3 ms·
No, the referred article doesn't claim that. In fact it draws a distinction between people having ADD and people with ADT. Have a look: https://hbr.org/2005/01
by dimitar 11y ago
No, the referred article doesn't claim that. In fact it draws a distinction between people having ADD and people with ADT.
Have a look: https://hbr.org/2005/01/overloaded-circuits-why-smart-people-underperform https://hbr.org/2005/01/overloaded-circuits-why-smart-people...
Unlike ADD, a neurological disorder that has a genetic component and can be aggravated by environmental and physical factors, ADT springs entirely from the environment. Like the traffic jam, ADT is an artifact of modern life. It is brought on by the demands on our time and attention that have exploded over the past two decades. As our minds fill with noise—feckless synaptic events signifying nothing—the brain gradually loses its capacity to attend fully and thoroughly to anything.
- whoopdedo 11y agoIf ADD is genetic in origin, why isn't a DNA test used to diagnose the condition?
- hyperion2010 11y agoJust because it is genetic (in this case they probably mean heritable and supported by twin studies) doesn't mean you can find the genes that cause it. RE: why we know that intelligence has genetic components but you will be laughed out of the room if you claim to have a genetics based IQ test.
- taco_emoji 11y agoA) Just because we know something is genetic (via identical twin studies, for example) doesn't mean we know which parts of the genetic sequence are responsible B) There might be a constellation of genetic polymophisms involved, such that anything short of full-genome sequencing & analysis wouldn't yield anything useful C) Even the cheapest genetic tests are likely more expensive and take longer than a 15-minute behavioral test.
- car 11y agoThat's a good question. There are a lot of conditions where twin and adoption studies have established a genetic predispositions decades ago, but the exact cause of these disorders is unknown, and understood to be more stochastic in nature. Rather then single gene mutations, such complex disease predispositions could be combinations of single base variations in the binding sites of transcription factors and/or slight variations in proteins, which elevate disease risk, but may still require environmental factors for an actual outbreak. Our understanding here is improving rapidly, while we are learning about the regulatory elements in our genome (see the ENCODE project), and the influence of the 3D arrangement of the genome into what is known as chromatin. However, teasing apart these variations and causal relationships is extremely complex, as you can imagine. Bottom line, there is still so much we don't know or understand, but progress is being made.