Too good to be true? Think twice


 

HAVE you ever grabbed an offer without any hesitation, simply because the price is too cheap to resist?

Many of us have this experience especially during sales or promotional campaigns. We tend to spend more at the end or buy things which we are uncertain of their quality when the deal seems too good to say no.

It may be harmless if the amount involved is insignificant. However, when we apply the same approach to big ticket items, it can cause vast implications.

Recently, I heard a case which reinforces this belief.

A friend shared that a property project which was selling for RM300,000 a few years ago is now stuck. Although the whole project was sold out, the developer has problem delivering the units on time.

The developer is calling all purchasers to renegotiate the liquidated and ascertained damages (LAD), a compensation for late delivery.

One of the homeowners said he is owed RM50,000 of LAD, which means the project is 1½ years late. When we chatted, we found that he purchased the unit solely due to its cheap pricing without doing much research in the first place.

The incident is a real-life example of paying too low for an item which can leave us as losers, especially when it involves huge sum of investment, such as property.

To many, buying a house maybe a once-in-a-lifetime experience, a decision made can make or break the happiness of a family.

A good decision ensures a roof over the head and a great living environment, while an imprudent move may incur long-term financial woes if the house is left uncompleted.

Nowadays, it is common to see people do research when they plan to buy a phone, household item, or other smaller ticket items.

Looking at the amount involved and implication of buying a house, we should apply the same discretion if not more.

It is always important for house buyers to study the background of a developer and project, consult experienced homeowners regarding the good and bad of a project before committing.

I have seen many people buy a house merely based on price consideration.

In fact, there are more to be deliberated when we commit for a roof over our heads. The location, project type, reputation of a developer, the workmanship, the future maintenance of the property etc, are all important factors for a good decision as they would affect the future value of a project.

Beware when a discount or a rebate sounds too good to be true, it may be just too good to be true and never materialised. If the collection or revenue of a housing project is not sufficient to fund the building cost, the developer may not be able to complete the project or deliver the house as per promised terms. At the end of the day, the “price” paid by homeowners would be far more expensive.

In general, the same principle applies elsewhere. It is a known fact that when we pay a premium for a quality product from a reliable producer, we have a peace of mind that the product could last longer and end up saving us money. Some lucky ones will end up gaining much more.

For instance, when we purchase a car, we should consider its resale value as some cars hold up well, while others collapse after a short period. Other determining factors include the specifications of the car, the after sales service, and the availability of spare parts.

Quality products always come with a higher price tag due to the research, effort, materials and services involved.

In addition to buying a house or big ticket items, other incidents that can tantamount to losing huge sums are like money games, get-rich-quick scheme, or the purchase of stolen cars or houses with caveats.

When an offer or a rebate sounds dodgy, the “good deal” can be a scam.

Years of experience tells me that when what is too good to be true, we should think twice. I always remind myself with a quote from John Ruskin (1819-1900) who was an art critic, an artist, an architect and a philosopher. “It’s unwise to pay too much, but it’s worse to pay too little. When you pay too much, you lose a little money – that’s all. When you pay too little, you sometimes lose everything, because the thing you bought was incapable of doing the thing it was bought to do.

“The common law of business balance prohibits paying a little and getting a lot – it can’t be done. If you deal with the lowest bidder, it is well to add something for the risk you run, and if you do that you will have enough to pay for something better.”

Food for thought by Alan Tong

Datuk Alan Tong has over 50 years of experience in property development. He was the world president of FIABCI International for 2005/2006 and awarded the Property Man of the Year 2010 at FIABCI Malaysia Property Award. He is also the group chairman of Bukit Kiara Properties. For feedback, please email feedback@fiabci-asiapacific.com.

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Can Malaysia’s household debt at 87.9% in 2014 be reduced to 54% ?
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Scientists Finally Discover How the Obesity Gene Works


https://news.yahoo.com/video/key-gene-tied-obesity-maybe-221910667.html?format=embed

Scientists have finally figured out how the key gene tied to obesity makes people fat, a major discovery that could open the door to an entirely new approach to the problem beyond diet and exercise.

The work solves a big mystery: Since 2007, researchers have known that a gene called FTO was related to obesity, but they didn’t know how, and could not tie it to appetite or other known factors.

Now experiments reveal that a faulty version of the gene causes energy from food to be stored as fat rather than burned. Genetic tinkering in mice and on human cells in the lab suggests this can be reversed, giving hope that a drug or other treatment might be developed to do the same in people.

The work was led by scientists at MIT and Harvard University and published online Wednesday by the New England Journal of Medicine.

The discovery challenges the notion that “when people get obese it was basically their own choice because they choose to eat too much or not exercise,” said study leader Melina Claussnitzer, a genetics specialist at Harvard-affiliated Beth Israel Deaconess Medical Center. “For the first time, genetics has revealed a mechanism in obesity that was not really suspected before” and gives a third explanation or factor that’s involved.

Independent experts praised the discovery.

“It’s a big deal,” said Dr. Clifford Rosen, a scientist at Maine Medical Center Research Institute and an associate editor at the medical journal.

“A lot of people think the obesity epidemic is all about eating too much,” but our fat cells play a role in how food gets used, he said. With this discovery, “you now have a pathway for drugs that can make those fat cells work differently.”

Several obesity drugs are already on the market, but they are generally used for short-term weight loss and are aimed at the brain and appetite; they don’t directly target metabolism.

Researchers can’t guess how long it might take before a drug based on the new findings becomes available. But it’s unlikely it would be a magic pill that would enable people to eat anything they want without packing on the pounds. And targeting this fat pathway could affect other things, so a treatment would need rigorous testing to prove safe and effective.

The gene glitch doesn’t explain all obesity. It was found in 44 percent of Europeans but only 5 percent of blacks, so other genes clearly are at work, and food and exercise still matter.

Having the glitch doesn’t destine you to become obese but may predispose you to it. People with two faulty copies of the gene (one from Mom and one from Dad) weighed an average of 7 pounds more than those without them. But some were obviously a lot heavier than that, and even 7 pounds can be the difference between a healthy and an unhealthy weight, said Manolis Kellis, a professor at MIT.

Related: More U.S. Adults Are Now Obese than Overweight

He and Claussnitzer are seeking a patent related to the work. It was done on people in Europe, Sweden and Norway, and funded by the German Research Center for Environmental Health and others, including the U.S. National Institutes of Health.

Researchers can’t guess how long it might take before a drug based on the new findings becomes available. But it’s unlikely it would be a magic pill that would enable people to eat anything they want without packing on the pounds. And targeting this fat pathway could affect other things, so a treatment would need rigorous testing to prove safe and effective.

The gene glitch doesn’t explain all obesity. It was found in 44 percent of Europeans but only 5 percent of blacks, so other genes clearly are at work, and food and exercise still matter.

Having the glitch doesn’t destine you to become obese but may predispose you to it. People with two faulty copies of the gene (one from Mom and one from Dad) weighed an average of 7 pounds more than those without them. But some were obviously a lot heavier than that, and even 7 pounds can be the difference between a healthy and an unhealthy weight, said Manolis Kellis, a professor at MIT.

Related: ‘Healthy Obesity’ Turns Unhealthy Over Time

He and Claussnitzer are seeking a patent related to the work. It was done on people in Europe, Sweden and Norway, and funded by the German Research Center for Environmental Health and others, including the U.S. National Institutes of Health.

“It’s a potential target” for drug development, said Dr. Sam Klein, an obesity researcher at Washington University in St. Louis. He called the work “an amazing study” and “a scientific tour de force.”

Dr. Rudolph Leibel, an obesity expert at Columbia University in New York, used the same term — “tour de force.” Still, some earlier research suggests the FTO gene may influence other aspects of obesity such as behavior and appetite.

“It’s possible there are several mechanisms being affected,” and that fat-burning is not the whole story, he said.

Read This Next: There Are 6 Types Of Obesity — And Each Should Be Treated Differently

– Associated Press

Malaysia’s richest four poorer by RM13b


Their net worth hit by challenging economic outlook and slump in oil prices

PETALING JAYA: The country’s top four tycoons in the latest Forbes Malaysia Rich List are “poorer” by a total of US$3.6bil (RM12.9bil) with last year’s challenging economic out­­look shrinking their wealth, ­albeit slightly.

Robert Kuok, 91, who controls a business empire which includes palm oil, shipping, media, hotels and real estate, topped the list for the 10th year in a row with an estimated net worth of US$11.3bil (RM40.5bil) as of February, down US$200mil (RM720mil) from 2013.

In second place was telecommunications tycoon T. Ananda Krishnan whose wealth is valued at US$9.7bil (RM35bil), a drop of US$1.6bil (RM5.7bil) from the previous year, with third spot taken by property mogul and Hong Leong Group chairman Tan Sri Quek Leng Chan with a net worth of US$5.6bil (RM20bil), down US$800mil (RM2.8bil).

Genting Malaysia Bhd chairman and chief executive Tan Sri Lim Kok Thay, who runs casinos in the Bahamas, London, Singapore, Manila and New York besides the home-grown casino in Genting Highlands, claimed fourth place with a net worth of US$5.5bil (RM19.8bil), down US$1bil (RM3.6bil).

“The wealth of some on the list was affected as the local stock market lost steam and the oil price collapse sent the Malaysian ringgit down 10% against the dollar,” according to a statement issued by the business magazine after the release of its latest rankings.

The statement said Ananda’s net worth decreased partly due to a slump in the shares of Bumi Armada Bhd, his offshore oilfield services provider, while Lim’s wealth was affected as China’s economic moderation affected the region’s casino gaming and entertainment sector.

The statement said tycoons with significant investments and ties to the oil sector also suffered a decline in their net worth.

SapuraKencana Petroleum Bhd vice-chairman Tan Sri Mokhzani Ma­­­­ha­­thir was knocked out of the billionaire’s list this year as his estimated net worth fell by US$500mil (RM1.8bil) to US$700mil (RM2.5bil).

The main investors in Sapura­Ken­cana – brothers Tan Sri Shahril Shamsuddin and Datuk Shahriman – also saw their fortunes drop to US$860mil (RM3.1bil) from a reported US$1.4bil (RM5bil) the year before.

It was not all bad news for some Malaysian tycoons as a weaker ringgit boosted exports.

Tan Sri Lau Cho Kun, who heads Hap Seng Consolidated Bhd, made it to the billionaire ranks with a net worth of US$1.08bil (RM3.8bil) on the back of robust plantation and trading revenues.

Software tycoon Goh Peng Ooi, the founder and executive chairman of Silverlake Group, saw his net worth rise by US$450mil (RM1.6bil) to US$1.55bil (RM5.5bil).

– The Star Asia News Network

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大家,看看我们聪明的政府们到底为人民做了什么好事。。。
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Living life to the fullest


living-life-to-the-fullest
Chan, an avid mountaineer and myelofibrosis patient, with a photo of himself (in red jacket) and fellow climbers at the summit of Mount Kinabalu. Photo: UU BAN/The Star >>

Despite having a rare blood disorder, Tan Sri Chan Choong Tak not only continued his active lifestyle , but also took up mountain-climbing.

FORMER Dewan Negara president Tan Sri Chan Choong Tak’s motto in life is to live it to the fullest.

Not surprising then that among his many accomplishments are two Malaysian Book of Records titles as the oldest Malaysian to reach the top of Mount Kilimanjaro’s Uhuru Peak (on Aug 31, 2003, at the age of 70) and the oldest Malaysian to reach the top of Mount Kinabalu’s King George Peak (on Aug 29, 2004, at the age of 71).

Uhuru Peak is the highest point on Mount Kilimanjaro, which is the tallest freestanding mountain in the world (from sea level) and the tallest mountain in Africa, while King George Peak is located on the more challenging and lessclimbed Eastern Plateau of Mount Kinabalu, Sabah.

What makes these two records more significant – aside from the impressive fact that Chan only took up mountain-climbing in his sixties – is that he was suffering from a rare bone marrow disorder at the same time.

His condition, primary myelofibrosis, is one of a group of diseases called myeloproliferative neoplasms, which are caused by abnormal production of blood cells in the bone marrow.

In the case of myelofibrosis, the problem lies in the abnormally-increased production of megakaryocytes, which are the cells that directly give rise to platelets. This results in an initial increased number of platelets in the body.

Cytokines – protein growth factors that are produced by megakaryocytes – are also correspondingly increased.

And as these cytokines are what stimulate the bone marrow’s fibroblasts to produce collagen, this results in an excessive amount of collagen being made.

The collagen deposits in the bone marrow as webs of fibre – similar to scar tissue on the skin – resulting in the disease’s characteristic fibrosis of the bone marrow.

With the collagen taking up so much space in the bone marrow, regular blood cell production is disrupted.

Red blood cells (RBCs) are usually decreased in number and abnormally formed, resulting in anaemia, while white blood cells (WBCs) are abnormal and immature, resulting in increased infection rates.

With production of blood cells in the bone marrow disrupted, the spleen, which is the body’s secondary supplier of blood cells, steps up to meet the body’s needs.

This extra work usually causes the spleen to enlarge (splenomegaly), resulting in pain or a feeling of fullness below the left rib.

Occurring commonly in those above 50 years of age, myelofibrosis is caused by a spontaneous genetic mutation (i.e. not inherited) in the affected person’s blood stem cells. This is what causes the uncontrolled production of megakaryocytes.

The cause of the mutation itself in primary myelofibrosis is, as yet, unknown.

Accidental discovery

As the symptoms of myelofibrosis, like fatigue, shortness of breath, pallor, frequent infections and easy bruising, are quite vague, diagnosis can be quite difficult.

In Chan’s case, he did not notice any signs or symptoms of myelofibrosis prior to his diagnosis.

In fact, it was a combination of a road accident and his wife, Puan Sri Cecelia Chia’s sharp eyes that alerted them to the possibility of a problem.

He shares: “My son gave me a racing bike for my 60th birthday – that was 21 years ago. So, I used to cycle around. Then, I met with a road accident.”

Chan was cycling along the narrow, winding roads of his hillside residential area in Seremban, Negeri Sembilan, when he suddenly met an oncoming car.

With no space to avoid the car, he braked hard and was thrown to the ground in a head-first fall.

“My helmet broke and I thought I would be paralysed. My friend, who is a doctor, straightaway rang up the hospital and they sent the ambulance,” he says.

Fortunately, Chan suffered no major injuries from the accident.

However, his cardiologist son insisted that he be checked more thoroughly for brain injuries, which resulted in him seeing a neurologist.

While his brain turned out to be fine, his wife noticed that his platelet count from the blood test were quite high – between 600,000 to 700,000 platelets per cubic millimetre, when the upper limit for normal is 400,000.

His son then sent him to consultant haematologist Dr Ng Soo Chin, who prescribed hydroxyurea to bring down his platelet count.

That seemed to work quite well for Chan, and it was, in fact, shortly after this that he began mountain-climbing with a group of fellow MBA (Masters of Business Administration) alumni from Tenaga Nasional Bhd.

Chan was then a director of the company, and had gone to Ohio University, United States, to study his MBA along with other Tenaga Nasional executives.

“So, as I climbed, I continued to take hydroxyurea and everything was normal.

“But Soo Chin said, hydroxyurea will eventually bring down your red corpuscles (another term for RBCs), and recommended anagrelide,” he says. Anagrelide is a platelet-reducing agent.

Accelerating disease

Chan continued happily with the two medications, until the year 2011, 18 years after his initial diagnosis.

By then, he was seeing consultant haematologist Datuk Dr Chang Kian Meng at Hospital Ampang, Selangor, as Dr Ng had advised him to continue his follow-ups at a public hospital as his medications are quite expensive.

Chan shares that Dr Chang started him on epoetin alfa and pegylated interferon that year as his blood cell levels were fluctuating.

While interferon decreases the production of blood cells in general, epoetin alfa stimulates the production of RBCs to counteract the effects of anaemia.

However, his haemoglobin levels dropped even further, and he started requiring blood transfusions about once every two months.

The transfusions made a big difference as he reports feeling “very energetic” after receiving the first one. (Fatigue is a common symptom of anaemia.)

The following year, it was the WBCs turn to go “completely haywire”, when a blood test revealed that they had dramatically increased to about 56 from the regular range of about 4 to 10.

He also started experiencing profuse night sweats and cramps, along with the occasional itchiness that had started in his seventies – all of which are among the symptoms of myelofibrosis.

“Then, both Dr Chang and Soo Chin agreed that I had entered into myelofibrosis in acceleration,” he says.

The only cure for myelofibrosis is a bone marrow transplant, but aside from the difficulty of finding a suitable donor and the riskiness of the procedure, Chan’s age rendered him unsuitable for such a treatment.

Fortunately for him, a new drug had recently been approved by both the European Commission and the United States Food and Drug Administration for use in myelofibrosis at that time.


A new drug

The drug, ruxolitinib, inhibits certain enzymes in the JAK pathway, which regulates blood cell production. Half of primary myelofibrosis cases are caused by mutations in the JAK genes, which results in the dysfunctional production of blood cells in the bone marrow.

However, the drug was not available in Malaysia then. (It was only launched in the Malaysian market in 2013.)

This is where his political connections as a Gerakan life member and former secretary-general came in useful.

Then Minister in the Prime Minister’s Department and Gerakan president Tan Sri Dr Koh Tsu Koon offered to help pass on the letter Chan had written to the Health Ministry requesting approval to use the drug on compassionate grounds, to the Health secretary-general.

Four days later, Chan received the approval he needed, and received his first dose of ruxolitinib in October 2012.

Since then, after some adjustments in dosage, Chan’s blood cells are back in the normal range and his last transfusion was in December 2013.

He is currently doing well enough for his doctor to lower his dosage of ruxolitinib, while still taking epoetin alfa and interferon.

Life goes on as normal for this active 81-year-old, who still climbs hills, reads newspapers of various languages and blogs daily, works out in the gym and does regular morning calisthenics.

Of his condition, Chan shares that he never felt the need to know about the disease, being only interested in his blood test results.

“I didn’t know what myelofibrosis was all about until I was asked to do this interview. That was the first time I went into Google to see what was myelofibrosis,” he says with a laugh.

“But I knew it was a dangerous disease, but I wasn’t bothered. I continued to carry on with my normal life.”

He adds: “I’m not bothered with what happens because I have full trust in my doctors.

By Tan shiow China The Star/ANN

Related:

101 Ways To Live Your Life To The Fullest personalexcellence.co/blog/101-ways-to-live-your-life-to-the-fullest/  – If your answer to any of the above is a no, maybe or not sure, that means you’re not living your life to the fullest.

Exercise can affect your DNA


DNA_ExcerciseExercise doesn’t only improve your appearance, it can alter your genes, cutting your risks of obesity and diabetes, a new Swedish study finds.Healthy_Body_Healthy_Mind

While inherited DNA cannot be altered, the way that genes express themselves can through exercise, diet, and lifestyle, researchers from Lund University Diabetes Center explained, noting that a workout can positively affect the way cells interact with fat stored in the body.

Lead author Charlotte Ling, associate professor, and her team looked at the DNA of 23 slightly overweight but healthy men aged around 35. The men previously didn’t exercise but attended indoor cycling and aerobics classes for six months. “They were supposed to attend three sessions a week, but they went an average 1.8 times,” says associate researcher Tina Rönn.

Using technology that analyses 480,000 positions throughout the genome, they could see that epigenetic changes had taken place in 7,000 genes (an individual has 20,000 to 25,000 genes). A closer look revealed genes linked to diabetes and obesity, also connected to storing fat, had also been altered.

“We found changes in those genes too, which suggests that altered DNA methylation as a result of physical activity could be one of the mechanisms of how these genes affect the risk of disease,” said Rönn.

“This has never before been studied in fat cells. We now have a map of the DNA methylome in fat,” Lind added.

The findings, announced this week, appear online in the journal PLOS Genetics.

A separate study published this March in the journal Cell Metabolism shows that when people exercise for as little as 20 minutes, it can alter their DNA almost immediately. – AFP Relaxnews

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Exercise for the brain


The therapeutic properties of exercise is well supported by a substantial amount of research.

Recent studies reported that an increase in the time dedicated to physical health-based activities is not associated with a decline in academic performance.Recent studies reported that an increase in the time dedicated to physical health-based activities is not associated with a decline in academic performance.

THE benefits of exercise are well publicised. Exercise is associated with a reduction in physical illnesses such as cardiovascular disease, colon and breast cancer, obesity and mental illness (including depression and anxiety disorders) across the adult lifespan.

The National Health and Morbidity Survey 2011 revealed that about 64.3% of Malaysians were physically active. The level of physical activity gradually decreased with increasing age, and this was particularly apparent in senior citizens.

Despite evidence of the importance of exercise, the prevalence of overweight and obese Malaysians was 29.4% and 15.1% respectively based on the World Health Organization (1998) classification.

Although some are aware of the benefits of exercise, there are many who are unaware that exercise has considerable benefits for the brain. This is put aptly by John Ratey, author of A User’s Guide to the Brain.

“Exercise is really for the brain, not the body. It affects mood, vitality, alertness and feelings of well-being.”

There is increasing evidence that exercise can improve learning and memory, delay age-related cognitive decline, reduce risk of neurodegeneration and alleviate depression.

Exercise and brain function

Exercise improves brain function in different ways. It enhances learning and plasticity, is neuroprotective, and is therapeutic and protective against depression

Exercise enhances learning and plasticity, which is the capacity of the brain and nervous system to continuously alter neural pathways and synapses in response to experience or injury.

Although some are aware of the benefits of exercise, there are many who are unaware that exercise has considerable benefits for the brain.

Although some are aware of the benefits of exercise, there are many who are unaware that exercise has considerable benefits for the brain.

The effects of exercise have been demonstrated in ageing human populations in which sustained exercise has augmented learning and memory, improved executive functions, impeded age-related and disease-related mental decline, and protected against age-related atrophy in parts of the brain areas that are vital for higher cognitive processes.

Physical activity has a positive effect on cognition, which includes every mental process that may be described as an experience of knowing (including perceiving, recognising, conceiving, and reasoning).

There is a significant relationship between physical activity and improved cognition in normal adults as well as those with early signs of Alzheimer’s disease (AD), in which there is mild impairment of memory or cognition.

There is a dose-response relationship between exercise and health-related quality of life, with moderate exercise associated with the best outcomes.

The literature on the effects of exercise on cognition during children’s development is less substantial. However, a meta-analysis by Sibley & Etnier reported a positive correlation between physical activity and cognitive performance in children aged between four and 18 years in eight categories, i.e. perceptual skills, intelligence quotient, achievement, verbal tests, mathematic tests, memory, developmental level/academic readiness and others.

A beneficial relationship was found for all categories, with the exception of memory, which was unrelated to physical activity behaviour, and for all age groups, although it was stronger for children in the ages of four to seven and 11 to 13 years, compared with the ages of eight to 10 and 14 to 18 years.

Recent studies have reported that an increase in the time dedicated to physical health-based activities is not associated with a decline in academic performance.

The literature on the impact of exercise on cognition in young adults is limited, probably because cognition peaks during young adulthood and there is little room for exercise-related improvement at this stage of the lifespan.

Although there is considerable evidence that exercise can facilitate learning in humans and other animals, there are gaps in knowledge regarding the types of learning that are improved with exercise.

Therapeutic exercise programmes after a stroke accelerates functional rehabilitation. Therapeutic exercise programmes after a stroke accelerates functional rehabilitation.

Exercise protects the brain (neuroprotective). It reduces the impact of brain injury and delays the onset and decline in several neurodegenerative diseases. For example, therapeutic exercise programmes after a stroke accelerates functional rehabilitation.

Furthermore, physical activity delays the onset and reduces the risk for AD, Huntington’s disease and Parkinson’s disease, and can even slow functional decline after neurodegeneration has begun.

There is evidence that exercise is therapeutic and protective in depression, which is associated with a decline in cognition.

Depression is considered to be a health burden that is greater than that of ischaemic heart disease, cerebrovascular disease or tuberculosis.

Clinical trials have reported the efficacy of aerobic or resistance training exercise in the treatment of depression in young and older patients, with benefits similar to that of antidepressant medicines. More exercise leads to greater improvements.

Trials have also reported improvement in depressive symptoms in AD compared to those non-exercising individuals whose depressive symptoms worsened.

Bipolar disorders do not appear to respond as well to exercise, but those with anxiety respond even faster.

There is a convergence of the concept that brain health and cognition are influenced by the interplay of various central and peripheral factors. Brain function is believed to be impaired by peripheral risk factors that lead to cognitive decline, including hypertension, hyperglycemia, insulin insensitivity and dyslipidemia, features that are commonly known as the “metabolic syndrome”.

Of these factors, hypertension and glucose intolerance play crucial roles. Exercise not only reduces all these peripheral risk factors but also improves cardiovascular health, lipid–cholesterol balance, energy metabolism, glucose use, insulin sensitivity and inflammation.

As such, exercise improves brain health and function by directly enhancing brain health and cognitive function, and indirectly, by reducing the peripheral risk factors for cognitive decline.

It is believed that exercise initiates an interactive cascade of growth factor signals which lead to the stimulation of plasticity, improvement of cognitive function, reduction of the mechanisms that drive depression, stimulation of neurogenesis and improvement of cerebrovascular perfusion.

Although much is known about the effects of exercise and physical activity on brain and cognition, there are many important questions that are unanswered.

They include questions like the design of exercise interventions which optimise the effects on cognition and brain health; when it is best to begin; what are the best varieties, intensities, frequencies and duration of exercise; is it ever too late to start an exercise programme; and can exercise be used to reduce the effects of neurodegenerative diseases.

Knowing the how

Exercise affects many sites in the nervous system and stimulates the secretion of chemicals like serotonin and dopamine, which make humans feel calm, happy, and euphoric. You do not have to wait for these feelings to occur – you can initiate them by exercising.

There is no shortage of advice on the various physical exercises that enhances cardiovascular health. Prior to embarking on exercise, a consultation with the doctor would be helpful, especially for senior citizens. This will help in choosing the appropriate exercise for one’s individual situation.

In general, what is good for the heart is also good for the brain.

The usual recommended minimum is half an hour of moderate exercise thrice a week. This can be walking, jogging, swimming, playing games, dancing etc.

The public is often reminded about a healthy lifestyle, which is focused on physical health. However, it is also important to exercise mentally and keep the brain healthy.

There are publications and activities available that can help you make a start and continue to improve cognition, memory, creativity and other brain functions.

Anyone at any age can do so, even senior citizens. It is moot to remember the adage: if you don’t use it, you lose it.

Malaysia Festival of the Mind 2013

The ninth Malaysia Festival of the Mind will be held from June 15-16, 2013, at Universiti Tunku Abdul Rahman (UTAR) Perak Campus in Kampar, and June 22-23 at Tunku Abdul Rahman University College (TARC) Main Campus in Setapak, Kuala Lumpur.

It is open to the public from 9.30am – 4.30pm. Talks, workshops, exhibitions and competitions will be held to create awareness about the human mind and its unlimited potential; as well as ways of tapping into and developing one’s brainpower to the fullest.

For further information, visit www.utar.edu.my/mmlm or email mmlm@utar.edu.my or call (03) 7625 0328 (Justin/Sin Yee) or (05) 468 8888 (Wei See/Jamaliah).

By Dr MILTON LUM

> Dr Milton Lum is a member of the board of Medical Defence Malaysia. This article is not intended to replace, dictate or define evaluation by a qualified doctor. The views expressed do not represent that of any organisation the writer is associated with. For further information, e-mail starhealth@thestar.com.my. The information provided is for educational and communication purposes only and it should not be construed as personal medical advice. Information published in this article is not intended to replace, supplant or augment a consultation with a health professional regarding the reader’s own medical care. The Star does not give any warranty on accuracy, completeness, functionality, usefulness or other assurances as to the content appearing in this column. The Star disclaims all responsibility for any losses, damage to property or personal injury suffered directly or indirectly from reliance on such information.

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A million-dollar dream?


What would you do if you have a million bucks?

Monday Starters – By Soo Ewe Jin

WHAT would you do if you have a million bucks? A poor government clerk from Bihar, a remote and poverty-stricken region of northern India, has become the first person to win 50 million rupees (RM3mil) on the popular Indian version of the gameshow Who Wants to be a Millionaire?

Sushil Kumar’s win is a classic case of life imitating art as the script is similar to that of the 2008 Oscar-winning film Slumdog Millionaire.

According to the Associated Press, Sushil said he would spend some of his prize money to prepare for India’s tough civil service examination, which could lead to a secure and prestigious lifetime job.

He would also buy a new home for his wife, pay off his parents’ debts, give his brothers cash to set up small businesses and build a library in Motihari so the children of his village would have access to books and knowledge.

Real life slumdog millionaire: Sushil (left) says thank you with clasped hands as he receives his US$1mil prize from Bollywood actor Amitabh Bachchan during the fifth season of the Indian version of the Who Wants to be a Millionaire? television quiz in Mumbai on Oct 25. Kumar, a computer operator who earns just US$130 a month, has become the first person to win the top prize. — AFP

Everyone loves a story like this. Although people can become instant millionaires by striking the lottery or pulling the lever on a one-armed bandit at a casino, using one’s talent at a tension-filled gameshow is more admirable.

And I applaud Sushil for his noble attitude in thinking of others to share in his newfound fortune. Bihar is one of the poorest states of India and its remoter areas, such as Motihari, have been largely untouched by India’s phenomenal recent economic growth.

Do you know that there are now at least 39,000 millionaires in Malaysia? According to a recent report by the Credit Suisse Group, 19,000 new millionaires were created over the past 18 months alone.

Meanwhile, the Asia-Pacific Wealth Report 2011 by Merrill Lynch Global Wealth Management and Capgemini, also released recently, revealed that Malaysia’s rich prefer splurging on a fancy new set of wheels, luxurious yachts or private jets.

Up to 46% invested their ringgit in luxury collectibles like cars, boats and jets, the highest percentage of any country within the Asia-Pacific region.

Their counterparts down south seem less interesting and still prefer jewellery and luxury watches.

I know that the CEOs who read the business section of this newspaper may consider a million ringgit small change but to most of us, it is a very faraway goal, not something one can possibly achieve as a regular salaried worker.

But we can all dream and I was wondering to myself, what would I do if I suddenly had a million ringgit in hand? I suppose our wishes would coincide very much with our age, status, and ultimately our character.

To those who believe material pursuits equate to real happiness, a shopping spree would be fantastic.

Those who do not focus too much on material things may want to travel around the world and complete their Bucket List, which may also include going on a religious pilgrimage.

I believe that God never gives us more than we can handle, just as He never lets us go through trials and tribulations beyond our capacity to endure.

And that was when I stopped dreaming. Because I know, seriously, I will never be able to handle so much money at any one time. So I shall be content and count my blessings. I hope you will too.

Deputy executive editor Soo Ewe Jin notes that the world’s population officially hits seven billion today. No one really knows who is Citizen Seven Billion, of course, but by the time he grows up, millionaires and billionaires will probably be a dime a dozen.

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