In A Simple Guide to Cholesterol on Low Carb Part I, I gave a very broad overview of LDL particles and their important cargo along with common misconceptions about this subject within a low carb, high fat diet.
Without question, the guide was the most visited post on my blog. And many of my followers have remarked on how helpful the graphics were in getting across the information. So I decided to get ambitious with Parts II and III and tell it more as a visual story. In short – more graphics, less blog text. Enjoy!
Simple and to the point. Look forward to the part 3.
Thanks — it will likely be soon after my presentation at Low Carb Breckenridge.
I’m still looking forward to part 3.
I know — I keep meaning to get to it and find other priorities pushing ahead. Hopefully soon…
Love this! This is honestly how they should have taught us in med school, learning so much more through your cartoon compared to some of the expensive classes i took! Waiting for part 3!
He could make an installment in the “Ridiculously Simple” series 🙂
To be honest, I really don’t think nearly this much was understood when I was in med school. As a surgeon, it’s not all that useful for me professionally- just to chastise my trainees when they present the old paradigms!
Did you ever do part III?
We need Part 3 still!
Using cartoons to explain lipid metabolism is so cool! really great work.
In case anyone’s interested (apart from the above series ^), this is probably one of the best explanations of this topic [https://www.youtube.com/watch?v=998r-MyEEPc] that i have come across.
Yeah, that happens to be one of the earlier videos I saw when I started to learn about the lipid system. Really informative.
Very interesting video, thank you !
Great article shared it in the Dutch Low Carb community.
Great! Thanks, Wim, I hope it proves very useful.
Thanks so much for this Dave. Am I right in understanding that the LDLs become small and dense when they are lacking in cholesterol and have a lot more trigs to drop off?
Hi Nicole,
Actually, I believe it’s the other way around, generally. Trigs are distributed mainly at first and VLDL goes to IDL, then to LDL with this last stage being the smallest and most dense (due to being higher protein vs lipid content) and *cholesterol rich*. The assumption with the establishment is that the longer those last stage LDL particles continue in the system, the more likely they are to get oxidized and end up in our arteries, or get retained in our arteries and then get oxidized, thus starting atherogenesis.
As we’ve discussed before, I have a very different leaning given my own data and research thus far. But more of that will be covered in my upcoming presentation at Low Carb Breckenridge.
I have been eating keto for 7 months now. I am also a T1 Diabetic. My Trigs are 100 and my HDL is 40. I have heard that a 2:1 ratio is where you want to be regarding Trigs:HDL. My remnant cholesterol is now 21 (was 28 on my last lab). However, my LDL particle sizes are the small, dense kind in large numbers. Anything to be concerned about here? Is it possible to reduce this in order to have more large, fluffy particles?
Can’t see any way to subscribe.
As I’m a bit new to WordPress blogging, I myself wasn’t aware subscribing would be possible — but even if it were, I may have to wait until I move this site to the new host (probably in Feb or March).
Excellent site and excellent illustration!!
Any info on Wellbutrin use and elevated cholesterol? Long and complicated history, but would love any leads if you have come across any associations in your research. Thanks again and keep it up! This information needs to get out!
Megan
Hi Dr Z-
No, I’m not familiar with Wellbutrin or it’s impact on cholesterol.
If one went on a low carb, high fat diet while also starting the medication at the same time, then it might be difficult to determine what impact each had along with what they do in combination. Is this what happened?
Hi Dave,
Thanks for the response.
Here is a brief hx:
At the time the 36 y/o female (now 40 y/o) pt started on 300mg/d bupropion (Rx’d by different dr) and within one month lost 5 pounds, going from 122-117 at 5’4″. She maintained that weight for 1.5 years as she was recovering from a foot injury that prevented her from being very active — even walking was not an option for about 6 months. Once the foot was healthy she resumed her previous exercise routine: weights, moderate cardio and in general significantly more mobility simply due to no longer being limited. The only dietary change she made was reducing alcohol intake. She said that she was drinking 2-3 beers/night, so she cut back to only twice per week and only 2 drinks at a time. After the reduction in alcohol and increase in activity level, she lost 10 pounds in 6 weeks. She stopped having her period and started to suffer insomnia, more depression and fatigue.
Dietary wise: honestly, it’s not terrible or specifically high fat, low carb, etc, but she definitely could stand reduce sugar intake. She admits to eating chocolate, daily, and often gets a pastry with her coffee in the AM. Otherwise, she adheres to a whole foods diet. Not heavy on meat, however. Nor is she big on the carb front (excluding the pastries and chocolate habit).
I ran some labs and sex hormones are in the tank — all postmenopausal. DHEA-s normal, testosterone – normal Thyroid markers are all low: TSH, T3, T4, free T3, free T4, all below RR. Anti-bodies are negative. Cortisol production is low, however, conversion to cortisone is high.
The cholesterol is the interesting bit:
Total: 308
HDL-C 151
Direct LDL-C 182
Tri 75
Non- HDL-C 157
She does carry the E3/E4 genotype
C/T MTHFR genotype
She also tested high on her Beta-sitosterol and campesterol absorption markers
I have 2 years worth of labs tracking her trends and the cholesterol numbers have slowing increased, the 308 was the most recent. Two years ago she was at 256 total.
My thoughts are the bupropion which inhibits norepinephrine and dopamine re-uptake, in time, overly taxed the adrenals, which lead to the menstrual and thyroid dysfunction. I suspect she was hyperthyroid for a bit. And the the end result is increase in cholesterol as it is the precursor to sex hormones. I can’t find any literature on this, however. She presents almost anorexic, but is not. Her lowest weight was 106 and was extremely lean, if I were to guess, single digits. She has gained about 10 pounds, yet still no cycle and is still suffering from the symptoms that drove her into my care: fatigue, insomnia, depression and unintentional weight loss. The logical or trial run approach would be to take her off of the bupropion, but she says she has tried that (slowly tapering) but ends up feeling worse.
Anyway … thanks for reading and for any thoughts or other minds that I could reach out to. It is disconcerting that so many medications are prescribed without truly knowing how they can impact the human system. Prior to the buproprion this pts cycles, sleep, energy, etc. were normal. Her only issue was depression and she says the bupropion has helped quite a bit.
Thanks again for your incredible site and work in this field!
Dr. Z
Hi Dr Z-
First, as always, I caveat that I’m not a medical professional and this doesn’t constitute medical advice.
– The first thing that popped out at me was her symptoms of insomnia, depression, and fatigue. Since going LCHF, I’ve found my biggest struggle was getting in the habit of consuming enough electrolytes and in particular sodium. I start my day with 3.5g of pink salt mixed in water and have one to two more of these drinks throughout the day along with salting many of my foods generously. If I don’t, I find I I have all the above mentioned symptoms, along with occasional cramps as well. It’s very unintuitive (more salt makes me less tired???) — but now that it is built into my routine, it is second nature. Given she’s actively eating better, she likely needs more sodium anyway as this is so common in processed foods.
– Lower thyroid numbers certainly can have an effect on lipid numbers, though I concede that one is more outside my wheelhouse.
– I too am a 3/4 and believe it to predispose me to higher lipid numbers. MTHFR genotype I’m still early on with research (and technically, everyone else is too – ha!)
I’ve regularly joked that if I were female, I’d have have stopped researching any further and this site wouldn’t exist. The reason is because I’ve come across so much research that shows higher cholesterol has the lowest all cause mortality with women in particular.
Here are some recent studies with very large population numbers:
Health Study (91,219) Norwegian HUNT study (52,087).
Key lines from the Japan study:
“Overall, an inverse trend is found between all-cause mortality and total (or low density lipoprotein [LDL]) cholesterol levels: mortality is highest in the lowest cholesterol group without exception. If limited to elderly people, this trend is universal. As discussed in Section 2, elderly people with the highest cholesterol levels have the highest survival rates irrespective of where they live in the world.”
http://www.karger.com/Article/Pdf/381654
Key lines from Norwegian study:
“Among women, cholesterol had an inverse association with all-cause mortality [hazard ratio (HR): 0.94; 95%”
https://www.ncbi.nlm.nih.gov/pubmed/21951982
Hi Dave,
Thanks for the article link. Great information! And thank you for your thoughts on my question. Even though you may not have any formal medical training you are 100 times more informed than many medical providers that I know! I figured I would ask for any input that you may have simply due to your extensive research on the subject. So thanks again for your wisdom and time in responding to me.
Megan
Oh, and she does have an MTHFR variant that causes her to not methylate as efficiently … but what that means in the cholesterol world. Who knows! 🙂
Thank you, Megan! 🙂
Hello Dave….
We chatted quickly on Twitter the other night, we had similar numbers and weight loss on LCHF. Here are my numbers again, before LCHF and one year later on LCHF. You said that you are taking no steps to lower your cholesterol at this point but told me to comment here for further explanation…Very interested!
Thanks….Joe
Jan 2016 Jan 2017
Weight 206 173
Cholesterol 223 373
HDL Cholesterol 65 92
Triglycerides 101 79
LDL / Cholesterol 138 265
Chol / HDLC Ratio 3.4 4.1
Non HDL Cholesterol 158 281
Hi Joe — I’m going to build this into a blog post by itself. But this week I’m burning the candle at both ends, the reason why I’ll also be putting into a post soon.
Please check back again next week…
Thanks Dave…
Very interested in what you have to say, I will keep an eye out.
Hey Dave,
Just wanted to say what a great job you did presenting at the Low Carb Conference.
Keep up the great work.
Gale Bernhardt
Thank you so much, Gale! I appreciate the encouragement.
Dave
Love your work also loving LCHF. Got Lab work back after being LCHF for several months. Stopped 10mg Lipitor after taking for 15 -20 years six months ago.
HDL-C 71 was 46 on HCLF +10mg Lipitor
LDL-C 170 was 95 on HCLF + 10mg Lipitor
Triglycerides 65 was120 on HCLF + 10mg Lipitor
HDL-P total 34.5unmol/L first time measured
Small LDL-P 625umol/L first time measured
Large LDL-P 1552umol/L first time measured
Total -C 254 was 161 on HCLF + 10mg Lipitor
Only number that I don’t like is the Small LDL-P which is just slightly out of range it’s 625 and reference high is 527. I know your not a MD but what’s your take?
Thanks
Eric
I’m probably a lot more skeptical than most on small LDL-P being causal of atherosclerosis specifically. I’ll have a blog post on this in the near future (I hope). This is not to say I’m sure it isn’t, only that my own data and research shows just how quickly these numbers change, showing the level of control the lipid system has in the first place.
Two points to consider:
1) Small LDL-P can be cleared far faster than is presumed (in as little as 3 days). I’ve shown this several times now, including my Extreme Drop experiment at the Ketogains Seminar (441 to <90 -- http://cholesterolcode.com/infographic-of-prediction-experiment/). The common assumption with atherosclerotic build up is that it is due a “traffic jam” of LDL-P (and in particular, smLDL-P) as the body can’t seem to clear it, yet my data is showing it can.
2) More importantly, the causal assumption also presumes the body wouldn’t intentionally upregulate LDL to meet an emergency state. But we already know this to be false. LDL has been shown to be upregulated in an infection event. Likewise, it can be increased to repair injury. In other words, it shouldn’t be surprising to find those near the end of their life to have more LDL given its immunological and reparative benefits. Which is why I’m actually surprised after learning of these factors that LDL levels are not actually *higher* when found near death in the aggregate.
But then, I also know the presence of doctors being frequently found in proximity to people who have died doesn’t mean they must be killers.
Do you have any concern over Large LDL-p?
Current thinking by lipidologists like Dr. Dayspring is that total LDL-P (large or small) is the factor that matters most. While I’m not as convinced, it’s definitely something I don’t rule out.
Dave
Thanks again! I am still losing weight since diet change have gone from 187 to 165 in 9 months very steady slow decline. I wonder if while losing weight some how LDL-p numbers go up?
Eric
Many in the LC community (like Volek and Phinney) will point out that subsets have shown higher LDL-P when losing weight. I’m actually more skeptical of it being a 1:1 with released TG now due to my data. It’s a bit technical to explain, but to simply state it — I think the body has more effective LDL-P clearance control than is currently believed in the medical community, and that the higher numbers could be transitory or even upregulated by preference of the body. (Again, it would take a bit of time to really break this out)
Just found your interview with Ketogains https://www.youtube.com/watch?v=QUjbvK2U1D8 My A1c was 5.7 when I started changing my diet. Did your A1c lower over time how long did it take?
Thanks Again!
Eric
My A1C being 6.1 was the reason I started the diet, actually. It was around 5.4 seven months after a started, but has since bounced up to around 5.5-5.6 in my most recent tests. This appears to be due to higher glucose sparing where my body keeps my glucose closer to 100 mg/dl (which is higher than usual for a keto diet), yet my fasting insulin is extremely low (typically 2-4 uiu/ml).
Dave
I’m suprised your A1c is not lower. I read on Dr. Attia’s blog his hemaglobin size was small giving him a higher A1c reading than his acutal blood glouse average. He compared his A1c to the Average BG from the Dexcom CGM he was wearing. Implying the CGM average blood glucose reading is more accurate. I wonder if your hemaglobin size also is small?
Thanks
Eric
Actually, I want to do an entire blog post on that. Both my A1C and fasting glucose is now higher than when I started (5.6 and 100-ish, respectively), but I suspect strongly this is due to glucose sparing on the part of my body. The reason is due to my low relative fasting insulin (typically 1.5 to 3.5).
OMG I’m so glad I found you. Just heard your Breckenidge talk. I’m Jill. I’m her. 7 months on keto and took the cholesterol test and almost fell off my chair. I couldn’t believe it had shot up so much. total cholesterol went up, LDL went up, HDL went up but not by much. My ratios were worse I couldn’t see a way to explain it favourably. I wrote to Dr Ken Sokardis, Gary Taubes, Jimmy Moore, Dom De’Agostino, Stephen Phinney, Malcolm Kendrick and a few others. Most wrote back some with good news others not so much. How can I email you please? I’ve encouraged my mother and sister onto this diet – I’ve even started a degree in Nutritional science and now I am feeling so deflated. Scared to eat fat. Scared not to and put on all the weight I lost. I don’t know what to do.
Hi Lita – I’ll reach out to you. But to be sure, my communication is sporadic these days as I’ve got quite a bit on my plate. 🙂
Hello Jill,
I have exactly the same situation. The important things are the two ratios: TotCl/HDL and TG /HDL
As long as they are ok, I don’t worry about cholesterol. You can improve HDL with fish oil EPA & DHA.
I use this for my guidelines: “Cholesterol Conundrum – Know Your Metrics” on Youtube https://www.youtube.com/watch?v=YRFRRqe0vrE
Good luck,
Brian
Do you follow Dr. Peter Attia at all? He has had quite a change of position on Ldl(a)-P in the last few years mainly I think through lots of feedback from Dr Tom Dayspring. Large particle number=arterial damage. Any comments?
Hi Dave–Do you follow Dr. Peter Attia’s Eating Academy blog? Nice detail and for sure he has an increasingly negative standpoint re Lp(a)-P. I think from more in-depth conversations with Dr Tom Dayspring. It is indeed a hot area of research but Dr Attia seems to be settiing the tone of high-P=artertial damage (no matter the particle (i.e. any Cholesterol). Any thoughts?
Yes, in fact I consider Attia and Dayspring the most read (and watched) in my core education on this topic. I have come to a few different conclusions mechanistically than they’re teachings, mainly due to my own experiments and the patterns that have emerged — but that’s for a different post.
The subject of risk is actually a pretty long one, but I intend to do a post on it in the near future.
Very cool illustration. One detail seems to need attention, though. Perhaps I’ve missed something somewhere, but from what I understand, small LDL particles and vLDL are not the same thing. I used to think they were, until I was called out on it, and did more some research on it.
Further research showed me that there are actually five major groups of lipoproteins: (1) chylomicrons, (2) vLDL, (3) LDL, (4) IDL (intermediate density lipoprotein) and (5) HDL.
LDL particles vary in size and density, as we know. Larger, less-dense particles are referred to as Pattern A LDL, whereas smaller, dense particles are referred to as Pattern B LDL (or “LDL-P small”).
vLDL is a completely different lipoprotein than LDL, and tends to have a direct relationship with trigylcerides. Higher triglycerides = higher vLDL, and smaller triglycerides = lower vLDL. However, I’ve seen cases in which small LDL particles can be high, even when trigylcerides are low.
I’d be interested to know your thoughts on this. Thanks!
Hi Ben-
– Note I don’t actually address “small LDL” particles as a classification in this story, only that as triglycerides are being dropped off, the particle continues to get smaller. In fact, this first portion pretty much covers their journey as a VLDL until the last couple pages where the run into the HDL and it gets remodeled (read: turned into IDL).
> vLDL is a completely different lipoprotein than LDL, and tends to have a direct relationship with trigylcerides. Higher triglycerides = higher vLDL, and smaller triglycerides = lower vLDL. However, I’ve seen cases in which small LDL particles can be high, even when triglycerides are low.
VLDL is characterized by the added apos and being more triglyceride rich and larger. LDL (as a classification) is really just a possible end stage of VLDL-origination (if it isn’t absorbed by the liver first).
And yes, there are definitely cases where trigs are low with high small LDL – Pattern B. I see a higher proportion of this with keto athletes.
Thanks for the clarification. It just seems easy to misunderstand from your sixth slide, which states that there are two types of LDL, and it seems to say that one form of LDL is vLDL. The 7th slide seems to state that the other form of LDL is the chylomixron. Glad to hear that this is not truly what you were trying to communicate.
I *am* trying to make that distinction between Chylomicrons and VLDLs. I consider those the two major classifications.
I know in the literature the term “LDL” is often in reference to a *stage* of the VLDL. (VLDL > IDL > LDL) And this is why I just typically say “LDL particle” in casual conversation given the blood test for LDL-P encompasses all apoB containing lipoproteins. It’s frustrating for many who are trying to learn this process how unintuitive these terms are.
What is apoB?
The identifying protein on lipoproteins like VLDL, LDL, and chylomicrons.
Hello, this is a great series! Any idea when Part 3 will be out?
Thanks!
Thanks — at the moment I’m spread pretty thin, but my hope is that I’ll have Part III out this summer.
So basically I don’t have to worry about having a 321 mg/dl cholesterol and a 240mg/dl LDL right now?
The short answer is: we don’t know.
Obviously, I’m operating at a higher level of cholesterol that came with my keto diet given all the information I have to this point and my low markers of inflammation. But If I see any signs of atherosclerosis, I’ll change gears with the data (and report it here, of course). But in short, I’m cautiously optimistic.
Foods like oatmeal, apples, prunes, and beans are high in soluble fiber, which keeps your body from absorbing cholesterol.
I plan to do some experiments with fiber soon. But in tracking the fiber intake I already have, I’m not seeing a significant change based on inputs.
To be sure, 85% of cholesterol is endogenous (produced within the body), and this is counterbalanced with existing absorption anyway. So while it might have some impact, I’m guessing it won’t be as significant as say 15 or 20% or more.
I sense in your comment that one should be worry about cholesterol intake, which is the mantra that the medical establishment has been imbuing to the public for decades. My first question would be: Why would I need to worry about intake cholesterol? Does cholesterol cause any harm to the body? If the answers were yes, then I would be diligent in taking my oatmeal, apples and prunes everyday. But what if high levels of cholesterol is not the cause of heart injury and metabolic syndrome? This site is dedicated to throw light on this issue.
Foods like oatmeal, apples, prunes, and beans are high in soluble fiber, which keeps your body from absorbing cholesterol.
I have been on LCHF for about a year. I have lost weight, feel good. I had a cholesterol PARTICLE test done. My doctor who ordered it then called, and said “we need to do something about your cholesterol”. Before I started LCHF, my cholesterol levels were moderate, NOT high (according to the standard cholesterol test and my doctors opinion). Now they are high. But I’m not able to interpret the results, and I’m a little fearful. My doctor won’t help me interpret the results…..he just sees “high”. If I give you the results, can you help me with deciphering them? I sent them to Dr. Andreas Eenfeldt at Dietdoctor.com and he said “As far as I can see these numbers are relatively average for the population. Hard to give a more useful reply without knowing your other health situation and what the numbers looked like before LCHF, etc.”. Not too helpful.
These are my results. I would sure like some peace of mind, one way or the other, if you would be so kind as to help me.
LDL-P = 1836
LDL-C = 208
HDL = 47
Tryglicerides = 65
Cholesterol = 268
HDL-P = 26.1
Small LDL-P = 371
LDL Size = 21.7
LP-IR Score = 33
Thank you so much.
This is the rabbit hole many of us have fallen into, finding out that establishment nutrition/health practitioners have serious flaws in their understanding of cholesterol, but not sure what to do about it.
If your concern is CVD, from my understanding of the research, the best test is to get a calcium score from a CAC. LDL is only very weakly predictive and possibly only so because its a marker for insulin resistance.
For me, my wife is in the category of concerned and not (yet?) well-read. Getting the CAC test (assuming my result is good) will be sufficient for her to let me KCKO. As far as my doc, I’m not sure if I want to switch, educate, or ignore. I’m gathering some data using the Feldman protocol so that my next appointment will be more interesting.
Your numbers are very similar to mine. I too have been LCHF for about a year and half now and feel great because of it. My reason was not so much weight loss ,but to get relief from post concussion syndrome, which it helped greatly.
I was concerned about the LDL-P being high after reading Dayspring/Attia thoughts on this, but Jimmy Moore says high LDL-P isn’t necessarily a problem as he has carried an absurdly high LDL-P (over 3000) with a CAC of 0 and CIMT scan showing no arterial blockage.
This doc also shares the same sentiment on LDL-P:
http://azsunfm.blogspot.com/2012/09/font-definitions-font-face-font-family.html
My numbers:
http://i.imgur.com/lyzQ7nr.png
Thanks for sharing that your numbers and that link, it was a great read. Certainly relevant for my situation.
My numbers are almost identical to yours and I, too, feel great with unintended weight and waist circumference lost. One other thing that gives me peace of mind is that there are no studies (which are not drug or genetic studies) that link high LDL or total cholesterol with heart injury, when Triglycerides (congratulations on your number) and HDL are good. (I am parroting Dave here).
Hi,
I am a medical doctor from South Africa. Hyper-responder on LCHF. Cholesterol now at 9mmol/l (360)
would like to partake in your study.
Pieta
I may have a write up for a remote one up pretty soon. Stay tuned. 🙂
Part 1 & 2 are really informative.
Thanks! I hope to have Part III up in the near future, but these take a lot of work, so no promises.
Foods like oatmeal, apples, prunes, and beans are high in soluble fiber, which keeps your body from absorbing cholesterol.
I’ll have some future experiments that will actually test that variable (soluble fiber) directly.
Hi Dave,
My mum have been on LCHF for close to 10 months now and a comparison of her lipid panels shown below (before and after LCHF):
(in mg/dL)
Total Cholesterol : 313 to 444
Triglyceride : 242 to 102
HDL : 50 to 60
LDL : 214 to 364
TG/HDL : 4.84 to 1.7
1. Is she what you would consider a “hyper-responder”?
2. Obviously the worry here is the upshoot in her LDL. But I told her that all her other important markers have improved – increased HDL, reduced Triglyceride, improved TG/HDL ratio. Her BP is normal and she has reduced her BP medication by half (50% less frequent intake of BP pills).
Are her worry confounded? Or am I too optimistic?
3. She also conducted a lipid sub-fraction test and she has about 27% small LDL (percentage excludes VLDL). Her VLDL number is 51 mg/dL. I.e. she has overall Pattern B particle size. Is that something to worry about?
Thanks.
kk
1. Yes — that definitely fits a Hyper-responder.
2. Yes, I’d consider her markers substantially improved, particularly triglycerides. BP, in particular, has a very strong association with CVD (where LDL does not).
3. 27% small LDL is actually in line with most hyper-responders. I’m not sure why they are coming to Pattern B unless it’s quantitative, not qualitative. Is she thin or average, but not overweight? The VLDL being at 51 is further indicative she is properly using triglycerides for energy (as would be appropriate for low carb) and isn’t likely very insulin resistant.
Honestly, I think this lab looks good from a lipid standpoint. I always want to see TG and HDL because they can tell the larger story as to whether LDL is high for a *bad* reason (IR, infection, injury), rather than a good one (energy transport due to being LC).
Oh — and by the way — let me cut paste these comments I made regarding women and high cholesterol. I’m confident you’ll find it quite powerful:
——————————————————————————
Health Study (91,219) Norwegian HUNT study (52,087).
Key lines from the Japan study:
“Overall, an inverse trend is found between all-cause mortality and total (or low density lipoprotein [LDL]) cholesterol levels: mortality is highest in the lowest cholesterol group without exception. If limited to elderly people, this trend is universal. As discussed in Section 2, elderly people with the highest cholesterol levels have the highest survival rates irrespective of where they live in the world.”
http://www.karger.com/Article/Pdf/381654
Key lines from Norwegian study:
“Among women, cholesterol had an inverse association with all-cause mortality [hazard ratio (HR): 0.94; 95%”
https://www.ncbi.nlm.nih.gov/pubmed/21951982
Dave,
Enjoying your blog, videos, and cartoons!
I had a couple questions regarding lipoproteins:
Are VLDLs/LDLs _delivering_ cargo to fat tissue, _picking up_ cargo from fat tissue, or a little bit of both?
During conditions of fasting and/or low carb dieting, what is the primary energy transport from fat tissue to other tissues of the body? LDLs? HDLs? Free fatty acids?
Thanks!
-Chuck W
Chuck,
Glad you found us! Fat is continually cycling through the body.
To adipose (fat tissue):
1. VLDLs deliver TG from the liver to various parts of the body, including adipose.
2. Chylomicrons deliver TG from the gut to various parts of the body, including adipose.
From adipose:
3. Adipose releases FFA (free fatty acid), which gets picked up by Albium and returned to the liver. Other tissues can tap into this stream of energy, but I’m not sure the exact uptake mechanism.
I don’t haven numbers or ratios, but I my guess is VLDL are going to be doing the bulk of the work during fasting. Especially during periods of energy demands, like exercise.
Craig
Craig,
Thanks for the reply, I had trouble finding this info from other sources.
So from the perspective of the adipose cell, release of FFA is the only “way out” for fat energy?
Thanks,
-Chuck W
Hi Dave –
I think that I’m a hyper-reponder as well and would be in a study if possible.
I realize that you’re not a Dr but you do have lots of experience reading the #s and I would love your opinion.
I’m 55, female and have been on a keto diet for 7 months. I’ve lost 35 lbs and am within 5 lbs of my maintenance weight. My bloodwork prior to keto was all great. Last week I had my first blood work since keto and some of the #’s are now through the roof.
Cholesterol 302
TG 60
HDL 78
VLDL calc 12
NonHDL Chol 210
LDL-P 2274
LDL-C 218
VLDL size 70
HDL-P 27.9
My Lipidologist (who is on keto but has normal bloodwork) thinks I’m possibly a hyper-absorber.
I’m seriously concerned about CVD and would love to hear your thoughts
Hi Annie,
Your numbers are actually very standard for a hyper-responder. VLDL count is low, TG are very low, yet your HDL is nice and high — everything IMO looks very solid.
Moreover, as a 55 year old female, you’d have more reason than not to *want* higher cholesterol. I actually address this in a comment earlier in this thread –> http://cholesterolcode.com/a-simple-guide-to-cholesterol-on-low-carb-part-ii/#comment-11199
I often joke that if I were female, I’d have long abandoned my research and probably continued doing software development given how much *stronger* the case is for high cholesterol with the opposite sex. 🙂
Thank you, I appreciate your response!
Just watched your presentation at Low Carb Breckenridge and thought it was great. I will be starting (again) a LCHF diet in January and will get some blood work for your “study”. I am going to lef.org to purchase the CBC panels for $35 each. I think that is the best price around for blood work. Do you know of another I should look into?
Just started following you on Twitter as well. Thanks for your work
CBC = Complete Blood Count. It’s great for a number of markers related to such things as White Blood Count (WBC) to check when sick, etc — but it isn’t a lipid panel.
I recommend seeing if you get a “Standard Lipid Panel” which is typically cheap ($20-40), or “Nuclear Magnetic Resonance” (aka “NMR”), which is typically not as cheap (typically $99). These will give you cholesterol markers. The former will be LDL-C, HDL-C, Triglycerides (and hopefully VLDL-C). The latter will give you all those and a complete breakdown of your LDL particles (total, small, etc).
Thanks for the info…and here is what Life Extension does for the $35…they do an annual sale too where you can buy a years wort of tests: http://www.lifeextension.com/Vitamins-Supplements/itemLC381822/Chemistry-Panel-Complete-Blood-Count-CBC-Blood-Test
Just noticed they call it this: Chemistry Panel & Complete Blood Count (CBC) .. Sorry for the confusion
Awesome
I’ve put my numbers into your calculator (total cholesterol 7, triglycerides 2.38, HDL 1.1, LDL 4.8 and the result seems to be “high risk”, which seems ominous! However, not sure what the implications are or what I can do about it. Been LCHF for 7 months. Was 198lbs, Hba1c of 68, cholesterol 5.6 (not sure of breakdown, but triglycerides around 7, despite long-term fenofibrate and simvastatin. In December (still on drugs, but low carb AND relatively low fat – due gall bladder flare) Hb1ac was 32, total cholesterol 3.7 and triglycerides 1.6. Since Xmas, have upped the fats, but still low carb (aim for about 50gms or less a day). I have stopped the fibrate and statin and the latest results (Hba1c up slightly but still “normal” at 35) are those given at the top of this post. Should I be concerned? Should I do something to improve the profile? If so, what? All help gratefully received!
Hi Liz–
Unfortunately, I don’t have as much experience with those who are on or have recently been on lipid-lowering medication. Anecdotally, there appears to be a period of time where the cholesterol numbers are varied and fluid in unpredictable ways. So it could well be that yours will “settle” more in another few months.
If you aren’t already, you might want to work with a low carb doctor to track these numbers more closely.
Many thanks for taking the time to reply. I can’t afford private medical care and I’m in the UK, where few GPs know anything about low carb! (in fact, having succeeded in putting my own Type 2 into remission (my Hba1c is 35) I’m about to start helping run a group for Type 2s in our medical centre hopefully inspiring them to change to LCHF! (naturally, against the standard govt guidelines, as we all know what those advise!)
On a personal note, I know I should exercise (I do none effectively) and I’m going to tweak my diet (remove fruit to a large extent – though I only eat red berries anyway) and try and up the omega 3s. Thanks again for your reassurances.
Sure thing, Liz — and a big congrats on getting your T2D down. 🙂
Hi Dave, thank you so much for the awesome research that you are doing. I’m a 56 yr old female. I’m a runner but have not been running much the last 3 months. I’d been training for a marathon and got up to 15 miles and crashed on energy levels. I also lift weights and do yoga. I’m not lean. 5’0 124lb. I’ve been doing keto for almost 5 months. BMI 24. I’ve only lost 3 lbs. I just got my fasting bloodwork results. glucose 59, ketones 2, A1C 5.0, CBC WBC 7.7, total cholesterol 494, Trig 79. HDL 153, LDL 322, non-hdl 341. I’m not sure why I’m not loosing weight, and get out of ketosis very easily. I eat very low carb, do intermittent fasting. And have started back on marathon training. Started back up with 6 miles and struggling on energy levels. Read your article on adding more carbs in. I’ve done low carb high protein for several years prior to LCHF
It’s *really* important to emphasize I don’t have any article about *adding* in carbs, rather, it’s typically about *swapping* in carbs instead of fat. It’s a very important distinction as an energy surplus can just simply make the numbers go higher (and add weight). And really, this is only to demonstrate changes in lipid numbers. (Not that this is even a desired result)
Fascinating lipid numbers. Of course your trigs are just a little shy of the Lean Mass Hyper-responder cut points. But even while you point out your BMI is 24, clearly your energy demands are higher as you’re remaining active (good for you!).
Given your descriptions with energy levels, I’m very curious if you’re getting enough electrolytes — particularly sodium. This problem I’ve struggled with like no other and now I regularly average between 8-10g of salt a day (not a misprint), 1g of potassium, and 1g of magnesium. Now while I expect I’m a corner case, like you, I’ve done a lot of distance running and found it was extremely relevant to me.
Thanks Dave for taking the time to reply. I will look more into electrolytes. I do the Trace Minerals 40,000 volt, and Concen Trace Mineral Drops. I also take potassium and magnesium. I’ll check my salt. Thanks for the suggestions.
Yeah– truly, I only came to the level of salt intake I have now through a lot of trial and error. I kept having stages of “it can’t be *this* much… surely it’s something else…” before finally giving in to my personal taste threshold. If you find (as I do) that you can heavily salt your steak/salmon/eggs and it continues to tastes great, then there might be something to that.
I’m ready for part III! Maybe you can also explain glucagon’s role in fatty acids?
I know, I know! My hope is that I’ll be getting around to pt III this summer.
Not sure if I can fit in glucagon into pt III as it will be mainly about the immunological and reparative aspects of LDLs, but I might hit it in a pt IV or later.
I just saw both posts part 1 & 2 and they’re amazingly simple! Great job Dave! Looking forward for part 3 =D
Thanks — I do hope to be getting to it later this summer.
I love your “disruptive” research Dave…I have been looking for answers to the cholesterol puzzle for many years…You have broken the code…I am not surprised that a systems engineer would be the one to do this…
Unless I missed it, I am trying to better understand the “inputs” that affect HDL-C blood levels…I am following your energy model with the LDL- and LDL-P, but I am still not clear on the factors that affect HDL-C?
That’s a tough question to answer for a few reasons. The biggest is that I suspect strongly that HDL goes up with a LCHF diet because it is actually sharing in the fat-based energy distribution (as TGs). But explaining this out would take a lot of comment space and I’d rather just get to it in a presentation or article.
Now that said, HDL is *usually* discussed for its “support” role and I often call them the “emergency vehicles” of the vascular system. But their actual setpoint can also be heavily influenced by genetics.
Sorry I am a little confused about some terminology, I hope you can help me.
Is LDL-C the Cholesterol or is it LDL in my blood work?
I wish I could include a graphic with my question. But I will try to explain why I am asking. In your cartoon picture on this site you show “everyone boarding a blue circle” that is being called Low Density Lipoprotein” also know as LDL and the passengers are Triglycerides, Cholesterol and Fat soluble vitamins.
Then in this presentation at https://www.youtube.com/watch?v=jZu52duIqno&t=2178s&list=WL&index=16 at min 12:33 you ask “What is the cholesterol in this?(the boat)” and you then label the life-rafts LDL-C.
I am really trying make some sense out of this because i think it could be very helpful I have been low carb since before it was popular (like 20 years now) and my lipid numbers aren’t great but they do fluctuate. I am so interested in this!!!
Last test for me 3/1/17 chol 292, LDL 222, HDL 56, Tri 70. now learning I probably didn’t fast long enough (not a full 12 hours) and wonder now how much being a coffee drinker mattered too.
Hi Dawn
– Generally, when they say “LDL” in your bloodwork, they mean “LDL-C” or “LDL Cholesterol” which does mean the cholesterol found in Low Density Lipoprotein “boats” ( as per the guide on this page, of course 😀 )
– The cruise ship is a bit of an oversimplification, but the gist is that I’m trying to emphasize how the lipoprotein is the “boat” (LDL-P, or LDL particle) and the cholesterol found in the boat is the LDL-C (the life rafts), which is cargo on the boats.
– So naturally I ran the numbers you mentioned through our tool and it looks very, very standard for a hyper-responder on LCHF (like hundreds of others on this site). See below:
–==== CholesterolCode.com/Report v0.9.2 ====– on – ::: …
…
Total Cholesterol: 292 mg/dL 7.55 mmol/L
LDL Cholesterol: 222 mg/dL 5.74 mmol/L
HDL Cholesterol: 56 mg/dL 1.45 mmol/L
Triglycerides: 70 mg/dL 0.79 mmol/L
–CHOLESTEROL REMNANTS–
Remnant Cholesterol: 14 mg/dL 0.36 mmol/L >>> Lowest Risk Quintile
Remnant Chol to HDL: 0.25 >>> Medium-Low Risk Quintile
Go to https://tinyurl.com/y8hokam2 for more on Cholesterol Remnants
–ATHEROGENIC INDEX OF PLASMA (AIP)–
AIP: -0.264 >>> Lowest Risk Third
Go to https://tinyurl.com/ycccmmnx for more on Atherogenic Index of Plasma
–CONVENTIONAL MARKERS AND RATIOS–
Friedewald LDL-C: 222 | Iranian LDL-C: 193
Total/HDL Ratio: 5.21
TG/HDL Ratio in mg/dL: 1.25 | in mmol/L: 0.54
Hi Dave.
First of all- this is an amazing resource that you created- thank you so much. It really is the best explanation of the science that I’ve ever seen on this topic.
Question: Male, 35, 6’1, 185 lbs with 14% body fat per recent dexa. Life long athlete and weight stable for 10 years +. Currently 4-5 cardio sessions per week plus 3-4 weight training sessions. Started keto 12 weeks ago for general health and some GI issues.
Baseline lipids: Total: 164; HDL 63, LDL 88, Trigs-64;
After 12 weeks of keto: Total-235; HDL 64, LDL 161, Trigs 52;
If I understand correctly this is somewhat expected on keto, especially if someone is a hyper-responder. I’m not sure, however, what criteria classifies me as such (besides the 3 you list). I.e. how do I know that this rise in LDL is just due to a higher transport needs for Trigs (for energy) vs. genetic pre-disposition?
What test would you recommend to do in order to properly assess if I’m at a higher risk of CV issues, and what would you be looking for on that test? Or is the fact that my trigs went down a good enough indication that I’m ok?
Again, thanks so much for this blog. Currently devouring every article on it and sending links to friends and family.
Dtree
Hi there, I’m handling comments while Dave is on a hiatus for a few weeks for his anniversary.
First off – glad you’re enjoying the site and that it has been helpful for you!
Based on your lower bodyfat percentage, and switch over to a fat based diet I’m not especially surprised by your lipid profile change – it fits pretty well with others in a similar situation that I’ve seen, and with Dave’s demonstration of how the system may be working. You’ll also notice that if you run your previous and current numbers through the report tool that your remnant cholesterol has gone from 13 to 10, so both in the lowest risk category but of different degrees. More on remnant cholesterol here.
As for checking for a genetic predisposition, one thing you could do to help figure that out, is just to change the energy input. In other words, you could try to do the Feldman Protocol, and see if you get a drop. If you do, it’s likely that your numbers are simply a reflection of how you’re getting energy to your cells. Not a guarantee, but would help to suss out which it is.
Just be sure to avoid common confounders like coconut and MCT oil, heavy coffee drinking or coffee drinking on the morning of the test, and make sure to fast 12-14 hours before each test.
Hi Siobhan.
Thanks so much for the response- makes a lot of sense. I will definitely plan on implementing the Feldman protocol to test that hypothesis in the next 2 weeks. I’ll post here with the results.
In terms of additional tests: Is it advisable to have an NMR done? Or will the confirmation via Feldman protocol be a sufficient indication (along with very low CRP-.3) that CV risks are likely low? Any other test you’d recommend looking at?
Thanks so much for taking the time!
Dtree
Awesome! We do appreciate people sharing their results 🙂
As for the NMR, personally I’m in the camp of “more information is better so long as it doesn’t overly confuse things”. The most reliable risk marker I’ve seen for CVD is available from the standard lipid panel (remnant cholesterol) but I also don’t like relying on one marker alone. An NMR, and fasting insulin would help provide a little more information on risk, if you’re worried about it (if you’re curious about why, check out Ivor Cummins work).
Perfect, thanks so much!
Last question- I promise:
I understand the mechanism of lowering LDL by switching to carbs (Feldman protocol). But what is the mechanism for lowering the LDL by increasing the calories with high fat? Wouldn’t additional fat increase the LDL available to transport TGs?
Thanks!
This is because the body balances two sources of fat energy – dietary fat you just ate (transported by chylomicrons), and fat from storage (transported by VLDL, which turn into LDL once they drop off the triglycerides). As access to dietary fat goes up, need for stored fat to be transported goes down.
Chylomicrons are cleared from the system by the 12 hour mark, and when you get bloodwork done you are (or we recommend you are) 12-14 hours fasted. At that point you’re measuring the VLDL (Remnant cholesterol) and LDL.
If you increase the amount of dietary fat you take in, you decrease the need to use fat from storage, and LDL goes down as a result. The nitty gritty is explained in an article I wrote here.
Brilliant article!! Thank you!
This is simply brilliant! Thanks for demystifying cholesterol and more important, removing the scary halo around it.
I am now in month 14 on keto. I just got back blood results and they were consistent with this blog post. I started in Mar 2017 with an HDL 35 mg/dl, LDL 152 mg/dl and TG 62 mg/dl. Last week’s (Apr 2018) results: HDL 64, LDL 136 and TG 44. This my highest HDL and lowest TG in the 10 years for which I have records. Remnant cholesterol has gone down from 12 to 8.8.
Also, I’ve lost 60 lbs and feel the best I have in years.
Glad to hear the site has been helping you on your health journey, Shantanu!
Congrats on the weight loss, and health gains!
Too many cartoons – part #1 was def better & easier to make sense of
Thanks for the feedback Dr. David! This is meant to be a “Simple Guide” so if there’s any part in particular that was confusing or needs expanding on or clarification please do comment with that, it would be appreciated 🙂
This initial thought was from someone who has read & studied a lot over the last year about all aspects of low carb lifestyle, ketosis, diabetes & metabolic syndrome + obesity, just so you know. My thought was simply that if someone like me is having some difficulty following everything you say, a lot if not most of your other readers must also have difficulty. I’ve read almost all the books written on these topics from Jason Fung’s 3, Phinney & Volek, Nina Teicholz, Dr. Perlmutter, Jimmy Moore, Dr. Bruce Fife, Dr. Mercola, Wilson & Lowery . . . I’ve got them all & they are all saying the same thing. So, thank you for confirming the science for me & making some of it easier to understand. I just think it was a lot easier to follow with only some cartoons. Great work though & from the look of it, no doubt a lot of work!
PS: The size of the print in those cartoons is so small, it’s hard to read which of course affects the reader’s willingness to keep going.
That’s a completely legitimate thought for sure! Feedback is highly appreciated, especially from someone who has already done their research into the nutrition science environment as a whole. Thank you! 🙂
How can you lower you remnant cholesterol? The calculator has me at medium risk – 25 remnant cholesterol. And 0.47 CHOL to HDL. – I’ve been doing LCHF for about 4 months having my #’s go up. Was at total cholesterol 258, LDL 177, Trig. 62 and HDL 69. Now Total 281, LDL 203, Trig 125 and HDL 53. Doctor wants to put me on a statin but I’m resisting. I just want to make sure I’m making the right choice but it’s all overwhelming and hard to find doctors that support Keto.
The higher remnants are due to the increase in triglycerides. Try starting here: http://cholesterolcode.com/high-triglycerides-on-low-carb-and-what-to-do-about-it/
Hi Dave.
great article very easy to understand for a non medical person
I just wanted to tell you my case
i am currently on keto since 2 months and i have blood test done, please check below and let me know if i need to take any precautionary measures
in mg/dl
HDL 35
LDL 279
VLDL 19
Total Cholestrol 334
Triglycerides 96
I like your trigs and VLDL, but I’m not super psyched about your HDL.
Now it’s quite possible given the pattern of your lipids that you have genetically influenced lower HDL. Do you know if one or both of your parents have had historically low HDL?
Hi Dave, thanks for the reply I am not sure…and i don’t think they got any blood tests done till now, but is it possible to find out if my parents have historically low hdl and if is it a genetically modified?
and in my case what is the solution to push up the HDL?
thanks
naren
I’m not sure about specifically “pushing up” HDL. Think of HDL as a status indicator more than ammo to shoot. What we’re looking for as a reason HDL could be lower and if that reason is bad. If you don’t know for sure on genetic influence, I tend to lean toward getting a wider spectrum of blood tests just to help rule out a challenge event of any kind (such as an asymptomatic illness).
Also consider getting a 23andMe and looking through different genes of yours to see if one or more are highly associated with lower HDL.
I got to say I love the low carb Community. You’ll understand why when you see my results and my question.
Before keto tc 204, hdl 51, ldl 120, tg 168
After 2 years keto tc 197 hdl 62 ldl 119 tg 76
After 5 mo. carnivore tc 182 hdl 56 ldl 113 tg76
Here are the other numbers ( no base line sorry)
Vldl 28 total LDL particles 903 rlp 121 small dense LDL lll 243 sn D’s LDL lv 70 total hdl particles 6994 large buoyant hdl 2388 Apo B100 82 Apo A1 157 Lp(a) 6.4 Metabolism syndrome traits 0 CRp 3.68 fasting insulin 9.4 homo cysteine 16.1 farthing glucose 90. my lovely zero carb Health Group pointed out that there may be a possibility of MTHFR variant and I just heard from one of my brother’s that he has been tested and found that he yes indeed has that very thing. I will be 62 next month and I have eaten a standard diet interspersed with periods of Adkins on and off for 40 years, I have been 60 to 70 lb overweight my entire adult life, and lost about 50 on keto. I have gained back 5 lb on Carnivore however I expected to because sarcopenia.. my question to you is do these look like decent numbers? I take 112 mcg. Thyroid daily and my thyroid numbers are . 61 TSH 11.7 t4 and 72 t3
Thank you
I can’t speak to your thyroid numbers, but I can say I like your lipid numbers overall. Your HDL is a solid 56 and TG 76, suggesting you’re definitely burning fat effectively. I’d like your VLDL a little lower, but I think that will come with time on your health journey.
Mega grats on your incredible success!
Hi Dave!
Awesome job! I wisk we have it also in Spanish!
Maybe is it possible to yranslate it? Co working with Diet Doctor?
It would be great enlightening for Spanish Spoken people. We are so hungry of learning and have right info!
That’s definitely something I’d love to have. We’re just tight on overall bandwidth. Perhaps we’ll have some help in that department soon. 🙂
Hi Dave
I’m part of the LCHF email group that I believe and most of your “LDL” images. I also speak Spanish so maybe I can collaborate with another expert to create this Spanish version of the cartoons?
Definitely feel free. Just let me know and I’ll also tweet/post it. 🙂
I know I am insulin resistant and have metabolic syndrome as a result of adipocyte and other physiological changes induced by radiation therapy as a child..I am very lean and take testosterone replacement plus synthroid. If triglycerides are very high after fasting (still above 500 after 12-16 hour fast, no coffee or tea), is this a VLDL issue? Doctor is recommending statins even though the LDL is 74 and LDL-P is ~1000? HDL is low of course..~30. The only way I have been able to get triglycerides down below 500 and HDL up above 40 is via low fat diet. LCHF improved the LDL-P with no improvement to Trigs. Is there a way for me to do high fat and to keep trigs down if there is a VLDL / insulin resistance issue?
Hi Robert — you may want to check out our article on high TGs here: http://cholesterolcode.com/high-triglycerides-on-low-carb-and-what-to-do-about-it/
This site has allowed for the best understanding of this issue that I have come across in the last 20 years. Thanks for creating this space! The only piece I’m not sure of is MCTs. Do they count as part of the fat bomb, liquid fat category, or are they independent of the VLDL (mobile adipocyte) non-usage issue that comes with the insulin resistance? I’m struggling to see how to get enough calories if I’m low carb/keto and have limited fat sources.
So technically, the literature emphasizes MCTs are generally broken down directly by the liver without going through the lymphatic system (and instead going through the portal vein). Thus, in theory, there would be less overall lipoprotein packaging and transport. How this applies to the bigger picture is still somewhat unknown with regard to lipid metabolism and cholesterol markers overall.
But with regard to not getting enough calories and having limited fat stores, I am not sure if I fully follow… do you eat to satiety and yet you feel you’re underfed/undernourished?
I have struggled with hyperlipidemia. I am a nurse practitioner so of course the plan of care has always been “use a statin”. I don’t tolerate them. I have tried using lowest dose 2-3 times a week etc. While it lowered my cholesterol and LDL I noticed my triglycerides always went up! I couldn’t make sense of it. This spring I was off meds while on vacation – had steak 3 times in a week. Labs done – Total cholesterol was 300 with LDL of 200, trigs were 100. I immediately decided no beef and tried to eat very little chicken etc. Mostly plant proteins – which are high in carbs. But it’s scary to see those numbers so made an effort to implement traditional methods. By the way I am very active – I typically bicycle gravel around 30 miles a week, sometimes more, walk every day at least 3-4 miles. In July – after 6 weeks of Zetia – cholesterol lowered to 230, LDL to 130, trigs 200. But I couldn’t lose weight, felt like crap. Went off meds. Added back chicken, beef maybe once a week, lowered my carb intake – felt much better. And I immediately lost 5#. Anyway – watched your video with Zdogg. Everything made sense. Looking forward to new changes – increasing fat , lowering carbs even more.
Your story sounds very much as though you’d be a Lean Mass Hyper-responder phenotype. You might check out our page on it here: http://cholesterolcode.com/lmhr/
Excellent description. Thank you!
Thank you so much Dave for all this amazing information. My LDL and total cholesterol jumped up after being on a low carb diet for 8 months. I’m not lean – still have quite a bit of weight to drop – so I don’t fall into your lean hyper responder category. But I’m hoping as I read more of your site I will figure out whats going on for me.
Thanks again – it’s wonderful of you to do all this research and share it with the rest of us (saving me from completely panicking about my numbers!!)
absolutely loved how simple this was to understand. Is there a part 3?
A part 3 is intended, yes 🙂