Autism: Maybe It's Not What We've Been Told

I felt a tear beginning to well up. As we sat on the floor, my 3-year-old little boy with autism was looking directly into my eyes, something he hadn’t done in almost a year. What’s more, he was smiling and calm. He seemed to be enjoying the moment. He wasn’t in his usual fog. There was a clarity in his face, as if he were saying. “I’m here, Dad. I’m with you.” I didn’t know what to do with the moment. I just sat there. “What in the world is going on?” I wondered. I was beginning to suspect it had something to do with the antibiotic he was taking, but that didn’t make any sense given what we had been told about autism to that point.

As I describe in my recent article in the peer-reviewed scientific journal Microbial Ecology in Health and Disease, our son had an unexpected, rapid, and dramatic improvement in his autism symptoms while taking a common antibiotic prescribed for his strep throat infection.

Starting on day four of the 10-day course, we saw great improvements in most of the areas where he had challenges: speech, mood, eye contact, energy level, even his gross motor skills.

One of the classic hallmarks of autism are speech delays, and our son was no exception. He rarely initiated speech and typically answered questions with one-word responses. Today he was stringing words together in unprecedented ways. He had lots of enthusiastic energy, almost hyper, which was very uncharacteristic of him. Each additional day he was on the amoxicillin brought greater improvements. On day six he did something remarkable; he rode a tricycle, which he had been unable to do since it was purchased six months earlier.

We had seen transient improvements in some of his autism symptoms before when he had a fever, but by this time his fever had been gone for several days, and we had never seen improvements of this magnitude.

Were we really seeing an improvement? Parents are very attuned to changes in their children, but memory can be unreliable, which is why I have used customized software to track changes in over 20 of my son’s autism symptoms on a daily basis, virtually since the day he was diagnosed. We felt confident we were seeing a dramatic improvement. The question I kept asking was: “why?”

After the first incidents of fever-related improvements, I fell back on my training as a medical venture capitalist and consulted medical literature, where I found one Johns Hopkins paper from 2007 that documented the presence of a “fever effect” in some children with autism. Estimates are that from 30 percent to 80 percent of children with autism experience improvements in some of their symptoms while they had a fever. Was there such a thing as an “antibiotic effect” too?

I went back to the medical literature. Bingo! I found a paper published in 2000 that documented a clinical trial at Chicago Rush Children’s Hospital where 8 out 10 young children with severe autism experienced marked improvements in their autism when they were given a powerful antibiotic called vancomycin.

We learned that many other parents of children with autism had experienced an antibiotic effect in their own children. So why just one research study from 15 years ago?

When our son was diagnosed we, like so many others, were told: “We don’t know what causes it. We have no treatments for it.”

From that meeting and subsequent meetings with neurologists and developmental pediatricians we had been led to believe that the behaviors we saw were a function of brain wiring that is ultimately driven by genes. In other words, he was “hard-wired” to be autistic. But if that were the case, why did his symptoms improve when he had a fever? Why were we witnessing such dramatic improvements while using an antibiotic? And why did so many parents report improvements from making various dietary changes? These reports and clinical studies seemed at odds with the “hard-wired” conventional view or paradigm of autism.

Something else seemed unusual: If autism were fundamentally driven by genetics, why was the incidence rising so rapidly? Genes take thousands of years to evolve. Was it really reasonable to think that autism has been around consistently at the recently reported rate of 1 in 68 children (1:42 for boys — almost 2.5 percent) but that we had just not noticed? There had to be something else going on.

Virtually all the autism medical research funding in this country is based on the hard-wired view and goes to gene-association studies and brain scans. However, there is an emerging view of autism as an acquired metabolic (biochemical) syndrome, in which the immune system and the microbiome (primarily gut bacteria) likely play a role. From this perspective, improvements such as the ones we and others have seen made more sense.

On an almost daily basis, we read of new research pointing to the important role that the microbiome plays in health and disease, from the surprising finding that gut bacteria were responsible for stomach ulcers, to their recently-implicated role in the development of food allergies and potentially even diabetes. The old view, of gut bacteria as free-loaders who simply help us digest some food, is outdated.

Could the conventional view of autism as genes>wiring>behaviors also be outdated?

In speaking with autism researchers who were at the forefront of the gut-brain connection, most were familiar with both the antibiotic effect and the 2000 vancomycin study, and indicated an intense desire to investigate this more fully. The issue, they told me was funding. Because this type of research fell outside of the conventional view, it was not well supported by the two or three governmental and charitable organizations that fund virtually all autism research in this country.

Could this conventional view of autism be getting in the way of making progress or breakthroughs in our understanding of autism?

Due to the lack of funding for research based on this emerging view of autism as a complex metabolic syndrome, I formed the non-profit N of One: Autism Research Foundation. We are focused on research that is grounded in the view that a child’s autism behaviors are not “hard-wired.” But this view needs more support from the public.

It’s been estimated that autism costs our country $126 billion per year. We are all paying a very high price for what we don’t know.

Our son’s symptoms improved while taking an antibiotic. That is anecdotal and not the basis for a wholesale shift in this country’s research strategy. However, the 2000 vancomycin study is not anecdotal. It was a rigorous study conducted by highly qualified researchers at a pre-eminent, mainstream medical institution. And it is a national embarrassment that additional funding has not been allocated to follow it up. To be clear, I am not advocating the use of antibiotics as a long-term treatment for autism, but rather arguing that we should use these findings as one of many potential clues for new directions in research.

I believe we are on the verge of a paradigm shift in autism where the new view is that, while some genetic factors may be important, the underlying condition is more of an acquired syndrome that arises from externally-induced changes in metabolism, immune function, and the microbiome. The encouraging thing about this view is there is reason to believe that many of these children can get better. We need to fund this kind of research. Our children deserve better answers.

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Carlsen Collects Another Chess Victory

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The world chess champion Magnus Carlsen, 24, scored another amazing victory with 7 points in 9 games at the Gashimov Memorial tournament in Shamkir, Azerbaijan. The Norwegian grandmaster finished a full point ahead of the former world champion Vishy Anand. The 45-year-old Indian grandmaster moves to second place behind Carlsen on the May FIDE rating list.

Carlsen’s 2876 rating is just 6 points shy of the record he established a year ago. But he is 72 points ahead of Anand. Bobby Fischer still has the record of the largest rating difference between the world’s top two players with 120 points over Boris Spassky in July 1972. When Garry Kasparov reached his highest rating of 2851 points in July 1999, he was 80 points ahead of Anand. It shows Anand’s class and durability.

The tournament in Shamkir was played in memory of Vugar Gashimov, a talented Azerbaijani grandmaster and world-class player who died last year at the age of 27.

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The biggest test for Carlsen came in the first round against Anand. The Indian grandmaster had the world champion on the ropes most of the game, but Magnus hung on and Vishy could not deliver the knockout. After that Carlsen scored five wins and finished undefeated with an incredible 78% performance.

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Carlsen played the best game against the former world champion Vladimir Kramnik. Inventive opening play and strong pressure in the middlegame led to material gain. Carlsen’s technique took it from there. Here is the final stage:

Carlsen,Magnus – Kramnik,Vladimir
Shamkir 2015

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46.Qb8!?
The most logical continuation, threatening 47.Qf8 and 48.Qg7 mate. The pawn breakthrough also wins: 46.f5 gxf5 47.g5 hxg5 (47…Rc2 48.g6+ Kh8 49.Qa8+ Rc8 50.Qxc8+ Bxc8 51.gxf7+-) 48.Qe7 (48.Qb8 Bc8 49.Qxc8 Rxb4 50.Kxf7+-) 48…Kg8 49.Qd8+ Kh7 50.Qf8 f4 51.Qg7#]
46…Rf2 47.f5! gxf5
After 47…Bxf5 48.Qa7! the double-attack on the rook and the f7-pawn wins.
48.Qg3!
Magnus chooses the faster win, finding another way to reach the square g7 with his queen.
48.g5 also wins: 48…Rg2 49.h4 hxg5 50.h5, renewing the threat 51.Qf8, White wins: 50…Kh6 51.Qh8 mate.
48…Rf1 49.g5
Black can’t cope with multiple mating threats. After 49…f4 50.Qh4; 49…Rc1 50.gxh6; 49…h5 50.g6+ wins.
Black resigned.

It was Kramnik’s third consecutive loss, a real blow to him. He used to be rather invincible, rarely losing. He became the world champion in 2000 without allowing Kasparov a single win.

Wesley So came to Shamkir straight from the U.S. Championship where he finished third after losing four games. He hoped things would go better at the Gashimov Memorial and they did. So begun with a furious pace 3.5/4, an incredible start in such an elite tournament. In the next round, Anand stopped the breakout, but he knew it wouldn’t be easy: “He had a huge year,” the former world champion said. “Except for one event, he hardly lost a game.”

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“It was a complicated, intense game,” Anand said after his victory against So. “We were both spending a lot of time. Those kinds of games are very satisfying to win.” It was another Vishy masterpiece.

Anand,Vishy – So,Wesley
Shamkir 2015

1.e4 e5 2.Nf3 Nc6 3.Bb5 a6 4.Ba4 Nf6 5.0-0 Be7 6.d3 b5 7.Bb3 0-0 8.Nc3 d6 9.a3 Nb8
Borrowing the idea from the Spanish Breyer: the knight goes to d7 and the bishop to b7. It also frees the c-pawn.
9…Bg4 is the computers’ main choice.
10.Ng5

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Anand’s prepared novelty. The computers don’t go near this devilish idea. In Wijk aan Zee this year, Fabiano Caruana played 10.a4 against So. They drew in 31 moves.
10…Nc6
I guess it didn’t work, we may say. But the knight is best placed on the square d4.
In a similar position Levon Aronian suggested:”Anyone who plays 11…Nc6 in this position should strip naked and undergo a full-body scan. Since this illogical move is considered by the computers to be the strongest…!” Of course, it is a different story here.
A. Black has to consider a combination known from the Philidor defense after 10…Nbd7 11.Bxf7+ Rxf7 12.Ne6 Qe8 13.Nxc7 Qd8 14.Nxa8 Bb7;
B. All kind of sacrifices are possible after 10…h6 11.f4 hxg5 (11…exf4 12.Nf3 (In King’s gambit style is 12.Nh3 g5 13.Nxf4 gxf4 14.Bxf4 the position of the black king is shattered and White has a big lead in development.) 12…g5 13.h4 Bg4 14.hxg5 hxg5 15.g3 Nc6 16.gxf4 Nd4 17.Be3 is unclear.)
12.fxg5 and now:
a) 12…Ng4 13.h3!? (Dangerous for White is 13.g6? d5! 14.Bxd5 (14.d4) 14…Bc5+ 15.Kh1 Qh4 16.h3 Qg3-+) 13…Bxg5 is roughly equal.;
b) 12…Bg4 13.Qe1 slightly favors White.
c) The strength of White’s attack is demonstrated in this line: 12…Nh7? 13.g6 Nf6 14.Rxf6! Bxf6 15.Qh5 Re8 16.Bxf7+ Kf8 17.Nd5 Be6 18.Qh8 mate.
11.Ba2
Anticipating 11…Nd4. The machines suggest 11.Nf3 reaching the same position as after 9.a3. But here Komodo 8 comes up with the move 11…Nb8 as played by So. Weird.
11.f4 Bg4 12.Nf3 Nd4.
11…Nd4 12.Ne2 Nxe2+
12…Bg4 13.f3 Nxe2+ 14.Qxe2 Bd7 15.f4 fits White’s plan.
13.Qxe2 h6
13…c5 14.f4 Qc7 was possible.

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14.f4?!
An amazing piece sacrifice with a nice geometry: the pawn on f7 is being attacked diagonally (Ba2), in a straight line (Rf1) and eventually by a pawn from g6.
14…hxg5
So takes the piece. After14…exf4 15.Nf3 g5 16.g3 g4 (16…fxg3 17.hxg3 c6 18.Nd4 White lands his pieces on the weak light squares.) 17.Nh4 (After 17.Bxf4 gxf3 18.Qxf3 Bg4 19.Qe3 Be6 Black has the advantage.) 17…f3 18.Qe3 White has the edge.
15.fxg5 Ng4 16.g6!
White may give the black horse more freedom, but the pawn on g6 is a vital thorn in Black’s position. Black is fine after 16.h3 Bxg5.
16…Bg5
After 16…Nh6 17.Bxh6 gxh6 18.Rxf7 Rxf7 19.Rf1 Kg7 20.Rxf7+ Kxg6 21.Qf3 h5 22.Rf5!? forces a draw.;
The white queen on e2 helps to create a simple defense in the line 16…d5 17.Bxd5 Bc5+ 18.Kh1 Qh4 19.g3!
17.h3 Bxc1 18.Raxc1 Nh6 19.Qh5
To prevent Black’s next move, the computers prefer 19.Rxf7 for example 19…Nxf7? (19…Rxf7 20.Qh5 (20.gxf7+) 20…Kf8 21.gxf7±) 20.Qh5 mates soon.
19…Be6 20.Bxe6 fxe6 21.g4
Threatening 22.g5, winning the piece back.
21…c6?
Black should have tried blocking the f-file with 21…Rf4 22.g5 Qf8 but White still has the edge.

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22.Rxf8+
Leads to a forced play. 22.g5 seems to be more precise because of the double attack on h6. Even after some acrobatics like 22…Qb6+ 23.Kg2 Rxf1 24.Rxf1 Qe3 25.gxh6 Qxh6 26.Qg4 (26.Qxh6 gxh6 27.Rf7) 26…Re8 27.Rf7 Qd2+ 28.Rf2 Qh6 29.h4 White has a clear advantage.
22…Qxf8 23.Rf1 Qe7 24.g5 Rf8 25.gxh6 Rxf1+ 26.Kxf1 Qf8+ 27.Ke2 gxh6 28.Qg4 Qf6 29.h4 d5?!
After 29…a5 30.b4 a4 31.h5 c5 32.Qg1 cxb4 33.Qa7 bxa3 34.Qa8+ Kg7 35.Qb7+ Kg8 36.Qxb5±
30.h5
With the protected passed pawn, White can go into a pawn endgame. He has to find a way of breaking through with his king.
30…d4 31.b4!
Fixing the queenside pawns.
31…Kg7 32.Qf3 Qe7
After the queen exchange White wins: 32…Qxf3+ 33.Kxf3 Kf8 34.c3 dxc3 (34…Kg7 35.cxd4 exd4 36.Kf4+-) 35.Ke2 Kg7 36.Kd1 Kf8 37.Kc2 Kg7 38.Kxc3 Kf8 39.d4+-.
33.Kd1 Kg8 34.Qf2 Kg7 35.c3!
Undermining the center leads to victory.
35…dxc3
35…Qd7 36.cxd4 exd4 37.e5 Kg8 38.Qf6 Black can hardly move. 38…Qe8 39.Qf4 wins a pawn and the game.
36.Kc2 Qc7 37.Qc5!

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Black is almost without moves.
37…Kg8 38.Qe3 a5 39.Qh3 axb4
39…Qe7 40.bxa5 creates a dangerous passed pawn.
40.Qxe6+ Kf8 41.axb4 Qa7 42.Kxc3 Qa3+ 43.Kc2 Qa4+ 44.Qb3 Qa7 45.d4

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After 45…exd4 (45…Qxd4 46.Qf7#) 46.Kd3 Kg7 47.Qf7+ Qxf7 48.gxf7 Kxf7 49.Kxd4 wins.
Black resigned.

April was rich in chess events.
China won the World Team Chess Championship in Tsaghkadzor, Armenia, ahead of Ukraine and Armenia. The U.S. team without its champion Hikaru Nakamura and So, woke up in the second half to share fourth place with Russia.
Georgia finished first at the Women’s World Team Championship in Chendu, China. Russia won the silver and China the bronze medals.
Three high-level established tournaments – Norway Chess in Stavanger, Sinquefield Cup in Saint Louis and London Chess Classic – have been united into the Grand Chess Tour. It will feature players from the world’s Top Ten list, vying for a total prize of $1,050,000. After the announcement in Saint Louis, Kasparov defeated Nigel Short 8.5-1.5 in an exhibition match.

Note that in the replay windows below you can click either on the arrows under the diagram or on the notation to follow the game.

Images by Shamkirchess

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