MALAYSIA INFLATION RATE AT 3.7%

Inflation rate stays at 3.7%

FMT Business - 24 Mar 2023, 2:01pm

PETALING JAYA: Increases in the prices of several items such as food and beverages, household essentials and health products continue to drive the inflation rate in Malaysia.

However, an easing in transport cost has helped to keep the rate at an even keel, according to the statistics department.

The opposing trend in the consumer price index (CPI) of various groups has kept the inflation rate at 3.7% in February, the same level as in the previous month.

 An increase in prices of food has been negated by a drop in transport costs, thus keeping the inflation rate unchanged.

Rise in consumer price index for some groups and drop for others keep the rate unchanged.

A recent poll of 22 economists by Reuters forecast a 3.6% inflation rate.

Chief Statistician Uzir Mahidin said today the restaurants and hotels sector recorded a 7.4% increase in the CPI while the food and non-alcoholic beverages saw a 7% rise.

However, a drop in the CPI for the transport group – from 4% in January to 3.7% in February – has helped to offset the rise in inflation.

Among other groups that also recorded increases in the CPI are miscellaneous goods and services, utilities, recreation services and education.

However, alcoholic beverages as well as clothes and footwear recorded marginal drops of 0.8% and 0.4% in their CPI respectively.

While the food and non-alcoholic beverages CPI recorded an increase overall, some items within the group saw a drop in the index.

Food away from home recorded a CPI of 8.9% compared with 9.3% in January.

The subgroup for milk, cheese and eggs rose but at a lower pace of 6.6% in February compared with 7% in January.

Meanwhile, transport inflation slowed to 3.7% in February from 4% previously.

The rate for unleaded petrol RON97 fell to 4.4% from 9.5% in January, as fuel price remained at RM3.35 per litre.

Japan inflation slows to 3.1% in February

24 Mar 2023, 11:32am

Singapore core inflation stays unchanged at 14-year high

23 Mar 2023, 2:58pm

HOW TO STAY MOTIVATED

How To Stay Motivated (Motivation Theories Explained)

By Steve Burns

NewTraderUniversity.com

Internal Motivation Vs. External Motivation

Internal motivation and external motivation are two different types of motivation that drive our behavior and actions. Internal motivation comes from within oneself and is driven by personal interests, values, and desires, whereas external motivation comes from external factors such as rewards, punishments, or social pressure.

Internal motivation is often seen as more sustainable and fulfilling in the long term, as it comes from a deep sense of purpose and passion. When internally motivated, we are more likely to enjoy what we are doing, fully engage in the task at hand, and persist even in facing obstacles. This type of motivation is often associated with activities we find inherently rewarding, such as hobbies, creative pursuits, or meaningful work.

Conversely, external motivation is often seen as less sustainable and less fulfilling in the long term, as it relies on rewards or punishments to motivate. While external motivation can effectively drive behavior in the short term, it can decrease motivation over time if the rewards or punishments are not sustained. This type of motivation is often associated with activities done for extrinsic reasons, such as work done for pay, papers written for grades, or social recognition for accomplishments.

While both internal and external motivation can effectively drive behavior, internal motivation is generally seen as more fulfilling and sustainable over the long term. In contrast, external motivation is more effective in driving behavior in the short term. Still, it may decrease motivation over time if the external rewards or punishments are not sustained.

If you want to be an entrepreneur or self-employed, you must find ways to motivate yourself to do the work needed, as you have no boss or company to motivate you externally.

Businesses look for what they call self-starters or employees driven by internal motivation, as it makes management so much easier. Companies, bosses, and leaders also have many ways to motivate people externally.

Motivation Theories Explained

Motivating people in an organization is crucial for achieving organizational success. Employees are likelier to be productive, engaged, and committed when encouraged. 

Motivation can also increase job satisfaction, leading to lower employee turnover rates. Motivated employees are more likely to take on challenges, be creative, and find innovative solutions to problems. They are also more likely to take ownership of their work and feel a sense of pride in their accomplishments.

 Ultimately, a motivated workforce can contribute to increased profitability, improved performance, and a positive organizational culture.

Motivation is crucial for every leader to understand. Let’s look at how scholars have developed various motivation theories to understand what motivates people.

Content Theories

Maslow’s Hierarchy of Needs:

 This theory describes needs as a hierarchy. The five levels include physiological needs, safety needs, social needs, esteem needs, and self-actualization needs. 

Maslow argued that needs at the bottom of the hierarchy must be satisfied before an individual can move to the next level and seek to satisfy those needs.

Herzberg’s Two-Factor Theory:

 According to this theory, two factors affect job satisfaction and dissatisfaction: hygiene factors and motivators. Hygiene factors are those that are necessary to prevent dissatisfaction in the workplace but do not necessarily contribute to satisfaction. 

Examples of hygiene factors include working conditions, salary, company policies, job security, and relationships with supervisors and coworkers. If these factors are not met, employees may become dissatisfied with their job, but if they are met, employees will not necessarily be satisfied.

 Conversely, motivators contribute to job satisfaction and motivate employees to perform at their best. Examples of motivators include achievement, recognition, responsibility, advancement, and the work itself.

Three Needs Theory:

 This theory argues that each of us has three needs on a scale: the need for achievement, affiliation, and power. Managers can use the three needs theory to set motivational targets tailored to each team member.

McGregor’s Theory X and Theory Y: 

This theory states that employees fall into two categories: theory X and theory Y. Theory X assumes that team members are intrinsically lazy and unmotivated and will avoid doing work if there is any opportunity to do so. Theory Y, on the other hand, assumes that team members are ambitious and self-motivated.

ERG Theory: 

ERG theory is a simplified version of Maslow’s hierarchy of needs. In ERG theory, there are three needs arranged as a hierarchy: existence needs, relatedness needs, and growth needs.

Mayo’s Motivation Theory:

 Mayo determined that how well a group of employees performs is defined by norms and group cohesiveness. Groups with high cohesiveness and positive models will be the most highly motivated and, therefore, the highest performing.

Process Theories

Adams’ Equity Theory: 

This theory says that high levels of employee motivation can only be achieved when each employee perceives their treatment as fair to others.

Expectancy Theory: 

This theory states that a person will choose their behavior based on what they expect the result of that behavior to be. For an employee to be motivated, three factors must be present: expectancy, instrumentality, and valence.

Taylor’s Scientific Management: 

Taylor believed employees were only motivated by one thing: money. Employers should monitor workers very closely to ensure they are not slacking off.

Self-Efficacy Theory of Motivation: 

The higher your self-efficacy, the greater your belief that you can perform a specific task and the more your motivation.

Reinforcement Theory of Motivation: Four factors influence motivation: positive reinforcement, negative reinforcement, punishment, and extinction.

Locke’s Goal Setting Theory:

This theory is based on the premise that setting the right goals can increase motivation and productivity.

How To Implement Motivational Theories

Successfully implementing motivational theories in an organization requires careful planning and execution. Here are some steps that can help to ensure successful implementation:

Assess the needs of employees: Understanding the needs and aspirations of employees is key to implementing effective motivational strategies.

 Conducting employee surveys and gathering feedback can help to identify areas of improvement.

Choose the right motivation theory: Selecting the most appropriate motivation theory for your organization and employees is crucial. Consider the unique needs and challenges of your organization when selecting a theory.

Set clear goals and expectations: Communicating goals and expectations is essential to ensure that employees understand what is expected of them and what they are working towards.

Resources and support: Providing employees with the help and support they need to achieve their goals is essential. This can include training, mentorship, and access to tools and technology.

Offer recognition and rewards: Recognizing and rewarding employees for their achievements can help to motivate them and encourage continued success.

Evaluate and adjust: Regularly evaluating the effectiveness of motivational strategies and changing as needed is essential to ensure continued success.

Conclusion

Motivation theories attempt to explain how to motivate employees in the workplace. Content theories look at motivation from the perspective of our needs and aspirations, whereas process theories look at how people are motivated. 

By understanding these theories, companies can create a work environment conducive to employee motivation, increasing productivity, job satisfaction, and organizational success. 

Entrepreneurs, traders, and the self-employed must be our own source of motivation to get things done.

 

 

7 HABITS OF HIGHLY SUCCESSFUL SECURITIES TRADERS

SUCCESSFUL TRADING

7 Habits of Highly Successful Traders

BySteve Burns

SEP 21, 2022

Just like Stephen Covey found the effective habits of successful people through his studies I have found the common habits of successful traders through research. Many similarities for what creates success in any field. Let me breakdown the seven habits common in most successful traders. 

1. Use A Positive Expectancy Model

What is Positive Expectancy?

The closest a trader can hope to come to a holy grail is a trading system with a positive expectancy. The first job of a trader is creating a quantified system with an edge that is repeatable and provides enough opportunities to be meaningful.  A positive expectancy model creates more profits than losses that average out to profitability over time.

A positive expectancy means you have an edge, that when you average out all the wins and losses you make money. If you divide your total profits by your total trades you have a profit factor and have a positive outcome. A successful trader expects that if they place a certain amount of trades that they will be profitable at the end of the sequence of entries and exits based on their statistical and systematic edge.

As an example a casino, sports bookmaker, horse handicapper, professional gamblers, and Black Jack card counters all have an edge they understand that makes them profitable in the long-term as their edge plays out.

Positive expectancy could be the most important part of trading. For every trader no matter what trading method they use on any timeframe, if they don’t have a positive expectancy trading model then they have no edge and will likely have no long term profits. Most traders lose money because they have a negative expectancy model and don’t even know it. Risk/reward ratios, trade management, and backtesting are ways to define your expectancy.

Before traders start putting any money at risk they should know if the trading system they are using has a positive expectancy. Without first having a positive expectancy system to trade that fits your own risk tolerance and return goals your trading psychology and risk management don’t matter much. If you use good position sizing and the right mindset on trading a system with a negative expectancy or high risk of ruin it just means you lose money at a slower pace with a better attitude.

Knowing we have a positive expectancy means we have done enough homework, backtesting, and validation to show ourselves our trading system will create profits over the long term based on our signals, win rate, and risk/reward ratio.

The first part of successful trading is in the research to validate your system. This is a lot of work and effort and why most traders don’t succeed. Too many new traders enter the market in pursuit of easy and fast money not to do hundreds of hours of research.

A win rate is not what creates a positive expectancy. It’s the size of all the wins and losses combined that create the expectancy. You can have a low win rate system that is profitable due to a few huge wins and a lot of small losses. Huge trading losses and large drawdowns due to bad position sizing are the primary factor that creates a negative expectancy system.

The first step to creating a positive expectancy system is removing big losses from your system and the second most important is to let your winners run. This is the purpose of your entry signals, exit signals, position sizing, trailing stops, and profit targets, to create a positive expectancy.

How can you calculate a trading system’s positive expectancy?

Positive Expectancy Formula:

E(R) = (PW x AW) – (PL x AL)

where:

E(R): Expectancy/ or Expected Return

PW: Probability of winning

AW: Average win

PL: Probability of losing

AL: Average loss

Positive Expectancy: is a positive “E(R)”

This is the first step in a new trader’s journey not something to do later. A lot of positive expectancy emerges from trade management after a trade entry with stops to minimize losses and trailing stops to maximize gains.

2. Use A Dynamic Trading Strategy

What is a dynamic trading strategy?

Trading dynamically, means reacting and adapting to what the market price action is telling you. It means following a plan created to maximize wins and minimize losses. It means managing a trade based on reactive technical analysis using entry signals, stop losses, trailing stops and profit targets.

No matter how much a trader believes that they can predict the future or how strong their conviction is, no individual trader or investor can control the outcome of a market move unless they have enough capital to move a market their self. Traders have the unique frustration that few other careers have, a lack of control on outcome. All a trader controls is their system development and execution, the market movement creates the outcome of wins and losses.

A trader can’t control:

1.The price movement.

2.The outcome of a trade.

Once a trader is in a trade the price movement is based on the collective actions of the market participants buying, selling, or holding not the trader’s predictions, hopes, and opinions. While a trader can manage a trade with size and exit strategies they can’t control whether their stop loss is triggered or their profit target is hit. A trader is at the mercy of the market to choose the outcome of each of their trades.

The good news is that a trader does have a lot of control.

A trader can control:

1. When they enter a trade.

2..When they don’t trade.

3. A trader can choose their own watchlist.

4. The price they exit to stop a loss.

5. The price target they will exit at to lock in a gain.

6. To use a trailing stop loss to let a winner run.

7. The position sizing for a trade.

8. Their plan to manage a maximum loss with the combination of position sizing and a stop loss.

9. The technical indicators to use for signals.

10. How their emotions are managed.

11. The lessons they learn from every trade.

12. Whether to keep trading or quit.

You can’t control what the market price action will do but you can control what you will do in response to the price action and how you manage each trade after entry. Before you’re in a trade you control how big and when you will get in. After you are in you control when and how you will get out. You will never control the markets but you can develop the discipline to have complete control of yourself. The dynamic of flexibility is a trait of most successful traders while stubbornness and arrogance is the factor that usually leads to ruin as opinions and trades become fixed.

3. Create Asymmetric Trades

Asymmetric trades

The key to profitable trading is creating asymmetrical risk/reward ratios that are in your favor. Successful traders risk $100 to make $200 or more to create at least a 1:2 risk/reward ratio. This can be very profitable with just a 50% win rate.

For example:

Win $200

Win $200

Win $200

Lose $100

Lose $100

Lose $100

Total ins are $600 and total losses are $300 for a $300 profit in a six trade sequence. This is what successful trading looks like as a basic example.

Equal profit targets along with the same level as your stop would be considered symmetrical. You shouldn’t be buying a stock at $100, and your profit target be $103, with your stop at $97. This is symmetrical because it has the same dollar target on both sides of your trade. This means you have to win over half the time to be profitable. This is difficult for most traders, and a string of losses can be devastating to your account if you don’t have large winning trades to offset the drawdowns in capital.

Most traders do the worst thing they could by creating asymmetrical risk against their self. They take large position sizing going after small moves but will hold losing trades hoping to get back to even creating large losses. Risking a lot to make a little is the opposite of a favorable risk/reward ratio.

Successful traders limit their downside risk tightly with stop losses but leave their upside profit potential open with trailing stops and profit targets. This is what is meant by cutting losses short and letting winners run.

4. Mental Model Of Success

The way a successful trader thinks can be at the core of their profitability. Their operating mental model is faith in their system to create profits and faith in their self to execute it with discipline and focus. They don’t waste time and energy with self-doubt and second guessing their trading method. They trade, they learn, they adjust, and they grow. They bring passion and energy to their trading and have confidence in their self to navigate the markets and create profits using their system.

A successful trader knows who they are and are not doubleminded. 

They have no Plan B just the Plan A of becoming and staying a successful trader by doing whatever it takes.

 Their passion creates the energy they need to do the work to achieve success and then maintain their level of high performance.

Successful traders think very differently from the majority that never make it. At their core you will find positivity, passion, focus, and love for the game.

5. Experts On Their Method

Successful traders are experts on their chosen method, markets, and time frame. They know their edge and stay within their circle of competence. They don’t try to beat all traders just their direct competitors. They let the traders in other markets and time frames battle it out why they stay in their own lane.

They are not a Jack-of-all-trades, they are the masters of just one. It’s easier to win at a method you are an expert in than pursue things you don’t fully understand due to the fear of missing out on opportunities.

They choose a method to master and they build a system to optimize their own success. Many unsuccessful traders chase every waterfall but never learn how to swim.

You can only win battles after you choose which one to fight with focus and long-term effort in one direction.

6. Confluence of Profitable Dynamics

Successful traders have created a confluence of the three required parameters for profitable trading. Trading a winning system using the right risk management along with correct trading psychology.

If any of these three building blocks are missing then profitable trading will not be achieved.

If you have a winning system with proper risk management but the wrong trading psychology you will have no discipline to follow it.

If you have a winning system with the right trading psychology but no risk management you eventually will lose your account in ruin.

If you have the right trading psychology and good risk management but no winning system you will have no edge leading to profitability.

If you combine a positive expectancy model, with proper position sizing, and mental discipline then only time separates you from profitable trading. This is what successful traders learned on their journey.

7. Hunger To Win

“The secret to being successful from a trading perspective is to have an indefatigable and an undying and unquenchable thirst for information and knowledge.” – Paul Tudor Jones

The successful traders had the hunger and desire to win. Trading was the game they chose and much like the greatest professional athletes their edge came from wanting to win. Their desire drove them to doing the necessary work to achieve their goals.

They weren’t satisfied with trading as a hobby, they wanted to go pro and make it their full time job. Hunger to reach goals is the primary driver of the energy to get there.

The biggest determinate of successful traders from everyone else who didn’t make it through the learning curve was their hunger to succeed.

How bad do you want it?

 

DR SONG BENG KAH: CAUSES OF AUTISM

 爱心餐导致自闭症，伊党议员说错了吗

Title: Does Rahmah Menu Cause Autism? Did the PAS MP say something wrong?"

Quote: 薄利多销的爱心餐单，对B40家庭来说，是很好的援助策略，前提是食材素质不成问题。但因政治因素而胡乱瞎说，就必须受到谴责。

Quote: "The Rahmah menu with small profits and high sales is a good aid strategy for B40 families, provided that the quality of the ingredients is not a problem. But if it is arbitrarily said due to political factors, it must be condemned."

爱心餐单（Menu Rahmah）的菜色品质会不会导致自闭症？这是这几天朋友们在群组的热门话题。

Can the quality of the dishes on the "Menu Rahmah" (Compassion Menu) cause autism? This has been a hot topic among my friends in our group chat in the past few days.

事缘伊斯兰党议员哈丽玛医生在国会下议院，对爱心餐单的质量问题“可能”让B40人口暴露于癌症、自身免疫疾病和自闭症潜在风险表示担忧，因而饱受民众和其他议员的批评。在人们的嘲笑、批判声中，连国会下议院副议长也说她的言论不可取，会对社会上特殊群体造成二度伤害。

"Recently, Dr. Halimah, a member of the Islamic Party, expressed concerns about the quality of the "Menu Rahmah" in the lower house of Parliament, suggesting that it may expose the B40 population to potential risks of cancer, autoimmune diseases, and autism. Her comments were criticized by the public and other members of Parliament. Even the deputy speaker of the lower house of Parliament said that her remarks were inappropriate and could cause secondary harm to vulnerable groups in society amid the ridicule and criticism."

爱心套餐的质量有保障，据说是毋庸置疑的，但哈丽玛说错了吗？

The quality of the Rahmah Menu is guaranteed and is said to be beyond doubt. However, is Halimah wrong?

一般互联网搜索引擎和ChatGPT，对这些科学讯息的搜寻会有所不足，甚至产生误导。

The general internet search engines and ChatGPT may be inadequate in searching for this scientific information and may even lead to misinformation.

但对读者而言，尤其是大学毕业生，使用PubMed和Google Scholar等学术文献库平台来核实公众人物的声明，应不是件难事；这不但可以取得较可靠信息，更能清楚理解诸如自闭症的复杂科学议题。

"However, for readers, especially college graduates, it should not be difficult to use academic literature databases such as PubMed and Google Scholar to verify public figures' statements. This can not only obtain more reliable information but also provide a clearer understanding of complex scientific issues such as autism.

既然民众对哈丽玛的批评多聚焦于自闭症，这里简单梳理一些研究文献，来协助大家釐清“自闭症和饮食之间”的关系，并分为三个组别来讨论。

Since the public's criticism of Halimah largely focuses on autism, here is a brief summary of some research literature to help clarify the relationship between autism and diet, divided into three groups for discussion.

（A）关于孕妇和新生儿的研究

(A) Studies on pregnant women and newborns

1。 美国University of California使用241个幼童数据的研究发现，已有自闭症孩子的孕妇在孕期服用各类维生素，可能降低第二次生下自闭症孩子的风险（引2019年2月《JAMA Psychiatry》论文）。

1. A study by the University of California in the United States, using data from 241 young children, found that pregnant women who had children with autism and who took various types of vitamins during pregnancy may reduce the risk of having another child with autism (citing a paper published in JAMA Psychiatry in February 2019).

2。 根据中国江苏师范大学（Jiangsu Normal University）评估310名自闭症患儿和1240个对照组的研究，维生素D水平较低的婴儿患自闭症的风险增加260%（引2017年11月《Journal of Bone and Mineral Research》论文）。

2. According to a study by Jiangsu Normal University in China, which evaluated 310 children with autism and 1,240 control groups, infants with lower levels of vitamin D have a 260% increased risk of developing autism (citing a paper published in the Journal of Bone and Mineral Research in November 2017).

3。 美国Drexel University School of Public Health发表的研究结果和过往研究一致，即新生儿维生素D低水平，可能与自闭症风险增加有关；新生儿样本包括1399个自闭症病例和1607个对照样本（引2021年5月《Molecular Psychiatry》论文）。

3. The research results published by Drexel University School of Public Health in the United States are consistent with previous studies, that low levels of vitamin D in newborns may be associated with an increased risk of autism; the newborn samples included 1,399 autism cases and 1,607 control samples (citing a paper published in Molecular Psychiatry in May 2021).

4。 以色列University of Haifa研究人员指出，在怀孕前和怀孕期间“服用叶酸和多种维生素补充剂”的孕妇，其孩子患自闭症风险比“没服用补充剂”的孕妇低。此研究共使用4万5300名儿童的数据，在出生后到8至12岁这段时间里，评估他们患自闭症的风险（引2019年2月《JAMA Psychiatry》论文）。

4. Researchers at the University of Haifa in Israel pointed out that pregnant women who took folic acid and multiple vitamin supplements before and during pregnancy had a lower risk of having children with autism than pregnant women who did not take supplements. This study used data from 45,300 children and evaluated their risk of developing autism between the ages of 8 and 12 after birth (citing a paper published in JAMA Psychiatry in February 2019).

5。 美国California Department of Public Health团队涉及563名新生儿的研究，并不支持“新生儿低维生素D水平与自闭症风险增加”之间存在关联的说法（引2019年3月《Autism Research》论文）。

5. A study by the California Department of Public Health team involving 563 newborns did not support the claim that there is a link between low vitamin D levels in newborns and an increased risk of autism (citing a paper published in Autism Research in March 2019).

（B）涉及儿童的研究

(B) Studies involving children

埃及Assiut University研究人员对109名自闭儿童进行双盲随机对照试验（double-blinded randomized controlled trial），显示补充维生素D可能有助于改善症状（引2016年11月《Journal of Child Psychology and Psychiatry》论文）。必须注意的是，该论文已被撤回，此研究的可靠性存疑；目前仍没有研究证明儿童营养不良会导致自闭症。

Researchers from Assiut University in Egypt conducted a double-blinded randomized controlled trial on 109 children with autism, and found that supplementing with vitamin D may help improve symptoms (cited in a November 2016 article in the Journal of Child Psychology and Psychiatry). However, it is important to note that this paper has been retracted and the reliability of this study is questionable. Currently, there is still no research to prove that malnutrition in children can lead to autism.

（C）综述和元分析

(C) Review and Meta-Analysis.

1。 中国北京大学团队对已发表的10项研究进行元分析（meta-analysis），发现缺乏维生素D的儿童患自闭症的可能性，比维生素D水平充足的儿童高出5.2倍（引2021年1月《Nutrients》文章）。然而，这些研究之间存在很大异质性，对“维生素D缺乏”的定义也不一致。

1. A team from Peking University in China conducted a meta-analysis on 10 published studies and found that children who lack vitamin D are 5.2 times more likely to develop autism than those with sufficient levels of vitamin D (according to an article published in Nutrients in January 2021). However, there is significant heterogeneity among these studies, and the definition of "vitamin D deficiency" is also inconsistent.

2。 美国Icahn School of Medicine at Mount Sinai研究人员分析自闭症环境风险因素后，显示维生素D与儿童自闭症之间存在因果关系，而缺乏叶酸和omega 3脂肪酸引起自闭症的影响则尚未确定（引2017年3月《Molecular Autism》文章）。

2. Researchers from the Icahn School of Medicine at Mount Sinai in the United States analyzed environmental risk factors for autism and found a causal relationship between vitamin D and autism in children. However, the impact of folate and omega-3 fatty acid deficiency on autism is yet to be determined (according to an article published in Molecular Autism in March 2017).

根据以上研究，我们可作出以下推论：

Based on the above studies, we can draw the following conclusions: 

（a）如果哈丽玛的“B40群体”指的是孕妇，那其论点其实有一些科学依据；但目前仍没有足够科学证据，能证明营养不良是自闭症的直接原因。

(a) If Halimah's "B40 group" refers to pregnant women, her argument actually has some scientific basis; however, there is still not enough scientific evidence to prove that malnutrition is a direct cause of autism.

（b）如果她指的是“B40儿童”，就更没有确凿的科学证据，来支持“饮食和自闭症的关联”论点。

(b) If she is referring to "B40 children", there is even less conclusive scientific evidence to support the argument that there is a link between diet and autism.

可惜，哈丽玛并没有上PubMed搜寻研究报告，也不懂得以研究数据为自己辩护，更在被希盟议员和民众轰炸后，自乱阵脚辩说“言论被歪曲原意”。

Unfortunately, Halimah did not search PubMed for research reports and did not know how to defend herself with research data. After being bombarded by Pakatan Harapan MPs and the public, she became disoriented and argued that her statement was misinterpreted.

自闭症是一种复杂的神经疾病，可能受各种遗传、环境和发育因素的相互影响。虽然产前营养素缺乏是可能风险因素，但它并不是自闭症的唯一原因，也需要进一步研究来确认其和自闭症的关联。值得注意的是，以上研究的自闭症儿童群体，可能因长期偏食等饮食因素，导致某些营养素（例：维生素B1、B6、B12、A、C、D、钙和锌）的缺乏，而不是营养缺乏引发自闭症。

Autism is a complex neurological disorder that may be influenced by various genetic, environmental, and developmental factors. While prenatal nutrient deficiencies may be a possible risk factor, they are not the sole cause of autism and further research is needed to confirm their association. It is worth noting that the autism children in the above studies may have lacked certain nutrients (such as vitamins B1, B6, B12, A, C, D, calcium, and zinc) due to long-term dietary factors such as picky eating, rather than a general lack of nutrition causing autism.

薄利多销的爱心餐单，对B40家庭来说，是很好的援助策略，前提是食材素质不成问题。但因政治因素而胡乱瞎说，就必须受到谴责。

A low-profit and high-turnover Rahmah Menu is a good assistance strategy for B40 families, provided that the quality of the ingredients is not an issue. However, making reckless and baseless statements due to political factors must be condemned.

https://research.monash.edu/en/persons/song-beng-kah

LINK BETWEEN DIET, NUTRITION AND CANCER

 Two Papers on Diet, nutrition and Cancer 

PAPER I

Diet, nutrition and the prevention of cancer

Published online by Cambridge University Press:  02 January 2007

Timothy J Key et al

Abstract

Objective:

To assess the epidemiological evidence on diet and cancer and make public health recommendations.

Design:

Review of published studies, concentrating on recent systematic reviews, meta-analyses and large prospective studies.

Conclusions and recommendations:

Overweight/obesity increases the risk for cancers of the oesophagus (adenocarcinoma), colorectum, breast (postmenopausal), endometrium and kidney; 

Body weight should be maintained in the body mass index range of 18.5–25?kg/m2, and weight gain in adulthood avoided. 

Alcohol causes cancers of the oral cavity, pharynx, oesophagus and liver, and a small increase in the risk for breast cancer; if consumed, alcohol intake should not exceed 2?units/d. 

Aflatoxin in foods causes liver cancer, although its importance in the absence of hepatitis virus infections is not clear; exposure to aflatoxin in foods should be minimised. 

Chinese-style salted fish increases the risk for nasopharyngeal cancer, particularly if eaten during childhood, and should be eaten only in moderation. 

Fruits and vegetables probably reduce the risk for cancers of the oral cavity, oesophagus, stomach and colorectum, and diets should include at least 400g/d of total fruits and vegetables.

 Preserved meat and red meat probably increase the risk for colorectal cancer; if eaten, consumption of these foods should be moderate. 

Salt preserved foods and high salt intake probably increase the risk for stomach cancer;

 Overall consumption of salt preserved foods and salt should be moderate. 

Very hot drinks and foods probably increase the risk for cancers of the oral cavity, pharynx and oesophagus; drinks and foods should not be consumed when they are scalding hot. 

Physical activity, the main determinant of energy expenditure, reduces the risk for colorectal cancer and probably reduces the risk for breast cancer; regular physical activity should be taken.

PAPER II

Nutrition and cancer: the current epidemiological evidence

Carlos A Gonzalez. 

Br J Nutr. 2006 Aug.

Abstract

We have examined the current scientific evidence on the relationship between nutrition and the most frequent tumours in the Spanish population: lung, colorectal, prostate, breast and stomach. 

Consumption of fruit is negatively associated with cancer of the lung and stomach, possibly with colorectal cancer, but probably not with prostate cancer and breast cancer. 

Consumption of vegetables probably reduces the risk of colorectal and stomach cancer, but probably is not associated with cancer of the lung, prostate and breast.

 Consumption of red and processed meat is positively associated with colorectal cancer and probably with stomach cancer. 

Animal fat is possibly associated with colorectal cancer and probably with prostate and breast cancer. 

High alcohol intake increases the risk of colorectal and breast cancer, while dairy products and calcium seem to decrease the risk of colorectal cancer. 

Obesity is a recognised risk factor of colorectal cancer and breast cancer in postmenopausal women, while foods with a high glycaemic index and glycaemic load possibly increase the risk of colorectal and prostate cancer. 

The relevance of nutrition on the cancer process is evident. Nevertheless important issues remain to be solved and further studies are needed. This accumulative knowledge should be used by public health authorities to develop recommendations and activities to reduce overweight and obesity and to promote healthy dietary intak

Public Health Nutrition , Volume 7 , Issue 1a , February 2004 , . 187 - 

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CUTTING EDGE RESEARCH: AUTISM

 

CAUSES OF AUTISM : AN OVERVIEW

Examining the Causes of Autism

David G. Amaral, Ph.D.

Introduction 

Autism is a broad, complex, and increasingly important brain disorder. New data from the Center for Disease Control and Prevention indicate that one in sixty-eight children is born with some degree of autism. Autism is also more common in males by a four to one ratio. 

Making it especially difficult to discuss in finite, conclusive terms is the fact that there is no biological test for autism; diagnosis is based on behavior, and the only verified treatment is intensive behavior therapy. Our author, one of the nation’s foremost researchers on autism, examines the prenatal factors that contribute to the disorder.

As an autism researcher, I often try to put myself in the shoes of parents who have just been told that their child has autism. More and more families in the United States and around the world are facing this difficult news. The families that I’ve seen go through this often respond emotionally at first. Some go through denial; others are sad or furious. But emotions soon give way to questions. What caused my child’s autism? Was I to blame? Which treatments will help? And what does the future hold?

Autism research has made tremendous progress over the last 20 years, but yet we still can’t provide definitive answers to most of these questions. I find the autism community to be proactive, combative, and opinionated. The complexity and ambiguity of autism has spawned myriad speculations about causes—many of which have little supportive evidence. It seems clear at this point, however, that when all is said and done, we will find that autism has multiple causes that occur in diverse combinations.

To begin with, many people struggle to understand the nature of a condition so wide ranging in its severity. Autism Spectrum Disorder (ASD) or autism is a behaviorally defined neurodevelopmental disorder characterized by 1) persistent deficits in social communication and interaction across multiple contexts, and 2) restricted, repetitive patterns of behavior, interests, or activities. 

Few would dispute that the causes of ASD include both genetic and environmental factors. Indeed, more than 100 genes are known to confer risk1,2 and 1,000 or more may ultimately be identified.3 A wide range of potential environmental challenges have also been associated with autism, although studies in this area lag behind genomics research. A short overview of data supports genetic and environmental contributions to ASD etiology. A focus on prenatal events will hopefully clarify that the cause of autism, in the vast majority of cases, occurs prenatally, even if behavioral signs first appear several years after birth.

Twin Studies

Strong evidence against the unfounded view that autism results from neglectful parenting came in 1977 from Folstein and Rutter and the first systematic, detailed study of twin pairs containing at least one child with autism.4 In this study, 11 of the twin pairs were monozygotic (nearly identical genetics) and 10 were dizygotic (shared approximately half of their genome with each other). The major finding was that four of the monozygotic twin pairs were concordant (both had autism), whereas none of the dyzygotic twins were. Beyond autism, nine of the eleven monozygotic pairs were concordant for some form of cognitive impairment, compared to one of ten of the dyzygotic pairs.

The researchers concluded that autism and other neurodevelopmental disorders have a strong genetic component. But environmental factors must also contribute to autism etiology, they pointed out. For the 17 twin pairs that were discordant for autism—one child had a diagnosis and the other did not—the authors speculated that direct damage to the brain might have affected the diagnosed twin. They identified five features known to be associated with brain damage, such as severe hemolytic disease, a delay in breathing of at least five minutes after birth, and neonatal convulsions. In six of the pairs, one twin—always the autistic one—experienced one or more of these insults. Looking further, they found that one of an expanded list of “biological hazards” (e.g., discrepancies in birth weight, a pathologically narrow umbilical cord) occurred in the autistic twin in 6 of the 11 remaining discordant pairs and never in the non-autistic twin. The authors concluded that “some form of biological impairment, usually in the perinatal period, strongly predisposed to the development of autism.”

Since the Folstein and Rutter paper cited above, there have been a total of 13 twin studies focused on autism. All find genetic and environmental contributions to autism, although conclusions about the proportions of the two factors and interpretations have varied substantially. One research team,5 for example, concluded that a large proportion of the variance in liability (55 percent for strictly defined autism and 58 percent under a broader definition) can be explained by shared environmental factors, whereas genetic heritability accounts for 37 percent. This somewhat surprising finding—that environmental factors contribute more substantially than genetics—has been challenged by a more recent, large-scale twin study,6 which found that the largest contribution to autism liability comes from additive genetic effects. And, a recent meta-analysis7 concludes that the causes of autism are due to strong genetic effects, and that shared environmental influences are seen only if autism is very narrowly defined. A brief synopsis of the history of autism twin studies8 finds that concordance for monozygotic twins is roughly 45 percent, versus 16 percent for dizygotic twins.

The reason for this short review of autism twin studies is to emphasize that even the best evidence for both genetic and environmental etiologies of autism leads to inconsistent conclusions about their proportional contributions. Moreover, twin studies do not typically consider that the cause of autism may involve genetic and environmental factors working together (the so-called gene by environment effect); i.e., certain environmental exposures only cause autism in individuals with a particular genetic composition. The second point is that if autism had a completely genetic etiology, we would expect a much higher concordance rate in monozygotic twins; the actual rate may reflect, in part, that even monozygotic twins do not share an identical environment prenatally.9,10 Therefore, one must seriously search for environmental factors that either alone, or in combination with genetic predisposition, can increase autism risk. What are these factors?

Maternal Infection

If twin studies provide the best evidence for a genetic basis of autism, then naturally occurring pathogen exposures offer the strongest evidence of environmental etiology. The best example is maternal rubella (German measles) infection during pregnancy.

 Before development and widespread dissemination of effective vaccines, major pandemics occurred every 10 to 30 years.11 The last of these was from 1963 to 1965 and infected an estimated 10 percent of pregnant women, resulting in more than 13,000 fetal or early infant deaths; 20,000 infants born with major birth defects and 10,000 to 30,000 infants born with moderate to severe neurodevelopmental disorders. Stella Chess, a child psychiatrist at New York University, studied 243 children exposed to rubella during pregnancy12,13 and found that the largest category of neurodevelopmental disorder was intellectual disability, which affected 37 percent of the sample. Nine of these children were also diagnosed with autism; another, without intellectual disability, had a possible diagnosis; and eight a partial syndrome of autism. These numbers would translate to an autism prevalence of 741 per 10,000 rubella-exposed children, just over seven percent. This is striking in comparison to published prevalence rates, at the time of the study, of two to three per 10,000 in the general population. Fortunately, rubella epidemics have ended due to widespread dissemination of the measles, mumps and rubella vaccines and the association of autism with other viral or bacterial infections is weaker than with rubella.14

Collier et al15 have pointed out that nearly 64 percent of women surveyed in the US have experienced an infection during their pregnancies. This obviously does not lead to autism or any other neurodevelopmental disorder in most cases.

Examining prenatal environmental factors is best conducted in very large cohorts of subjects that have excellent health care records. This can be done in Scandinavian countries with their nationalized health care systems, and in large health care providers in the US.

One such study, conducted in Denmark, found no association between maternal bacterial or viral infection during pregnancy and diagnosis of ASD in the offspring,16 although viral infection during the first trimester, or admission to the hospital due to infection during the second trimester were associated with the diagnosis. 

In a more recent study17 Atladottir and colleagues found little evidence, overall, that common infectious diseases or fevers (lasting more than seven days) during pregnancy increased the risk of autism—noting, however, that influenza increased the risk of having an autistic child twofold. Use of antibiotics also increased risk. The link between influenza exposure during fetal life and increased risk for autism is in line with a series of animal studies18, 19 suggesting that the influenza virus activates the maternal immune system, which may be harmful to fetal brain development. But the Danish researchers seem to downplay even their statistically significant findings, suggesting that their results do not indicate that either mild infection or the use of antibiotics represent strong risk factors for autism.

A parallel set of studies has been carried out by Zerbo and colleagues in California. The first,20 based on 1,122 children, found no association between maternal influenza and ASD but (in contrast to Atladottir et al), the occurrence of maternal fever did increase risk. A second study21 of 2,482 children (407 with ASD) found that mothers of children with ASD were diagnosed with viral infections during pregnancy no more often than mothers of non-autistic children. Maternal bacterial infections during the second trimester and the third trimester, however, were associated with a twofold increase in ASD risk, and two or more infections diagnosed in the third trimester with even higher risk, again suggesting a link with more severe infection during pregnancy. The most recent study,22 based on a large cohort of children (196,929) born between 2000 and 2010, found that neither maternal influenza infection during pregnancy nor influenza vaccination were associated with increased risk for ASD.

In conclusion: Some infections during pregnancy, such as German measles, clearly increase the risk of ASD. However, there seems relatively little evidence that today’s widely experienced infectious illnesses, such as influenza, during pregnancy substantially increase the risk of ASD. Perhaps the signal is weak because of gene by environment effects [as seems to be the case for different strains of mice23, 24]. If so, evidence will need to come from studies that combine large scale epidemiology with sophisticated genomic analyses.

Maternal Antibodies

Autoimmune diseases (in which immune cells erroneously identify cells in the body as foreign and attack them) mediated by circulating antibodies currently affect as much as nine percent of the world’s population,25 and the notion that autoimmunity may be associated with neurological and psychiatric disorders goes back to the 1930s. 

Reviewing this contentious area of research, Goldsmith and Rogers26 conclude that the literature, though conflicting, “contains a large amount of circumstantial, but not conclusive, evidence for immune dysfunction in patients with schizophrenia.” Interestingly, an auto-immune disorder with antibodies directed at the NMDA receptor causes an encephalopathy, which in its early stages can be indistinguishable from schizophrenia.27

Precedents for antibody-related CNS disorders include Rasmussen encephalitis, stiff-person syndrome, neuromyelitis optica, post streptococcal movement disorders (Sydenham’s chorea and PANDAS), and systemic lupus erythematosus.28 Judy Van de Water, of UC Davis, the main proponent of the idea that circulating antibodies may cause some forms of autism, first reported in 2008 that 12 percent of mothers of children with ASD have unusual antibodies directed at fetal brain proteins.29 Based on more specific assays for these antibodies, she has since proposed that Maternal Antibody-Related (MAR) causes may be associated with as many as 22 percent of autism cases, suggesting that this may be a preventable form of ASD.30 This area of research is exciting because it suggests potential therapeutic targets. Although many questions remain (e.g., how antibodies would enter the fetal brain, what neurodevelopmental processes they may alter), it is entirely possible that circulating antibodies represent prenatal environmental risk factors for ASD.

Drugs

Efforts to understand the increased prevalence of autism spectrum disorder have led some to wonder whether the use of various drugs during pregnancy might be partly responsible. 

Historically, a strong case could be made for an association between autism and thalidomide, a potent sedative that was used (for several years around 1960) during pregnancy for the relief of nausea. A study of 100 adult Swedish patients whose mothers had taken thalidomide while pregnant31 found that at least four had clear autistic characteristics. This was the first evidence that a drug ingested during pregnancy could substantially increase autism risk. More recently, concerns have been raised about valproic acid and serotonin reuptake inhibitors.

Valproic acid, an approved drug since the early 1960s, is primarily prescribed for epilepsy and seizure control, but also used for ailments ranging from migraine headaches to bipolar disorder. Both animal and human epidemiological studies have raised concerns that valproic acid is a teratogen. The largest epidemiological study to date32 tracked 415 children, 201 of whom were born to mothers who took antiepileptic medication during their pregnancies. Nearly 7.5 percent of the children of the treated women had a neurodevelopmental disorder, primarily some form of autism, versus 1.9 percent in the non-epileptic women.

A recent concern has been the use of serotonin reuptake inhibitors (SSRIs) for the treatment of depression during pregnancy. Serotonin is an important brain neurotransmitter that plays a significant role in functions ranging from sleep to mood to appetite, and whose dysregulation during early fetal life can have serious negative consequences for brain development.33 As the name implies, SSRIs, which have been in use since the late 1980s, delay the reuptake of serotonin from the synaptic cleft into the presynaptic terminal and thus enhances its effect on the postsynaptic receptors. A recent review and meta-analysis of six case-control studies and four cohort studies concluded that SSRI use during pregnancy34 was significantly associated with increased risk of ASD in offspring.

The effect was most prominent with use of the drugs during the first and second trimesters of pregnancy. Interestingly, the researchers found that preconceptual exposure to SSRIs was also associated with increased ASD risk—as was the use of non-SSRI antidepressants. They note that a large cohort study found that, while ASD rates in the SSRI-exposed group were significantly higher than in the unexposed group, the rates in the SSRI-exposed group did not significantly differ from those among mothers with unmedicated psychiatric disorder and those who had discontinued SSRIs. It currently appears impossible to disentangle the deleterious effect of SSRIs from the fact of a maternal condition that necessitates the drug. Many authors also comment on the potentially worse effect on pregnancies of untreated maternal depression.

In sum, a brief review of the literature indicates that ingesting some drugs during pregnancy increases the risk of ASD, suggesting the need for more careful evaluation of drug safety during fetal development prior to widespread medical use.

Environmental Toxicants

Beyond viral and bacterial pathogens and medically prescribed drugs, researchers have begun investigating environmental toxicants. These range from automobile-produced air pollution to cigarette smoke to heavy metals and pesticides.35,36 Small increases in autism risk have been reported if, for example, a family lives closer to a freeway or to an agricultural area during pregnancy. The field of autism environmental epidemiology is still in its infancy and techniques to comprehensively establish a prenatal “exposome” (i.e., all environmental factors affecting a fetus during pregnancy) are still under development. That said, given the unlikelihood that all autism will be explained by genetic factors, the determination of environmental causes, some of which might be avoided or minimized, may have far greater translational impact than the much better funded genetic studies. Strategies for exploring gene-by-environment interactions need to be enhanced with haste.

Postnatal Factors

Since autism is a neurological disorder that undoubtedly reflects altered brain function, it is possible that the insult to the brain occurs after birth. There is currently very little evidence for this. One historical concern was that vaccines, such as the measles, mumps, and rubella (MMR) vaccine, administered initially when the child is about one-year old, might transform a healthy child into one with autism. This fear was fueled by regressive onset in some cases—a child seems fine for the first year or so, then loses social and language function and regresses into a classical autistic syndrome. But we have found that even in children who demonstrate this regressive form of autism, brain changes begin by four to six months, long before behavior changes.37 Moreover, many large-scale epidemiologic studies have unequivocally demonstrated no link between MMR administration and the risk of ASD (summarized in 38), the same conclusion that the US National Academy of Sciences reached in a thorough review carried out in 2011.39

The only other postnatal experience that has been linked to the onset of ASD is profound social isolation in institution-reared children, such as those in the Romanian orphanage system.40 Rutter and colleagues41 found that nearly 10 percent of children raised in Romanian orphanages and adopted by British families showed some features of autism. These children were very poorly treated in the orphanage (most were underweight and had intellectual disability and various medical problems). While fully qualifying for an autism diagnosis at age 4, they showed substantial improvement and less severe autism symptoms by age 6. Is this truly autism? The authors conclude: “The characteristics of these children with autistic features, although phenomenologically similar in some respects to those found in “ordinary” autism, differed sharply in the marked improvement evident between 4 and 6 years of age and in the degree of social interest... The quasi-autistic pattern seemed to be associated with a prolonged experience of perceptual and experiential privation, with a lack of opportunity to develop attachment relationships, and with cognitive impairment.”

This sad epoch demonstrates both the potential for severely abnormal rearing practices to influence brain regions that are affected by typical causes of autism, and the resilience of the brain in compensating and restoring once the individual is placed in a more normal environment. But it does not provide evidence for the postnatal genesis of autism.

The research picture regarding the causes for Autism Spectrum Disorder remains complex, although there is certainly a very strong genetic component. While there are some genes, such as CHD8, the mutation of which almost always cause autism in a very low percentage of cases42 most mutations seem to confer small increases in risk. 

Similarly, while some environmental factors, such as rubella infection or fetal exposure to valproic acid, have been highly associated with autism risk, the increase in risk associated with others, such as living close to a highway, is small. It is very likely that the answer to what causes autism will not reside solely in genetics or in environment but in a combination of the two. Whatever factors go into the mix, they most likely have their effect during fetal life: a person with autism is born with autism.

Biography

• 

David G. Amaral, Ph.D., is a Distinguished Professor in the Department of Psychiatry and Behavioral Sciences at UC Davis. He is also the Beneto Foundation Chair and Research Director of the MIND Institute, which is dedicated to studying autism and other neurodevelopmental disorders. As research director, he coordinates a multidisciplinary analysis of children with autism called the Autism Phenome Project to define clinically significant subtypes of autism. More recently, Amaral has become Director of Autism BrainNet, a collaborative effort to solicit postmortem brain tissue to facilitate autism research. In April of 2015, Amaral became editor-in-chief of Autism Research, the journal of the International Society for Autism Research. In 2016, he was appointed to the Interagency Autism Coordinating Committee by the Secretary of Health and Human Services. Amaral received a joint Ph.D. in neuroscience and psychology from the University of Rochester and conducted postdoctoral research at the Department of Anatomy and Neurobiology at Washington University. He also conducted research at the Salk Institute for Biological Studies and served as an adjunct professor in the Department of Psychiatry at UC San Diego.

David G. Amaral, Ph.D.

Copyright 2017 The Dana Foundation All Rights Reserved

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