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afraid of animal fats and cholesterol?
Replies
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When someone says to do your own research it's a red flag to me. Can you imagine going to a class to learn, but all the teacher says is to do your own research?
Having been in graduate school in multiple disciplines, yes, that's precisely what the teachers would tell us.
One has to wonder ... Ten pages of back and forth, everyone spouting the same positions they've put forward in other similar threads ... what exactly are we supposed to take away from this kind of thread, other than boredom?
Did the professors tell you to look it up on the internet? They never gave lectures? Never took questions from students?
Give me a break. That's not at all what I was saying.
Case in point: a professor writes down an equation and says something like, "it follows then that ..." or "it's intuitively obvious that ..." followed by another equation; then studying with friends you spend two hours figuring out what he was getting at. This happened to me many times in grad school.
Usually any equations put on the table are themselves following from earlier rules that have been stated. And at least at my university, claims have always been shown to be true in maths classes unless the professor intended them to be homework, they were obvious or largely irrelevant.
He could tell us to just look it up ourselves, but if understanding it is integral to understanding what follows in the same lecture, there's no way around explaining it.
But regardless, that's not what happens here, we're not at a university. We're people in a discussion about things with differing levels of knowledge of the subject, not having a lecturer who you can largely trust knows what he's talking about implicitly. Asking online person X to back up claims they made, especially if those claims go against things like official guidelines, is to be expected.
So the situation is more like your fellow student telling you "Yeah, the solution is 42! Just trust me on that." and you asking them the steps they went through.2 -
@vingogly
It occurs to me that my two posts directed to you sound harsher than I intended and I apologize. I mean you no disrespect. I enjoy reading your contributions since you are often a voice of reason and clarity in threads that tend to get wild and crazy.
I'm sorry I wasn't more careful to moderate my tone.1 -
AlabasterVerve wrote: »aqsylvester wrote: »aqsylvester wrote: »@aqsylvester what is your endgame? That we all follow the diet you think best for all? Clearly we are all doing fine as we are.
@J72FIT Thanks for the question. I really appreciate these forum conversations for how they push me to ask new questions, explore more research, and really understand the breadth and depth of ignorance/misinformation (and its sources). My eyes have really been opened up in so many ways.
In considering your question, I could probably write a book. Working as a nurse, I feel as if I'm on the front lines, witnessing the--I guess you could call it--"endgame" of human suffering related to diseases of lifestyle (diabetes, obesity, heart disease, stroke, cancer, dementia, the list goes on...). I care about my patients, and I want to help people prevent disease. So empathy is a major driving force. When you say, "we are all doing fine as we are," I'm not sure who all you include in the word "we." I believe that "we" are not doing fine, not at all.
If I can help point one person in the right direction by sharing evidence-based nutrition, I have done enough. It certainly changed my life.
If I could have it my way, mainstream nutrition, health, and pharmaceutical organizations would not be influenced by profit, but would instead put people, our future, and our planet first--I guess just a basic understanding that we are all connected, whether we realize it or not. In light of that, they would practice with ethics and empathy, and they would promote the truth. They would, for example, publish all research done, whether it showed a benefit to the profit of a company or not. They would promote healthy eating and treatment advice based on evidence, and not whether or not they can make money off us.
I guess, in my "endgame," if I could give you a big picture summary (as there are certainly lots and lots of details), people would 1. not be afraid to eat real food, even foods high in fat, saturated fat, and cholesterol--as they have been so unjustly demonized (and to our detriment); 2. they would understand the real dangers of processed foods and have an effective fear of them--as they have become so ubiquitous in our culture without much prudence or investigation (this connects us back to the real major causes of heart disease)
I started this thread to share real evidence about fat, saturated fat, and cholesterol, and that is just one small piece of the puzzle. Most people nowadays back off on the meaningfulness of restricting fat, the mainstream organizations have stopped pushing restricting cholesterol, and lastly, we are debating over saturated fat. I shared a plethora of meaningful, compelling data.. and I hope it reaches one person out there looking for truth because I used to be that person.
Well one area I certainly agree with you on is not being afraid of saturated fat. That said, I have no desire to make it the bulk of my calories. 30% is enough IMO.
Humans are multi variant creatures living in a multi variant environment. To that point, I think we have the capacity to thrive on many diets, some high carb and some high fat. Which is best? I guess we really won't know until the end.
I do appreciate your passion on this topic (albeit a little one sided) as I am passionate on the topic as well. My take: eat mostly whole real nutrient dense food, get adequate protein, fat and fiber and fill in the rest with carbs. Get plenty of exercise and sleep. Try to live in the moment and keep stress at bay. I think stressing about eating a perfect diet is probably worse then eating a not so perfect diet and not stressing about it.
As I tell all my friends and clients, "train hard, eat well, get plenty of rest and go live your life..."
I believe the rest will take care of itself.
What's funny is, it sounds like we are basically in agreement.
I also think humans do well eating mostly whole real nutrient dense food. I never once said, nor do I think everyone needs to eat a ketogenic diet. I do, however, believe it is a highly effective treatment for IR and obesity, among other things--and also excellent for disease prevention.
The state of ketosis is very beneficial to the human body, but even just going in and out of it can still provide substantial benefits. I imagine our ancestors went in and out of it depending on the time of day or the season of the year (whether or not starchy foods were available). In fact, most normal, healthy people go into a mild ketosis during the prolonged fast of sleeping (after 14 hrs or so). I'm sure I often go out of ketosis after meals, but quickly get back into it. Eating nutrient dense, whole foods probably does just as much for me as regular ketosis does when it comes to the newfound ease (did not have at all on a low fat plant-focused diet--no butter, no eggs, only lean meats and fish) I have with skipping meals or fasting.
I agree with much of what you're saying but I think it's important to point out that everyone does not respond favorably to forced nutritional ketosis. Or saturated fat. Regardless of the recent reviews and favorable low carb studies I think a little less certainty is in order.
Here's some thoughts from Peter Attia:
March 2015
Peter Attia clarifies his position on saturated fat on his blog Eating Academy. He cautions that high saturated fat intake -- 25% of calories and up high -- may not be benign for everyone. This coincides with the recent articles regarding bullet proof coffee.
"And contrary to what some (perhaps many) of you might think, I don’t believe this is a settled debate across the board. What do I mean by that (i.e., “across the board”)? Certainly in this presentation I try to make the case that the continually falling recommendations for SFA—from 12% to 10% to 8% to 5% of total calories—are not supported by convincing science. In fact, such recommendations likely do harm, courtesy of the “substitution effect,” i.e., people end up eating more of other things—namely, sugars and omega-6 polyunsaturated fats (n-6 PUFA)—that likely cause greater metabolic derangement.
However, some readers may interpret the data I present to mean it’s perfectly safe to consume, say, 25% (or more) of total calories from SFA. I realize I may have to turn in my keto-club card, but I am convinced that a subset of the population—I don’t know how large or small, because my “N” is too small—are not better served by mainlining SFA, even in the complete absence of carbohydrates (i.e., nutritional ketosis). Let me repeat this point: I have seen enough patients whose biomarkers go to hell in a hand basket when they ingest very high amounts of SFA. The leads me to believe some people are genetically equipped to thrive in prolonged nutritional ketosis."
Short excerpt above; the full post is worth a read for those of us who eat a LCHF diet:
Evidence for (and against) the dietary guidelines restricting saturated fat
http://eatingacademy.com/cholesterol-2/random-finding-plus-pi
May 2016
23:30: Ketogenic diets do not work for everyone. The efficacy of the ketogenic diets may have a genetic basis and it does not seem appropriate for everyone.
It's frustrating to a lot of patients because they just want this so badly to work and it doesn't. And there's no denying that. When you see their LDL-P skyrocket to 3500nmol/L, when you see their CRP skyrocket, when you see all of these changes that go in the wrong direction from a lipoprotein standpoint, inflammatory standpoint, from a hormonal standpoint. You can tweak it all you want you can say maybe there's too much omega 6 or maybe you gotta go more monounsaturated versus saturated fat but, you know, you've only got a handful of levers to pull there and in the end you sometimes just acknowledge that this diet is not optimal for this person. And yet, interestingly, I'll take that patient and I'll put them on a relatively carbohydrate restricted non-ketogenic diet and can have amazing results.
Episode 1: Peter Attia on how to live longer and better
http://www.ihmc.us/stemtalk/episode001/
Thanks, @alabasterverve
Yes, I have read this article once already. This is a reality that LCHF docs encounter, and why they are conducting research on it atm. You may have heard this talk from Dr. Sarah Hallberg:
https://youtu.be/w8jUmCe3zDs
The phenomenon seems to be common in the most insulin resistant patients--those with the greatest metabolic damage. This may be related to damaged ApoB receptors on the cells (meaning they can't uptake the LDL particles) or the effects of rapidly lowering serum insulin concentrations in insulin resistant patients, since insulin does play a role in down-regulating production of VLDL.
However, elevated LDL is not the main issue in heart disease, since LDL in itself is normal and not dangerous--it's oxidized LDL that is atherogenic (http://www.ncbi.nlm.nih.gov/pubmed/25318456)--mechanisms include: endothelial damage; alteration in vascular tone; monocyte/macrophage recruitment; increased uptake of LDL by macrophages, with foam cell formation; induction of growth factors; increased platelet aggregation; and formation of autoantibodies to oxidized LDL. Elevated plasma concentrations of oxidized LDL are associated with CHD (http://www.ncbi.nlm.nih.gov/pubmed?term=16000355). That's why the greatest risk factors are more tied to inflammation--like insulin resistance. The problem is, it's very difficult to measure oxidized LDL in the blood (http://circ.ahajournals.org/content/103/15/1930.full).
This is ultimately why--I think--that Cochrane Review showed no effect on hard end points (what really matters, i.e. death) with reducing SFA intake. We can increase PUFAs (in place of SFA... because replacing SFA with carbohydrates doesn't show benefit) in the diet in order to lower our LDL, but at what risk? What is causing the lowering LDL? While we need PUFAs (they are also present in meat and dairy, more so in grassfed, of course), they are also unstable and easily oxidized, especially from heating (for example, in the harsh production of vegetable and seed oils). If we are going to consume them, we need antioxidants to prevent oxidation. PUFAs interact with reactive oxygen species in the bloodstream to create these PUFA oxidation products, and since these products are not measurable with a standard lipid panel, it looks like LDL is going down, when in fact this is not a safe situation (another reason why a NMR lipid panel can be more helpful in determining what is going on).
"I have seen enough patients whose biomarkers go to hell in a hand basket when they ingest very high amounts of SFA."
"When you see their LDL-P skyrocket to 3500nmol/L, when you see their CRP skyrocket, when you see all of these changes that go in the wrong direction from a lipoprotein standpoint, inflammatory standpoint, from a hormonal standpoint. You can tweak it all you want you can say maybe there's too much omega 6 or maybe you gotta go more monounsaturated versus saturated fat but, you know, you've only got a handful of levers to pull there and in the end you sometimes just acknowledge that this diet is not optimal for this person."
Yes, I'm familiar with Sarah Hallberg. But don't statements like these give you any pause? Not about your own diet - I'm sure you do just as well eating a LCHF whole foods based diet as I do - but about recommending nutritional ketosis to any and everyone as a powerful cure all for metabolic issues without reservations?
I think your confidence that it's a-ok for all of these biomarkers to "go to hell in a handbasket" that some people experience on a ketogenic diet or with high intake of SFA's is premature.3 -
AlabasterVerve wrote: »AlabasterVerve wrote: »aqsylvester wrote: »aqsylvester wrote: »@aqsylvester what is your endgame? That we all follow the diet you think best for all? Clearly we are all doing fine as we are.
@J72FIT Thanks for the question. I really appreciate these forum conversations for how they push me to ask new questions, explore more research, and really understand the breadth and depth of ignorance/misinformation (and its sources). My eyes have really been opened up in so many ways.
In considering your question, I could probably write a book. Working as a nurse, I feel as if I'm on the front lines, witnessing the--I guess you could call it--"endgame" of human suffering related to diseases of lifestyle (diabetes, obesity, heart disease, stroke, cancer, dementia, the list goes on...). I care about my patients, and I want to help people prevent disease. So empathy is a major driving force. When you say, "we are all doing fine as we are," I'm not sure who all you include in the word "we." I believe that "we" are not doing fine, not at all. If I can help point one person in the right direction by sharing evidence-based nutrition, I have done enough. It certainly changed my life.
If I could have it my way, mainstream nutrition, health, and pharmaceutical organizations would not be influenced by profit, but would instead put people, our future, and our planet first--I guess just a basic understanding that we are all connected, whether we realize it or not. In light of that, they would practice with ethics and empathy, and they would promote the truth. They would, for example, publish all research done, whether it showed a benefit to the profit of a company or not. They would promote healthy eating and treatment advice based on evidence, and not whether or not they can make money off us.
I guess, in my "endgame," if I could give you a big picture summary (as there are certainly lots and lots of details), people would 1. not be afraid to eat real food, even foods high in fat, saturated fat, and cholesterol--as they have been so unjustly demonized (and to our detriment); 2. they would understand the real dangers of processed foods and have an effective fear of them--as they have become so ubiquitous in our culture without much prudence or investigation (this connects us back to the real major causes of heart disease)
I started this thread to share real evidence about fat, saturated fat, and cholesterol, and that is just one small piece of the puzzle. Most people nowadays back off on the meaningfulness of restricting fat, the mainstream organizations have stopped pushing restricting cholesterol, and lastly, we are debating over saturated fat. I shared a plethora of meaningful, compelling data.. and I hope it reaches one person out there looking for truth because I used to be that person.
Well one area I certainly agree with you on is not being afraid of saturated fat. That said, I have no desire to make it the bulk of my calories. 30% is enough IMO.
Humans are multi variant creatures living in a multi variant environment. To that point, I think we have the capacity to thrive on many diets, some high carb and some high fat. Which is best? I guess we really won't know until the end.
I do appreciate your passion on this topic (albeit a little one sided) as I am passionate on the topic as well. My take: eat mostly whole real nutrient dense food, get adequate protein, fat and fiber and fill in the rest with carbs. Get plenty of exercise and sleep. Try to live in the moment and keep stress at bay. I think stressing about eating a perfect diet is probably worse then eating a not so perfect diet and not stressing about it.
As I tell all my friends and clients, "train hard, eat well, get plenty of rest and go live your life..."
I believe the rest will take care of itself.
What's funny is, it sounds like we are basically in agreement.
I also think humans do well eating mostly whole real nutrient dense food. I never once said, nor do I think everyone needs to eat a ketogenic diet. I do, however, believe it is a highly effective treatment for IR and obesity, among other things--and also excellent for disease prevention.
The state of ketosis is very beneficial to the human body, but even just going in and out of it can still provide substantial benefits. I imagine our ancestors went in and out of it depending on the time of day or the season of the year (whether or not starchy foods were available). In fact, most normal, healthy people go into a mild ketosis during the prolonged fast of sleeping (after 14 hrs or so). I'm sure I often go out of ketosis after meals, but quickly get back into it. Eating nutrient dense, whole foods probably does just as much for me as regular ketosis does when it comes to the newfound ease (did not have at all on a low fat plant-focused diet--no butter, no eggs, only lean meats and fish) I have with skipping meals or fasting.
I agree with much of what you're saying but I think it's important to point out that everyone does not respond favorably to forced nutritional ketosis. Or saturated fat. Regardless of the recent reviews and favorable low carb studies I think a little less certainty is in order.
Here's some thoughts from Peter Attia:
March 2015
Peter Attia clarifies his position on saturated fat on his blog Eating Academy. He cautions that high saturated fat intake -- 25% of calories and up high -- may not be benign for everyone. This coincides with the recent articles regarding bullet proof coffee.
"And contrary to what some (perhaps many) of you might think, I don’t believe this is a settled debate across the board. What do I mean by that (i.e., “across the board”)? Certainly in this presentation I try to make the case that the continually falling recommendations for SFA—from 12% to 10% to 8% to 5% of total calories—are not supported by convincing science. In fact, such recommendations likely do harm, courtesy of the “substitution effect,” i.e., people end up eating more of other things—namely, sugars and omega-6 polyunsaturated fats (n-6 PUFA)—that likely cause greater metabolic derangement.
However, some readers may interpret the data I present to mean it’s perfectly safe to consume, say, 25% (or more) of total calories from SFA. I realize I may have to turn in my keto-club card, but I am convinced that a subset of the population—I don’t know how large or small, because my “N” is too small—are not better served by mainlining SFA, even in the complete absence of carbohydrates (i.e., nutritional ketosis). Let me repeat this point: I have seen enough patients whose biomarkers go to hell in a hand basket when they ingest very high amounts of SFA. The leads me to believe some people are genetically equipped to thrive in prolonged nutritional ketosis."
Short excerpt above; the full post is worth a read for those of us who eat a LCHF diet:
Evidence for (and against) the dietary guidelines restricting saturated fat
http://eatingacademy.com/cholesterol-2/random-finding-plus-pi
May 2016
23:30: Ketogenic diets do not work for everyone. The efficacy of the ketogenic diets may have a genetic basis and it does not seem appropriate for everyone.
It's frustrating to a lot of patients because they just want this so badly to work and it doesn't. And there's no denying that. When you see their LDL-P skyrocket to 3500nmol/L, when you see their CRP skyrocket, when you see all of these changes that go in the wrong direction from a lipoprotein standpoint, inflammatory standpoint, from a hormonal standpoint. You can tweak it all you want you can say maybe there's too much omega 6 or maybe you gotta go more monounsaturated versus saturated fat but, you know, you've only got a handful of levers to pull there and in the end you sometimes just acknowledge that this diet is not optimal for this person. And yet, interestingly, I'll take that patient and I'll put them on a relatively carbohydrate restricted non-ketogenic diet and can have amazing results.
Episode 1: Peter Attia on how to live longer and better
http://www.ihmc.us/stemtalk/episode001/
Thanks, @alabasterverve
Yes, I have read this article once already. This is a reality that LCHF docs encounter, and why they are conducting research on it atm. You may have heard this talk from Dr. Sarah Hallberg:https://youtu.be/w8jUmCe3zDs
The phenomenon seems to be common in the most insulin resistant patients--those with the greatest metabolic damage. This may be related to damaged ApoB receptors on the cells (meaning they can't uptake the LDL particles) or the effects of rapidly lowering serum insulin concentrations in insulin resistant patients, since insulin does play a role in down-regulating production of VLDL.
However, elevated LDL is not the main issue in heart disease, since LDL in itself is normal and not dangerous--it's oxidized LDL that is atherogenic (http://www.ncbi.nlm.nih.gov/pubmed/25318456)--mechanisms include: endothelial damage; alteration in vascular tone; monocyte/macrophage recruitment; increased uptake of LDL by macrophages, with foam cell formation; induction of growth factors; increased platelet aggregation; and formation of autoantibodies to oxidized LDL. Elevated plasma concentrations of oxidized LDL are associated with CHD (http://www.ncbi.nlm.nih.gov/pubmed?term=16000355). That's why the greatest risk factors are more tied to inflammation--like insulin resistance. The problem is, it's very difficult to measure oxidized LDL in the blood (http://circ.ahajournals.org/content/103/15/1930.full).
This is ultimately why--I think--that Cochrane Review showed no effect on hard end points (what really matters, i.e. death) with reducing SFA intake. We can increase PUFAs (in place of SFA... because replacing SFA with carbohydrates doesn't show benefit) in the diet in order to lower our LDL, but at what risk? What is causing the lowering LDL? While we need PUFAs (they are also present in meat and dairy, more so in grassfed, of course), they are also unstable and easily oxidized, especially from heating (for example, in the harsh production of vegetable and seed oils). If we are going to consume them, we need antioxidants to prevent oxidation. PUFAs interact with reactive oxygen species in the bloodstream to create these PUFA oxidation products, and since these products are not measurable with a standard lipid panel, it looks like LDL is going down, when in fact this is not a safe situation (another reason why a NMR lipid panel can be more helpful in determining what is going on).
"I have seen enough patients whose biomarkers go to hell in a hand basket when they ingest very high amounts of SFA."
"When you see their LDL-P skyrocket to 3500nmol/L, when you see their CRP skyrocket, when you see all of these changes that go in the wrong direction from a lipoprotein standpoint, inflammatory standpoint, from a hormonal standpoint. You can tweak it all you want you can say maybe there's too much omega 6 or maybe you gotta go more monounsaturated versus saturated fat but, you know, you've only got a handful of levers to pull there and in the end you sometimes just acknowledge that this diet is not optimal for this person."
Yes, I'm familiar with Sarah Hallberg. But don't statements like these give you any pause? Not about your own diet - I'm sure you do just as well eating a LCHF whole foods based diet as I do - but about recommending nutritional ketosis to any and everyone as a powerful cure all for metabolic issues without reservations?
I think your confidence that it's a-ok for all of these biomarkers to "go to hell in a handbasket" that some people experience on a ketogenic diet or with high intake of SFA's is premature.
No, it's not A-OK, IMO, especially not the CRP; however, exploring the root cause is important--which is what I'm talking about here. A LCHF doc can help tease out what's happening, especially with more advanced tests and diet inventory. In the meantime, tweaking the diet by introducing more whole food carbs might help. I personally doubt it's a genetic problem, most likely the cause of existing metabolic damage.0 -
They're saying the same thing about diabetes now; it's not you eating sugar but rather your overall lifestyle: overweight and inactive.
Same goes for blood pressure; don't Blame the salt. It's you're lifestyle.2 -
JeromeBarry1 wrote: »I've used an 81mg "baby" aspirin daily for several years. Let's call it a hypothetical that it will reduce inflammation, reduce atherosclerosis, and at the slight risk of induced bleeding on the brain and stomach ulcers be generally harmless. It was my own idea, as my GP seems to be hook-line-and-sinker in with the Cholesterol Theory of Heart Disease. The aspirin wasn't her idea. It was mine in response to reports several years ago explaining the inflammation root of atherosclerosis. I'm still alive. I have type B+ blood. I've read that B-type blood is a little thicker than other types. I do not subscribe to the Blood Type Diet. Still, I was regularly using 81 mg aspirin one day 4 years ago when I experienced an arhythmia of my heart. While seated at rest it suddenly began beating at 200 bpm. I was confused and didn't know what to do. I sat around the house for an hour with my heart running wild before I decided to go to the hospital. I drove myself. When I checked-in at the ER they sprang into action doing all the proper things and then, just as suddenly as it began, it stopped before the medical staff actually got any drug into me. They kept me a day before releasing me, finding no sign of damage. A cardiologist explained that the rapid contractions of the arhythmia can prevent oxygenated blood from reaching the heart muscle, directly causing heart damage and often death. We know that the risk of brain bleeds from aspirin is a result of the fact that aspirin thins the blood. I do believe that the thinning effect on my blood allowed just enough oxygenated blood to reach my entire heart muscle in that hour of indecision that I survived the event with no damage. I know this isn't a direct response to the "cholesterol' purpose of the discussion, but the first video did mention inflammation and I hope this story can help several someones survive surprises.
Aspirin doesn't thin blood, but reduces platelet aggregation. The lack of oxygen to the heart is because with the heart beating so fast, the chambers of the heart don't have enough time to fill properly with each beat, therefore reducing cardiac output (or blood flow aka oxygen) to the rest of your body. And the first place blood goes when it leaves your heart is the heart muscle itself. The action of the aspirin is actually to reduce the risk of atherosclerosis within the cardiac arteries themselves, thereby reducing risk of a heart attack or stroke. I'm glad you didn't wait around to go to the ER. Too many people die at home because they take too long to seek help for things like that.1 -
Another thread where feelings got hurt, hearts got broken, food plates got taken away yet still stays inconclusive.
At the end of the day this thread is like almost other big debates that ended on the note of
1. Life style matters
2. Good vs bad is based on how that certain food reacts with your body
3. Stay in your specific normal weight zone
4. Move/exercise/increase physical activity
5. Only bad food group or item or condiment is the one that gives YOU an adverse response.
However-I am tested a Keto diet on myself and all the FATS are coming from vegetables or flax seed or virgin coconut oil. I'm logging it daily and I'll post my results for interested parties.
See how I'm conducting research on myself !!2 -
So basically my takeaway is this: At best, SFA does not increase the chances of CVD, unless there is a genetic propensity but worse case, it can contribute. Or you can monitor/maintain SFAs at 10-15% of your diet, increase plant based carbs, increase things like fish and other unsaturated fats, exercise and lose weight and call it a day.
If I have time, I need to go back and look at all the studies that suggest that SFA didn't contribute to see what their average threshold was for SFA intake.2 -
So basically my takeaway is this: At best, SFA does not increase the chances of CVD, unless there is a genetic propensity but worse case, it can contribute. Or you can monitor/maintain SFAs at 10-15% of your diet, increase plant based carbs, increase things like fish and other unsaturated fats, exercise and lose weight and call it a day.
If I have time, I need to go back and look at all the studies that suggest that SFA didn't contribute to see what their average threshold was for SFA intake.
some more homework?
http://ajcn.nutrition.org/content/103/2/356.long
0 -
Gianfranco_R wrote: »So basically my takeaway is this: At best, SFA does not increase the chances of CVD, unless there is a genetic propensity but worse case, it can contribute. Or you can monitor/maintain SFAs at 10-15% of your diet, increase plant based carbs, increase things like fish and other unsaturated fats, exercise and lose weight and call it a day.
If I have time, I need to go back and look at all the studies that suggest that SFA didn't contribute to see what their average threshold was for SFA intake.
some more homework?
http://ajcn.nutrition.org/content/103/2/356.long
It definitely adds a bit more complexity. At 15% of your calories from SFA, it would suggest that where the SFA comes from matters (appears that the Dutch get a large portion of their SFA from dairy; ~33%).0 -
Gianfranco_R wrote: »So basically my takeaway is this: At best, SFA does not increase the chances of CVD, unless there is a genetic propensity but worse case, it can contribute. Or you can monitor/maintain SFAs at 10-15% of your diet, increase plant based carbs, increase things like fish and other unsaturated fats, exercise and lose weight and call it a day.
If I have time, I need to go back and look at all the studies that suggest that SFA didn't contribute to see what their average threshold was for SFA intake.
some more homework?
http://ajcn.nutrition.org/content/103/2/356.long
Nice, more than 97% of the population exceeded the upper intake limit of 10% of energy as recommended by the Health Council of the Netherlands--good for them! 15% was the population mean, and higher intake was associated with lower risk for heart disease. Replacing SFA with PUFA, MUFA, protein, or carbohydrates increased risk of heart disease.
If SFA came from dairy or solid fats, the risk was lower; if from meat, no difference--I suspect this is because any other source of SFA is likely to be more refined fats/processed foods.2 -
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