Juliegee wrote:Most resources suggest that the body makes up about somewhere between 2/3 and 80% of the cholesterol we need to stay healthy. The rest comes from food.
Do you have any references for “most resources”? I can’t find any evidence to suggest that we need any dietary sources of cholesterol. There are no lower limits set on dietary cholesterol. The European Food Safety Authority certainly doesn’t set a lower limit:
http://onlinelibrary.wiley.com/doi/10.2 ... .1461/epdf I’m sure we’d see a lot of health issues in vegetarians, especially vegans, if this was the case.
Juliegee wrote:My understanding is that’s the reason we need essential fatty acids- precisely because our bodies CAN'T make them.
It is true that we need essential fatty acids, of which there are two: alpha-linolenic acid (omega-3 PUFA) and linoleic acid (omega-6 PUFA). There is no requirement for saturated fatty acids or MUFAs, as the body can make these. Also, essential fatty acids don’t seem to be a part cholesterol synthesis. There is no mention here:
https://en.wikipedia.org/wiki/Essential_fatty_acid, here:
https://en.wikipedia.org/wiki/Essential ... teractions or here:
https://en.wikipedia.org/wiki/Cholesterol
My belief is that your essential fatty acid needs can be met by eating wholefoods, without the need to add extra oils, otherwise how did our ancestors manage? That said, our ancestors would have a got a lot of omega-3 from eating insects, so it may be best to supplement this if you don’t eat oily fish (or insects!). Vegetarians/vegans can use algal dha omega 3, but milled flax seeds can also provide AHA, which is converted into DHA.
Juliegee wrote:It’s interesting to consider hypobetalipoproteinemia. When I look up "symptoms," however, I see that they vary vary widely among sufferers of this disorder. Some are quite severe including neurological problems, blood clotting issues, vitamin deficiencies, fatty liver disease, failure to thrive, etc. Hardly the picture of health.
Only homozygotes with undetectable LDL levels have these problems. Heterozygotes are asymptomatic. Please understand that no matter how hard you try, you will never get your LDL as low as these people, probably not even via the use of drugs. The bottom line; unless you are a hypobetalipoproteinemia homozygote with virtual zero LDL or suffer Abetalipoproteinemia (again, virtual zero LDL) then you do not need to worry about low LDL.
Juliegee wrote:...he’s methodically demonstrated how our current thinking regarding cholesterol metabolism is backwards.
Do you really trust this one person, who has obvious biases, with his n=1 experiments, over thousands of research centres, universities and public health institutions across the globe? Is it really plausible that the entirety of the research community and the hundred years of accumulated research is all wrong, but yet he is right?
Do you know of Brown and Goldstein? In 1985, they won the Nobel Prize in physiology and medicine for their research into cholesterol and discovering the mechanisms of our LDL receptors. Their research has spanned over 40 years. Dave Feldman is software engineer that went on a low carb diet two or three years ago. Do you really trust this guy or think he’s more qualified on this topic than the likes of Brown and Goldstein?
Juliegee wrote:Dave has shown that a very low fat diet drives his LDL-P dramatically upwards and conversely, a hypercaloric high fat diet drives his LDL-P downwards.
I don’t know of Dave’s low-fat experiments, nor how they were composed. When I spoke to him recently he said he was trying to set up a low-fat vegan experiment, which I’ll be interested to see. From my understanding of the literature, LDL-P improves on low-fat, wholefood diets. In this paper, 73 participants on a low fat (< 10%) diet was shown to make significant changes to lipoprotein subclasses in the right direction. I recommend you look at the graphs in this paper;
Effects of cardiovascular lifestyle change on lipoprotein subclass profiles defined by nuclear magnetic resonance spectroscopy
https://lipidworld.biomedcentral.com/ar ... -511X-8-26
Effects of lifestyle changes on lipoproteins
The lifestyle intervention led to significant changes in NMR-defined lipoprotein subclasses, in particular, clinically important LDL variables that contribute to CAD risk (Figure 1). There was a clear beneficial effect on the total number of LDL particles, which decreased 8.3% overall in participants (p < 0.05 compared to controls). Likewise, sdLDL particles, which have been associated with CAD risk in several studies, decreased 9.5% during the program (p < 0.05 versus controls). Lifestyle changes also were effective in increasing both HDL (+1.0%; p < 0.01) and LDL (+0.8%; p < 0.05) particle size, while decreasing very-low-density lipoprotein (VLDL) size (-9.7%; p < 0.01) and large VLDL and chylomicron concentrations (-29.4%; p < 0.05)
And in this study, comparing two low carb diets, one high in saturated fat and the other low in saturated fat, everything was worse for the high saturated fat group;
Changes in Atherogenic Dyslipidemia Induced by Carbohydrate Restriction in Men Are Dependent on Dietary Protein Source
http://jn.nutrition.org/content/141/12/2180.full
Interestingly, small LDL concentrations were significantly reduced following the LCLSF diet period compared to the LCHSF diet period.
Total cholesterol, LDL-C, nonHDL-C, apoB, and total LDL were reduced following the LCLSF diet period compared to both the baseline and LCHSF diet periods.
But as I’ve mentioned before, you don’t need to worry about LDL-P if you’re not suffering metabolic syndrome. LDL-P is really only relevant in those suffering metabolic syndrome, something you very probably wouldn’t be suffering from if you have a healthy body weight and following a low-fat lifestyle.
But if LDL-P is decreased on a high fat diet and LDL-C is high then you are still in trouble. You’ve got less LDL particles, but the ones you do have are large and jam-packed full of cholesterol. As I’ve also mentioned, all LDLs are atherogenic, so do you really want big LDLs crashing into your artery walls, dumping their huge cargo?
In Brown and Goldstein’s work, they explain the workings of the LDL receptor and how it pulls back into the cell once the cell has received enough cholesterol. Cells can only accept so much cholesterol and can actually die if they receive too much. So what happens when your cells have all the cholesterol they need? There will be no or few cells accepting LDLs, so the LDLs just end up floating around in your arteries for extended periods, oxidizing and attaching to artery walls. And remember, SFA down regulates the liver’s LDL receptor activity. No cells taking up cholesterol and the liver not taking up cholesterol is a recipe for disaster. And, of course, this is even worse in ApoE4 carriers as our liver’s LDL receptors see impaired activity as well as increased LDL synthesis.
Just think about FH suffers, their liver’s LDL receptors function poorly, resulting in very high LDL and heart attacks at an early age. They tend to have low LDL-P with larger, ‘fluffy’ LDLs. Doesn’t sound too different to what I’ve described in the paragraph above, does it?
Evan A. Stein is another lipid researcher that, like Brown and Goldstein, has over 4 four decades of expertise in this area. This is a quote by him, which I got from the video I linked, and I pasting it here as it’s brilliant and very relevant here;
For the practicing clinician, however, the major argument for extending measurement of subclasses into the mass market is the hypothesis that one subclass is more atherogenic than another. Because evidence clearly indicates that all Apo B–containing particles are atherogenic, this reasoning is akin to the argument that an Uzi submachine gun is more deadly than an M16 or an AK47. Obviously all are potentially lethal, and although this assertion may interest gun aficionados, it matters little to law enforcement or to general public safety if the sole objective is disarmament!
Subclass studies have proliferated over the last few years, but many of these studies were funded or subsidized either by suppliers of the assays as a method to expand their use and move them into mainstream practice, or by pharmaceutical companies in an attempt to claim some advantage over other therapeutic agents, especially when the LDL-C or Apo B reducing ability of their drug was less competitive. Although these studies have created more heat, they provide little additional light.
Juliegee wrote:To my knowledge, no one has done more diet/cholesterol interaction investigations.
There are hundreds of metabolic ward studies that have studied the effects of SFA on lipids. Here is one meta-analysis of 395 of them:
https://www.ncbi.nlm.nih.gov/pmc/articl ... 006469.pdf The scientific community have done this to death. I really don’t see how Dave has done anything in his n=1 experiments that hasn’t already been done in the vast body of lipid research, spanning circa 100 years.
I’ve talked to Dave over social media and, to be honest, he seems like nice guy. More than I can say for the rest of the low-carb/keto crowd, as he does seem to be a little open to contrasting ideas. But I have to say, he has all the hallmarks of someone who has been misled by low carb pseudoscience and has become personally and emotionally invested in the low carb ideology. For example, he mentioned Ancel Keys in one of his videos, describing him as a cherry picker and the reason for the unfounded demonization of saturated fat. If he’d bothered to properly research this topic, he’s understand that virtually everything stated about Keys in the low carb community is just misrepresentation and complete lies. Anyone, including doctors, who mention these falsehoods about Keys should be immediately viewed with scepticism because either they haven’t done their research on this or they are using it as a way to confuse you and sell you a diet book. The worst of these lies were propagated by Gary Taubes and Nina Teicholz, but they seem to have their origin in Uffe Ravnskov’s book, The Cholesterol Myths. All of these authors have been completely debunked by various sceptics. If anyone reading this believes in the lies about Keys, then let me know and I’ll send you everything I know of that completely debunks these claims. (Sorry, went off on a bit of a tangent there).
Juliegee wrote:Functional HDL aids in reverse cholesterol transport and abeta clearance; both problems already associated with the E4 allele. Additionally, HDL delivers antioxidants to protect our slower transiting LDL from oxidation. You can play with our search engine to find topics surrounding this.
I do understand the role and importance of HDL. However, having lower HDL in a low LDL environment doesn’t seem to be a problem. This hasn’t shown to predict heart disease or events. High LDL combined with low HDL is definitely a problem and, combined with high triglycerides, usually represents metabolic syndrome.
Ok, I’ve spent a lot of time on this now, so I really need to get back to spending time with my family. I wish everyone on these forums the best of health.