Before I go into the research that shows that all LDL can cause arteriosclerosis, let me give you a little history. The argument that only small particle LDL particles cause arterial issues almost always comes from those who want to justify having high LDL numbers. Western societies have notoriously high LDL numbers and we all want to feel good about the way we eat. So it’s very convenient to ignore LDL. However, below I will show you many reasons from the research why this is very naive thinking.
CAUTION: Some researchers have noted that it is the LDL-P that really counts and not the the LDL-C. LDL-C is the traditional LDL number that you and I are used to and that physicians commonly pull for our annual physical. LDL-P is known as the “particle count” and it is this nummber that correlates most powerfully with heart disease and atherosclerosis. So why do we use LDL-C? Well, the reason, at least in my mind is simple: most people who have hgih LDL-C problem usually have an LDL-P problem as problem. Now that is certainly not always true, especially for men who are on lower fat diets like myself, and who can sometimes have low LDL-C but higher LDL-P.
Also, many readers do not understand why I repeatedly emphasize arterial health. Again, as Dr. Steven Lamm emphasized: what’s good for the heart is good for the penis. Common sense tells you that you have to keep those penile arteries plaque-free if you want to maintain your erectile strength. Remember: that plaque will harden the arteries and limit nitric oxide – both of which are bad for erections.
1. Unoxidized LDL. Another apologetic argument of LDL disbelievers: “inflammation and oxidation are the causes of arteriosclerosis, not LDL!” Unfortunately, this simply does not hold in real life. One study noted that “native, unoxidized LDL has direct atherogenic effects, for example to enhance activated monocytes to produce the inflammatory mediators TNF-Î± and IL-8.”  Of course, TNF-alpha is the inflammatory cytokine playing a role in heart disease and dozens of other nasty chronic conditions.
2. Large, “Fluffy” LDL. Not only is large LDL plaque-building, but it is also a major player. The same study above stated:
“Finally, large cholesterol-rich LDL is the predominant type of LDL in familial hypercholesterolemia (44), and it is firmly established that this LDL is responsible for their premature atherosclerosis. Thus, large and small LDL are atherogenic, and it is not possible to judge which if any is more harmful, overall.” 
3. Intermediate LDL. Yes, there are all different sizes of LDL and even ones in the middle. Researchers call this kind IDL. And some kinds of IDL can be artherogenic: “These data suggest that IDL CE content may be a determinant of progression of coronary lesions and may be influenced by compliance with or metabolic response to lipid-lowering dietary advice in patients with coronary artery disease during simvastatin treatment.” 
- “long residence time in plasma
- enhanced oxidizability
- arterial proteoglycan binding
- permeability through the endothelial barrier”
And the research does indeed show that this kind of LDL is particularly viscious.  A number of studies have shown this clearly: “Particularly atherogenic forms of LDL include small, dense LDL particles and oxidized LDL. All lipoproteins that contain apolipoprotein B, such as LDL, very-low-density lipoprotein, and intermediate-density lipoprotein, tend to promote atherosclerosis.” 
5. All Arterial Plaque Reversers. There are a number of well-known doctors out there who are actually reversing arteriosclerosis. This is a remarkable accomplishment if you think about it, because heart disease is the number one killer of men. Every one of these clinicians includes in their practice a strong LDL-lowering in strategy. This includes the famous physicians Drs. Davis, Esselstyn and Gould for example. Each of them has their own protocol for lowering LDL, but all of them have a proven track record of reducing arteriosclerosis by starting with LDL as their base technique.
And what LDL levels do they want? Is LDL of 120+ like the typical American okay? Each of them wants LDL to be in the 60-85 range, something I document in my link on LDL Thresholds for Arterial Health. By the way, the books of these authors are a fascinating read and not all of them are traditional Low Fat. One rule that I really like Dr. Davis’ “Rule of 60” for plaque reversal: LDL < 60; HDL > 60; Triglycerides < 60.
6. Primal Cultures. Loren Cordain documented, in one of his early papers, how every modern primal culture with no heart disease had cholesterol below 150.  Of course, Loren Cordain is the founder and cheif apostle of the Paleo Diet, and many Paleo followers will be shocked to learn that Loren Cordain originally advocated LDL in the 50-70 range, because of the overwhelming eviden’ce of good health from these supposedly “primitive” peoples that were so heart healthy. 
Now cholesterol is not that relevant of a number, but cholesterol of 150 will almost always mean low LDL. If your cholesterol is low, then your LDL is very likely to be low as well and this is why Loren Cordain came to his original conclusions. Even the Masai, who ate boatloads of saturated fat had cholesterol right at 150. Some people say the Eskimo/Intuits had cholesterol greater than 150, but they also ate mountains of fish and suffered with severe osteoporosis-related issues because of their diet.
So what can you do? It is simple. I have a link with good starter information called How to Clear Your Arteries and I also highly recommend that you read the books of the above doctors. Particularly relevant is Prevent and Reverse Heart Disease by Dr. Esselstyn, both of whom generally advocate a drug-free approach.
1) https://thepaleodiet.com/wp-content/uploads/2012/11/JACC-LDL-Final.pdf, JACC, June 2, 2004:2142â€“62004, 43(11), “Optimal Low-Density Lipoprotein Is 50 to 70 mg/dl: Lower Is Better and Physiologically Normal”
2) The Journal of Clinical Endocrinology & Metabolism, Oct 1 2003, 88(10), “Low-Density Lipoprotein Size and Cardiovascular Disease: A Reappraisal”
3) Circulation, 2004, 109:III-2-III-7, “Atherosclerosis: Evolving Vascular Biology and Clinical Implications: Atherogenic Lipoprotein Particles in Atherosclerosis”
4) Can J Cardiol, 2001 Aug, 17(8):859-65, “A prospective, population-based study of low density lipoprotein particle size as a risk factor for ischemic heart disease in men”
5) Arteriosclerosis, Thrombosis, and Vascular Biology, 1998, 18:577-583, “IDL Composition and Angiographically Determined Progression of Atherosclerotic Lesions During Simvastatin Therapy”