Moderate physical activity performed in midlife or later appears to be associated with a reduced risk of mild cognitive impairment — and a six-month high-intensity aerobic exercise program can improve cognitive function in individuals who already have the condition.
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Each year, 10 percent to 15 percent of individuals with mild cognitive impairment will develop dementia, as compared with 1 percent to 2 percent of the general population.
Physical exercise may protect against mild cognitive impairment by means of the production of nerve-protecting compounds, greater blood flow to the brain, improved development and survival of neurons and the decreased risk of heart and blood vesseldiseases.
Taking more exercise and eating the right foods may help increase levels of an enzyme vital for guarding against age-related cell damage, work suggests.
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Among 24 men asked to adopt healthy lifestyle changes for a US study in The Lancet Oncology, levels of telomerase increased by 29% on average.
Telomerase repairs and lengthens telomeres, which cap and protect the ends of chromosomes housing DNA.
As people age, telomeres shorten and cells become more susceptible to dying.
It is the damage and death of cells that causes ageing and disease in people.
Several factors such as smoking, obesity and a sedentary lifestyle are associated with shorter-than-average telomeres.
Professor Dean Ornish, from the Preventive Medicine Research Institute in California, and his team wanted to find out if improvements in diet and lifestyle might have the opposite effect.
They asked 30 men, all with low-risk prostate cancers, to take part in a three-month trial of comprehensive lifestyle changes.
These consisted of a diet high in fruit and vegetables, supplements of vitamins and fish oils, an exercise regimen and classes in stress management, relaxation techniques and breathing exercises.
Telomerase activity was measured at the beginning of the trial and again at the end.
Among the 24 men who had sufficient data for analysis, blood levels of telomerase increased by 29% on average.
Increases in telomerase activity were linked with decreases in “bad” LDL cholesterol and decreases in one measure of stress – intrusive thoughts.
The researchers say it is too early to tell if the boost in telomerase levels will translate to a change in telomere length.
But there is evidence to suggest that telomere shortness and low telomerase activity might be important risk factors for cancer and cardiovascular disease.
“This might be a powerful motivator for many people to beneficially change their diet and lifestyle,” they told The Lancet Oncology.
Professor Tim Spector, from King’s College London, who has been researching ageing and telomeres, said: “This work builds on what we already know.
“Lifestyle can affect your telomeres. It would be interesting to find out whether it is diet, stress or both that is important.”
“This might be a powerful motivator for many people to beneficially change their diet and lifestyle ”
Definition:
Skin cancer is the uncontrolled growth of abnormal skin cells. If left unchecked, these cancer cells can spread from the skin into other tissues and organs.It is a malignant growth on the skin which can have many causes. Skin cancer generally develops in the epidermis (the outermost layer of skin), so a tumor is usually clearly visible. This makes most skin cancers detectable in the early stages. There are three common types of skin cancer, each of which is named after the type of skin cell from which it arises. Cancers caused by UV exposure may be prevented by avoiding exposure to sunlight or other UV sources, and wearing sun-protective clothes. The use of sunscreen is recommended by medical organizations as a measure that helps to protect against skin cancer (see sunscreen).
Unlike many other cancers, including those originating in the lung, pancreas, and stomach, only a small minority of those afflicted will actually die of the disease.[citation needed] Skin cancers are the fastest growing type of cancer in the United States. Skin cancer represents the most commonly diagnosed malignancy, surpassing lung, breast, colorectal and prostate cancer. Melanoma is the least common skin cancer but it is potentially the most serious: there are over 8,000 new cases each year in the UK and 1,800 deaths. More people now die of Melanoma in the UK than in Australia. It is the second most common cancer in the young population (20 – 39 age group). It is estimated that approximately 85% of cases are caused by too much sun. Non-melanoma skin cancers are the commonest skin cancers. The majority of these are called Basal Cell Carcinomas. These are usually localised growths caused by excessive cumulative exposure to the sun and do not tend to spread.
Types:-
There are different types of skin cancer. Basal cell carcinoma is the most common. Melanoma is less common, but more dangerous.
More rare types of skin cancer include:
*Dermatofibrosarcoma protuberans
*Merkel cell carcinoma
*Kaposi’s sarcoma
The BCC and the SCC often carry a UV-signature mutation indicating that these cancers are caused by UV-B radiation via the direct DNA damage. However the malignant melanoma is predominantly caused by UV-A radiation via the indirect DNA damage.[citation needed] The indirect DNA damage is caused by free radicals and reactive oxygen species. It has been shown, that the absorption of three sunscreen ingredients into the skin, combined with a 60-minute exposure to UV, leads to an increase of free radicals in the skin.
Skin cancer as a group:-
Many laymen and even professionals consider the basal cell carcinoma (BCC), the squamous cell carcinoma (SCC) and the malignant melanoma as one group – namely skin cancer. This grouping is problematic for two reasons:
*the mechanism that generates the first two forms is different from the mechanism that generates the melanoma. The direct DNA damage is responsible for BCC and SCC while the indirect DNA damage causes melanoma.
*the mortality rate of BCC and SCC is around 0.3 causing 2000 deaths per year in the US. In comparison the mortality rate of melanoma is 15-20% and it causes 138001 deaths per year.
Even though it is rare, malignant melanoma is responsible for 75 % of all skin cancer related death cases.
While sunscreen has been shown to protect against BCC and SCC it may not protect against malignant melanoma. When sunscreen penetrates into the skin it generates reactive chemicals. It has been found that sunscreen use is correlated with malignant melanoma. The lab-experiments and the epidemiological studies indicate that sunscreen use causes melanoma.
Causes:
The outer layer of skin, the epidermis, is made up of different types of cells. Skin cancers are classified by the types of epidermal cells involved:
Basal cell carcinoma develops from abnormal growth of the cells in the lowest layer of the epidermis and is the most common type of skin cancer.
Squamous cell carcinoma involves changes in the squamous cells, found in the middle layer of the epidermis.
Melanoma occurs in the melanocytes (cells that produce pigment) and is less common than squamous or basal cell carcinoma, but more dangerous. It is the leading cause of death from skin disease.
Skin cancers are sometimes classified as either melanoma or nonmelanoma. Basal cell carcinoma and squamous cell carcinoma are the most common nonmelanoma skin cancers. Other nonmelanoma skin cancers are Kaposi’s sarcoma, Merkel cell carcinoma, and cutaneous lymphoma.
Skin cancer is the most common form of cancer in the Unites States. Known risk factors for skin cancer include the following:
*Complexion: Skin cancers are more common in people with light-colored skin, hair, and eyes. *Genetics: Having a family history of melanoma increases the risk of developing this cancer. *Age: Nonmelanoma skin cancers are more common after age 40. *Sun exposure and sunburn: Most skin cancers occur on areas of the skin that are regularly exposed to sunlight or other
*ultraviolet radiation. This is considered the primary cause of all skin cancers.
Skin cancer can develop in anyone, not only people with these risk factors. Young, healthy people — even those with with dark skin, hair, and eyes — can develop skin cancer.
Symptoms:
Skin cancers may have many different appearances. They can be small, shiny, waxy, scaly and rough, firm and red, crusty or bleeding, or have other features. Therefore, anything suspicious should be looked at by a physician. See the articles on specific skin cancers for more information.
Here are some features to look for:
*Asymmetry: one half of the abnormal skin area is different than the other half *Borders: irregular borders *Color: varies from one area to another with shades of tan, brown, or black (sometimes white, red, blue) *Diameter: usually (but not always) larger than 6 mm in size (diameter of a pencil eraser)
Any skin growth that bleeds or will not heal
Use a mirror or have someone help you look on your back, shoulders, and other hard-to-see areas.
Risk factors:-
Skin cancer is most closely associated with chronic inflammation of the skin. This includes:
1.Overexposure to UV-radiation can cause skin cancer either via the direct DNA damage or via the indirect DNA damage mechanism. UVA & UVB have both been implicated in causing DNA damage resulting in cancer. Sun exposure between 10AM and 4PM is most intense and therefore most harmful. Natural (sun) & artificial UV exposure (tanning salons) are associated with skin cancer.[citation needed] Since sunbeds cause mostly indirect DNA damage (free radicals) their use is associated with the deadliest form of skin cancer, malignant melanoma.
2.UVA rays affect the skin at a deeper level than UVB rays, reaching through the epidermis and the dermis to the hypodermis where connective tissues and blood vessels are located. UVA activates the melanin of the epidermis causing changes in pigmentation as well as loss of elasticity of the skin, which contributes to premature wrinkling, sagging and aging of the skin.
3.UVB rays primarily affect the epidermis causing sunburns, redness, and blistering of the skin. The melanin of the epidermis is activated with UVB just as with UVA; however, the effects are longer lasting with pigmentation continuing over 24 hours.
Chronic non-healing wounds, especially burns. These are called Marjolin’s ulcers based on their appearance, and can develop into squamous cell carcinoma.
4.Genetic predisposition, including “Congenital Melanocytic Nevi Syndrome”. CMNS is characterized by the presence of “nevi” or moles of varying size that either appear at or within 6 months of birth. Nevi larger than 20 mm (3/4″) in size are at higher risk for becoming cancerous.
5.Skin cancer is one of the potential dangers of ultraviolet germicidal irradiation.
Skin can be protected by avoiding sunlight entirely, or wearing protective clothing while outdoors. Skin cancer is usually caused by exposing skin to UV rays excessively.
Treatment:-
Most skin cancers can be treated by removal of the lesion, making sure that the edges (margins) are free of the tumor cells. These excisions provide the best cure for both early and high-risk disease.
For low-risk disease, radiation therapy and cryotherapy (freezing the cancer off) can provide adequate control of the disease; both, however, have lower overall cure rates than surgery.
Mohs’ micrographic surgery is a technique used to remove the cancer with the least amount of surrounding tissue and the edges are checked immediately to see if tumor is found. This provides the opportunity to remove the least amount of tissue and provide the best cosmetically favorable results. This is especially important for areas where excess skin is limited, such as the face. Cure rates are equivalent to wide excision. Special training is required to perform this technique.
In the case of disease that has spread (metastasized), further surgical procedures or chemotherapy may be required.
Scientists have recently been conducting experiments on what they have termed “immune- priming”. This therapy is still in its infancy but has been shown to effectively attack foreign threats like viruses and also latch onto and attack skin cancers. More recently researchers have focused their efforts on strengthening the body’s own naturally produced “helper T cells” that identify and lock onto cancer cells and help guide the killer cells to the cancer. Researchers infused patients with roughly 5 billion of the helper T cells without any harsh drugs or chemotherapy. This type of treatment if shown to be effective has no side effects and could change the way cancer patients are treated. You may click to see Best herbs for skin.
Prognosis:-
The outlook depends on a number of factors, including the type of cancer and how quickly it was diagnosed. Basal cell carcinoma and squamous cell carcinoma rarely spread to other parts of the body. However, melanoma is more likely to spread. See the specific skin cancer articles for additional information.
Prevention :-
Minimizing sun exposure is the best way to prevent skin damage, including many types of skin cancer:
*Protect your skin from the sun when you can — wear protective clothing such as hats, long-sleeved shirts, long skirts, or pants.
*Try to avoid exposure during midday, when the sun is most intense.
*Use sunscreen with an SPF of at least 15. Apply sunscreen at least one-half hour before sun exposure, and reapply frequently.
*Apply sunscreen during winter months as well.
*Reapply sun block every 2 hours and after swimming
Although it is generally accepted that UV exposure is the greatest risk factor in melanoma development, some sceptics say that there is no proven data that links moderate sun exposure with the appearance of melanoma.
Disclaimer: This information is not meant to be a substitute for professional medical advise or help. It is always best to consult with a Physician about serious health concerns. This information is in no way intended to diagnose or prescribe remedies.This is purely for educational purpose.
From a swollen thumb to a bruise to food poisoning, good old grandma has often had a single remedy: a dash of turmeric. Indian researchers have now found that this dietary supplement plays a positive role in taming cancers too.
The ubiquitous spice of the typical Indian kitchen has of late been a subject of much curiosity among medical researchers because of its well-known wound healing and anti-inflammatory properties.
Researchers stumbled upon the anti-cancer potential of curcumin, the active ingredient of turmeric, recently. Since then, a number of research groups all over the world have been engaged in animal studies to prove curcumin’s efficacy.
Reported in the latest issue of Carcinogenesis, the work by a team of Indian medical scientists led by Girish Maru of the Advanced Centre for Treatment, Research and Education in Cancer (ACTREC), Mumbai, is one of first studies on the subject.
More importantly, the Mumbai scientists were able to unravel the exact mechanism behind curcumin’s action. They found that curcumin not only inhibits the enzymes that directly help a cancer-causing agent to damage the DNA but also increases the availability of yet another set of enzymes that helps the body fight the carcinogenic compound.
For their studies the ACTREC researchers used the carcinogen benzo[a]pyrene (B[a]P), a compound commonly found in cigarette smoke and wood smoke and that is implicated in lung cancer. They fed mice with curcumin for 16 days. Then the animals were given a relatively high quantity of B[a]P enough to induce DNA damage that can lead to tumour growth.
Subsequent studies on how the carcinogen interacted with various sets of enzymes inside the animals gave interesting results. The mice fed with curcumin had much depleted levels of cancer-promoting enzymes compared with the control group. Also, they showed higher levels of friendly enzymes such as glutathione S-transferase, indicating increased detoxification of B[a]P.
But is the quantity of turmeric, which one consumes through food, enough to have a protective effect against cancers? Scientists do not think so.
Though very potent, the levels of curcumin in turmeric are as low as 0.01 per cent. Moreover, curcumin uptake by the human body is relatively low. However, scientists are trying to increase curcumin uptake by the human body. For instance, they have already found that adding one part of piperine, the compound responsible for black pepper’s pungency, to 20 parts of curcumin can increase the uptake by several hundred-fold.
A meeting between two ordinary men in a remote locale in Mongolia hit the headlines all over the world in July last year. But neither Bao Xishun, 56, nor He Pingping, 19, holds a position of eminence. Nor are they film or sports celebrities. The encounter grabbed world attention because of the two men’s contrasting statures. While Xishun, at 2.36m, is the world’s tallest living man, the 74-cm Pingping claims he is the shortest.
Modern science may not be able to explain the yawning gap between the heights of these two men — both hailing from Inner Mongolia — but it has gained some genetic insight into the varying stature of billions of others who fall between Xishun and Pingping in terms of height.
For nearly a century, scientists have believed that genes handed down from parents are responsible for 90 per cent of the normal variation in human height in a population. And it is not just one gene but probably a few hundred that contribute towards making a person tall or short. But until last year, scientists were clueless about their location on the human genome, which consists of more than 3 billion DNA base pairs.
In September 2007, researchers from both sides of the Atlantic, while foraging through DNA from 35,000 people, stumbled upon a difference in a gene called HMGA2, which plays a decisive role in making people taller or shorter, albeit marginally. They found that if a person had two copies of a longer variant of HMGA2, he or she would be 1cm taller than one who has two shorter versions of it.
The HMGA2 gene thus became the first reliable genetic link to human height. Later, scientists zeroed in on yet another gene, GDF5, which makes for an average height difference of 0.4cm.
What made the discovery of such genes possible is what scientists call genome-wide association studies. This is a relatively new way of identifying genes involved in human diseases. Made possible by advances in genetics and sophistication in scientific tools, this method searches the genome for small variations, called single nucleotide polymorphisms (SNPs). The tools are so advanced that researchers can search for hundreds or thousands of SNPs simultaneously. Such studies pinpoint genes that may contribute to a person’s risk of developing a certain disease or those associated with a trait such as height or eye colour.
If 2007 saw a beginning in understanding the role played by genes in deciding how tall a person will be, 2008 has so far proved to be a watershed. The same consortium of scientists who discovered the HMGA2 and GDF5 genes, now split into two groups, recently discovered 40 more genetic locations. Combined, they may be able to explain a height difference of up to 6cm, or 5 per cent of the population variation in height.
The number and variety of genetic regions discovered so far show that height is determined not just by a few genes operating in the long bones, notes Thomas Frayling of Peninsula Medical School in the UK. Frayling is the lead author of the one of the two studies that appeared in Nature Genetics last month.
Joel Hirschhorn, a paediatric endocrinologist at Broad Institute in the US, who led the other study, says that the new findings account for only a small fraction of the variation in height among people and that there is a lot more to discover. “This is much more than we had even last year. But we are not close to predicting adult height,” Hirschhorn told Knowhow.
The study of genes involved in determining adult height stems from more than sheer curiosity. By identifying which genes affect normal growth, it is easy to understand the processes that lead to abnormal growth, the scientists say. “There appears to be a definite correlation between height and some diseases,” says Michael Weedon, a colleague of Frayling. Weedon was not only part of the original team that discovered the HMGA2 gene but was also instrumental in the latest discovery of 20 new genetic locations linked to height. For instance, there is a strong association between shortness and a slightly increased risk of conditions such as heart disease. Similarly, tall people are more prone to certain cancers and, possibly, osteoporosis.
A predominant factor that determines one’s height may be heredity, but diet too has a role to play. In fact, improved nutrition means that each generation gets successively taller, as has been shown by a recent study on Indians.
That said, Indians still have some catching up to do: an average Indian man (165.3cm) is two centimetres shorter than an average Czech woman who stands 167.3cm tall.
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