering technology and arms race that attends the power struggles in the Middle East and the economic instabilities of the former Soviet Union. Although the 1975 Biological Weapons Convention (BWC) has demilitarized the main drivers of bioweaponry technical advance, in the U.S. and in the overt activities of other formidable powers, the BWC has not been enforced successfully against Iraq and is more or less openly flouted in a handful of other countries. The United Nations (UN) Security Council is too splintered on other issues to take a firm stand on the defiance by Iraq of the UN-mandated inspections. It would not be child's play for defiant small countries to adopt advanced biotechnology into their weapons programs. But we have seen that the climactic high-science successes in one decade become fodder for high-school projects in the next. Influenza is an unlikely candidate for rational weapons development, because new strains promptly embrace the world. But that logic is insufficient reason to neglect the contingency. More likely similar principles would be applied to more governable bioagents, but any bioagents in warfare are an affront and a threat to the entire human species. Informed professionals throughout the world should be leading campaigns to insist on universal compliance with the BWC as a major bulwark of human health and associating that with the most positive measures to apply advanced biotechnology in a constructive way for dealing with nature's continued scourges.

Read More »»

A/H1N1 influenza like human illness in Mexico and the USA: OIE statement

A virus circulating in Mexico and the USA and involving person to person transmission appears to cause in some cases severe disease in certain people infected by this virus. There is no evidence that this virus is transmitted by food.

It is not a classical human influenza virus called seasonal influenza, which causes every year millions of human cases of influenza worldwide but a virus which includes in its characteristics swine, avian and human virus components.

No current information in influenza like animal disease in Mexico or the USA could support a link between human cases and possible animal cases including swine. The virus has not been isolated in animals to date. Therefore, it is not justified to name this disease swine influenza. In the past, many human influenza epidemics with animal origin have been named using geographic name, eg Spanish influenza or Asiatic influenza, thus it would be logical to call this disease “North-American influenza”.

Urgent scientific research must be started in order to know the susceptibility of animals to this new virus, and if relevant to implement biosecurity measures including possible vaccination to protect susceptible animals. If this virus would be shown to cause disease in animals, virus circulation could worsen the regional and global situation for public health.

Currently, only findings related to the circulation of this virus in pigs in zones of countries having human cases would justify trade measures on the importation of pigs from these countries. The OIE will continue its alert function and will publish in relation with its Members, Reference Laboratories and Collaborating Centres all appropriate information in real time.

OIE and FAO underline the great value of the influenza veterinary laboratory network called OFFLU, in charge of the surveillance of the evolution of influenza viruses in animals. There is a strong need to reinforce this network whose members are urged to put immediately in the public domain any genetic sequence of influenza virus they obtain.

This influenza event underlines in all countries the crucial importance of maintaining worldwide veterinary services able to implement in animals early detection of relevant emerging pathogens with a potential public health impact. This capacity is fully linked with veterinary services good governance and their compliance with OIE international standards of quality.

April 2009

Read More »»

Spanish flu,Russian flu,Mexican influenza

The Spanish flu, also known as La Gripe Española, or La Pesadilla, was an unusually severe and deadly strain of avian influenza, a viral infectious disease, that killed some 50 million to 100 million people worldwide over about a year in 1918 and 1919. It is thought to be one of the most deadly pandemics in human history. It was caused by the H1N1 type of influenza virus.

The Spanish flu caused an unusual number of deaths because it caused a cytokine storm in the body. (The recent epidemic of bird flu, also an Influenza A virus, had a similar effect.) The Spanish flu virus infected lung cells, leading to overstimulation of the immune system via release of cytokine bursts into the lung tissue. This leads to extensive leukocyte migration towards the lungs, causing destruction of lung tissue and secretion of liquid into the organ, making it difficult for the patient to breathe. People with strong immune systems (such as young adults) were more susceptible to the disease than young children and the elderly.


The term "Spanish" flu was coined because Spain was at the time the only European country where the press were printing reports of the outbreak, which had killed thousands in the armies fighting the First World War. Other countries suppressed the news in order to protect morale.
Russian flu
The more recent Russian flu was a 1977–1978 flu epidemic caused by strain Influenza A/USSR/90/77 (H1N1). It infected mostly children and young adults under 23 because a similar strain was prevalent in 1947–57, causing most adults to have substantial immunity. Some have called it a flu pandemic but because it only affected the young it is not considered a true pandemic. The virus was included in the 1978–1979 influenza vaccine.

Mexican influenza
The Mexican influenza virus isolated from patients in the United States was found to be made up of genetic elements from four different flu viruses – North American Mexican influenza, North American avian influenza, human influenza, and swine influenza virus typically found in Asia and Europe – "an unusually mongrelised mix of genetic sequences."[10] This new strain appears to be a result of reassortment of human influenza and swine influenza viruses, in all four different strains of subtype H1N1. However, as the virus has not yet been isolated in animals to date and also for historical naming reasons, the World Organisation for Animal Health (OIE) suggests it be called "North-American influenza".[11]

Several complete genome sequences for U.S. flu cases were rapidly made available through the Global Initiative on Sharing Avian Influenza Data (GISAID).[12][13] Preliminary genetic characterization found that the hemagglutinin (HA) gene was similar to that of swine flu viruses present in U.S. pigs since 1999, but the neuraminidase (NA) and matrix protein (M) genes resembled versions present in European swine flu isolates. The six genes from American swine flu are themselves mixtures of swine flu, bird flu, and human flu viruses.[14][15] While viruses with this genetic makeup had not previously been found to be circulating in humans or pigs, there is no formal national surveillance system to determine what viruses are circulating in pigs in the U.S.[16]

Read More »»

Influenza A virus subtype H1N1

Influenza A virus subtype H1N1, also known as A(H1N1), is a subtype of influenzavirus A and the most common cause of influenza in humans. Some strains of H1N1 are endemic in humans, including the strain(s) responsible for the 1918 flu pandemic which killed 50–100 million people worldwide. Less virulent H1N1 strains still exist in the wild today, causing roughly half of all flu infections in 2006.[1] Other strains of H1N1 are endemic in pigs and in birds.



1.In March and April 2009, an outbreak of H1N1 influenza in Mexico led to hundreds of confirmed cases and a number of deaths.
2. As of April 28, the new strain was suspected to have infected more than 2,500 individuals worldwide, with 152 attributed deaths. The U.S. Centers for Disease Control and Prevention warned that it was possible the outbreak could develop into a pandemic.
3. On April 27, 2009, the World Health Organization raised their alertness level from 3 to 4 (on a scale of 6) worldwide in response to sustained human-to-human transfer of the virus. The situation was raised to level 5 (pandemic imminent) on April 29, 2009 by the World Health Organization.
4.
Influenza A virus strains are categorized according to two viral proteins, hemagglutinin (H) and neuraminidase (N). All influenza A viruses contain hemagglutinin and neuraminidase, but the structure of these proteins differs from strain to strain due to rapid genetic mutation in the viral genome. Influenza A virus strains are assigned an H number and an N number based on which forms of these two proteins the strain contains.

Read More »»