"Why do some British people not like Donald Trump?" by Nate White

"A few things spring to mind. Trump lacks certain qualities which the British traditionally esteem. For instance, he has no class, no charm, no coolness, no credibility, no compassion, no wit, no warmth, no wisdom, no subtlety, no sensitivity, no self-awareness, no humility, no honour and no grace - all qualities, funnily enough, with which his predecessor Mr. Obama was generously blessed.

“So for us, the stark contrast does rather throw Trump’s limitations into embarrassingly sharp relief. Plus, we like a laugh. And while Trump may be laughable, he has never once said anything wry, witty or even faintly amusing - not once, ever.

“I don’t say that rhetorically, I mean it quite literally: not once, not ever. And that fact is particularly disturbing to the British sensibility - for us, to lack humour is almost inhuman. But with Trump, it’s a fact. He doesn’t even seem to understand what a joke is - his idea of a joke is a crass comment, an illiterate insult, a casual act of cruelty.

“Trump is a troll. And like all trolls, he is never funny and he never laughs; he only crows or jeers. And scarily, he doesn’t just talk in crude, witless insults - he actually thinks in them. His mind is a simple bot-like algorithm of petty prejudices and knee-jerk nastiness. There is never any under-layer of irony, complexity, nuance or depth. It’s all surface.

“Some Americans might see this as refreshingly upfront. Well, we don’t. We see it as having no inner world, no soul. And in Britain we traditionally side with David, not Goliath. All our heroes are plucky underdogs: Robin Hood, Dick Whittington, Oliver Twist.

“Trump is neither plucky, nor an underdog. He is the exact opposite of that. He’s not even a spoiled rich-boy, or a greedy fat-cat. He’s more a fat white slug. A Jabba the Hutt of privilege. And worse, he is that most unforgivable of all things to the British: a bully. That is, except when he is among bullies; then he suddenly transforms into a sniveling sidekick instead.

“There are unspoken rules to this stuff - the Queensberry rules of basic decency - and he breaks them all. He punches downwards - which a gentleman should, would, could never do - and every blow he aims is below the belt. He particularly likes to kick the vulnerable or voiceless - and he kicks them when they are down.

“So the fact that a significant minority - perhaps a third - of Americans look at what he does, listen to what he says, and then think 'Yeah, he seems like my kind of guy’ is a matter of some confusion and no little distress to British people, given that: 1) Americans are supposed to be nicer than us, and mostly are; 2) You don't need a particularly keen eye for detail to spot a few flaws in the man.

“This last point is what especially confuses and dismays British people, and many other people too; his faults seem pretty bloody hard to miss. After all, it’s impossible to read a single tweet, or hear him speak a sentence or two, without staring deep into the abyss. He turns being artless into an art form; he is a Picasso of pettiness; a Shakespeare of shit. His faults are fractal: even his flaws have flaws, and so on ad infinitum.

“God knows there have always been stupid people in the world, and plenty of nasty people too. But rarely has stupidity been so nasty, or nastiness so stupid. He makes Nixon look trustworthy and George W look smart. In fact, if Frankenstein decided to make a monster assembled entirely from human flaws - he would make a Trump. And a remorseful Doctor Frankenstein would clutch out big clumpfuls of hair and scream in anguish: ‘My God… what… have… I… created?’”

“A new culprit has emerged in the quest to understand how Alzheimer’s attacks the human brain”

“A team of scientists at the Fisher Center for Alzheimer’s Research laboratory at Rockefeller University managed to isolate a metabolite called C99 and found — quite unexpectedly — that it seems to cluster in regions of the brain that are most susceptible to Alzheimer’s.

“‘It was a total surprise because we saw the places where C99 accumulates in the brain of Alzheimer’s patients are exactly the places where neurons later are going to die,’ says Victor Bustos, senior research associate at the Fisher Center for Alzheimer’s Research. ‘C99 becomes a very good marker for neurodegeneration.

“In the world of dementia research, having a new ‘marker’ is important because these are the targets scientists go after when they test drugs in the hopes of finding a cure for Alzheimer’s. So far, that cure has been elusive, and this discovery suggest a possible reason why. Perhaps researchers have been aiming at the wrong target.

“The markers most associated with Alzheimer’s are the so-called ‘plaques’ and ‘tangles’ that accumulate in the brain of people with this disease. The plaques are clumps of beta-amyloid protein that coat neurons as the disease advances, and the tangles are tau proteins that go awry inside the neurons.

“Alzheimer’s research has focused heavily on medicines that seek to clear way amyloid plaque, but those efforts have led to a long string of disappointing results. Even when the drugs have reduced plaque, the memory of Alzheimer’s patients has not improved. Bustos says some regions of the brain are heavily affected by Alzheimer’s, while other regions aren’t. For someone suffering from the disease, beta-amyloid is present in high amounts in both regions, he says. ‘So that is kind of an argument to say beta-amyloid may not be well-enough related to Alzheimer’s disease to be the cause of Alzheimer’s,’ Bustos says.

“What he and his colleagues did was go in search of other potential culprits, using a technique that includes sophisticated super-resolution microscopy. ‘We decided to look at C99 because it is the precursor of beta-amyloid,’ Bustos says. ‘Before beta-amyloid becomes beta-amyloid, it is first called C99. You can call it an intermediate in the production of amyloid.’

“Bustos and his colleagues knew they had found something important when C99 showed up in high concentrations in areas of the brain most involved in memory, but not in other areas of the brain less susceptible to Alzheimer’s. ‘The hippocampus is one of the first areas to degenerate in Alzheimer’s disease, and we observed an early accumulation of C99 in the hippocampus,’ he says. ‘Later, after the hippocampus has degenerated, the frontal cortex starts to degenerate. We observed the same pattern. There was a secondary accumulation of C99 in the frontal cortex. Those are areas that are vulnerable to Alzheimer’s.’

“The significance of this result led the research team to post its findings online, rather than wait out the lengthy process of getting it published in a peer-review journal. ‘That way, people can know about these findings,’ Bustos says. ‘We have had an extraordinary response. In less than a week after it was public, I could see that already 3,600 people had looked at the paper, which is an extraordinary number.’

“Dr. Michelle Papka, founder and director of the Cognitive and Research Center of New Jersey, has read the paper and describes it as ‘a very interesting finding and a very worthwhile hypothesis to pursue.’ Papka was not involved in this study, but has been treating people with Alzheimer’s and engaging in dementia research for more than two decades. She describes the finding just published as a ‘pilot study, a preliminary first step.’

“If further research were to confirm that C99, not amyloid, is a primary driver of neurological damage in Alzheimer’s patients, that could open new avenues of research that might bring better results. ‘If it turns out this is correct, some of these anti-beta preventions may have been going after the wrong targets, and that may be why some have led to futile results,’ Papka says. ‘This type of research might help us determine more specifically what we need to target.’

“Based on his research, Bustos is not suggesting that amyloid is the wrong target. ‘I believe both C99 and amyloid contribute to the disease because amyloid is a toxic substance,’ he says. However, he says past efforts may have been flawed because many of the medicines used to attack beta-amyloid in clinical trials have done so in a way that actually raises the level of C99 in the brain.

“‘We believe C99 is the most toxic substance, so what we propose is that instead of reducing amyloid and increasing C99, we should aim at strategies that decrease both C99 and amyloid,’ he says. ‘What this study is telling the pharmaceutical companies is, please focus your resources on lowering C99; it’s a much better target than amyloid alone.’”

The Fisher Center lab at Rockefeller University is a leading scientific center focusing on Alzheimer’s disease. The research involving C99 was funded by the Fisher Center for Alzheimer’s Research Foundation, whose mission is to understand the causes of Alzheimer’s, improve the care of those living with it and find a cure. For more information, visit the foundation’s website at www.alzinfo.org

SCIENTISTS GET A ‘TOTAL SURPRISE’ AND A PROMISING NEW CLUE FOR HOW TO CURE ALZHEIMER’S 

Stress Linked to an Increased Risk of Dementia

“Men and women who had high blood levels of cortisol, the so-called stress hormone, performed worse on tests of memory than those with normal cortisol levels. They also had smaller brains volumes, which has been linked to an increased risk of dementia later in life.

“‘Cortisol affects many different functions, so it is important to fully investigate how high levels of the hormone may affect the brain,’ said study author Dr. Justin B. Echouffo-Tcheugui of Harvard Medical School. Cortisol, produced by the adrenal glands, helps the body respond to stress. It helps to control inflammation, blood sugar and blood pressure levels, among other body functions. Persistently high cortisol levels are a sign of chronic stress.

“For the study, researchers looked at 2,231 men and women, most in their 40s or 50s. All were part of a larger study and free of dementia. Study participants were given tests of memory and thinking skills at the start of the study, and again eight years later. Doctors also collected blood tests to measure cortisol levels, and most had MRI brain scans to assess brain size.

“Participants were divided into three groups: low, middle and high cortisol levels. Those with the highest cortisol levels, a sign of stress, had lower scores on tests of memory and thinking skills than those with normal levels of cortisol. They also had slightly smaller brain volumes. No links were found between low cortisol levels and memory or brain size.

“The researchers controlled for smoking, high blood pressure, blood vessel disease and other factors that can impact brain health. Still, the ties between cortisol levels and memory impairment and brain size persisted. The findings were published in Neurology.

“‘Our research detected memory loss and brain shrinkage in middle-aged people before symptoms started to show,’ said Dr. Echouffo-Tcheugui. As a result, ‘It’s important for people to find ways to reduce stress, such as getting enough sleep, engaging in moderate exercise, incorporating relaxation techniques into their daily lives, or asking their doctor about their cortisol levels and taking a cortisol-reducing medication if needed.’”

By ALZinfo.org, The Alzheimer’s Information Site. Reviewed by Marc Flajolet, Ph.D., Fisher Center for Alzheimer’s Research Foundation at The Rockefeller University.

Source: Justin B. Echouffo-Tcheugui, MD, PhD; Sarah C. Conner, MPH; Japyandra J. Himali, PhD; et al: “Circulating Cortisol and Cognitive and Structure Brain Measures: The Framingham Heart Study.” Neurology October 24, 2018

Stress May Affect Memory and Brain Size

A State of the Union Gesture, February 5, 2019

Gum Disease Could Be a Contributing Factor of Alzheimer’s Disease

“AFTER decades of disappointment, we may have a new lead on fighting Alzheimer’s disease. Compelling evidence that the condition is caused by a bacterium involved in gum disease could prove a game-changer in tackling one of medicine’s biggest mysteries, and lead to effective treatments or even a vaccine.

“As populations have aged, dementia has skyrocketed to become the fifth biggest cause of death worldwide. Alzheimer’s constitutes some 70 per cent of these cases (see “What is Alzheimer’s disease”), yet we don’t know what causes it. The condition, which results in progressive loss of memory and cognitive function, usually over a decade or so, is devastating both to those who have it and to their loved ones.

“The condition often involves the accumulation of two types of proteins – called amyloid and tau – in the brain. As these are among the earliest physical signs of the disease, the leading hypothesis since 1984 has been that the condition is caused by the defective control of these proteins, especially amyloid, which accumulates to form large, sticky plaques in the brain.

“The bulk of research into understanding and treating Alzheimer’s has centered on this ‘amyloid hypothesis.’ Huge sums of money have been invested in experiments involving mice genetically modified to produce amyloid, and in developing drugs that block or destroy amyloid proteins, or sometimes degraded tangles of tau.

“It has become clear that this approach isn’t working. In 2018 alone, the US National Institutes of Health spent $1.9 billion on Alzheimer’s research. But according to a recent study, the failure rate of drug development for Alzheimer’s has been 99 per cent.

“Some have begun to question the amyloid hypothesis. The lack of results has been compounded by the discovery that people – including some in their 90s with exceptional memories – can have brain plaques and tangles without having dementia. In a review of the research to date last year, Bryce Vissel at the University of Technology Sydney, Australia, concluded that there isn’t sufficient data to suggest that ‘amyloid has a central or unique role in Alzheimer’s.’

“In 2016, researchers discovered that amyloid seems to function as a sticky defense against bacteria. They found that the protein can act as an anti-microbial compound that kills bacteria, and when they injected bacteria into the brains of mice engineered to make Alzheimer’s proteins, plaques developed round bacterial cells overnight.

“At the time, the team said it still believed that amyloid itself went on to cause the brain damage of Alzheimer’s, not bacteria. But a spate of subsequent studies have looked at microbes. Bacteria have been found in the brains of people who had Alzheimer’s when they were alive. But it hasn’t been clear whether the bacteria caused the disease or were simply able to enter brains damaged by Alzheimer’s.

“Multiple teams have been researching Porphyromonas gingivalis, the main bacterium involved in gum disease, which is a known risk factor for Alzheimer’s. So far, teams have found that P. gingivalis invades and inflames brain regions affected by Alzheimer’s; that gum infections can worsen symptoms in mice genetically engineered to have Alzheimer’s; and that it can cause Alzheimer’s-like brain inflammation, neural damage and amyloid plaques in healthy mice.

“A whole new hypothesis: ‘When science converges from multiple independent laboratories like this, it is very compelling,’ says Casey Lynch of Cortexyme, a pharmaceutical firm in San Francisco. Now researchers from Cortexyme and several universities have reported finding the two toxic enzymes that P. gingivalis uses to feed on human tissue in 99 and 96 per cent of 54 human Alzheimer’s brain samples taken from the hippocampus – a brain area important for memory (Science Advances, doi.org/gftvdt). These protein-degrading enzymes are called gingipains, and they were found in higher levels in brain tissue that also had more tau fragments and thus more cognitive decline.

“The team also found genetic material from P. gingivalis in the cerebral cortex – a region involved in conceptual thinking – in all three Alzheimer’s brains they looked for it in. ‘This is the first report showing P. gingivalis DNA in human brains, and the associated gingipains co-localising with plaques,’ says Sim Singhrao at the University of Central Lancashire, UK, who wasn’t involved in the study. Her team has previously found that P. gingivalis actively invades the brains of mice with gum infections.

“When Lynch and her colleagues looked at brain samples from people without Alzheimer’s, they saw that some had P. gingivalis and protein accumulations, but at low levels. We already know that amyloid and tau can accumulate in the brain for 10 or 20 years before Alzheimer’s symptoms begin. This, says the team, shows that P. gingivalis doesn’t get into the brain as a result of Alzheimer’s – but could be the cause.

“When the team gave P. gingivalis gum disease to mice, it led to brain infection, amyloid production, tangles of tau protein and neural damage in the regions and nerves normally affected by Alzheimer’s. This suggests causation, says Lynch.

“She adds that P. gingivalis fulfils an updated set of criteria for attributing a disease to a particular pathogen. These conditions are named Koch’s postulates, after Robert Koch, a founder of the germ theory of disease.

‘The study does address most of Koch’s postulates,’ says Robert Genco of the University at Buffalo, New York. ‘Future studies need to be in humans to be convincing.’

“We don’t know how P. gingivalis gets into the brain, but there are plausible routes it could take. Your mouth normally hosts a diverse and relatively stable community of bacteria, but when dental plaque builds under the edge of your gums, it can form inflamed pockets in which P. gingivalis can thrive and release toxins.

“This inflammation can lead to chronic periodontitis and tooth loss, and some studies have shown that people with fewer teeth are more likely to have dementia. The inflammation and toxins caused by P. gingivalis damage the lining of your mouth, which may make it possible for oral bacteria to enter the bloodstream and then other organs. Even if you don’t have gum disease, transient damage to your mouth lining from eating or tooth-brushing can let mouth bacteria into your blood, says Lynch.

“As to how P. gingivalis might cause dementia after it arrives in the brain, there are two clear possibilities. It may trigger the release of amyloid, the brain’s method of trying to contain the infection, and this may then kill neurons.

“Hope for treatments: The speed at which damage accumulates is a key factor in the disease. Although many people harbour P. gingivalis in their mouths, only some develop Alzheimer’s. Because it can be decades before Alzheimer’s symptoms appear, whether a person develops the condition could come down to how much damage occurs before they die of other causes.

“The blood-brain barrier should protect your brain from microbes, but P. gingivalis can invade white blood cells and the cells lining blood vessels, so might cross it that way. It may also invade cranial nerves near the mouth, then spread from cell to cell towards the brain over a period of years.

“Or P. gingivalis may directly damage the brain. We already know that Alzheimer’s involves inflammation, an excessive immune response that ends up killing neurons instead of protecting them. P. gingivalis is known to cause inflammation in gum tissue, and it may do so in the brain as well. In response to the new findings, David Reynolds of the Alzheimer’s UK charity said he is dubious that P. gingivalis causes Alzheimer’s, because of the evidence showing that a person’s genes play a crucial role in the disease.

“‘Strong genetic evidence indicates that factors other than bacterial infections are central to the development of Alzheimer’s, so these new findings need to be taken in the context of this existing research,’ he said in a statement. But a bacterial hypothesis for Alzheimer’s doesn’t conflict with genetic evidence. The human body’s propensity for inflammation can vary according to genetic variations that affect our immune systems, and this may influence how much damage P. gingivalis induces in a brain.

“The biggest genetic risk factor for Alzheimer’s is a variant of the gene that makes the ApoE immune protein. Last year, a team in Sweden found that the gingipains released by P. gingivalis break up the ApoE protein into fragments, cleaving it at the site of a particular amino acid within the protein, and that these fragments may harm nerves. The ApoE4 variant of this protein contains more of this amino acid, suggesting that the reason people who make this variant are at a higher risk of developing Alzheimer’s may be because harmful levels of ApoE protein fragments build up more quickly in their brains than in those of other people.

“‘Alzheimer’s strikes people who accumulate gingipains and damage in the brain fast enough to develop symptoms during their lifetimes,’ says Lynch. She says her team’s findings are a ‘universal hypothesis of pathogenesis,’ fully explaining the causes of Alzheimer’s disease. But Vissel warns that Alzheimer’s is a complex disease. ‘The answer is unlikely to be one-cause-fits-all. We need to keep open eyes.’

“However, the new study is ‘very exciting,’ he says. ‘Alzheimer’s is so common in people at advanced age that I think it can only be either some intrinsic property of the brain, or an infection.’

“If this new hypothesis of Alzheimer’s is borne out, the good news is that it could lead to effective treatments for the condition. Although there is plenty you can do to reduce your risk of gum disease, Cortexyme is hoping it can stop or even reverse Alzheimer’s using molecules it has developed that block gingipains. The firm found that giving some of these to mice with P. gingivalis infections reduced brain infection, halted amyloid production, lowered brain inflammation and even rescued damaged neurons. ‘This provides hope of treating or preventing Alzheimer’s disease one day,’ says Singhrao.

“Cortexyme reported last year that the best of its gingipain blockers had passed initial safety tests in people, and entered the brain. It also seemed to improve symptoms in participants with Alzheimer’s. The firm will launch a larger trial later this year.

“The company also plans to test the drug against gum disease itself. Efforts to fight that have led a team in Melbourne to develop a vaccine for P. gingivalis that started tests in 2018. A vaccine for gum disease would be welcome – and if it also stops Alzheimer’s the impact could be enormous.

It is early days for this new hypothesis, and if the pursuit of amyloid-busting drugs over the past few decades has taught us anything, says Vissel, it is that a complex disease may not have a simple mechanism.

“Even if P. gingivalis is confirmed as a cause of Alzheimer’s, we don’t know yet whether it will turn out to be the only cause or one of several factors contributing to the disease. ‘This paper is very important,’ says George Perry at the University of Texas at San Antonio. ‘The view that pathogens might be one of several paths leading to Alzheimer’s disease fits my current thoughts of amyloid and tau being critical brain responses to injury, instead of the initiators.’

“That, he says, is why years of efforts to treat Alzheimer’s by removing those proteins have seen few results: they are symptoms of the disease, not its cause. ‘This is a further turning point in the understanding that infections and inflammation can be at the heart of Alzheimer’s disease.’”

We may finally know what causes Alzheimer’s – and how to stop it by Debora MacKenzie 

Pensionomics 2018: Measuring the Economic Impact of Defined Benefit Pensions by the National Institute on Retirement Security

Economic gains attributable to defined benefit (DB) pensions in the U.S. are substantial. Retiree spending of pension benefits in 2016 generated $1.2 trillion in total economic output, supporting some 7.5 million jobs across the U.S. Pension spending also added a total of $202.6 billion to government coffers, as taxes were paid at federal, state and local levels on retirees’ pension benefits and their spending in 2016.

Pensionomics 2018: Measuring the Economic Impact of Defined Benefit Pension Expenditures reports the national economic impacts of public and private pension plans, as well as the impact of state and local plans on a state-by-state basis.

This study finds that in 2016:

$578.0 billion in pension benefits were paid to 26.9 million retired Americans, including:

·         $294.7 billion paid to some 10.7 million retired employees of state and local government and their beneficiaries (typically surviving spouses);

·         $83.0 billion paid to some 2.7 million federal government beneficiaries; and

·         $200.3 billion paid to some 13.5 million private sector beneficiaries.

Expenditures made out of those payments collectively supported:

·         7.5 million American jobs that paid nearly $386.7 billion in labor income;

·         $1.2 trillion in total economic output nationwide;

·         $685.0 billion in value added (GDP); and

·         $202.6 billion in federal, state, and local tax revenue.

DB pension expenditures have large multiplier effects:

·         Each dollar paid out in pension benefits supported $2.13 in total economic output nationally.

·         Each taxpayer dollar contributed to state and local pensions supported $8.48 in total output nationally. This represents the leverage afforded by robust long-term investment returns and shared funding responsibility by employers and employees.

The largest employment impacts occurred in the real estate, food services, health care, and retail trade sectors.

The purpose of this study is to quantify the economic impact of pension payments in the U.S. and in each of the 50 states and the District of Columbia. Using the IMPLAN model, the analysis estimates the employment, output, value added, and tax impacts of pension benefit expenditures at the national and state levels. Because of methodological refinements explained in the Technical Appendix, the state level results are not directly comparable to those in previous versions of this study.

from Pensionomics 2018: Measuring the Economic Impact of Defined Benefit Pension Expenditures by Ilana Boivie

For the full report, Click Here.

Commentary:

What is the difference between a Defined-Benefit Pension Plan and a Defined-Contribution Savings Plan? (Posted on this blog Sept. 30, 2011; June 10, 2013; Jan. 4, 2015; March 17, 2017; March 7, 2018):  

A Defined-Benefit Pension Plan:

1)  You cannot outlive your benefit;
2) Your defined-benefit pension plan is more cost efficient than the defined-contribution savings plan;
3)  Your defined-benefit pension plan offers predictable, guaranteed monthly benefits for life;
4)  Funds are invested by professional asset managers in a diversified portfolio that follows long-term investment strategies;
5)  The large-pooled assets reduce asset management and miscellaneous fees;
6)  Your defined-benefit pension plan provides spousal (survivor) financial benefits;
7)  Your defined-benefit pension plan provides disability benefits;
8)  The state is responsible for funding, investment, inflationary and longevity risks;
9)  Because you are not affected by Market volatility, your defined-benefit pension plan is a more effective protection than the defined-contribution savings plan;
10) Because teachers understand the value of such a plan, they are willing to give up higher wages;
11) A defined-benefit plan encourages a long-term career and stable workforce;
12) Your defined-benefit pension plan provides you with self-sufficiency in retirement; it is associated with far fewer households that experience food privation, shelter adversity and health-care hardship;
13) Your defined-benefit pension plan is less expensive for taxpayers than Social Security – a reason why legislators, et al. had negotiated for Illinois teachers to not pay into Social Security;
14) The Teachers Retirement System of Illinois is the 37th largest in the U.S. with 406,855 members (TRS, 2017);
15) The average investment returns for TRS: 8.8% (for 1986-2016) (TRS, 2016) and 7.54% (for 1996-2016) (TRS, 2017);
16) Your defined-benefit pension plan has an economic impact of over $4 billion on Illinois; the effect on Gross Domestic Product is $2.38 billion; jobs that are created: 30,448 (TRS, 2013).

A Defined-Contribution Savings Plan:

1) A defined-contribution savings plan (401(k), 403(b), 457) was not initially created as a retirement vehicle but rather as a supplementary savings account;
2) A defined-contribution savings plan shifts all the responsibilities and all of the risk from the employer to you; thus, your benefit is not guaranteed for life;
3)  Your benefit ceases when your account is exhausted;
4) There are no survivor or disability benefits and guarantees;
5)  Your benefit is based upon individual investment earnings;
6)  You assume all funding, investment fees, and inflationary and longevity risks;
7)  A defined-contribution savings plan does not have the pooled investments, professional asset managers, and shared administrative costs that a defined-benefit pension plan provides;
8) Though you bear no portability risks, accounts are not always rolled over when you change jobs;
9) Changeover costs to this plan could be significant;
10) Your employer (state) will have to bear the administrative costs of both defined-benefit pension and defined-contribution savings plans when you switch over;
11) “Payments to amortize unfunded liabilities for the defined-benefit pension plan may be accelerated” (National Institute on Retirement Security (NIRS, 2011);
12) The Governmental Accounting Standards Board “requires [an] acceleration of unfunded liability payments when the defined-benefit pension plan is closed to be recognized on financial statements” (NIRS, 2011);
13) “No unfunded obligations [liabilities] for existing members are reduced when new members go into a defined-contribution savings plan” (NIRS, 2011);
14) “The loss of new members makes it difficult to finance the unfunded obligations of the defined-benefit pension plan” (NIRS, 2011);
15) The State of Illinois will not save money. Most of the State’s obligation to TRS is for contributions not paid during the past several decades; therefore, the deferred cost of underfunding cannot be eliminated by switching to a defined-contribution savings plan;
16) Shifting to a defined-contribution savings plan can raise annual costs by making it more difficult for Illinois to pay down existing liabilities. The plan will include fewer employees and fewer contributions going forward;
17) Even with a defined-contribution savings plan option, states and localities are still left to deal with past underfunding;
18) There is a several trillion dollar deficit between what 401(k) account holders should have and what they actually have;

19) “...The truth is this: the concept of a do-it-yourself retirement (401(k)s) [is] a fraud. It [is] a fraud because to expect people to save up enough money to see themselves through a 20- or 30-year retirement [is] a dubious proposition in the best of circumstances. It [is] a fraud because it allow[s] hustlers in the financial sector to prey on ordinary people with little knowledge of sophisticated financial instruments and schemes.

20) “And it [is] a fraud because the mainstream media, which increasingly relies on the advertising dollars of the personal finance industry, [sells] expensive lies to an unsuspecting public. When combined with stagnating salaries, rising expenses and a stock market that [does] not perform like Rumpelstiltskin and spin straw into gold, do-it-yourself retirement [is] all but guaranteed to lead future generations of Americans to a financially insecure old age. And so it [will].” To read the complete article, Click Here.

Sources: the National Institute on Retirement Security (NIRS), Center for Retirement Research at Boston College, National Conference on Public Employee Retirement Systems, Center on Budget and Policy Priorities, and the Teachers' Retirement System of Illinois (TRS) 

Retirees and Current Teachers: If You Are Not a Member of the Illinois Retired Teachers Association, You Should Be

“...[T]oday is the day that TRS deposits our next pension payment. More importantly, this February pension payment is the first one of 2019 to include our annual 3% raise, if you’re over the age of 60, of course.

“Speaking on behalf of the IRTA, I’d like to remind you that it was the leadership of this organization that saved your yearly 3% cola when the state legislature voted to restrict it several years ago. It was the IRTA lawsuit in the case, Heaton vs. Quinn that ultimately guaranteed our retirement benefits. 

“Without the efforts of the IRTA we would be poorer and our futures less assured. So, as a reminder, if you haven’t yet paid your 2019 IRTA annual dues, now is a great time to do so. With that in mind, remember that you can save $10.00 a year by switching over to dues deduct by going to the new and improved IRTA website.   

“And when you run into retired school colleagues [and current teachers], ask them to join the IRTA, if they haven’t done already. After all, we belong to the only state-wide organization solely dedicated to protecting the retirement benefits promised to us by the state…”

Thank you for your membership.

Mike Schmidt,

IRTA Membership Committee, Chair

Joining or Renewing IRTA Membership is Easy. Just click here on your phone, tablet or computer! 


P.S.

To all current teachers, 

We are smart enough to know that the attacks on our pensions will never end. The IRTA is also protecting your future retirement pension! Please join too. Thank you.

-Glen Brown