Hello, I'm trying to determine if higher LDL cholesterol levels that result from the fat burning cycle when fasted present the same risk as elevated LDL levels that result from eating a diet high in saturated fat that then causes elevated LDL cholesterol.
Putting it another way, if someone eats a healthy diet but does regular fasting or time restricted eating, during which the body consumes its own saturated fat (which I understood accounts for 1/3 of the body's fat stores), is that the same as eating the equivalent saturated fat?
Is there any actual research about this that people can to?
elevated LDL from fasting versus exogenous fat consumption
Re: elevated LDL from fasting versus exogenous fat consumption
Hi,
Good question,
I'm not aware of any direct study.
My gut feeling is that caloric restriction or fasting may act differently (immunosuppressive)
than dietary fat intake (especially saturated fat - immunosupportive).
Here is one study on keto and immunity which I think is very interesting.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8350890/
Very‐low‐carbohydrate diet enhances human T‐cell immunity through immunometabolic reprogramming
Good question,
I'm not aware of any direct study.
My gut feeling is that caloric restriction or fasting may act differently (immunosuppressive)
than dietary fat intake (especially saturated fat - immunosupportive).
Here is one study on keto and immunity which I think is very interesting.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8350890/
Very‐low‐carbohydrate diet enhances human T‐cell immunity through immunometabolic reprogramming
The question is whether APOE4 really needs that...Our data suggest KD as a feasible and effective clinical tool to augment human T‐cell immunity
BJ56 wrote: ↑Mon Jan 22, 2024 10:35 am Hello, I'm trying to determine if higher LDL cholesterol levels that result from the fat burning cycle when fasted present the same risk as elevated LDL levels that result from eating a diet high in saturated fat that then causes elevated LDL cholesterol.
Putting it another way, if someone eats a healthy diet but does regular fasting or time restricted eating, during which the body consumes its own saturated fat (which I understood accounts for 1/3 of the body's fat stores), is that the same as eating the equivalent saturated fat?
Is there any actual research about this that people can to?
JNB
ApoE 4/4, Male, Age 40+
ApoE 4/4, Male, Age 40+
Re: elevated LDL from fasting versus exogenous fat consumption
Really good question.
I'm in the same boat with high-ish LDL (4/150 to 5/190) and having all sorts of statins being waved in my face!
HDL is 1.3/52 ish
Trigs are 0.6/50 - 0.9/80
I'm in the same boat with high-ish LDL (4/150 to 5/190) and having all sorts of statins being waved in my face!
HDL is 1.3/52 ish
Trigs are 0.6/50 - 0.9/80
Apo E4/E4, Male, Age 61
Re: elevated LDL from fasting versus exogenous fat consumption
Honestly I was not bothering with my elevated LDL levels much as recent keto/carnivore hype says CVD is not caused by LDL, they say its all about insulin sensitivity and glucose, which might be true under some circumstances.
I personally don't believe humans evolved in keto, not even Eskimo are in keto.
Now I think that what is more determinantal is how diet and APOE type influences functions of immune system.
As I love Tsimane (they have no APOE2) yet the best hearts ever documented on the planet, and the decrease in their brain volumes with age is 70% slower than in Western populations.
Their energy levels, now mainly lipids and especially LDL are super low (but also glucose and triglyceride levels) compare to western populations. Their mean LDL for APOE 3/4 & 4/4 <100/2.6 across the whole spectrum of BMI!
the paper here, https://elifesciences.org/articles/68231 already mentioned on the forum
I suspect that APOE4 allocates its energy surplus to support its defense system (rather than store it).
It all sounds good until some threat appears... It seems as if the immune system of APOE4 runs hot (fueled by higher levels of LDL), it can easily get frenzy (if not tame well) destroying its own tissues rather than doing nothing.
Worms seem to know how to damp these reactions.
Tsimane are always under attack (of pathogenic bacteria, much higher levels of CRP, not like us) on a daily bases but worms calming down immune system that is especially more beneficial (cognition improved) for APOE4 with hotter arsenal.
The evidence here, Eosinophilia as hallmark of worms presence (the more the better, in a constantly hammering environment)
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5349792/
Actually to my taste, cognitive differences are tiny (but their differences of LDL between APOE types are also small).
I believe immune system is the key to neurodegeneration (apart of atherosclerosis).
What especially bothers me on very high LDL levels (e.g. being on keto) is
My personal strategy for near future is to lower my LDL levels as much as possible, with lifestyle and diet (no processed foods),
Tsimane have no statins.
I personally don't believe humans evolved in keto, not even Eskimo are in keto.
Now I think that what is more determinantal is how diet and APOE type influences functions of immune system.
As I love Tsimane (they have no APOE2) yet the best hearts ever documented on the planet, and the decrease in their brain volumes with age is 70% slower than in Western populations.
Their energy levels, now mainly lipids and especially LDL are super low (but also glucose and triglyceride levels) compare to western populations. Their mean LDL for APOE 3/4 & 4/4 <100/2.6 across the whole spectrum of BMI!
the paper here, https://elifesciences.org/articles/68231 already mentioned on the forum
I suspect that APOE4 allocates its energy surplus to support its defense system (rather than store it).
It all sounds good until some threat appears... It seems as if the immune system of APOE4 runs hot (fueled by higher levels of LDL), it can easily get frenzy (if not tame well) destroying its own tissues rather than doing nothing.
Worms seem to know how to damp these reactions.
Tsimane are always under attack (of pathogenic bacteria, much higher levels of CRP, not like us) on a daily bases but worms calming down immune system that is especially more beneficial (cognition improved) for APOE4 with hotter arsenal.
The evidence here, Eosinophilia as hallmark of worms presence (the more the better, in a constantly hammering environment)
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5349792/
Actually to my taste, cognitive differences are tiny (but their differences of LDL between APOE types are also small).
I believe immune system is the key to neurodegeneration (apart of atherosclerosis).
What especially bothers me on very high LDL levels (e.g. being on keto) is
We show that ketone bodies profoundly impact human T‐cell responses. CD4+, CD8+, and regulatory T‐cell capacity were markedly enhanced,
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8350890/CD8+ T‐cell response displayed markedly increased levels of interferon γ (IFNγ)
Chen found that, in cell culture, microglia activate T cells when given interferon-γ. Immune cells produce IFNγ in a range of infectious and other sickness conditions, and scientists have detected interferon-response microglia in models of neurodegeneration and in the AD brain (Mathys 2017; Sala Frigeiro et al., 2019).
https://www.alzforum.org/news/research- ... ts-t-cellsAn answer—at least for these mice—came when Chen ablated T cells by injecting tau/ApoE4 mice every five days with anti-CD4 and anti-CD8 antibodies, beginning at 6 months of age. By 9.5 months, their parenchymas were devoid of T cells. Strikingly, the pattern of phospho-tau staining placed them at a much earlier stage of disease than untreated littermates, and their microgliosis and atrophy were but a fraction (see image below)
My personal strategy for near future is to lower my LDL levels as much as possible, with lifestyle and diet (no processed foods),
Tsimane have no statins.
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JNB
ApoE 4/4, Male, Age 40+
ApoE 4/4, Male, Age 40+
Re: elevated LDL from fasting versus exogenous fat consumption
and regulatory T‐cell capacity were markedly enhancedJNB wrote: ↑Sat Jan 27, 2024 12:57 pm
We show that ketone bodies profoundly impact human T‐cell responses. CD4+, CD8+, and regulatory T‐cell capacity were markedly enhanced,
CD8+ T‐cell response displayed markedly increased levels of interferon γ (IFNγ)
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8350890/
But also to defend keto, Treg cells expression seems to be enhanced.
That would actually counteract the effect of increased T Cells expression, that would be good.
I don't know personally whether that is actually good. I cannot quantify the results, as I'm not a specialist.
Despite that, I still want to lower my LDL levels...
I'm still convinced immune system of APOE4 tends to be more overreacting and needs cushioning.
That's why worms help to improve cognition in APOE4 Tsimane.
https://en.wikipedia.org/wiki/Effects_o ... une_systemRook postulates that different parasitic worms suppress different Th types, but always in favor of regulatory T (Treg) cells
Worms should help with life extension similar to rapamycin (via their immunosuppressive effects), but they are way more gross than rapa.
JNB
ApoE 4/4, Male, Age 40+
ApoE 4/4, Male, Age 40+
Re: elevated LDL from fasting versus exogenous fat consumption
The only study I’m aware of is from the so-called “Lean Mass Hyperesponder” crowd: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9048595/
This is a very controversial area of study, with one crowd claiming that ultra-high cholesterol in otherwise metabolically healthy people following a ketogentic diet is not risky. With the other side being the bulk of the scientific community who believe in the LDL hypothesis. It gets pretty spicy on Twitter/X.
This is a very controversial area of study, with one crowd claiming that ultra-high cholesterol in otherwise metabolically healthy people following a ketogentic diet is not risky. With the other side being the bulk of the scientific community who believe in the LDL hypothesis. It gets pretty spicy on Twitter/X.
Dan
ε4,ε4
ε4,ε4
Re: elevated LDL from fasting versus exogenous fat consumption
Thank you for all the insights shared. Regarding the "lean mass hyperesponder" study, I wonder about ketosis without following a ketogenic diet: if 2/3 of the time you are in a fasted state, you're going to be partly in ketosis in that time regardless of diet. So assuming the established view where elevated LDL is an indicator of risk for heart disease, it seems like any kind of diet that raises fat metabolism will raise that risk. Maybe this risk is trivial, though, compared to other lifestyle choices (like high saturated fat consumption).
Also interesting points about auto-immune conditions based on factors (like diet) for ApoE4 types.
Also interesting points about auto-immune conditions based on factors (like diet) for ApoE4 types.
Re: elevated LDL from fasting versus exogenous fat consumption
This always goes in my mind, because we see slightly more prevalence in atherosclerosis with age in men than in women while opposite is true for AD. Why the difference if AD goes with CVD?
https://www.nature.com/articles/nri.2016.90Generally, adult females mount stronger innate and adaptive immune responses than males. This results in faster clearance of pathogens and greater vaccine efficacy in females than in males but also contributes to their increased susceptibility to inflammatory and autoimmune diseases.
And also we see a tendency for higher cholesterol in women.
JNB
ApoE 4/4, Male, Age 40+
ApoE 4/4, Male, Age 40+
Re: elevated LDL from fasting versus exogenous fat consumption
One could probably self-test this over a period of time (say 60 days) by doing the two routines 1. Intermittent fasting (say one meal a day, 3-8% or less SFA intake) and 2. diet higher in SFA, regular eating. (three meals a day, 15%+ SFA).
Then go get a NMR lipoprofile after each 60 day period and see the difference in the LDL particle size and count for comparison. I would think if the count comes in higher and the particle size lower, that would argue against the protocol -- irrespective of the LDL-C total.
Then go get a NMR lipoprofile after each 60 day period and see the difference in the LDL particle size and count for comparison. I would think if the count comes in higher and the particle size lower, that would argue against the protocol -- irrespective of the LDL-C total.
Re: elevated LDL from fasting versus exogenous fat consumption
Hmmm: that's a good point about LDL particle size and I agree that a self-directed study like this would resolve the question.