Asking Richard Morris for clarification

(jketoscribe) #1

On the FB page, @Richard said:

For someone who has stalled but still not at maintenance weight - their fat cells have become insulin sensitive enough to sequester energy, and they still overproduce insulin. MCTs may be a way to maintain sufficient ketones in circulation to prevent your brain demanding more glucose and/or slowing your metabolic rate in an apparent drought, to spare energy for essential services.

Richard, do you mind elaborating? Are you saying that MCT’s may feed the brain so that your body can use the stored energy better? It might help those of us whose weight loss has been stuck?


Not speaking got Richard but…
The brain is capable of running on 80% ketones and 20% glucose. If ketones are reduced, the brain will demand more glucose from the liver via hormonal signaling (glucagon). Glucagon is counter-regulated by secreting more insulin. A person who is over-producing insulin will benefit from maintaining ketone levels where the brain is happy at lower glucose levels.

(Richard Morris) #3

As I understand it one of the first breakdowns on the road to type 2 diabetes is that your fat cells become insulin resistant. Normally when insulin is high, fat cells respond by turning off the spigot of energy they supply to the rest of the body. That makes sense because if Insulin is high then you [normally] have OTHER caloric options and can hold the fat in reserve for when you have exhausted those other options and insulin goes low.

When you hear that insulin blocks lipolysis (fat burning) that’s one half of that story - fat cells hoovering up fat and holding onto it. The other half of that story is at the other end of the process where your cells are making energy from fuel in the blood … insulin inhibits their ability to rapidly burn fat.

So as we become insulin resistant our fat cells lose the ability to hold onto fat, but our cells still don’t use it well so we end up with a surplus of unused lipids in circulation.

So what happens when a person like that goes low carb? Their insulin drops, their cells all become better at burning fat for energy, circulating triglycerides drop, and their body fat not holding onto fat is now not a problem - it fuels a massive weight loss. These people draw down massive amounts of body fat and burn 60-80 lbs of the stuff. But then their fat cells are no longer stuffed they become more willing to listen to the signal of insulin.

This is why some people who are less insulin resistant go keto and get to their ideal range, and some of us who are more insulin resistant go keto, drop a massive amount quickly and then stall out. People who are insulin resistant make more insulin even when fasted. We stall when we run into the level of our insulin resistance … and it’s that our fat cells have become HEALTHY and doing their job that stalls us out.

How we get off that stall, is we spend more time in as low an insulin state as we possibly can and slowly we make less insulin for the same response – we become more insulin sensitive the longer we are not eating things that raise insulin.

So how does MCT help in this state? They turn into ketones even when insulin is high because they bypass that inhibition at the cellular level against burning fat when insulin is high. As Carol said if you have ketones your brain needs less glucose. If you are ketogenic then the ratio of glucose to ketones for your brain is 1:4. So every 1% reduction in ketones means a 4% increase in demand for glucose. Make less ketones, you have to make much more glucose, and therefore you need to make more insulin. And we’re trying to reduce insulin, chronically.

(Kathy L) #4

So, if weight loss has stalled-lower carbs more?

(jketoscribe) #5

And/or if weight loss is stalled raise MCT to increase ketones?

(Richard Morris) #6

If you have stalled then you need to lower insulin.

Carbs raise insulin. But what if you are eating almost no carbs.
Protein raises insulin. But you need a minimum amount of protein just to maintain your body.
Some people make too much insulin even when they eat nothing.

So the next step is to reduce your insulin resistance and that takes time on a low insulin diet (ketogenic) and the less insulin resistant you are the faster that reduction will be.

And then there are strategies and hacks for lowering insulin such as intermittent and extended fasting, muscle building and regular muscle depletion.

I believe that keeping ketones high enough to reduce the amount of glucose you need to make for your brain may reduce the amount of insulin you have to make. Eating some medium and short chained triglycerides can increase the amount of ketones you make.

(Ross Daniel) #7

I was thinking it was just the opposite effect which was the problem. Every cell in your body except fat cells become increasingly insulin resistant as you go down the road to T2D, so your fat cells become a sink for the energy your other cells “refuse” to take in. Because it has to go somewhere, it goes to fat cells and you get fat.

I’m certainly not saying @richard is wrong here, I may have my understanding turned around. This is gathered from a few books I’ve read over the past few months, so I could be mis-remembering the facts!


There are two stages. First, the high insulin levels cause increased fat storage, then the fat cells become resistant and dysfunctional and eventually fail to uptake the glucose. This is the stage when the liver becomes a fat repository and systemic IR becomes much worse.
Even non-obese people can be highly IR if their fat cells do not function correctly.

“Increased adipocyte size correlates with serum insulin concentrations, insulin resistance, and increased risk of developing type 2 diabetes (3–10). Obese subjects with few large adipocytes are more glucose intolerant and hyperinsulinemic than those having the same degree of obesity and many small fat cells…”

(Ross Daniel) #9

Awesome! thanks @carolT for the info.

This makes a ton of sense to me. The point at which the fat cells become resistant is basically where your weight would plateau and then that would be your “new normal” until they either get worse (more resistant) or better (less resistant). Us on the ketogenic diet are moving towards the less resistant fat cells, thus moving our homeostasis point lower. Whereas glucose burners are moving the needle in the opposite direction. Makes sense :grin:

(Kathy L) #10

Thank you -less carbs = more ketones -I think I have been a little lax which may be cause of stall. KCKO

(Richard Morris) #11

That’s how I used to view it too - fat cells being the energy consumer of last resort, and all other tissue becoming insulin resistant in the face of increasing amounts of insulin.

Then @erdoke gave me studies about a year ago that showed that the progressive failure of fat cells to sequester fat drives insulin up. This is a much simpler mechanism than those proposed for increasing systemic insulin resistance; namely;

whenever there is free fatty acids AND glucose in circulation, we need more insulin to shut off the free fatty acids so we can focus on the glucose.

Free fatty acids in circulation along with high insulin cause ectopic fat deposition in other tissues and that drives insulin resistance. This is something that has been experimentally shown in MRIs in England where they saw that reducing as little as 1g of ectopic fat in the pancreas is sufficient to completely reverse diabetes. And intramyocellular lipids in skeletal cells have been shown to be a trigger for them to develop insulin resistance. And as with all models, once compensatory hyperinsulinemia develops there will come a point where the pancreas can no longer keep up with demand for insulin - and glucose rises.

I believe it’s really just a nuance of the understanding of the progression of hyperinsulinemia.

(Ross Daniel) #12

Makes total sense to me now, that is great information to have. Especially the part about fat cells driving insulin up as they fail to hang on to the free fatty acids!

(Gabor Erdosi) #13

People like to think about fat cells (adipose tissue) as the place for long term energy storage that is only used when we cannot get enough food for longer periods. This was a dangerous misinterpretation of physiology. In fact, adipose tissue is the main regulator of metabolism both by providing place for continuous depositing and release of energy and by releasing hormones and cytokines (adipokines). There is a very delicate balance shifting between adipose tissue and the liver, more or less handing over direction of metabolism from the fasted to the fed state, respectively. Then there are different types and even subcategories of adipose tissues with specific roles. It’s been one of the biggest mistakes of modern medicine to vastly underestimate its roles.
In general, the more time you let your adipose tissue govern systemic metabolism the healthier you are and the better outlook you have on longevity.


Can you copy-paste that into a podcast for us? Pleeeese?