Originally Posted by YNot
I think it's different now - with our thinning ozone layer, melanomas are becoming much more common. Doesn't matter to me either way, though - I'm a fair skinned red head. I look at the sun and I burn.
That ozone layer is thinning mostly at the poles. Most people live closer to the equator where the layer is pretty much full thickness. Therefore, it's unlikely that this is a major cause, if at all, of any particular skin disorder for most of us. On the other hand, cancer of all forms (indeed, diseases of all forms), including skin cancers, has increased in parallel to our collective adoption of a high-carb diet all over the world.
It's important to keep in mind that cancer doesn't just need an initial trigger, it also needs a continuous favorable environment for its growth. This is not a fire-and-forget kind of thing, like a homing missile or something like that, where merely pulling the trigger is it. Anyways, this is achieved mostly by two agents - glucose and insulin (glucose is the fuel, insulin is the growth signaling just as growth hormone is the growth signaling for normal growth in kids for example) - both of which can be done simultaneously just by eating a high-carb diet. Cancerous cells are said to have as much as 10x the number of insulin receptors (not sure on the exact number, but the principle is the same, there's more insulin receptors).
Even without an initial trigger, if we establish this favorable environment a priori, then the initial trigger will be that much more effective at creating cancer. Conversely, the absence of this favorable environment will not allow any trigger to eventually turn single cancerous cells into tumors - there is no growth. For our purpose, the Atkins diet should be effective enough to create an environment most unfavorable for cancer growth.
Additionally, it's possible that certain causes of cancer, in and of themselves, act positively to cause both glucose and insulin to remain higher, if these causes are living things like bacteria or virus for example, as they would have evolved to make their preferred environment more favorable, just as we have evolved to make ours more favorable to us. And thus, this makes the Atkins diet a diagnostic tool to discover the presence of such an active agent. I.e., if the diet works, then the high-carb diet was the only thing keeping cancer growing, but if the diet doesn't work as it should, then there must be something else going on.
For the latter, Richard Feinman et al did an experiment with a ketogenic diet and cancer. They found that not all subjects responded equally. There's a bunch of hypotheses to explain this, but the most likely, in my opinion, is that in those that did not respond, there still remains an active agent that diet alone cannot fix. Link to discussion on the experiment: http://forum.lowcarber.org/showthread.php?t=447278
As for the topic of skin disorders caused by the Atkins diet via methylglyoxal (and then through glycation of skin tissue), this is very unlikely. Ketones stimulate the process chaperone-mediated autophagy (CMA), the recycling of glycated protein inside cells. From the drop in HbA1c, ketones must obviously also stimulate this process elsewhere in the body outside cells. Mike Eades of Protein Power wrote about this here: https://proteinpower.com/drmike/200...eans-our-cells/
Glycation is a normal process, but then CMA is also a normal process to take care of the normal glycation that occurs. But as soon as we eat a high-carb diet, CMA can't keep up (in fact CMA is shut down because insulin shuts down ketogenesis in the liver, so no ketones to stimulate CMA), glycation accumulates above and beyond what we can handle otherwise, disease takes over. For example, HbA1c is noted as being associated with - as being a marker for - diabetes type 2. In conjuction with CMA, a low-carb diet contains few(er) carbohydrates, so little fuel and little insulin for cancer growth. This is a double whammy for cancer, either way, whether we eat a high-carb diet or a low-carb diet, respectively.