The ingredients can be combined in hundreds of ways, to make a delicious dinner. It takes just 15 minutes of prep, and ten minutes of cooking!
Start – pick one protein
Chicken breast or thigh meat, sliced
Vegan chik’n (such as Trader Joe’s or Gardein Chik’n)
Beef strips/tips, sliced
Vegan beef (such as Trader Joe’s or Gardein Beef-less tips)
Gardein Mandarin Orange Crispy Chik’n
Gardein Beefless tips
(If you use real meat, stir fry first for about 4 minutes, then add to the rest of the stir fry. If you use faux meat or tofu, then it all cooks at the same time.)
Pick a carbohydrate to lay your stir fry over
Spaghetti, or angel hair pasta
Mung bean vermicelli
Pick a few veggies
Have a different combination each time
Red bell peppers, green bell peppers, yellow or orange bell peppers
Yellow onions, vidalia onions
If you like, add nuts
Stir fry sauce
Red curry sauce and coconut milk
Sesame ginger sauce
Thai Peanut Satay (House of Tsang Bangkok Padang)
Panda Express Orange Sauce
Szechuan Spicy stir fry sauce (House of Tsang)
Island Mango sauce (World Harbors)
How can we protect Boston from rising sea levels? Various proposals
I. Metro Boston DikeLANDS – 14 mile dike around the harbor
A 14-mile dike could protect Greater Boston from sea level rise. The barrier would run from Cohasset to Swampscott
…The metropolitan Boston estuary is uniquely different from many others around the nation. It is protected on its flanks by the shoulder highlands of Swampscott and Cohasset. The Metro Boston DikeLANDS proposal takes advantage of the estuary’s unique geological characteristics.
We propose building a 14-mile dike barrier between the shoulder highlands of Cohasset and Swampscott. The dike would be located some eight miles out from Deer Island, complete with residential and commercial developments, windmills, solar collector farms, and recreational areas.
A simple dike barrier with a 200-foot-wide top and reaching 120 feet from seafloor to storm-surge top would require some 246 million cubic yards of material. Bi-directional locks could provide access for all crafts, protecting Boston’s commercial activity and its waterfront integrity.
The new dike system will prevent storm tides from inundating the entire metropolitan estuary while allowing rivers to discharge their water into a harbor reservoir capable of holding more than 10 billion gallons of river-fed water… By lowering the reservoir level to half the current tidal range, the cherished Boston Harbor Islands and their recreational potential would be protected.
At a cost of $100 per cubic yard, with two bi-directional shipping locks of $500 million each (plus soft and contingency costs), this macro-engineering and macro-economic project would probably cost between $30 billion and $50 billion. The 200-foot wide top of the 14-mile stretch would create 68 acres of new dike lands, which in turn would need to be supported by a complete infrastructure system of water, sewer, electricity, and transportation …
The project could help pay for itself if the newly-created, flat-top area of the dike, amounting to some 68 acres, was sold as waterfront property at between $3 and $7 million per acre. That would raise between $100 billion and $400 billion (after return on invested capital)
Source: 14-mile dike could protect Greater Boston from sea level rise, Commonwealth Magazine, Jan 2018, Peter Papesch, Franziska Amacher and A. Vernon Woodworth, members of the Boston Society of Architects
Plan details Metro-Boston-Dike-Barrier.pdf
II. Climate Ready Boston: Planning three possible harbor dikes
The team, led by Paul Kirshen, a professor of climate adaptation at UMass’ School for the Environment, is weighing three harbor barrier configurations. The barrier study was recommended in the city’s Climate Ready Boston report.
The smallest would connect Logan Airport in East Boston with Castle Island in South Boston, protecting the city’s inner harbor and downtown from tidal flooding.
The medium-sized solution is a barrier from Deer Island, in the harbor, to Quincy, which would wall off all of Boston’s neighborhoods.
The largest of the proposed harbor barriers would protect not just Boston, but also Weymouth, Hingham, Quincy and Hull.
III. Make parts of Boston a city of canals, to live with the flooding
From the Urban Land Institute of Boston/New England’s “The Urban Implications of Living with Water”
With the future unclear about exactly when the full impacts of sea level rise will occur, designing now for flexibility and the ability to adapt becomes critical. For example, with major street sections to be rebuilt, the typical 60 or 75 foot cross-section can be planned to be able to change when conditions warrant.
The goal is to provide for current urban linkages across the district without limiting the ability to accommodate future needs. Such needs could take the form of green infrastructure or surface channels to move water safely and quickly back to the ocean.
Build canals through Boston’s Back Bay
A street view of what this could look like
IV. Like we did in the past, literally raise the land level of parts of Boston
Can lessons from Boston’s landfill, 250 years ago, help Boston deal with sea level rise today?
Alex Wilson, in A Bold Idea for Addressing Sea Level Rise, writes
… I was struck by the realization that 250 years ago Boston was an island, connected by just a single land-bridge …there must have been a fairly massive effort to build the current land base of Boston. Might strategic land-building be an option for us as we are forced over the next century to address sea level rise as global warming melts the huge ice masses in Greenland and Antarctica?
…Rising seas are making life increasingly difficult in low-lying portions of dozens of U.S. cities today. The journal Nature Climate Change published a paper projecting the number of people in coastal regions of the U.S. who would be affected by sea level rise of 0.9 meters (3 feet) and 1.8 meters (5 feet). Unlike previous assessments of impact, this study considered not only current populations, but also projected population growth in these regions.
Populations in U.S. states that would be affected by 0.9 and 1.8 meter sea level rise.
Source: Nature Climate Change paper, “Millions Projected To Be At Risk From Sea-Level Rise in the Continental United States,” by Matthew Hauer, et. al., published online March 14, 2016.
By the year 2100, U.S. residents affected by 0.9 m and 1.8 m sea level rise would total 1.46 million and 3.85 million, respectively. Factoring in projected population growth in these regions, however, the number of people affected increases to 4.31 million and 13.1 million, respectively.
Can lessons from Boston’s landfill, 250 years ago, help with sea level rise today?
The comprehensive book, Gaining Ground: A History of Landmaking in Boston, by Nancy S. Seasholes, describes more than three centuries of effort to the Boston area to create new land and raise the elevation of existing land.
Beginning fairly early in Boston’s history—certainly by the 1700s—there was a massive effort to fill in the tidal flats around Boston. These efforts ultimately created some 5,250 acres of new land in Boston, East Boston, and Charlestown. In other areas, the land was significantly raised with fill. The original peninsula of Boston, known as Shawmut by the Native Americans, was just 487 acres. Today, merged with surrounding land, it is many times that size.
…Boston’s well-known Back Bay region was originally the back bay of the Charles River—an extensive estuary on the western side of the Shawmut Peninsula. The Fenway and Fenway Park (the Boston Red Sox’s home stadium) get their names from the fens or bogs in the area. It was only after extensive filling that building here was possible.
Logan Airport was open water in the 1930s. Today it is part of the extensive new land in East Boston.
I haven’t seen estimates of the amount of fill been used in Greater Boston over the last three centuries. If one assumes an average fill of six feet over the 5,250 acres of made land, that would total roughly 1.4 billion cubic feet or 50 million cubic yards.
I was particularly intrigued to learn in Gaining Ground that not only was new land made on the tidal flats of Boston, but in some places the elevation of existing land was raised. In the Church Street and Suffolk Street Districts (new Bay Village and Castle Square), sewage back-up was a problem in the mid-1800s, because there wasn’t enough pitch to the sewers (which no doubt dumped into the Bay).
The solution was to elevate the land and the buildings that were located there. In the 1860s, the City decided to raise the grade of the entire District. They would fill basements and abandon them, elevate buildings on cribbing and build new foundations beneath them.
On Church Street, starting in July 1868, the City hired contractors to bring in more than 150,000 cubic yards of fill and elevate 296 brick buildings by as much as 14 feet and 56 wooden buildings by as much as 17 feet. Remarkably (by today’s standards), this work was virtually completed by October 1869—ahead of schedule and under budget.
A similar project was carried out in the Suffolk Street District starting in July 1870 and being completed by the end of 1872. Nearly 250,000 yards of fill were brought in, and 600 buildings were elevated—also under budget.
Boston isn’t alone in having seen extensive landmaking over the centuries. In Manhattan, several thousand acres of land were created using fill, and more than 3,000 acres were created in Chicago. But nowhere in the U.S. has the landmaking been as extensive as in Boston.
What this suggests about our long-term response to rising sea levels is that we shouldn’t rule out the idea of raising the grade in our most important cities. I was astounded to learn just how significant the earthmoving was centuries ago; with today’s equipment and engineering prowess, one can imagine raising a low-lying city by tens of feet.
Of course, there would be huge challenges and tremendous costs with such an initiative, not to mention environmental risks. Our buildings are bigger than those in Boston were in the 1860s; they are closer together and more complex. Our infrastructure—streets and highways, bridges, sewers, power grids, pipelines—are tremendously complex. And, we’re much more conscious of ecological damage today than we were 150 years ago.
But consider the alternative. Are we ready to abandon cities like Boston, New York, Philadelphia, and Charlestown? It could well be easier to raise a city than to move it. And we will have to figure this out before the end of this century. I don’t know if raising the elevation of our low-lying cities will make sense, but I think we should begin that discussion.
We can start by looking at past experience, and Gaining Ground provides a good starting point in doing so. In some cases, it may be possible to fill in basements, compacting the fill to equalize the pressure on the outside of those walls, and turn first floors into basements—essentially eliminating an occupied floor of a building.
In other cases, entire buildings may have to be elevated and new foundations built on compacted fill 15 or 20 feet higher. Streets would have to be covered and rebuilt on fill. Very challenging will be the need for such modifications to be coordinated on a neighborhood-by-neighborhood basis. You can’t raise one building 20 feet and not do anything with the building next door.
This would be an extraordinarily complex process in terms of phasing, implementation, and environmental protection. But it’s time to take sea level rise seriously and begin looking at our options. Raising land mass may be one such option.
Source: Alex Wilson, Resilientdesign.org, A bold idea for addressing sea level rise, Mar 28, 2016
Explore the spatial data used in Climate Ready Boston – This app allows you to learn more about the data layers used in the Climate Ready Boston recommendations for protecting our City from a changing climate, and helps you better understand how projections are influencing resiliency solutions. Read the introduction to this interactive tool.
Sasaki : Sea Change Boston. Designing in the Face of Climate Change– Sasaki is a global design firm specializing in architecture, planning, urban design, landscape architecture.
HS-ESS2-6. Use a model to describe cycling of carbon through the ocean, atmosphere, soil, and biosphere and how increases in carbon dioxide concentrations due to human activity have resulted in atmospheric and climate changes.
HS-ESS3-1. Construct an explanation based on evidence for how the availability of key natural resources and changes due to variations in climate have influenced human activity.
HS-LS2-7. Analyze direct and indirect effects of human activities on biodiversity and ecosystem health, specifically habitat fragmentation, introduction of non-native or invasive species, overharvesting, pollution, and climate change. Evaluate and refine a solution for reducing the impacts of human activities on biodiversity and ecosystem health.*
High School Technology/Engineering
HS-ETS1-1. Analyze a major global challenge to specify a design problem that can be improved. Determine necessary qualitative and quantitative criteria and constraints for
solutions, including any requirements set by society.*
HS-ETS1-2. Break a complex real-world problem into smaller, more manageable problems that each can be solved using scientific and engineering principles.*
HS-ETS1-3. Evaluate a solution to a complex real-world problem based on prioritized criteria and trade-offs that account for a range of constraints, including cost, safety, reliability, aesthetics, and maintenance, as well as social, cultural, and environmental impacts.*
This intro is lightly adapted from thelogicofscience.com
Many people mistakenly believe that there are two fundamentally different types of evolution: microevolution and macroevolution. They argue that microevolution does actually occur, but only produces small changes within a species or “kind” of animal. For example, they’re okay with the concept that all finches evolved from a common ancestor, all crows evolved from a common ancestor, all ducks evolved from a common ancestor, etc.
However, they draw the line roughly at the taxonomic level of family (e.g., ducks are in the Anatidae family), and they argue that evolution beyond that level (what they call macroevolution) is impossible and has never and can never happen. Thus, they dismiss the notion that finches, crows, and ducks all share a common ancestor.
However, this distinction is completely arbitrary and meaningless: the exact same evolutionary mechanisms that caused the evolution of finch species could (and indeed did) cause the evolution of all birds. In other words, macroevolution is simply the accumulation of microevolutionary steps, and one inherently leads to the other.
Here is a visual explanation. The image below shows a hypothetical pathway through which turtles could have evolved from their lizard-like ancestors.
Several of these images are renderings of actual fossils: B6 = Milleretta, A15 = Eunotosaurus, C22 = Odontochelys, B30 = Proganochelys, D37 = Chelydra [modern turtles]; these are just screen shots from Dr. Tyler Lyson’s excellent video.
This full progression is, of course, what creationists would consider to be macroevolution, and creationists are adamant that today’s turtle families were uniquely created and did not evolve from a lizard-like ancestor. However, because they accept microevolution, most creationists would have no problem with any particular pair of images, and they would accept that A1 could evolve into B1, B1 could evolve into C1, etc.
In other words, each pair of images shows “microevolution” (which creationists almost universally accept), but when we string all of those steps together, we get “macroevolution” (which they say is impossible).
You can probably see where I am going with this, but just to be sure, I will state it explicitly. If you are going to say that macroevolution is impossible and turtles could not have evolved from lizard-like ancestors, then which step do you think is impossible?
Please show me which step could not have occurred, and justify that claim. Additionally, please explain the obvious transitional fossils. Remember, B6, A15, C22, B30, and D37 are actual fossils, and they perfectly match the expectations for what a transitional fossil should look like (details here). So, if turtles and their lizard like ancestors were uniquely created kinds, then at what point in this progression do lizard-like reptiles end and turtles begin?
Image from “Evolutionary Origin of the Turtle Shell” by Tyler Lyson
And here is the amazing video
Continued from “The Logic of Science”
Some people will likely be inclined to ignore my questions and harp instead on the fact that this pathway is hypothetical, but that argument completely misses the point in several ways. First, this pathway is only partially hypothetical because B6, A15, C22, B30, and D37 are actual fossils that we have found.
Additionally, of course the pathway is partially hypothetical. We will never find every single one of these steps, and we don’t need to: Evolution is very much like the visible light spectrum. Each color gradually fades into the next color without a clear breaking point. In other words, there is a point along the spectrum that is clearly red, and there is a point that is clearly blue, and there is a point that is clearly violet, but there is a spectrum of change in between those points – and it is not possible to pick an exact point where the blue ends and violet begins, just as you cannot pinpoint the exact step at which the reptile becomes a turtle as we know it.
Evolutionary Origin of the Turtle Shell
Tyler R. Lyson, Gabe S. Bever, Torsten M. Scheyer, Allison Y. Hsiang, Jacques A. Gauthier
Current Biology, Published Online: May 30, 2013
Articles by cognitive scientists Daniel Willingham
Why transfer is hard
Why students remember or forget
Why students think they understand when they don’t
Why practice is important
Why people love and remember stories
Why knowledge is important
How to teach critical thinking
Why reading comprehension strategies are less useful than most people think
What will improve a student’s memory?
What goes into mathematical thinking?
Motivation–role of praise
Motivation–role of rewards
Has technology changed how students think?
Can teachers increase students self-control?
Why does family wealth affect student outcomes?
The role of sleep in schooling and learning
Excerpt of Raising Kids Who Read
Can Reading Comprehension Be Taught?
How Do Manipulatives Help Students Learn?
Evaluation of Theories
Visual, auditory, kinesthetic learners
Using neuroscientific data in education theories
Developmentally appropriate practice
Mel Levine’s A Mind at a Time
How should we think about student differences?
21st century skills
Healthy plant-based diets – “A diet based on fruits, vegetables, tubers, whole grains, and legumes; and it excludes or minimizes meat (including chicken and fish), dairy products, and eggs, as well as highly refined foods like bleached flour, refined sugar, and oil.”
Changes to the American diet over the last century and health effects thereof
Old American diet
* Near the start of the 20th century, Americans each ate about 120 lbs if meat per year. By 2007, we ate about 222 lbs.
* About 1913, Americans ate about 40 lbs of processed sugar per person. By 1999, it had increased to 147 lbs per person.
* About 1909, Americans ate about 294 lbs of dairy products per person. By 2006, that number was over double…605 lbs of dairy per person!!
* This information came from the companion book to Forks Over Knives.
Write about health effects due to these changes
The China Study
The China Study is a book by T. Colin Campbell (2005.) The China Study examines the relationship between the consumption of animal products (including dairy) and chronic illnesses such as coronary heart disease, diabetes, breast cancer, prostate cancer, and bowel cancer. The authors conclude that people who eat a predominantly whole-food, plant-based diet—avoiding animal products as a main source of nutrition, including beef, pork, poultry, fish, eggs, cheese, and milk, and reducing their intake of processed foods and refined carbohydrates—will escape, reduce, or reverse the development of numerous diseases. … The book is loosely based on the China–Cornell–Oxford Project, a 20-year study—described by The New York Times as “the Grand Prix of epidemiology”—conducted by the Chinese Academy of Preventive Medicine, Cornell University, and the University of Oxford. (Wikipedia)
Dean Ornish Diet – tba
Ornish is known for his lifestyle-driven approach to the control of coronary artery disease (CAD) and other chronic diseases. He promotes lifestyle changes including a whole foods, plant-based diet, smoking cessation, moderate exercise, stress management techniques including yoga and meditation, and psychosocial support. Ornish does not follow a strict vegetarian diet and recommends fish oil supplements; the program additionally allows for the occasional consumption of other animal products. (Wikipedia)
The Engine 2 Diet/Rip Esselstyn
– Details tba
Jeff Novick diet
The Five Pillars of Healthy Eating: “A Common Sense Approach To Nutrition”
1) Plant-Centered – Center your plate and your diet around minimally processed plant foods (fruits, vegetables, starchy vegetables, roots/tubers, intact whole grains, and legumes (beans, peas & lentils).
2) Minimally Processed – Enjoy foods as close to “as grown in nature” with minimal processing that does not detract from the nutritional value &/or add in any harmful components.
3) Calorie Dilute – Follow the principles of calorie density choosing foods that are calorie adequate, satiating and nutrient sufficient.
4) Low S-O-S – Avoid/minimize the use of added Salts/sodium, Oils/Fats and Sugars/sweeteners
5) Variety – Consume a variety of foods in each of the recommended food groups.
This excerpt from an interview summarizes Jeff Novick’s view:
Consume a variety of foods in each of the recommended food groups. Now, if there were ten of us in the room, we could each implement these pillars slightly differently and still each have a healthy diet and great health results. That’s because when we look at the research evidence, there’s no one specific diet that is “best.” Instead, there are common denominators across healthy diets that combine to make up a healthy dietary pattern, and these are reflected in my five guidelines/principles of healthy eating.
What foods do you recommend that people incorporate into their diets? The healthiest foods are minimally processed fruits, vegetables, starchy vegetables, roots/tubers, intact whole grains, and legumes. These should make up most—if not all—of our daily calories. I recommend that people start right where they are and just keep adding in more of these foods each day.
It seems today that the topic of nutrition and health has become a war with sides drawn and no discussion. I am disappointed in the conversation I see happening on social media because a lot of it is very judgmental, confrontational, and elitist. The message out there seems to be that if the food you eat is not fresh, organic, local, shade-grown, GMO-free, and picked yourself or picked up at a local farmer’s market or purchased from some elite health food store, then all blended together in some expensive hi-tech blender, you are not doing well enough. And, if you buy any frozen or canned foods, you might as well be eating bacon and cheeseburgers.
We need to have compassion, not only for the animals and the environment, but also for our fellow humans, particularly in the way we treat each other, especially those who may not follow the exact same dietary pattern we do.
source: An interview with healthy eating expert Jeff Novick, posted on Jewishfoodherocom, Dec. 2015
Virginia Messina’s Vegan for Life
“Given what we know about the benefits of plant foods that are rich in healthful fats, it’s reasonable to expect that higher-fat, plant-based diets would be just as beneficial and perhaps have even more benefits,” says Virginia Messina, MPH, RD, vegan expert and coauthor of Vegan for Life. A Czech Republic study found benefits for people with diabetes who followed a high-fat (38%) almost-vegan diet.6 Messina also highlights that Esselstyn’s study didn’t include a control group or look at effects of weight loss and other potentially confounding variables, making it difficult to draw conclusions about the true effects of fat restriction. “We just don’t have the data to suggest that restricting dietary fat intake is necessary for good health and for treating disease. It’s much more likely that building a diet around healthful plant foods and choosing healthful fats is important,” Messina adds.
Dietary Approaches to Stop Hypertension (DASH) diet
The popular Dietary Approaches to Stop Hypertension (DASH) diet was created to lower blood pressure, but new research says it can also reduce the risk of depression later in life. A study, to be presented at the American Academy of Neurology’s 70th Annual Meeting in April, shows that the popular diet — rich in vegetables, fruit, whole grains, fat-free or low-fat dairy products and very few foods that are high in saturated fats and sugar — does more than what has been shown in multiple studies: Lowering blood pressure, bad cholesterol (LDL) and body weight….
The odds of becoming depressed over time was 11 percent lower among the adults who followed the DASH diet more closely. The group that followed a Western diet — high in saturated fats and red meats, low in fruits and vegetables — were more likely to develop depression.
The Mediterranean diet recommends emulating how people in the Mediterranean region have traditionally eaten, with a focus on foods like olive oil, fish and vegetables. U.S. News and World Report called the diet a “well-balanced eating plan” when placing it at the top of its best diets for 2018 list in January.
The DASH diet has been ranked as the No. 1 overall diet by U.S. News and World Report for eight consecutive rankings. Originally started by the National Heart, Lung, and Blood Institute (NHLBI) as a diet to help reduce blood pressure, the DASH diet is made up of low-sodium and healthful foods. The NHLBI publishes free guides on the plan so you can see if it is right for you.
“The thing about the DASH diet is you’re eating specifically the foods you’ve always been told to eat, pretty much fruit, vegetables, whole grain, lean protein and low-fat dairy,” Angela Haupt, assistant managing editor of health at U.S. News and World Report, told ABC News in January. “And it eliminates foods high in fat and sugar-sweetened drinks and sweets.”
Dr. Jay Sheree Allen, ABC News
Do vegetarians need to engage in protein combining?
Protein combining is a dietary theory for protein nutrition that purports to optimize the biological value of protein intake. According to the theory, vegetarian and vegan diets provide insufficient content of essential amino acids, making protein combining necessary. The theory has been roundly discredited by major health organizations. Studies on essential amino acid contents in plant proteins has shown that vegetarian and vegans in fact do not need to complement plant proteins in each meal to reach the desired level of essential amino acids as long as their diets are varied. The terms complete and incomplete are misleading in relation to plant protein. Protein from a variety of plant foods, eaten during the course of a day, supplies enough of all essential amino acids when caloric requirements are met.
Our related articles
External related articles
Students will gain the knowledge and skills to select a diet that supports health and reduces the risk of illness and future chronic diseases. PreK–12 Standard 4
Through the study of Improving Nutrition students will
3.1 Identify the key nutrients in food that support healthy body systems (skeletal, circulatory) and recognize that the amount of food needed changes as the body grows
3.2 Use the USDA Food Guide Pyramid and its three major concepts of balance, variety, and moderation to plan healthy meals and snacks
3.3 Recognize hunger and satiety cues and how to make food decisions based upon these cues.
3.8 List the functions of key nutrients and describe how the United States Dietary Guidelines relate to health and the prevention of chronic disease throughout the life span.
3.9 Describe a healthy diet and adequate physical activity during the adolescent growth spurt.
3.20 Identify and analyze dietary plans, costs, and long-term outcomes of weight management programs.
3.21 Identify how social and cultural messages about food and eating influence nutrition choices.
Increased knowledge about nutrition has led to the development of diets containing the variety of foods that can help people live longer and healthier lives. 8F/M7** (SFAA)
HS-LS1-2. Develop and use a model to illustrate the key functions of animal body systems, including (a) food digestion, nutrient uptake, and transport through the body; (b) exchange of oxygen and carbon dioxide; (c) removal of wastes; and (d) regulation of
Idea: The “Autism-Asperger’s Spectrum” is just a convenient way to talk about many different conditions. Scientists studying autism say that this spectrum actually is a combination of many different conditions; each condition now appears t0 have a different genetic origin. See Is a ‘Spectrum’ the Best Way to Talk About Autism?
Idea: Autism usually isn’t caused by one mutation by itself. Many mutations increase the chances of some condition developing, but the condition is often due to the gene plus some other triggering factor, perhaps:
a) exposure to a pathogen or hormone during gestation
b) There are molecular switches on top of the genes, epigenes. Sometimes genes only have a significant effect if the epigenetic switches are engaged in one way; but otherwise that gene variation might have little noticeable effect.
Autism genetics, explained
by Nicholette Zeliadt, June 27, 2017
Spectrum. [Spectrum began in 2008 as the News & Opinion section of SFARI.org. Simons Foundation Autism Research Initiative (SFARI). In the summer of 2015, we spun off to create an independent online identity.
How do researchers know genes contribute to autism? Since the first autism twin study in 1977, several teams have compared autism rates in twins and shown that autism is highly heritable. When one identical twin has autism, there is about an 80 percent chance that the other twin has it too. The corresponding rate for fraternal twins is around 40 percent.
However, genetics clearly does not account for all autism risk. Environmental factors also contribute to the condition — although researchers disagree on the relative contributions of genes and environment. Some environmental risk factors for autism, such as exposure to a maternal immune response in the womb or complications during birth, may work with genetic factors to produce autism or intensify its features.
Is there such a thing as a [single] autism gene? Not really. There are several conditions associated with autism that stem from mutations in a single gene, including fragile X and Rett syndromes. But less than 1 percent of non-syndromic cases of autism stem from mutations in any single gene. So far, at least, there is no such thing as an ‘autism gene’ — meaning that no gene is consistently mutated in every person with autism. There also does not seem to be any gene that causes autism every time it is mutated.
Still, the list of genes implicated in autism is growing. Researchers have tallied 65 genes they consider strongly linked to autism, and more than 200 others that have weaker ties. Many of these genes are important for communication between neurons or control the expression of other genes.
How do these genes contribute to autism?
Changes, or mutations, in the DNA of these genes can lead to autism. Some mutations affect a single DNA base pair, or ‘letter.’ In fact, everyone has thousands of these genetic variants. A variant that is found in 1 percent or more of the population is considered ‘common’ and is called a single nucleotide polymorphism, or SNP.
Common variants typically have subtle effects and may work together to contribute to autism. ‘Rare’ variants, which are found in less than 1 percent of people, tend to have stronger effects. Many of the mutations linked to autism so far have been rare. It is significantly more difficult to find common variants for autism risk, although some studies are underway.
Other changes, known as copy number variations (CNVs), show up as deletions or duplications of long stretches of DNA and often include many genes.
But mutations that contribute to autism are probably not all in genes, which make up less than 2 percent of the genome. Researchers are trying to wade into the remaining 98 percent of the genome to look for irregularities associated with autism. So far, these regions are poorly understood.
Are all mutations equally harmful?
No. At the molecular level, the effects of mutations may differ, even among SNPs. Mutations can be either harmful or benign, depending on how much they alter the corresponding protein’s function. A missense mutation, for example, swaps one amino acid in the protein for another. If the substitution doesn’t significantly change the protein, it is likely to be benign. A nonsense mutation, on the other hand, inserts a ‘stop’ sign within a gene, causing protein production to halt prematurely. The resulting protein is too short and functions poorly, if at all.
How do people acquire mutations?
Most mutations are inherited from parents, and they can be common or rare. Mutations can also arise spontaneously in an egg or sperm, and so are found only in the child and not in her parents. Researchers can find these rare ‘de novo’ mutations by comparing the DNA sequences of people who have autism with those of their unaffected family members. Spontaneous mutations that arise after conception are usually ‘mosaic,’ meaning they affect only some of the cells in the body.
Can genetics explain why boys are more likely than girls to have autism?
Perhaps. Girls with autism seem to have more mutations than do boys with the condition. And boys with autism sometimes inherit their mutations from unaffected mothers. Together, these results suggest that girls may be somehow resistant to mutations that contribute to autism and need a bigger genetic hit to have the condition.
Is there a way to test for mutations before a child is born?
Clinicians routinely screen the chromosomes of a developing baby to identify large chromosomal abnormalities, including CNVs. There are prenatal genetic tests for some syndromes associated with autism, such as fragile X syndrome. But even if a developing baby has these rare mutations, there is no way to know for sure whether he will later be diagnosed with autism.
Article source https://spectrumnews.org/news/autism-genetics-explained/
Most Autism Cases Can Be Explained by Faulty Genes, New Research Confirms: We understand it better than ever. By Mike Mcrae, Sept 27, 2017.
A fresh look at data from earlier research has reaffirmed what many researchers had thought – autism is primarily in the genes.
Other studies have shown autism spectrum disorder (ASD) tends to cluster in families and is associated with particular genes, but nailing down the risks with precision is a complex task. This new research has put a figure on the chances, claiming 83 percent of autism cases are inherited.
The study led by researchers from the Ichan School of Medicine in New York reanalysed a Swedish longitudinal study that involved over 2.6 million pairs of siblings, 37,570 pairs of twins, and just under a million half-sibling pairs.
Of these, 14,516 children had an ASD diagnosis.
Autism and its associated spectrum of conditions is a rather complex disorder, distinguished by difficulties in communicating and engaging in social interactions.
The signs usually aren’t all that clear until a child might be expected to develop advanced communication skills, around age 2 to 3, making it hard to untangle genetic and environmental causes.
In fact, as recently as just half a century ago, physicians thought it could be the result of a lack of maternal love and affection.
Studies that have focussed on finding links between family relationships have come up with a variety of figures on the genetics of ASD.
Twin studies have suggested as many as 9 out of 10 children with autism inherited the condition through their combination of genes, though other studies have also put a more conservative estimate down towards 60 percent.
One study published in 2011 conducted by researchers from Stanford University in California put the chances of genetic heritability at around 38 percent for ASD.
An analysis conducted in 2014 also calculated a lower number, nearer to just 50 percent.
Which of these numbers are more accurate?
The researchers were skeptical of how the 50 percent figure was determined, suspecting that by taking into account the precise timing of the autism diagnosis, the estimate was being distorted.
So the researchers took the same massive data-set on Swedish children and used another method that had previously proven itself in the field, identifying a model that fitted best.
Their conclusion of 83 percent is closer to the 90 percent determined by earlier twin studies than the 38 percent of the California research, and was estimated with higher precision.
“Like earlier twin studies, shared environmental factors contributed minimally to the risk of ASD,” write the researchers.
While we can be confident that genes play a key role in the development of the traits associated with ASD, we can also be sure that this won’t be the final word on the matter.
For one thing, just one in 68 children is diagnosed with the disorder. While not extraordinarily rare, it’s uncommon enough to make it hard to find a large enough sample size for precise predictions.
The condition isn’t cut and dried, either, with the spectrum covering a range of behaviours and functions. It affects just 1 in 189 girls, while 1 in 42 boys are diagnosed.
Progress is being made in determining which genes are responsible for the neurological variations that give rise to autism-like functions, but it’s slow going.
New research suggests a small fraction of the genes responsible might not be present in parents at all.
A recent study published in the American Journal of Human Genetics reported on the systematic analysis of genetic mutations among 2,300 families who had a single child affected by autism.
They found genetic changes that occur after conception – called postzygotic mosaic mutations – could be responsible for autism in around 2 percent of the individuals in their sample.
“This initial finding told us that, generally, these mosaic mutations are much more common than previously believed. We thought this might be the tip of a genetic iceberg waiting to be explored,” says researcher Brian O’Roak from Oregon Health & Science University.
We’re still a long way off mapping and understanding the role genes play in how our brains interact socially. And for all of this research, the environment can’t be ruled out completely. The more we discover, however, the clearer it is that ASD isn’t a condition we can easily prevent by simply making the right choices as a parent.
This research was published in JAMA. Source: https://www.sciencealert.com/researchers-find-most-autism-cases-can-be-explained-by-faulty-genes
Primary source: Research Letter. September 26, 2017
The Heritability of Autism Spectrum Disorder
Sven Sandin, PhD1; Paul Lichtenstein, PhD2; Ralf Kuja-Halkola, PhD2; et al Christina Hultman, PhD2; Henrik Larsson, PhD3; Abraham Reichenberg, PhD1
JAMA. 2017;318(12):1182-1184. doi:10.1001/jama.2017.12141
Half of all autism cases trace to rare gene-disabling mutations
Researchers identify short list of high-impact genetic causes of autism; see potential to guide personalized treatments
New research suggests that, in at least half of cases, autism traces to one of roughly 200 gene-disabling mutations found in the child but neither parent.
Many of these “high-impact” mutations, the investigators found, completely disable genes crucial to early brain development. In addition, they appear to be more common among people who are severely disabled by autism versus those only mildly affected.
The study, by scientists at Cold Spring Harbor Laboratory, New York, appears this week in the Proceedings of the National Academy of Sciences. (Download the full paper here.)
The DNA analysis of 1,866 families affected by autism looked at the growing list of more than 500 gene changes known to increase autism risk. It identified 239 genes with the greatest likelihood of causing autism if any one of them was disabled by a mutation.
The study’s findings also run counter to the commonly held idea that autism almost always results from a complex interplay of common and subtle gene changes and environmental influences – none of which would cause autism by itself.
This shortened “priority list” may prove particularly helpful to doctors and geneticists using genetic screens to guide diagnosis and personalized treatment, comments Mathew Pletcher, head of Autism Speaks’ genomic discovery program. Dr. Pletcher was not involved in the research.
“These findings argue strongly that genetics can provide meaningful answers for a significant portion of individuals with autism,” Dr. Pletcher explains. “From this extends the idea we can provide better care and support by deepening our understanding of the health risks that arise from each person’s specific genetic disruption.”
Most of the high-impact mutations identified in the new study occurred in the child but neither parent. Such newly arising, or de novo, mutations first occur in the mother’s egg, the father’s sperm or early in embryo development.
Some of the first research out of the Autism Speaks MSSNG project implicated de novo mutations in the higher rates of autism seen among children of older parents. With age, a woman’s eggs and a man’s sperm-producing cells tend to accumulate these mutations. And one potential source of these accumulating mutations, Dr. Pletcher notes, is lifetime exposure to environmental “insults” such as radiation and toxic chemicals (naturally occurring or otherwise).
Scientific paper: Low load for disruptive mutations in autism genes and
their biased transmission. Authors: Ivan Iossifova, Dan Levya… and Michael Wiglera.
PNAS 2015 October, 112 (41) E5600-E5607.
Fathers bequeath more mutations as they age
Genome study may explain links between paternal age and conditions such as autism.
Ewen Callaway, 22 August 2012
In the 1930s, the pioneering geneticist J. B. S. Haldane noticed a peculiar inheritance pattern in families with long histories of haemophilia. The faulty mutation responsible for the blood-clotting disorder tended to arise on the X chromosomes that fathers passed to their daughters, rather than on those that mothers passed down. Haldane subsequently proposed1 that children inherit more mutations from their fathers than their mothers, although he acknowledged that “it is difficult to see how this could be proved or disproved for many years to come”.
That year has finally arrived: whole-genome sequencing of dozens of Icelandic families has at last provided the evidence that eluded Haldane. Moreover, a study published in Nature finds that the age at which a father sires children determines how many mutations those offspring inherit2. By starting families in their thirties, forties and beyond, men could be increasing the chances that their children will develop autism, schizophrenia and other diseases often linked to new mutations. “The older we are as fathers, the more likely we will pass on our mutations,” says lead author Kári Stefánsson, chief executive of deCODE Genetics in Reykjavik. “The more mutations we pass on, the more likely that one of them is going to be deleterious.”
Haldane, working years before the structure of DNA was determined, was also correct about why fathers pass on more mutations. Sperm is continually being generated by dividing precursor cells, which acquire new mutations with each division. By contrast, women are born with their lifelong complement of egg cells.
Stefánsson, whose company maintains genetic information on most Icelanders, compared the whole-genome sequences of 78 trios of a mother, father and child. The team searched for mutations in the child that were not present in either parent and that must therefore have arisen spontaneously in the egg, sperm or embryo. The paper reports the largest such study of nuclear families so far.
Fathers passed on nearly four times as many new mutations as mothers: on average, 55 versus 14. The father’s age also accounted for nearly all of the variation in the number of new mutations in a child’s genome, with the number of new mutations being passed on rising exponentially with paternal age. A 36-year-old will pass on twice as many mutations to his child as a man of 20, and a 70-year-old eight times as many, Stefánsson’s team estimates.
The researchers estimate that an Icelandic child born in 2011 will harbour 70 new mutations, compared with 60 for a child born in 1980; the average age of fatherhood rose from 28 to 33 over that time.
Most such mutations are harmless, but Stefánsson’s team identified some that studies have linked to conditions such as autism and schizophrenia. The study does not prove that older fathers are more likely than younger ones to pass on disease-associated or other deleterious genes, but that is the strong implication, Stefánsson and other geneticists say.
Previous studies have shown that a child’s risk of being diagnosed with autism increases with the father’s age. And a trio of papers3–5 published this year identified dozens of new mutations implicated in autism and found that the mutations were four times more likely to originate on the father’s side than the mother’s.
The results might help to explain the apparent rise in autism spectrum disorder: this year, the US Centers for Disease Control and Prevention in Atlanta, Georgia, reported that one in every 88 American children has now been diagnosed with autism spectrum disorder, a 78% increase since 2007. Better and more inclusive autism diagnoses explain some of this increase, but new mutations are probably also a factor, says Daniel Geschwind, a neurobiologist at the University of California, Los Angeles. “I think we will find, in places where there are really old dads, higher prevalence of autism.”
However, Mark Daly, a geneticist at Massachusetts General Hospital in Boston who studies autism, says that increasing paternal age is unlikely to account for all of the rise in autism prevalence. He notes that autism is highly heritable, but that most cases are not caused by a single new mutation — so there must be predisposing factors that are inherited from parents but are distinct from the new mutations occurring in sperm.
Historical evidence suggests that older fathers are unlikely to augur a genetic meltdown. Throughout the seventeenth and eighteenth centuries, Icelandic men fathered children at much higher ages than they do today, averaging between 34 and 38. Moreover, genetic mutations are the basis for natural selection, Stefánsson points out. “You could argue what is bad for the next generation is good for the future of our species,” he says.
Nature 488, 439 (23 August 2012) doi:10.1038/488439a
Male biological clock possibly linked to autism, other disorders
Nature Medicine 14, 1170 (2008) doi:10.1038/nm1108-1170a
Over the last few years, epidemiological evidence has suggested that as men age their odds of having a child with autism, schizophrenia or bipolar disorder might increase. The findings, along with more recent genetic data have led researchers to ask whether the mutations that accumulate in sperm DNA with age might underlie this observed association. âIf this paternal age effect has something to do with mutations, then that opens up all sorts of interesting and sort of scary possibilities,â says Jonathan Sebat, a human geneticist at Cold Spring Harbor Laboratory in New York State. He says it is conceivable that the trend of delaying fatherhood might contribute to an increased incidence of mutations in the population that can give rise to neuropsychiatric disorders. In a study of more than 100,000 people, along with records about their parentsâ ages, Avi Reichenberg at Kingâs College London and his colleagues found that 33 out of every 10,000 offspring of men 40 years or older had autism spectrum disorderâa 475% increase compared to offspring of men younger than 30, who fathered afflicted children at a rate of 6 per 10,000 (Arch. Gen. Psychiatry 63, 1026â 1032; 2006). This association is now being tested in a larger study, says Reichenberg. A study this September showed a similar but less pronounced association of parental age with bipolar disorder (Arch. Gen. Psychiatry 65,1034â1040; 2008). Spontaneous mutations can arise in both sperm and eggs. As women age, for example, they have an increased risk of delivering a child with Downâs syndrome and other disorders caused by large-scale chromosome problems in eggs, such as trisomy. But unlike eggs, sperm arise from stem cells that continuously divideâabout 840 times by the time a man is 50 years old (Cytogenet. Genome Res. 111, 213â228; 2005). The theory is that the chances of mutations increase with each round of DNA replicationâa process that could underlie estimates that the mutation rate in males is about five times that in females (Nature 416, 624â626; 2002). âAny mutation you can think of occurs more frequently in the sperm of older men,â says Sebat. Meanwhile, recent genetic surveys of people with autism and other neuropsychiatric disorders have bolstered this controversialâ and still tenuousâhypothesis. The DNA studies have suggested that âspontaneousâ mutations contribute to schizophrenia and autism. This type of mutation can arise in the sperm or egg of the parents.
Sebat and his colleagues, for instance, looked at spontaneous deletions and duplications measuring about 100,000 DNA base pairs and longerâa length that often contain dozens of genesâin the genome of people with of autism spectrum disorders (Science 316, 445â449; 2007). Such spontaneous mutations occurred in only 1% of unaffected people, but they occurred in about 10% of subjects with sporadic forms of the disorder, meaning they had no family history. The researchersâ methods only pick up a fraction of mutations, so the effect of sporadic mutations is probably substantially larger, says Sebat. Similar studies this year have shown that people with nonfamilial forms of schizophrenia also have a higher rate of spontaneous duplications and deletions, and Sebat says his unpublished data show a similar association in bipolar disorder. But whether the mutations that arise spontaneously in neuropsychiatric disorders come mainly from mom or dad is still unclear, as is their association with parental age. Sebat says larger studies underway should help clarify these questions. And researchers caution that they have very little idea how the disrupted genes in eggs and sperm might potentially give rise to neuropsychiatric disease. âIt is not established, and it can put a class of individuals in a negative light,â says Rita Cantor, a human geneticist at the University of California, Los Angeles. Moreover, other, even more tenuous explanations could underlie the parental age effectâsuch as the idea that fathers who delay parenthood somehow have genes that affect their social behavior and make their offspring more prone to neuropsychiatric disorders.
Says Cantor, âI think itâs a delicate subject.â Charlotte Schubert, Washington, DC 1170 volume 14 | number 11 | novmeber 2008 nature medicine Male biological clock possibly linked to autism, other disorders New techniques preserve fertility hope for women For a man battling cancer, preserving the option to have children later in life is simple: store samples of semen. Even a single ejaculate contains millions of sperm that can later be used to fertilize an egg. A woman facing cancer, on the other hand, has far fewer choices, which depend on her age, how much time she has before treatment must begin and the availability of a partner who can provide sperm. Oocytes, or eggs, are particularly vulnerable to chemotherapy and radiation, leaving many women infertile after being treated for cancer. The most successful option for a woman of child-bearing age is to create embryos through in vitro fertilization and freeze them. (Even if the womanâs ovaries are removed, her uterus can still carry a transplanted embryo to term.) Doctors have turned to this method for over two decades, with a success rate of up to 40%. âThatâs a procedure that doesnât need improvement,â says Kutluk Oktay, director of reproductive medicine and infertility at New York Medical College. Women who donât have a partner can try to freeze unfertilized eggs. But, unlike hardy embryos, eggs are sensitive to chilling. Hundreds of babies have been born with this technique, but the success rate overall hovers around 3%.
above text from https://dokumen.tips/documents/male-biological-clock-possibly-linked-to-autism-other-disorders.html
Strong Association of De Novo Copy Number Mutations with Autism
Authors: Jonathan Sebat, B. Lakshmi… and Michael Wigler
Science 15 Mar 2007: DOI: 10.1126/science.1138659
We tested the hypothesis that de novo copy number variation (CNV) is associated with autism spectrum disorders (ASDs). We performed comparative genomic hybridization (CGH) on the genomic DNA of patients and unaffected subjects to detect copy number variants not present in their respective parents. Candidate genomic regions were validated by higher-resolution CGH, paternity testing, cytogenetics, fluorescence in situ hybridization, and microsatellite genotyping. Confirmed de novo CNVs were significantly associated with autism (P = 0.0005). Such CNVs were identified in 12 out of 118 (10%) of patients with sporadic autism, in 2 out of 77 (3%) of patients with an affected first-degree relative, and in 2 out of 196 (1%) of controls. Most de novo CNVs were smaller than microscopic resolution. Affected genomic regions were highly heterogeneous and included mutations of single genes. These findings establish de novo germline mutation as a more significant risk factor for ASD than previously recognized.
Rare De Novo and Transmitted Copy-Number Variation in Autistic Spectrum Disorders
Authors: Dan Levy, Michael Ronemus, … and Michael Wigler
Neuron 70, 886–897, June 9, 2011
To explore the genetic contribution to autistic spectrum disorders (ASDs), we have studied genomic copy-number variation in a large cohort of families with a single affected child and at least one unaffected sibling. We confirm a major contribution from de novo deletions and duplications but also find evidence of a role for inherited ‘‘ultrarare’’ duplications. Our results show that, relative to males, females have greater resistance to autism from genetic causes, which raises the question of the fate of female carriers. By analysis of the proportion and number of recurrent loci, we set a lower bound for distinct target loci at several hundred. We find many new candidate regions, adding substantially to the list of potential gene targets, and confirm several loci previously observed. The functions of the genes in the regions of de novo variation point to a great diversity of genetic causes but also suggest functional convergence.
Autism spectrum disorder: Genetics Home Reference
Many of the genes associated with ASD are involved in the development of the brain. The proteins produced from these genes affect multiple aspects of brain development, including production, growth, and organization of nerve cells (neurons). Some affect the number of neurons that are produced, while others are involved in the development or function of the connections between neurons (synapses) where cell-to-cell communication takes place, or of the cell projections (dendrites) that carry signals received at the synapses to the body of the neuron. Many affect development by controlling (regulating) the activity of other genes or proteins.
The specific ways that changes in these and other genes relate to the development of ASD are unknown. However, studies indicate that during brain development, some people with ASD have more neurons than normal and overgrowth in parts of the outer surface of the brain (the cortex). In addition, there are often patchy areas where the normal structure of the layers of the cortex is disturbed. Normally the cortex has six layers, which are established during development before birth, and each layer has specialized neurons and different patterns of neural connection. The neuron and brain abnormalities occur in the frontal and temporal lobes of the cortex, which are involved in emotions, social behavior, and language. These abnormalities are thought to underlie the differences in socialization, communication, and cognitive functioning characteristic of ASD.
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from CBS News, Feb 11, 2018
We like to think that good work is always rewarded. But what if some people who could do good work can’t their foot in the door in the first place? That’s where recent hiring initiatives that look beyond unfair stereotypes come in, as Lee Cowan reports in our Cover Story:
Twenty-seven-year-old Christopher Pauley thought he had it all figured out when it came to looking for a job.
He had a detailed spreadsheet of each and every position he applied for — at least 600.
But despite his degree in computer science from California Polytechnic State University, he went two years with barely a nibble.
Did he get discouraged? “Oh my gosh, my morale really started to drop towards the end,” he said. “In fact, there were days where I would either hardly fill out any applications at all, or just simply not apply on anything.”
He knew he had the smarts for most jobs; he was a former Spelling Bee Champ, after all. But Pauley struggles with social and communications skills because he’s also autistic.
While precise numbers are hard to come by, by some estimates at least 80% of adults with autism are unemployed, even though their IQs are often well above average.
Sometimes their job skills can present themselves in unique ways. For Christopher, it’s video games. His ability to recognize patterns and his acute attention to detail — both hallmarks of autism — make his playing the video game Rock Band look pretty easy. And they are the same skills he was hoping would impress prospective employers in the computer programming world. But he always had to get past that interview, which was a challenge at best.
Cowan asked, “Was there, in any of those interviews, a time where you just wanted to tell somebody, ‘Look, I know my social skills maybe aren’t quite what you expect, but I know I can do this job, and I know I can do a really good job if you give me a chance’?”
“But you never said that to anybody?”
“Most of the time, no,” he replied.
“I just wasn’t comfortable. It makes me come across as desperate.”
At Microsoft, however, there was no need to hide his autism; they were looking for it.
“It’s a talent pool that really hasn’t been tapped,” said Jenny Lay-Flurrie, the chief accessibility officer at tech giant Microsoft outside Seattle. “There really is, and was, a lot of data on the table that said to us that we were missing out. We were missing out on an opportunity to bring talent in with autism.”
Cowan said, “So in a way, it sounds like this was almost a business imperative.”
“Heck, yeah!” she laughed. “People with disabilities are a strength and a force of nature in this company, myself included.”
Lay-Flurrie, who is profoundly deaf, communicates by reading lips and working with an interpreter. She helped create a hiring program for Microsoft back in 2015 designed to better identify candidates with autistic talents.
Instead of the traditional job interview focusing so heavily on social skills, the company has replaced it with a vetting process that lasts for weeks, and team building exercises like one called the Marshmallow Challenge.
“Being able to watch a candidate in that environment as opposed to sitting across the table interviewing them makes all the difference in the world,” said Cowan.
“Every difference,” said Lay-Flurrie. “Every day, in any company, in any role, you’re going to be asked to work with someone else to figure out a problem or a challenge, or a project.”
“And yet in that scenario, they’re not as self-conscious that they’re being observed for a job — they’re just doing a task.”
After Christopher Pauley went through a similar, unconventional interview process back in 2016, Microsoft quickly hired him as a software engineer. His manager Brent Truell says he was immediately impressed by Christopher’s “out of the box” thinking.
“When we are faced with really complicated problems, the solutions to those aren’t always simple,” said Truell. “And Christopher always kind of brings new insights. And having that creative mind, he always brings something new to the team, which is really exciting.”
“Which is exactly why you hired him, right?
It’s an idea that’s catching on.
Last April, 50 big-name companies — including JP Morgan, Ford and Ernst & Young — came together for a summit on how to bring more autistic adults into the workforce.
It was hosted at the Silicon Valley campus of German software maker SAP, which was one of the first large companies to reach out to the autistic community.
It started its Autism at Work Program almost five years ago, and since then it’s hired 128 people on the spectrum, with the goal of hiring more than 600.
“I have been in this industry for close to 30 years, and I can tell you it’s probably the single most rewarding program that I have been involved with,” said Jose Velasco, who heads the program.
The biggest surprise for him, he says, has been the variety of candidates applying. “Very quickly we started getting resumes from people that had degrees in history, and literature in graphic design, attorneys … the whole gamut of jobs,” Velasco said.
“So really, you went into this thinking that people with autism would be good at certain jobs, and what you ended up discovering is they’re good at all jobs?” asked Cowan.
“They are good at just about every role.”
And they’re expected to perform in those roles, just like anyone else.
Mike Seborowski, for example, was hired three years ago and works in cybersecurity in SAP’s office outside of Philadelphia. When Cowan was visiting, Jose was helping Mike get ready for a long stint at the company world headquarters in Germany. “If you would had told me six years ago that we would have an employee who was openly autistic in the company, going on a business trip to Germany for a month, I would have not believed you,” said Velasco.
Almost everyone has been a surprise, he says. He points to 26-year-old Gloria Mendoza.
She told Cowan, “You should see some of the videos I had when I was a child. I was not very socially skilled with the other kids. Not showing interest with other people, displaying some of the challenging behaviors that a child on the autism spectrum would have.”
Her parents, Rosaura and Enrique Mendoza, helped get Gloria years of speech and occupational therapies, as well as access to top doctors. “When she was very young, I used to worry so much because I never thought she will overcome all what she has done,” said Rosaura. “So, it was like a very dark cloud.”
Gloria made huge strides in her childhood, but her parents were still concerned about how autism might affect her future.
“We worry about her adult life — well, first of all, could she make it through high school?” said Enrique. “Then, once she does that, you know, can she make it through college? Can she be independent?”
She made it through both high school and college; in fact, she got two degrees from Gettysburg College in Pennsylvania — one in music (she has a beautiful singing voice), and another in computer science. And yet, a year after graduating — and hundreds of resumes later — she still couldn’t find a job … until she applied to SAP.
“Probably the best part about working here is that I can use the skills which I have studied whilst being among people that understand who I am and how I’m different from everybody else,” she said.
SAP put Mendoza through five weeks of training, which included working on her social skills.
She’s now in something called Digital Business Services, where she deals directly with customers.
Cowan asked, “What’s the one dream you really want to come true?”
“Probably that I can be really up there in my department, earning a lot of money, and still keeping the friends that I have,” she replied.
Her new friends are mostly co-workers in the autism program, and they try to get together regularly. Cowan watched as Mendoza and her friends participated in Game Night.
“And that, CBS, is how you play Smash Brothers!” said Gloria.
She told Cowan, “I never really had that many friends when I was younger, and having this wide variety of friends that understands me really makes all the difference for me.”
How so? “‘Cause I can express myself in ways that people won’t look at me weird. And it turns out that a lot of people have common interests as I do.”
SAP boasts a retention rate of about 90% for their autistic employees. Part of that may be due to the fact they’re not just set adrift in the workplace all alone. Each participant in the program is assigned a mentor from within the company — like an on-site guardian angel.
Gabby Robertson-Cawley, who has a cousin on the spectrum, volunteered to work with Gloria. “I think it’s just the rewards of getting to be friends with these colleagues who have autism — it’s not something you get in your typical corporate day-to-day experience,” Robertson-Cawley said.
Microsoft also has mentors. Melanie Carmosino, who works with Christopher Pauley, has a personal connection as well; she has a son who’s autistic.
Cowan asked, “What have you taken away from this whole experience, personally?”
“Hope,” Carmosino replied. “I think that this program gives hope to the autism community. It gives hope to parents like me, and it gives hope to people like my son that a company can, and will, look past their differences and see their gifts and let them contribute to society just like everybody else.”
Christopher Pauley is now independent, living on his own in a high-rise apartment, something he’s always wanted.
Cowan said, “I don’t want to ask how much you’re making, but you’re doing pretty good, it sounds like, yeah?”
“Yes,” he said.
“Could you ever imagine you’d be making this much money?”
“No, I never did! Honestly I would have been perfectly happy with, like, half the money I’m making now.”
He bought a car and drives himself to work — and for the first time, he says, looks forward to arriving at a place where he’s accepted for who he is.
He knows there are still challenges ahead, but given a chance to prove his worth, says Christopher, has given him an optimism he never had.
Cowan asked, “If other kids, or young adults, or adults with autism are watching this, what’s your message to them?”
“Don’t give up, and make sure to always aim high,” he replied. “Don’t aim in the middle You know, shoot for the stars every time, ’cause you never know what might happen.”