filmov
tv
I was wrong about saturated fat.
Показать описание
#JohnnyColeDickson #Saturatedfat #Cholesterol
I was wrong about saturated fat. (read on below).
🟣If you read this, leave a like, it's free!
🟡🔋LMNT - get a free sample pack with any purchase!
CITES
📺Videos: mentioned:
- Ancel keys (butter) video:
- Livestreams:
- Sugar's sneaky impact on your blood:
Personal notes:
It's worth noting that lipids don't exclusively represent structure in the body. They are "concrete and bricks", but they are not ONLY concrete and bricks! Lipids are involved in energy production (think the fat on our bodies) and cell signaling (think membranes of our cells, trafficking, development, regulation + more). Although unlikely (and I haven't found anything of this nature), let's say cholesterol levels are increased by a specific lipid signaling pathway as a direct result of dietary saturated fat intake. Consider again, the weight of cholesterol in the overall conversation. We can rest assured that in the event dietary saturated fat causes more cholesterol production by way of our hypothetical signaling pathway that this would mean, for some reason, the body NEEDS that cholesterol. We must remember, cholesterol is not inherently bad- scratch that, we must remember cholesterol is vital to our existence. And if cholesterol is increased due to this proposed mechanism, we can't assume saturated fat is inherently bad either. Not to mention: cholesterol is a signaling lipid in and of itself.
Okay, what about lipid signalling on the immune system or oxidation production? Everything in the body represents a signal, every action the body takes warrants a pathway. When it comes to lipid signaling, we're regarding a vast and complex array of processes that affect many things, so let's hone it a bit. It's a great thing to know that lipids play crucial roles in communication. Saturated fat and unsaturated fat as we could imagine, don't communicate the same thing in every instance. This system/thought trail of lipid signaling on immunity, (for example, look into PUFA and SFA and macrophage signaling), would propose, I'd argue, the biggest merit for lipid signaling to be involved in the conversation of atherosclerosis (if we're talking specifically lipid signaling). But once we go there, we start to drift from the initial point of any of this: analyzing the most influential scientific message in American food history: the diet heart theory.
Regarding the context, the most relevant mechanism of cholesterol levels changing due to saturated or unsaturated fat intake has much more to do with what's proposed in this video than they do energy production (virtually irrelevant) or lipid signaling (bike shedding).
"Despite their ubiquitous presence, it is rare that a signaling
lipid is diagnosed as a causative agent in disease." [C]
Okay, but Johnny, aren't you being a bit too specific when you say things like "there is no mechanism for the saturation of a fat to influence cholesterol directly?" What about the interventional studies that show saturated fat increases cholesterol levels? For starters, consider the study's details, are they measuring by comparison[D] (SFA replaced by carb, protein, or PUFA)? Are they measuring quantity of LDL/cholesterol at all? or are they measuring quality?[E]. Were participants given ungodly amounts of SFA that wouldn't translate into "real world" application?[F (although, I do think this experiment is pretty cool!)]. Did the participants already have a preexisting condition?[G]. Were humans measured? We also must be careful to differentiate between LDL and cholesterol. But let's say we're talking about LDL (I'd argue most research is), remember LDL is benign until modified. There are types of LDL particles that are more susceptible to this "modification". So, the question to ask is: does saturated fat increase the chance of LDL becoming modified? Here's a narrative review of where the conversation is currently:[H].
Personal notes cont.
I was wrong about saturated fat. (read on below).
🟣If you read this, leave a like, it's free!
🟡🔋LMNT - get a free sample pack with any purchase!
CITES
📺Videos: mentioned:
- Ancel keys (butter) video:
- Livestreams:
- Sugar's sneaky impact on your blood:
Personal notes:
It's worth noting that lipids don't exclusively represent structure in the body. They are "concrete and bricks", but they are not ONLY concrete and bricks! Lipids are involved in energy production (think the fat on our bodies) and cell signaling (think membranes of our cells, trafficking, development, regulation + more). Although unlikely (and I haven't found anything of this nature), let's say cholesterol levels are increased by a specific lipid signaling pathway as a direct result of dietary saturated fat intake. Consider again, the weight of cholesterol in the overall conversation. We can rest assured that in the event dietary saturated fat causes more cholesterol production by way of our hypothetical signaling pathway that this would mean, for some reason, the body NEEDS that cholesterol. We must remember, cholesterol is not inherently bad- scratch that, we must remember cholesterol is vital to our existence. And if cholesterol is increased due to this proposed mechanism, we can't assume saturated fat is inherently bad either. Not to mention: cholesterol is a signaling lipid in and of itself.
Okay, what about lipid signalling on the immune system or oxidation production? Everything in the body represents a signal, every action the body takes warrants a pathway. When it comes to lipid signaling, we're regarding a vast and complex array of processes that affect many things, so let's hone it a bit. It's a great thing to know that lipids play crucial roles in communication. Saturated fat and unsaturated fat as we could imagine, don't communicate the same thing in every instance. This system/thought trail of lipid signaling on immunity, (for example, look into PUFA and SFA and macrophage signaling), would propose, I'd argue, the biggest merit for lipid signaling to be involved in the conversation of atherosclerosis (if we're talking specifically lipid signaling). But once we go there, we start to drift from the initial point of any of this: analyzing the most influential scientific message in American food history: the diet heart theory.
Regarding the context, the most relevant mechanism of cholesterol levels changing due to saturated or unsaturated fat intake has much more to do with what's proposed in this video than they do energy production (virtually irrelevant) or lipid signaling (bike shedding).
"Despite their ubiquitous presence, it is rare that a signaling
lipid is diagnosed as a causative agent in disease." [C]
Okay, but Johnny, aren't you being a bit too specific when you say things like "there is no mechanism for the saturation of a fat to influence cholesterol directly?" What about the interventional studies that show saturated fat increases cholesterol levels? For starters, consider the study's details, are they measuring by comparison[D] (SFA replaced by carb, protein, or PUFA)? Are they measuring quantity of LDL/cholesterol at all? or are they measuring quality?[E]. Were participants given ungodly amounts of SFA that wouldn't translate into "real world" application?[F (although, I do think this experiment is pretty cool!)]. Did the participants already have a preexisting condition?[G]. Were humans measured? We also must be careful to differentiate between LDL and cholesterol. But let's say we're talking about LDL (I'd argue most research is), remember LDL is benign until modified. There are types of LDL particles that are more susceptible to this "modification". So, the question to ask is: does saturated fat increase the chance of LDL becoming modified? Here's a narrative review of where the conversation is currently:[H].
Personal notes cont.
Комментарии