Dr. Ben Bikman

One, it starts to reach a point of maximum dimension that it can't grow anymore, otherwise the cell membrane starts to lose its integrity and literally start to pop, which would be a very messy inflammatory process. And at the second, the fat cell, as it's swollen up to 10 or 20 times bigger than it used to be, is now suffocating. It's getting pushed too far from capillaries.

In other words, blood vessels where it can get oxygen and give it CO2 and get nutrients. So the fat cell starts to get too big and it starts to suffocate. This elicits two responses. When the fat cell starts to get so big, it starts to tell insulin, insulin, you are trying to make me big and yet I can't grow anymore. And so while you are trying to block me from breaking down my fat,

In other words, blood vessels where it can get oxygen and give it CO2 and get nutrients. So the fat cell starts to get too big and it starts to suffocate. This elicits two responses. When the fat cell starts to get so big, it starts to tell insulin, insulin, you are trying to make me big and yet I can't grow anymore. And so while you are trying to block me from breaking down my fat,

In other words, blood vessels where it can get oxygen and give it CO2 and get nutrients. So the fat cell starts to get too big and it starts to suffocate. This elicits two responses. When the fat cell starts to get so big, it starts to tell insulin, insulin, you are trying to make me big and yet I can't grow anymore. And so while you are trying to block me from breaking down my fat,

I'm not listening, and I'm going to start leaking fats. To say that in a more precise term, insulin normally inhibits lipolysis, which is the term for breaking down fat. That's the primary mechanism whereby insulin promotes the growth of a fat cell. Not necessarily force-feeding it, but preventing it from breaking it down.

I'm not listening, and I'm going to start leaking fats. To say that in a more precise term, insulin normally inhibits lipolysis, which is the term for breaking down fat. That's the primary mechanism whereby insulin promotes the growth of a fat cell. Not necessarily force-feeding it, but preventing it from breaking it down.

I'm not listening, and I'm going to start leaking fats. To say that in a more precise term, insulin normally inhibits lipolysis, which is the term for breaking down fat. That's the primary mechanism whereby insulin promotes the growth of a fat cell. Not necessarily force-feeding it, but preventing it from breaking it down.

So the fat cell says insulin fats are still coming in or glucose is still coming in but now I'm going to start breaking down fat even though you're trying to tell me not to. So one, the fat cell, the hypertrophic or swollen fat cell becomes insulin resistant to prevent further growth.

So the fat cell says insulin fats are still coming in or glucose is still coming in but now I'm going to start breaking down fat even though you're trying to tell me not to. So one, the fat cell, the hypertrophic or swollen fat cell becomes insulin resistant to prevent further growth.

So the fat cell says insulin fats are still coming in or glucose is still coming in but now I'm going to start breaking down fat even though you're trying to tell me not to. So one, the fat cell, the hypertrophic or swollen fat cell becomes insulin resistant to prevent further growth.

Leaking free fatty acids into the blood in the midst of elevated insulin and those two things should not be high at the same time. High insulin and high free fatty acids now means you're going to start storing fat in other places throughout the body, most especially the liver, getting fatty liver and excess fat in the pancreas, creating insulin resistance in those tissues.

Leaking free fatty acids into the blood in the midst of elevated insulin and those two things should not be high at the same time. High insulin and high free fatty acids now means you're going to start storing fat in other places throughout the body, most especially the liver, getting fatty liver and excess fat in the pancreas, creating insulin resistance in those tissues.

Leaking free fatty acids into the blood in the midst of elevated insulin and those two things should not be high at the same time. High insulin and high free fatty acids now means you're going to start storing fat in other places throughout the body, most especially the liver, getting fatty liver and excess fat in the pancreas, creating insulin resistance in those tissues.

But the second problem, as I mentioned, is that the fat cell becomes hypoxic. It starts to suffocate, if you will, as it's gotten pushed too far from the capillary. The fat cell has a potential solution for that too, and that is by secreting a bunch of pro-inflammatory cytokines into the bloodstream.

But the second problem, as I mentioned, is that the fat cell becomes hypoxic. It starts to suffocate, if you will, as it's gotten pushed too far from the capillary. The fat cell has a potential solution for that too, and that is by secreting a bunch of pro-inflammatory cytokines into the bloodstream.

But the second problem, as I mentioned, is that the fat cell becomes hypoxic. It starts to suffocate, if you will, as it's gotten pushed too far from the capillary. The fat cell has a potential solution for that too, and that is by secreting a bunch of pro-inflammatory cytokines into the bloodstream.

So the hypertrophic fat cell becomes very pro-inflammatory because some of those cytokines that it's secreting have the ability to promote the growth of new capillaries. And so it starts to correct its hypoxia by stimulating the growth of new fat cells, which is a better outcome than suffocating and becoming necrotic. You know, once again, a very messy, inflamed death if that were to happen.

So the hypertrophic fat cell becomes very pro-inflammatory because some of those cytokines that it's secreting have the ability to promote the growth of new capillaries. And so it starts to correct its hypoxia by stimulating the growth of new fat cells, which is a better outcome than suffocating and becoming necrotic. You know, once again, a very messy, inflamed death if that were to happen.

So the hypertrophic fat cell becomes very pro-inflammatory because some of those cytokines that it's secreting have the ability to promote the growth of new capillaries. And so it starts to correct its hypoxia by stimulating the growth of new fat cells, which is a better outcome than suffocating and becoming necrotic. You know, once again, a very messy, inflamed death if that were to happen.

So the hypertrophic fat cell, in order to ensure its own survival, becomes insulin resistant to prevent further growth, inadvertently thereby flooding the body with free fatty acids to be stored elsewhere, and two, becomes very pro-inflammatory in order to correct its own hypoxia, but in the process flooding the body with pro-inflammatory cytokines, things like C-reactive protein, for example, which is increasingly measured on blood tests.