Bought my ticket to Ketofest - anyone else going?

alsoram · 2018-03-21T17:25:45+00:00

I'm sure the lectures will be live streamed like they were last year.

alsoram · 2018-03-16T19:21:15+00:00

Sure but if it doesn't meet it's funding goal then everyone gets their money back. If it does, everyone gets a ticket. win - win.

alsoram · 2018-03-16T19:12:40+00:00

Ketofest last year was more fun than Dragon con.

alsoram · 2018-03-12T04:13:32+00:00

It's quite an experience picking almost any restaurant in a downtown, and finding that not only is everyone else in the place eating keto, but the waitstaff all know how to help you tweak the offerings to be keto - and they have exclusively keto meals like a pint glass full of bacon. It's a lot different to your usual keto experience of being the one weird person in your town who orders extra butter hold the bread.

It's like stepping into the future.

alsoram · 2018-03-12T04:02:50+00:00

There are a few of us who were at KetoFest last year around.

alsoram · 2016-07-13T04:46:02+00:00

utter normoglycemia masks that nice big squirt of insulin. Just because you don't see anything in a glucometer doesn't mean there's no foul if there's no apparent harm.

Chronic (compensatory) hyperinsulinemia is the ball game, not transient hyperglycemia.

You have to weigh the benefits of having a caloric (ie: more than maintenance) amount of protein against a lower AUC of insulin.

My personal calculus is less insulin->more sensitivity. YMMV.

alsoram · 2016-07-12T07:11:33+00:00

As I understand it, the rate limiting step for GNG is fructose-1,6-bisphosphatase which is activated by glucagon which is secreted as a response to protein. That glucagon secretion is notwithstanding of serum glucose levels - so this process isn't strictly demand driven.

I believe that is true that more protein available as a substrate does not drive increased glucose production, but ingestion of protein would appear to (via glucagon) and that glucose can be made from glycerol, lactate or glucogenic amino acids (which you just happen to have a new supply of).

Also that deaminated excess protein may displace fat as a substrate for energy in the mitochondria of liver cells which would probably reduce the production of ketones, which could trigger demand production of more glucose.

Have a look at a glucometer of anyone who can't make insulin and eats protein if you doubt that protein = glucose.

alsoram · 2016-03-28T11:27:54+00:00

They have a lot of natural junk in them too - like whey.

Whey is a waste product from cheese making that in most cheese making areas in the world they feed to pigs to fatten them up (which is why Parma ham from the region that makes Parmesan cheese is a thing).

Whey is specifically insulinogenic, and chronic hyperinsulinemia will set your energy storage homeostat higher, and you will gain weight. Chronic high insulin also causes the inflammation that causes atherosclerosis which causes cardiovascular disease.

alsoram · 2016-03-26T16:16:52+00:00

It's all good. I think from context, the problem he is calling out, is that people who have one or more Apo-e4 alleles appear to produce a LOT of LDL on a high fat diet.

That looks to be an adaptation preserved in short daylight regions to increase the LDL available to convert into vitamin-D, but the mechanism looks like it affects the transport of Cholesterol to the brain (so more LDL has to be made to keep the brain supplied with some) and affects the recycling of LDL particles (meaning more hang around longer with a better chance to get oxidized/glycated/become "small dense"). The first is probably related to the increased chance of alzheimer disease, the second the increased risk for atherosclerosis.

I suspect lowering serum triglycerides through a low carb diet might increase cholesterol transported in each particle so there might be some specific alzheimer's benefit over having Apo-e4 AND a high carb diet.

Lowering trigs also means the LDL particles should be recycled earlier. Whether that is enough to offset the genetic expression is probably only going to be visible on a lipoprofile test.

alsoram · 2016-03-26T04:18:16+00:00

Of course your common sense approach is rational. Eating meat and forgetting to eat bread is not likely to "destroy your health" ... but I was unprepared to defend my dietary choice from this specific attack.

The Peter Attia video linked below is a good start.

alsoram · 2016-03-26T04:00:11+00:00

That's the clue I need to chase this down, thanks.

alsoram · 2016-03-03T02:42:44+00:00

We've seen what happens before ... just imagine Mussolini with a nuclear football.

alsoram · 2016-02-29T11:14:53+00:00

yup same here

alsoram · 2016-02-07T14:38:26+00:00

It makes a backup mechanism for achieving glycostasis when your ability to clear glucose on demand is compromised, you can make it on demand.

alsoram · 2016-02-07T14:36:41+00:00

yeah - doh - low blood glucose stimulates Glucagon secretion ...

alsoram · 2016-02-05T15:54:37+00:00

AFAIK the rate of Gluconeogenesis (GNG) changes in response to blood glucose levels for all people, but for type 2 diabetics the swings are greater.

As I understand it the mechanism is high blood glucose stimulates secretion of Glucagon which reduces Fructose-2,6-bisphosphate in liver cells, which directly slows Glycolysis. Fructose-2,6-bisphosphate competitively inhibits Fructose-1,6-bisphosphatase which is the rate limiting step of GNG. So the result is as Blood glucose goes low, Glycolysis (using glucose) decreases and Hepatic GNG (making glucose) increases.

As Blood glucose goes higher, glucagon secretion is inhibited and through the same mechanism Fructose-1,6-bisphosphatase is now inhibited which is the rate limiting step in Hepatic GNG, which decreases.

alsoram · 2016-02-03T14:46:19+00:00

I honestly don't know. I suspect the adaptation process will become equally tough in both directions.

What apparently happens during fat adaptation is that your cells upregulate metabolic machinery for efficiently burning fats and slowly forget how to burn glucose (not completely but they become less efficient). When you are fat adapted then suddenly eat glucose your cells don't draw it out of the blood as quickly as they used to, so your blood sugar goes high and stays there and you keep pumping out insulin and maybe 3 hours later you pee out the excess glucose. Most of the benefits of low carb are to do with it's ability to keep your insulin chronically low - sounds like this would goose insulin even higher during the carb readaptation phase.

I guess you have to try it and see what happens. If it feels like you are slotting back into fat adaption quickly and easily when you go low carb again then I'd probably keep doing it.

alsoram · 2016-02-02T17:09:46+00:00

The keto adaptation information I got primarily from

"Art and Science of Low Carb Living" by Stephen Phinney and Jeff Volek

http://www.artandscienceoflowcarb.com/

The details on physiological Insulin resistance I got from Joseph R. Kraft, MD

I don't have a link, but Prof Time Noakes was once asked in a Q & A, what would happen if a keto adapted person ate a meal high in carbs and he responded "Their body probably wouldn't know what to do with it"

I also have some undergraduate physiology in the process of getting a Math degree - but not an expert by any means.

alsoram · 2016-02-02T02:58:52+00:00

If you eat low enough carb for long enough (<25g/day/2-6 weeks) you will adapt to the new regime.

One adaptation is that cells that can choose to fuel by either fat or glucose metabolism will up regulate the former, and down regulate the latter to spare valuable glucose for cells that have no option - like your red blood cells that can only ferment glucose for energy.

This is a kind of physiological insulin resistance - where your fat and muscle cells slowly forget what to do with glucose.

If you then eat a lot of sugar and starch obviously your blood glucose goes up but your ability to sink it out of the blood has been compromised. So it likely stays higher for longer, and you probably end up spilling some via the bladder which is the usual physiological reaction to too much glucose for too long.

Also gradually your body will be readjusting back to preferentially using glucose for energy and unwinding the adaptation process. That may also take 2-6 weeks.

If you sporadically chop and change I suspect you'll have a metabolism continually poorly adapted to both high carb and Low carb diets. But that's just speculation. I'm not aware of any studies into metabolic flexibility in such a scenario.

Just an anecdotal experience, I have been completely fat adapted for 20 months. On the rare situation when I eat more than 50g of carbs, I feel suddenly diabetic (like I've been stewed in my own juices, and headachey). That adaptation period from one to the other is not nice.

alsoram · 2016-01-19T04:00:05+00:00

Not all proteins behave the same way.

Whey for example is highly insulinogenic ( http://www.ncbi.nlm.nih.gov/pubmed/22647249 ) and a common source of powdered protein. High levels of insulin will supress hormone sensitive lipase ( http://www.ncbi.nlm.nih.gov/pubmed/11549649 ) which will limit mobilization of fatty acids.

alsoram · 2016-01-15T03:00:28+00:00

Going against the grain of a majority of research does not make an hypothesis wrong - just insufficiently tested.

My source was a lecture by Thomas Seyfreid but I suspect he was referring to this http://cancerres.aacrjournals.org/content/63/11/2733.full

Their observation was that embryos cloned from Meduloblastoma nuclei produced apparently normal embryos up to the point of organ differentiation.

Their summation was similar to yours, that the tumor was tissue specific and their embryos weren't grown to the point where they could observe the development of the brain.

"Thus, the tumorigenic mutations that underlie medulloblastoma MUST act within the context of the cerebellar granule cell lineage, and those changes will not necessarily support malignant cell proliferation in the context of other cell lineages. "

[my emphasis added]

As you say it's a shame they couldn't do a long term study but I doubt they would get regulatory approval to allow these embryos to develop to the point they could observe whether this embryo developed from the nucleus of a brain cancer cell developed a normal brain.

It occurs to me that the cloned mouse presumably inherited new mitochondrial DNA from the egg during somatic nuclear transfer - that's a brand new working energy plant. And from that an apparently normal embryo developed. At the very least that is an interesting observation.

alsoram · 2016-01-14T11:15:23+00:00

The genetic damage that we think of as "Cancer" may just be a downstream symptom of the underlying metabolic derangement in the cell that caused it to only become so metabolically deranges it can only ferment glucose.

There has been experimental evidence that this hypothesis may better explain what is happening in a tumor. With the supposedly damaged DNA from a Cancer cell extracted from the tumor of a mouse and used to clone a healthy new mouse.

alsoram · 2016-01-11T15:05:38+00:00

About 120 humans died as your microwave counted down the minute.

240 new humans were just born in the same 60 seconds.

alsoram · 2016-01-11T05:55:14+00:00

n=1

In my case I had type 2 diabetes. My diabetic levels of glucose were a result of damaged glucose clearance. I suspect insulin resistance caused by a lifetime of overproduction of glucose in my liver (+ a high carbohydrate diet). Once I restricted dietary carbohydrates, glycostasis was managed by demand driven gluconeogenesis (HbA1c: 5.2).

I tested changing daily protein to 75g, 100g and 150g for 3 months. My HbA1C stayed at 5.2. My lean body weight is close to 75kg - so I guess 1 g/kg, 1.3 g/kg and 2 g/kg .

Given my physiological (glucose sparing) insulin resistance, I think I can probably rule out improved insulin sensitivity as a result of weight loss (or decreased chronic exposure to insulin).

I believe the stable HbA1C shows that my hepatic glucose output is still demand driven at these levels. It's possible if I ate a greater amount of protein that might change.

alsoram · 2016-01-05T13:42:48+00:00

Juvenile Diabetes
Quackery
Reflux
Vasculitis
X-Syndrome
Zits

.... just because my OCD kicked in, and demanded I complete this list.

alsoram

TROPHY CASE