I've had a bias in this direction for quite a while. When learning about neurodegenerative diseases back in college over a decade ago my conclusion at the time was that something metabolic was going on. Nothing else made sense to me as an explanation for how symptoms and pathology for a disease could show up after 60ish years. At that time I couldn't figure out how to make the link though, so it was a leap.
I was in a lab meeting maybe 4 years ago or so and my PI had just come back from a conference on Alzheimer's. He reported back that groups had started investigating the role of mitochondrial dysfunction in the disease and had been able to find that lineages with variants in genes related to mitochondria and energy homoeostasis were far more likely to have or develop Alzheimer's. I haven't kept an eye on progress in that line of research, but it is in line with what is being reported/speculated here.
Finally, a couple of years ago I ran into the father of someone I went to middle school with and I learned that he was a biochemist. Somehow the conversation wound around to the challenge of understanding neurodegenerative diseases. I asked him for his take on a disease that only presents after 60ish years. His immediate answer was DNA damage during mitosis. But neuron's don't divide. And then it hit me. There IS something that is still dividing inside the neurons! It is the mitochondria! The other possibility is the astrocytes, the microglia, or some other mitotic cell population in the brain, but the mitochondria really stand out as fitting both the fact the neurons don't divide and the instinct from a veteran biochemist that something that takes so long to appear must be related to DNA damage.
Like the article says: "“It’s too soon to make any firm conclusions about a lot of this stuff, but it sure looks like the mitochondria are disrupted in many kids with autism,” Frye says. “And environmental exposures, especially early on, may be programming the mitochondria to have different types of respiratory physiology.”"
You might find this of interest too from eleven years ago:
https://drhyman.com/blog/2010/12/09/breakthrough-discovery-o...
"Let’s look more closely at what this new study in The Journal of the American Medical Association tells us about mitochondrial dysfunction and how this may lead us to new methods of treatment—methods similar to the ones I used to help reverse Jackson’s autism. ...
This study forces the question: How do children acquire energy deficits that affect their whole system, not just the brain?
The causes of mitochondrial dysfunction are well known, specifically as it relates to metabolism and the brain, and I have documented them in my books UtraMetabolism and The UltraMind Solution. They include environmental toxins(iv)—mercury, lead and persistent organic pollutants(v)—latent infections, gluten and allergens (which trigger inflammation) sugar and processed foods,(vi) a nutrient-depleted diet,(vii) and nutritional deficiencies.(viii) These are all potentially treatable and reversible causes of mitochondrial dysfunction that have been clearly documented.
I found all these problems in Jackson, and over a period of 2 years we slowly unraveled and treated the underlying causes of his energy loss which included gut inflammation, mercury, and nutrient deficiencies. Over time, the tests for his mitochondrial function and oxidative stress (as well as levels of inflammation and nutrient status) all normalized. When they became normal, so did Jackson. He went from full-blown regressive autism to a normal, bright beautiful 6-year-old boy.
This is just one story, but if autism can be reversed in one child, if there is any possibility of effective treatments or a potential cure, it forces us to ask critical questions: How did this happen? Can it happen in other children? What were the biological patterns found and how were they treated?"
And if it applies to young brains, why would it not apply to older brains?
My pet theory on autism is the Back to Sleep campaign that began in the 90s. (1) Babies don’t like back sleeping. It disrupts their sleep. Sleep is important in brain development. Constantly disrupted sleep means a higher percentage of brain development issues.
I can back up my pet theory with studies. Bottom line is, stomach sleeping with good air circulation (2) reduces SIDS at similar rates to back sleeping without the side effect of autism.
Care to cite a study or data? I know sleep researches studying this issue at UCLA and elsewhere and would love to share it with them.
We were looking for natural experiments. Ideally somewhere that babies are still stomach slept. Much like Israel and peanut snacks in the study of peanut allergies, it’s hard to change a protective paradigm without a natural experiment.
The WaPo article is very illuminating re: how Chinese babies were raised. As it was published almost 30 years ago, those babies are now established Chinese adults. Makes you wonder how much they're shaped by how they were reared.
I’m referring to data on autism rates in China. The WaPo article makes it seem highly likely that kids have developmental issues. The question really is whether autism is measured in China in any reliable way.
Other researchers claim autism is an emotional evolution.
I’m disinclined to trust our contemporary society with deciding whether autism is good or bad.
A difficult scenario for parents, perhaps, but I feel that’s better handled by society pulling its head out of its ass and providing a system that supports such situations.
It's not like autism is a bacteria or a virus. It's a syndrome. Syndromes are just a grouping of a bunch of symptoms, in the case of autism, a bunch of disorders (things that aren't normal.)
The difference between (vi) a nutrient-depleted diet and (vii) nutritional deficiencies is supplementation, non-dietary factors affecting absorption, or something else?
There aren't good candidates for highly non-linear processes that can accumulate but take decades to hit some threshold. Biological systems are full of homeostatic mechanisms that prevent such slow accumulation and if and when they break they do so suddenly, so virtually all the other candidates don't fit the profile because you expect incidence to be distributed evenly as a function of age or occurring early (e.g. embryonic lethal).
I was in a lab meeting maybe 4 years ago or so and my PI had just come back from a conference on Alzheimer's. He reported back that groups had started investigating the role of mitochondrial dysfunction in the disease and had been able to find that lineages with variants in genes related to mitochondria and energy homoeostasis were far more likely to have or develop Alzheimer's. I haven't kept an eye on progress in that line of research, but it is in line with what is being reported/speculated here.
Finally, a couple of years ago I ran into the father of someone I went to middle school with and I learned that he was a biochemist. Somehow the conversation wound around to the challenge of understanding neurodegenerative diseases. I asked him for his take on a disease that only presents after 60ish years. His immediate answer was DNA damage during mitosis. But neuron's don't divide. And then it hit me. There IS something that is still dividing inside the neurons! It is the mitochondria! The other possibility is the astrocytes, the microglia, or some other mitotic cell population in the brain, but the mitochondria really stand out as fitting both the fact the neurons don't divide and the instinct from a veteran biochemist that something that takes so long to appear must be related to DNA damage.