If one were to hear the words “lipoprotein” or “cholesterol” in a sentence, it might be expected that the next words would be “heart disease”, or “diabetes” or “metabolic syndrome”. However, while working alongside Dave and digging deeper into research on the lipid system, I found that surprisingly the next words were sometimes “infection” or “immune system” or even “protective”.
Immunological Velcro
The one who first pointed me towards the connection between lipoproteins and the immune system was Dave, back in 2017. He described how LDL could, in a sense, velcro itself to pathogens, binding to them. Just like a security guard tackling someone trying to cause harm, lipoproteins appear to be able to do the same with bacteria, viruses, and even with some parasites. By binding to the pathogen in this way, LDL can block its entry into our cells, leaving the pathogen vulnerable to clearance by immune cells. This appears to be the case with salmonella, where a 7-fold increase in LDL in the test mice resulted in a 95% survival rate, compared to a 0% survival rate in the controls.1 This difference was assigned to the high levels of LDL in itself, due to its binding capacity. This binding capacity is not common among all viruses and bacteria, but has been seen with the Herpes virus, as well.2
Calming the Storm
Beyond infecting cells directly, pathogens can cause damage in other ways – including exposing cells to toxins that they carry. One example is an endotoxin, called lipopolysaccharide (or LPS, for short), found in the membrane of some bacteria.3 High levels of exposure to LPS can result in immune activation that is so severe it cause problems like sepsis, which can be fatal.4
Lipoproteins, like VLDL and LDL, can circumvent this problem by binding to LPS, neutralizing it and lessening the need for further immune activation.5 Animal studies have shown that mice with low cholesterol, compared to those with normal levels, are more at risk of fatal sepsis when exposed to LPS6, and higher levels of cholesterol are even more protective.7 Lipoproteins have also been found to neutralize an endotoxin, lipoteichoic acid (LTA), found on the bacteria that cause staph infections.8
Help From the Sidelines
Endotoxins from bacteria aren’t the only thing that lipoproteins may help clean up, though. While fighting pathogens, immune cells use something called oxidative burst, where they use Reactive Oxygen Species (ROS) to harm or kill the invading organism.9 Reactive Oxygen Species are often painted as bad things, because they can cause damage and oxidative stress if they are allowed to run rampant. However, it has been proposed that LDL can be one way we keep our own cells safe during times where levels of ROS need to be higher for our own protection.10
“Lipoprotein oxidation during APR initially is likely to serve a beneficial purpose. Reactive oxygen species and free radicals are part of the local host defense mechanisms, […] Thus, lipoproteins may scavenge these free radicals to prevent systemic toxicity and membrane damage.”
Memon RA, et al (2000); PMID: 10845869
I also learned another way LDL can be used to fight infection from the sidelines – Nadir Ali was the first to bring to my attention that LDL can interrupt bacterial scouting missions. In order to determine if an environment is ideal for replication, bacteria will essentially send out probes to gain information and figure out if the environment is hostile or not, a process called quorum sensing. If the probe doesn’t come back, it’s determined the environment is not ideal, and replication does not occur. LDL can attach itself to these probes, ensuring they never return to the bacteria that sent them out, and giving the impression that it isn’t the best place for the bacteria to settle into.11
Musical Chairs
Lipoproteins can also indirectly block pathogens from entering cells – in this case, the lipoprotein may not be interacting with the bacteria or virus directly, but may instead be using something that the pathogen needs to get into the cell. Some examples of this are LDL preventing the virus that causes the common cold from entering through the LDL receptor12, or VLDL preventing invasion of Malaria into the liver via the VLDL receptor.13 Essentially, it’s a game of musical chairs, where the lipoproteins are taking up some of the seats, resulting in a higher chance of the pathogen being the one to be “out” – making it more likely that our own immune cells can capture them.
Passive Accomplices or Active Participants?
After reading over these potential uses of lipoproteins, a question came to mind: if lipoproteins can be used as a defense against various assaults, as the literature seems to suggest, is this only a passive defense? In other words, are only the VLDL and LDL that you already have around used, or are there ways to get more of them onto the field if needed?
It didn’t take long before I started to come upon terms like “the hypertriglyceridemia of infection”14, which gave a hint to the answer. Why would high triglycerides be important? Because these triglycerides are, by necessity, carried by lipoproteins! During infection, more fat is coming from fat tissue to the liver, and there is an increase in new fat being made in the liver, as well as an increase in production of cholesterol – all materials necessary for making lipoproteins like VLDL.15
This is the result of many changes during infection, however, not just one solitary cause. For one, some infections cause transient insulin resistance as a protective mechanism16, which could lead to high triglycerides in-and-of itself, but inflammatory signalling can also set off a cascade of reactions that ultimately result in high triglycerides, and high cholesterol during infection.17
“VLDL production during infection most likely represents a part of the acute phase response. […] In this manner, the anti-infective, protective effects of lipoproteins are maintained.”
Grunfeld C, Feingold KR. (1992); PMID: 1374564
During infection, more VLDL being made is paired with a longer residence time of the lipoproteins, due to a combination of factors.18 This increase in production and decrease in clearance would result in a higher total levels of lipoproteins in the blood, which may be beneficial. Similar to a dozen policemen more quickly being able to capture multiple criminals compared to half a dozen, the same principle may apply here, as well.19
A Small Part of the Whole
The mechanisms discussed here only cover a tiny part of the whole – the focus remained on VLDL and LDL, and some has still been left out for the sake of brevity, but immune involvement has also been seen with HDL, chylomicrons, and even lipoprotein(a). Further posts on the topic are sorely needed, but until then a question is left – with no certain answer. Although the mechanisms outlined here are intriguing, and some have been seen in both animal and human studies, whether this has any noticeable impact in the day-to-day human is unknown.
While there are some observational studies, which tie lower cholesterol to death from infection20, it is possible this is due to conditions that can result in lower cholesterol, such as cancer, also being linked to a weaker immune system.21 Although it’s clear that there is much more to investigate on this topic, the plausibility of LDL – and other lipoproteins – acting as a part of the innate immune system, in a protective role in humans is certainly an interesting one worth exploring further.
Citations
1 Netea, Mihai G et al. “Circulating lipoproteins are a crucial component of host defense against invasive Salmonella typhimurium infection.” PloS one vol. 4,1 (): e4237. doi:10.1371/journal.pone.0004237
2 Huemer H, P, Menzel H, J, Potratz D, Brake B, Falke D, Utermann G, Dierich M, P: Herpes Simplex Virus Binds to Human Serum Lipoprotein. Intervirology 1988;29:68-76. doi: 10.1159/000150031
3 Morrison, D C, and R J Ulevitch. “The effects of bacterial endotoxins on host mediation systems. A review.” The American journal of pathology vol. 93,2 (1978): 526-618.
4 Bone, R. C. “Gram-Negative Sepsis. Background, Clinical Features, and Intervention.” Chest, vol. 100, no. 3, Sept. 1991, pp. 802–08. PubMed, doi:10.1378/chest.100.3.802.
5 Cavaillon, J. M., et al. “Cytokine Response by Monocytes and Macrophages to Free and Lipoprotein-Bound Lipopolysaccharide.” Infection and Immunity, vol. 58, no. 7, July 1990, pp. 2375–82.
6 Feingold, K. R., et al. “Role for Circulating Lipoproteins in Protection from Endotoxin Toxicity.” Infection and Immunity, vol. 63, no. 5, May 1995, pp. 2041–46.
7 Netea, M. G., et al. “Low-Density Lipoprotein Receptor-Deficient Mice Are Protected against Lethal Endotoxemia and Severe Gram-Negative Infections.” Journal of Clinical Investigation, vol. 97, no. 6, Mar. 1996, pp. 1366–72. Crossref, doi:10.1172/JCI118556.
8 Sigel, Stefanie, et al. “Apolipoprotein B100 Is a Suppressor of Staphylococcus Aureus-Induced Innate Immune Responses in Humans and Mice.” European Journal of Immunology, vol. 42, no. 11, Nov. 2012, pp. 2983–89. PubMed, doi:10.1002/eji.201242564.
9 Amulic, Borko, et al. “Neutrophil Function: From Mechanisms to Disease.” Annual Review of Immunology, vol. 30, 2012, pp. 459–89. PubMed, doi:10.1146/annurev-immunol-020711-074942.
10 Memon, R. A., et al. “Infection and Inflammation Induce LDL Oxidation in Vivo.” Arteriosclerosis, Thrombosis, and Vascular Biology, vol. 20, no. 6, June 2000, pp. 1536–42.
11 Peterson, M. Michal, et al. “Apolipoprotein B Is an Innate Barrier against Invasive Staphylococcus Aureus Infection.” Cell Host & Microbe, vol. 4, no. 6, Dec. 2008, pp. 555–66. PubMed, doi:10.1016/j.chom.2008.10.001.
12 Hofer, F., et al. “Members of the Low Density Lipoprotein Receptor Family Mediate Cell Entry of a Minor-Group Common Cold Virus.” Proceedings of the National Academy of Sciences of the United States of America, vol. 91, no. 5, Mar. 1994, pp. 1839–42. PubMed, doi:10.1073/pnas.91.5.1839.
13 Sinnis, P., et al. “Remnant Lipoproteins Inhibit Malaria Sporozoite Invasion of Hepatocytes.” The Journal of Experimental Medicine, vol. 184, no. 3, Sept. 1996, pp. 945–54. PubMed, doi:10.1084/jem.184.3.945.
14 Grunfeld, C., and K. R. Feingold. “Tumor Necrosis Factor, Interleukin, and Interferon Induced Changes in Lipid Metabolism as Part of Host Defense.” Proceedings of the Society for Experimental Biology and Medicine. Society for Experimental Biology and Medicine (New York, N.Y.), vol. 200, no. 2, June 1992, pp. 224–27. PubMed, doi:10.3181/00379727-200-43424.
15 Beisel, W. R., and R. W. Wannemacher. “Gluconeogenesis, Ureagenesis, and Ketogenesis during Sepsis.” JPEN. Journal of Parenteral and Enteral Nutrition, vol. 4, no. 3, June 1980, pp. 277–85. PubMed, doi:10.1177/014860718000400307.
16 Šestan, Marko, et al. “Virus-Induced Interferon-γ Causes Insulin Resistance in Skeletal Muscle and Derails Glycemic Control in Obesity.” Immunity, vol. 49, no. 1, July 2018, pp. 164-177.e6. Crossref, doi:10.1016/j.immuni.2018.05.005.
17 Glass, Christopher K., and Jerrold M. Olefsky. “Inflammation and Lipid Signaling in the Etiology of Insulin Resistance.” Cell Metabolism, vol. 15, no. 5, May 2012, pp. 635–45. Crossref, doi:10.1016/j.cmet.2012.04.001.
18 Feingold, K. R., et al. “Endotoxin Rapidly Induces Changes in Lipid Metabolism That Produce Hypertriglyceridemia: Low Doses Stimulate Hepatic Triglyceride Production While High Doses Inhibit Clearance.” Journal of Lipid Research, vol. 33, no. 12, Dec. 1992, pp. 1765–76.
19 Netea, M. G., et al. “Bacterial Lipopolysaccharide Binds and Stimulates Cytokine-Producing Cells before Neutralization by Endogenous Lipoproteins Can Occur.” Cytokine, vol. 10, no. 10, Oct. 1998, pp. 766–72. PubMed, doi:10.1006/cyto.1998.0364.
20 Shor, Renana, et al. “Low Serum LDL Cholesterol Levels and the Risk of Fever, Sepsis, and Malignancy.” Annals of Clinical and Laboratory Science, vol. 37, no. 4, 2007, pp. 343–48.
21 Sharp, S. J., and S. J. Pocock. “Time Trends in Serum Cholesterol before Cancer Death.” Epidemiology (Cambridge, Mass.), vol. 8, no. 2, Mar. 1997, pp. 132–36.
What an enlightening, well-written post. Thanks Siobhan!
Thank you! I’m glad you enjoyed. 🙂
As someone with selective IgA deficiency, it makes me glad to have very high LDL reading this… it’s probably all that’s saving me from being sick all the time!
I have a very high LDL (over 300) and low white blood count. I wonder if it is connected?
Not sure – could you post a little more detail (if you’re comfortable doing so)? E.g. HDL, trigs, and WBC count? 🙂
Great post!
Thanks! 🙂
Siobhan . . . the following piece of history may interest you . . .
THE NATURE OF ANTISTREPTOLYSIN ” S ” IN THE SERA OF MAN AND OF OTHER SPECIES: ANTISTREPTOLYSIN TITRES IN NORMAL AND DISEASED STATES.
J H Humphrey 1949
This was before lipoprotein fractions had been identified . . . . that was a year or 2 away.
He noted evidence that showed the haemolytic toxins were produced by streptococci. – 2 identified (1938)
(a) Toxin: Streptolysin “O” – was known as a strong antigen, inactivated by O2 – produced antibodies (anti-streptolysin “O”) – On infection there was sharp rise in titre of the anti-streptolysin “O”antibody.
(b) Toxin: Streptolysin “S” – not give rise to antibodies – but there was clear evidence of some inhibitory agent in the blood. (1931)
Called this unidentified serum agent anti-streptolysin “S” (AS-S) . . [We would identify as a lipoprotein]
AS-S did not appear to be an antibody
Describes studies (1939) trying to see the effect of AS-S against infections but had difficulties because they found AS-S in several species of animals that clearly had not had a streptococcal infection.
[It would appear AS-S is not highly specific for pathogens]
Describes some evidence of AS-S titres lowering on infection
From Humphrey’s study – – – – – –
Did a load of work on infected rabbits and horses to test his assay of AS-O and AS-S anti-sera.
Measured the AS-S and AS-O levels in people with various illnesses
No of sera AS-S AS-O
Range. Mean. Mean.
Scarlet fever – acute . . 8 3 – 2-8 6.3 35
Convalescent . . (14-16 days). 8 4 – 8 6.2 240
Streptococcal pharyngitis – acute 4 4.6 – 7 5.2 410
Sub-acute and convalescent . 4 2 – 9.5 6.1 240
Rheumatic fever – acute . . 8 5.6 – 7 6.3 428
Sub-acute . . . . I6 4 – 10 6.7 261
Convalescent . . . I5 5.3 – l2.5 8.4 275
Rheumatoid arthritis – acute . 4 5.3 – 9.5 6.5 92
Sub-acute . . . . 4 4.7 – 8 6-3 130
Normals (Controls) . . . . 14 8 – 12-5 9.7 48
Points from table . . .
• AS-O behaves like antibody: lower in normals . . . rises in ill people – falls on convalescence
• AS-S is lower in all infections than the average level in ‘normals’
• AS-S rises in convalescence
• AS-S Not behave like antibody
Also . . .
Noted that the AS-S appears to have properties of “lipo-nucleoproteins”.
Also noted that AS-S had no immunization properties unlike AS-O
—————————————
In 1950 a paper by Gene Stollerman . . .
“The association of lipoproteins with the inhibition of streptolysin S by serum.”
Showed that one particular fraction was most potent . . . VLDL? LDL?
Damien
That’s very interesting, thanks for posting! I will have to look into that a bit more. 🙂
Fascinating that this was showing up so long ago, even before we knew further details.
Insightful and thought provoking. Thank you.
You are welcome! Glad you enjoyed 🙂
Do we know if the protective effect is predominently linked to higher levels of LDL-C or LDL-P?
LDL-P is what is binding to pathogens/endotoxin/etc. Although the cholesterol content may be helpful to immune cells in certain situations.
What is happening in regard to CoVid19 ?
Hi, is this a general question or did you have something specific in mind? Dave has been the one to mostly cover COVID-19 info, and although I don’t discuss COVID-19 specifically I do have a post more relevant to viral infections here.
I hope that helps, but if not feel free to clarify and I’ll see if I can help a bit better. 🙂
New study in Spain confirms protección against sars-2, published yesterday.
Interesting – would you mind linking the study?
The flood of evidence that high levels of LDL are possibly protective does not appear to making any inroads to mainstream medical thinking? I honestly wonder why this is.
Stephen,
My guess is, inconvenient information! Not good optics to report that avoiding what we thought would kill you might just kill you instead!
beautifully put. Thx
Not good for Big Pharma statin producers. Big Pharma controls.
Because virus spikes are lipoproteins themselves, and the more lipoproteins in the system the more competition there is for receptors.
Reasons: Wilful ignorance, group thinking, and not being well-educated in simple biostatistics.
As a physician, I have come over to the anti-statin side a decade ago when I noticed quite a few patients having side effects with statins I used to prescribe. Quite risky to go against the crowd…
In addition to ref 20 above, see doi: 10.1186/s13054-016-1579-8 “In this large, prospective cohort study, low LDL-C was associated with increased long-term rates of community-acquired sepsis.”
and
doi: 10.1016/j.jcrc.2015.01.001 “Low levels of plasma lipids, particularly low HDL and LDL cholesterol on day 7, was predictive of adverse outcomes in patients with severe community-acquired pneumonia who needed ICU admission.”
— more evidence that low levels of LDL are associated with sepsis risk.
Then this: doi: 10.1001/jamanetworkopen.2018.7223 published this year using measured LDL-c, and genetic risk score which they say correlated with measured LDL-C levels (though no reference is given). Although measured LDL-c was inversely associated with sepsis, the genetic model did not, which led to the conclusion “Levels of LDL-C do not appear to alter the risk of sepsis or poor outcomes directly in patients hospitalized with infection.” — a conclusion I can’t get my head around. ????? I still can’t see how they generate a ‘genetic risk score’ or what this means????
Two of the authors declare they have previously received grants from Amgen — who make the PCSK9 inhibitor evolocumab (Repatha). Could it be that the manufacturers of drugs to drastically lower LDL wouldn’t want the possible link between LDL and immunity known too widely particularly as their drugs could lower a patient’s LDL greatly? Just saying.
I’ll have to look at the studies you mentioned, I’m curious as to the genetic factor as well.
Now I am wondering about the lipid profiles of those with tuberculosis, malaria, ebola, HIV, and essential thrombocytosis… among other issues…
genetic risk score i am led to believe is all about lifestyle choices which tend to run in families
This is a great article and a breath of fresh air, because it add art, music and engineering sense to the dry science most physicians just pass on without any intention to dig deep into or make something off of
Glad you enjoyed 🙂
Dave-I’m a hyper-responder. Are you still doing a study on this? I heard or read you were looking for people to enroll in this study. Is this still true? Is so how can I do this?
Currently not recruiting but you may want to join the Lean Mass Hyper-responder and/or cholesterolcode facebook groups as news would be posted there if there are any updates. 🙂
[…] Article I found interesting: LDL and the Immune System. […]
Thanks, that is very clear, concise and easy to read without getting a headache 🙂
So are you saying that the research is suggesting that high LDL may be an indication that the immune system is “fighting off” infection and disease… NOT causing it ?
In an analogy, if we used conventional medicine’s reasoning, doctors would be saying that because there are lots of police cars found near the site of a crime, it must be that police cars cause crime which is the kind of ludicrous and faulty reasoning which can be inferred by naive researchers who tie correlation to causation. Yes, there are police cars at crime scenes but unless you know why they are there, you can’t conclude they cause crimes.
Is there research as to “why” atherosclerosis occurs? Is the cholesterol plaque building up at sites because it is trying to attach to a pathogen or virus or cell wall damage in order for it to be
carried away by the immune system ?
And here’s another question? If an elevated LDL is part of the immune system response,
does taking a statin suppress our immune system’s ability to fight heart disease ?
I know that in my own N=1 experiments, when I stopped taking my statin, I felt “less sickly” and my health improved. Then, when I began Keto and stuck with it for a few months, my health
improved even more, my lymphedema in my legs went away. I stopped being sick and tired and felt energy returning. It is only N=1 but it is consistent with the idea that conventional medicine and pharmaceutical companies may be very wrong about the role of lipids in the human body.
Glad you enjoyed. 🙂
I think it is possible that there are harmful and plausibly benign environments that can lead to higher LDL. The harmful environments would be something like chronic immune activation, metabolic syndrome, etc. I would not find it surprising if these were harmful because of what is causing the symptoms (e.g. the environment causing the disease), not the symptoms themselves (including high LDL).
The plausibly benign reasons include energy transport, and self-resolving infection/injury.
Injury/infection and metabolic syndrome can look similar, but the main difference is one resolves itself and the other does not (possibly because of a constant trigger). I find it useful to look at this context.
There is a lot of research, but I don’t think it is conclusive yet.
Although there can be bacteria/pathogens found in atherosclerotic plaque it’s important to remember that the immune system is more than just pathogen clearance, as you mentioned. The immune system is also involved in injury repair, protection against oxidation (such as induced by smoking), and healing. There are indeed some models of induced atherosclerosis that involve intentionally injuring the artery, so it may be that this is akin to what we’re seeing just over a longer timespan.
I don’t know. Statins actually have multiple methods of action (reduction in inflammation, direct effects on immune cells) beyond just LDL reduction, so it would be difficult to say. Not only that but our compensatory pathways during infection (e.g. increased cholesterol recycling/recirculation) may be sufficient to function properly regardless. It is tough to speculate on this as I’ve not seen studies on it.
Possibly, but it could also be overall increased health from the diet change, not necessarily the cholesterol in itself – just to play devil’s advocate. It is something I commonly hear from low carbers though – that they get sick much less often. I don’t know why that is, but I would love research to be done on it, it is definitely interesting.
Meanwhile, back in 2003 Uffe Ravnskov wrote:
High cholesterol may protect against infections and atherosclerosis | QJM: An International Journal of Medicine | Oxford Academic
https://academic.oup.com/qjmed/article/96/12/927/1533176
Sure! Plenty of people have been relaying the same information back for quite a while before I was even aware of it. 🙂
Sometimes it’s just helpful to restate things.
Great post!
[…] Article I found interesting: LDL and the Immune System. […]
Great article. Iam assuming this is why people on a LCHF lifestyle are less prone to get sick.
It might be – but there might be other parts to it too. Definitely more research needed on that front, for sure!
Hello Siobhan and Dave and the team. A question (set of questions) I wanted to ask during the conference, Thursday-Saturday was the relationship between body shape, physical presentation, and lipids. For example (Eric Berg has 4 body types); round belly, thin legs, thinner through the truck from the rearview (Santa Clause type?); rounded hips on the rearview, thick thighs, thin over knees and smaller ankles; thicker/solid and broad spread fat over the rib cage/shoulder/lung area view from rear, with smaller hips, thin legs/ankles, bust wider than shoulders; and thick and broad thighs, streaming down to thick knees and ankles, but thinner view of chest over rib cage and smaller bust, slim waist no rounding over intestines but broad across hips
(possibly lipedema) . Do the LDL, HDL, Triglycerides triangle vary noticeably between these body types and are the all-cause mortality and risk profiles for CVD?
My other set of questions that came to mind during the conference over the past few days was in relation to Dr William Davis’s focus on colon bacteria and diversity of colonies, and Craig Emmerich’s presentation on bowel flora (or bowel fauna?) … if there is very low breadth of diversity in the lower colon and someone is eating higher seed oil, refined/dried and/or liquified fruit, predominantly processed/refined grains, limited fresh vegetables and unnatural meat, and rarely get natural sunlight in their eyes or on their spine… is their bacteria colony in the lower colon different to people who eat natural fats, no factory-produced seed oils, natural meat, a variety of leafy greens and bright natural, recently picked, freshly sliced savory fruit and get outdoor sunshine in the eyes and on the spine… AND what do these people have in regards to the Triangle LDL HDL and Triglycerides and what does colon bacteria and leaky gut have to do with all-cause mortality and liver conditions including hyperinsulinemia …. not questions that can be answered easily, just something that I was asking myself during the conference.
[…] in the bloodstream (potentially immune/repair) for 2-4 […]
I wonder if my heterozygous FH, on a low-carb diet, is what keeps me from getting sick? I’m 49 years old, been keto for about 2 years now, and I NEVER get sick. My ApoB receptor efficacy is at 60%. So that means roughly 40% of my VLDL/LDL just float around in my blood, waiting to tag invaders, until they get recycled – all because they can’t dock properly with the LDL-R sites on my cells. And that could mean an evolutionary advantage for low-carb diets. It’s an interesting rabbit-hole…
I love the discussion! I just hope that one dose of Repatha I took, does not destroy my immunity in these times of covid-19.
Hi – while we can’t say whether or not certain medications would impact your immunity in particular, I am actually working on an update post that focuses on viral immunity and the lipid system in particular. There’s some complexity and nuance involved when addressing viruses in general that you might find interesting, although there’s no way to say how this may apply to the current situation without more information/data (hopefully forthcoming). It might still be of interest, regardless, and fun to learn about at least. Keep an eye out!
Hi, great article. Do you have any insight to how high LDL cholesterol could affect Covid-19?
Thank you!
Hi, unfortunately I don’t think we have enough data to even speculate. Hopefully once everything settles down there will be some nice datasets from big populations and we can look into it from there.
As far as during the infection, it does seem to lower cholesterol acutely as described in the post, though, so there is that similarity.
But how LDL levels relate to risk of getting it – I’ve not seen anything yet that says much one way or the other.
Hi- I tested positive for covid19 on 4/14. My symptoms started on March16. It’s been over 50 days that I’m battling the virus. I get a good day every 2 weeks or so and then another cycle starts. Each cycle varies in intensity and normally lasts 2 weeks. My LDL/VLDL are 55/15. I diet and take medication to lower my cholesterol. Let me know what you think.
Hi – thanks for sharing your data and experience. I hope you get well soon!
As I said in the prior comment it’s too soon, in my opinion, to speculate and we certainly can’t comment on medication either (especially as we have little information on it). If you wouldn’t mind though, would you mind sharing what your HDL and triglycerides are, for added context?
And have you gotten your cholesterol measured while sick – or is this from before? Just wondering – thanks again!
HDL 40
Triglycerides 73
These numbers are from end of October last year. Thx
Gotcha – thanks for sharing the additional info! Would be interested if you get updated bloodwork once you recover to see if it has changed much/at all.
My LDL it’s 496 my triglycerides or 48 my hcl is 95 my CRP is .3 my insulin is 4. Should I be worried.
Hi – we can’t say whether you should worry or not, because we’re not doctors. However, we can point you to some resources that may be helpful.
For example. Based off of your cholesterol numbers, it looks like you fit the profile of a Lean Mass Hyper-responder. In other words, someone who is generally lean, and/or active. You may want to check out the Lean Mass Hyper-responder facebook group as there are many in the group with similar profiles who may be able to share their experience and viewpoints.
What I find helped me in a similar position, was to look at the evidence from various viewpoints and decide for myself what I was comfortable with. For example, we have this presentation from Dave from a cautiously optimistic perspective about high LDL in a low carb context, and this post from a cautiously pessimistic viewpoint – both making the strongest case for their perspective.
Dave also has this presentation going through his proposed mechanisms for why this can happen (e.g. the lipid energy model).
very informative…leads to more questions
My WBC is 6800 and LDL is 53, HDL is 57, Trig is 47. I’m on 40mg of Atorvastatin. Is my immunity weakened?
Hi, we can’t say whether you are or not as we’re not doctors and can’t give medical advice. As with any health concern, you could discuss with your doctors and see if there are any indications of this, if you feel it’s a legitimate concern. They have the full picture of your health and history and would be able to comment better.
Regarding the broader question of lipid levels and immunity in general – it’s worth noting that although the post is discussing the potential role of lipoproteins in the immune system, it’s talking about mechanisms of specific interaction – not implying that any level of LDL is more “desirable” over others in terms of immunity. In the post it’s discussing active infections, where lipoproteins may be upregulated in response, and interactions that have been noted when lipoproteins are present in general. Although lipoproteins in terms of immunity was the focus of the post, highlighting the fascinating research on the subject, it’s always worth likewise highlighting that there are other facets of the immune system which help shape the larger picture – lipoproteins are only one proposed part of it (and we don’t know how big that part is yet, as there’s a lot yet to be studied with regards to it).
As of yet I haven’t seen a study where the question of lipoprotein levels in isolation (e.g. in healthy people, excluding confounding factors like metabolic syndrome or other conditions that can impact other health factors beyond lipid levels) with regards to immunity and infection rates (not just infection mortality) has been investigated, so I wouldn’t even really want to speculate at this point with so little data available in humans (in a healthy context).
I recently went on the Ketogenic diet, lost 30lbs, feel amazing, loads of energy. Had my bloodwork done and expected my cholesterol to look better but all my numbers went up considerably! LDL 350, HDL 101, Triglycerides 80, total Cholesterol 467. I was shocked but now wondering if I need to be concerned?? All my other markers are perfect. My Dr wanted me to go on a statin before, now she will for sure! I’m afraid to even go back to her!
Hi Kathy,
It looks like you fit the profile of a Lean Mass Hyper-responder e.g. someone who is typically lean, active, and powered by fat (e.g. on a low carb/ketogenic diet). You may be interested in the Lean Mass Hyper-responder facebook group as there are many there with similar profiles who explore the latest research regarding it, their experience, their perspective, and how they’ve approached having the profile (e.g. taking steps to move away from the profile and how they did so, sticking with it but getting additional testing to keep an eye on things, etc).
We can’t say whether this profile is of concern or not (as we’re not doctors and can’t give medical advice), but we can offer some resources to explore different perspectives on the topic. For example there’s this presentation from Dave looking at high LDL in the context of high HDL and low triglycerides from a cautiously optimistic perspective, plus this post from Dr. Nadolsky looking at the same topic from a cautiously pessimistic perspective.
For those who decide they are not comfortable with it for the longterm, or would just like to confirm it is dietarily induced, the most consistently effective method (presuming it is dietarily induced) that we’ve seen demonstrated by people thus far is to decrease fat and proportionally increase carbs (e.g. isocaloric carb swapping), which is discussed here.
Interesting because I have had high cholesterol and LDL for years. I am very rarely ill. First I’ve heard of this correllation.