First, thank you to everyone who commented on the quiz. I enjoyed reading your thoughts.
Is High LDL Something to Worry About?
Perhaps this ought to be the first question. Jack Kronk says “I don’t believe that high LDL is necessarily a problem” and Poisonguy writes “Treat the symptoms, Larry, not the numbers.” Poisonguy’s comment assumes that the LDL number is not a symptom of trouble. Is it?
I think so. It helps to know a little about the biology of cholesterol and of blood vessels.
When cells in culture plates are separated from their neighbors and need to move, they make a lot of cholesterol and transport it to their membranes. When cells find good neighbors and settle down, they stop producing cholesterol.
The same thing happens in the body. Any time there is a wound or injury that needs to be healed, cholesterol production gets jacked up.
When people have widespread vascular injuries, cholesterol is produced in large quantities by cells lining blood vessels. Now, to repair injuries cells have to coordinate their functions. Endothelial cells are the coordinators of vascular repair: they direct other cell types, like smooth muscle cells and fibroblasts, in the healing of vascular injuries.
To heal vascular injuries, these cells not only need more cholesterol for movement; they also need to multiply. It turns out that LDL, which carries cholesterol, also causes vascular cells to reproduce (“mitogenesis”):
The best-characterized function of LDLs is to deliver cholesterol to cells. They may, however, have functions in addition to transporting cholesterol. For example, they seem to produce a mitogenic effect on endothelial cells, smooth muscle cells, and fibroblasts, and induce growth-factor production, chemotaxis, cell proliferation, and cytotoxicity (3). Moreover, an increase of LDL plasma concentration, which is observed during the development of atherosclerosis, can activate various mitogen-activated protein kinase (MAPK) pathways …
We also show … LDL-induced fibroblast spreading … [1]
If endothelial cells are the coordinators of vascular repair, and LDL particles their messengers to fibroblasts and smooth muscle cells, then ECs should be able to generate LDL particles locally. Guess what: ECs make a lipase whose main effect is to decrease HDL levels but can also convert VLDL and IDL particles into LDL particles and remove fat from LDL particles to make them into small, dense LDL:
Endothelial lipase (EL) has recently been identified as a new member of the triglyceride lipase gene family. EL shares a relatively high degree of homology with lipoprotein lipase and hepatic lipase …
In vitro, EL has hydrolyzed phospholipids in chylomicrons, very low density lipoprotein (VLDL), intermediate density lipoprotein and LDL. [2]
Immune cells, of course, are essential for wound healing and they should be attracted to any site of vascular injury. It turns out that immune cells have LDL receptors and these receptors may help them congregate at sites of vascular injury. [3]
I don’t want to exaggerate the state of the literature here: this is a surprisingly poorly investigated area. But I believe these things:
1. Cholesterol and LDL particles are part of the vascular wound repair process.
2. Very high LDL levels are a marker of widespread vascular injury.
Now this is not the “lipid hypothesis.” Compare the two views:
- The lipid hypothesis: LDL cholesterol causes vascular injury.
- My view: LDL cholesterol is the ambulance crew that arrives at the scene of the crime to help the victims. The lipid hypothesis is the view that ambulance drivers should be arrested for homicide because they are commonly found at murder scenes.
So, to Poisonguy, on my view high LDL numbers are a symptom of vascular injury and are a cause for concern.
Big-Picture View of the Cause of High LDL
So, on a micro-level, I think vascular damage causes high LDL. But what causes vascular damage?
Here I notice a striking difference in commenters’ perspectives and mine. I tend to take a big-picture, top-down view of biology. There are three basic causes of nearly all pathologies:
1. Toxins, usually food toxins.
2. Malnutrition.
3. Pathogens.
The whole organization of our book is dictated by this view. It is organized in four Steps. Step One is about re-orienting people’s views of macronutrients away from high-grain, fat-phobic, vegetable-oil-rich diets toward diets rich in animal fats. The other steps are about removing the causes of disease:
1. Step Two is “Eat Paleo, Not Toxic” – remove food toxins.
2. Step Three is “Be Well Nourished” – eliminate malnutrition.
3. Step Four is “Heal and Prevent Disease” – address pathogens by enhancing immunity and, where appropriate, taking advantage of antibiotic therapies.
So when someone offers a pathology, any pathology, my first question is: Which cause is behind this, and which step do they need to focus on?
In Larry’s case, he had been eating low-carb Paleo for years. So toxins were not a problem.
Pathogens might be a problem – after all, he’s 64, and everybody collects chronic infections which tend to grow increasingly severe with age – but Larry hadn’t reported any other symptoms. More to the point, low-carb Paleo diets typically enhance immunity, yet Larry had fine LDL numbers before adopting low-carb Paleo and then his LDL got worse. So it wouldn’t be infectious in origin unless his diet had suppressed immunity through malnutrition – in which case the first step would be to address the malnutrition.
Step Three, malnutrition, was the only logical answer. The conversion to Paleo removes a lot of foods from the diet and could easily have removed the primary sources of some micronutrients.
So I was immediately convinced, just from the time-course of the pathology, that the cause was malnutrition.
Micronutrient Deficiencies are Very Common
In the book (Step Three) we explain why nearly everyone is deficient in micronutrients. The problems are most severe for minerals: water treatment removes minerals from water, and mineral depletion of soil by industrial agriculture leads to mineral deficiencies in farmed plants and grain-fed animals.
This is why our “essential supplements” include a multimineral supplement plus additional quantities of five minerals – magnesium, copper, chromium, iodine, and selenium. Vitamins get a lot of attention, but minerals are where the big health gains are.
Copper Deficiency and LDL
Some micronutrient deficiencies are known to cause elevated LDL.
Readers of our book know that copper causes vascular disease; blog readers may be more familiar with an excellent post by Stephan, “Copper and Cardiovascular Disease”, discussing evidence that copper deficiency causes cardiovascular disease. As I’ve just argued that cardiovascular disease causes high LDL, it shouldn’t be a surprise that copper deficiency also causes hypercholesterolemia:
Copper and iron are essential nutrients in human physiology as their importance is linked to their role as cofactors of many redox enzymes involved in a wide range of biological processes, as well as in oxygen and electron transport. Mild dietary deficiencies of both metals … may cause long-term deleterious effects in cardiovascular system and alterations in lipid metabolism (3)….
Several studies showed a clear correlation among copper deficiency and dyslipidemia. The main alterations concern higher plasma CL and triglyceride (TG) concentrations, increased VLDL-LDL to HDL lipoproteins ratio, and the shape alteration of HDL lipoproteins. [4]
The essentiality of copper (Cu) in humans is demonstrated by various clinical features associated with deficiency, such as anaemia, hypercholesterolaemia and bone malformations. [5]
Over the last couple of decades, dietary copper deficiency has been shown to cause a variety of metabolic changes, including hypercholesterolemia, hypertriglyceridemia, hypertension, and glucose intolerance. [6]
Copper deficiency is, I believe, the single most likely cause of elevated LDL on low-carb Paleo diets. The solution is to eat beef liver or supplement.
So, was my advice to Larry to supplement copper? Yes, but that was not my only advice.
Other Micronutrient Deficiencies and Elevated LDL
Another common micronutrient deficiency that causes elevated LDL cholesterol is choline deficiency that is NOT accompanied by methionine deficiency. That is discussed in my post “Choline Deficiency and Plant Oil Induced Diabetes”:
Choline deficiency (CD) by itself induces metabolic syndrome (indicated by insulin resistance and elevated serum triglycerides and cholesterol) and obesity.
A combined methionine and choline deficiency (MCD) actually causes weight loss and reduces serum triglycerides and cholesterol …
I quote both these effects because it illustrates the complexity of nutrition. A deficiency of a micronutrient can present with totally different symptoms depending on the status of other micronutrients.
Julianne had a really nice comment, unfortunately caught in the spam filter for a while, with a number of links. She mentions vitamin C deficiency and, with other commenters, noted the link between hypothyroidism and elevated LDL. As one cause of hypothyroidism is iodine or selenium deficiency, this is another pathway by which mineral deficiencies can elevate LDL.
UPDATE: Mike Gruber reduced his LDL by 200 mg/dl by supplementing iodine. Clearly iodine can have big effects!
Other commenters brought up fish oil. They may be interested to know that fish oil not only balances omega-6 to modulate inflammatory pathways, it also suppresses endothelial lipase and thus moderates the LDL-raising and HDL-lowering effect of vascular damage:
On the other hand, physical exercise and fish oil (a rich source of eicosapentaenoic acid and docosahexaenoic acid) suppress the activity of EL and this, in turn, enhances the plasma concentrations of HDL cholesterol. [7]
Whether this effect is always desirable is a topic for another day.
My December Advice to Larry
So what was my December advice to Larry?
It was simple. In adopting a low-carb Paleo diet, he had implemented Steps One and Two of our book. My advice was to implement Step Three (“Be well nourished”) by taking our recommended supplements. Eating egg yolks and beef liver for copper and choline is a good idea too.
Just to cover all bases, I advised to include most of our “therapeutic supplements” as well as all the “essential supplements.”
Since December, Larry has been taking all the recommended supplements and eating 5 ounces per week of beef liver. As I noted yesterday, Larry’s LDL decreased from 295 mg/dl to 213 mg/dl, HDL rose from 74 mg/dl to 92 mg/dl, and triglycerides fell from 102 to 76 mg/dl since he started Step Three. This is all consistent with a healthier vasculature and reduced production of endothelial lipase.
Conclusion
Some people think there is something wrong with a diet if supplements are recommended. They believe that a well-designed diet should provide sufficient nutrition from food alone, and that if supplements are advised then the diet must be flawed.
I think this is quite mistaken. The reality is that Paleolithic man was often mildly malnourished, and modern man – due to the absence of minerals from treated water and agriculturally produced food, and the reduced diversity and higher caloric density of our foods – is severely malnourished compared to Paleolithic man.
We recommend eating a micronutrient-rich diet, including nourishing foods like egg yolks, liver, bone broth soups, seaweed, fermented vegetables, and so forth. But I think it’s only prudent to acknowledge and compensate for the widespread nutrient depletion that is so prevalent today. Even when nutrient-rich food is regularly eaten, micronutrient deficiencies are still possible.
Eating Paleo-style is not enough to guarantee perfect health. Luckily, supplementation of the key nutrients that we need for health and that are often missing from foods will often get us the rest of the way.
References
[1] Dobreva I et al. LDLs induce fibroblast spreading independently of the LDL receptor via activation of the p38 MAPK pathway. J Lipid Res. 2003 Dec;44(12):2382-90. http://pmid.us/12951358.
[2] Paradis ME, Lamarche B. Endothelial lipase: its role in cardiovascular disease. Can J Cardiol. 2006 Feb;22 Suppl B:31B-34B. http://pmid.us/16498510.
[3] Giulian D et al. The role of mononuclear phagocytes in wound healing after traumatic injury to adult mammalian brain. J Neurosci. 1989 Dec;9(12):4416-29. http://pmid.us/2480402.
[4] Tosco A et al. Molecular bases of copper and iron deficiency-associated dyslipidemia: a microarray analysis of the rat intestinal transcriptome. Genes Nutr. 2010 Mar;5(1):1-8. http://pmid.us/19821111.
[5] Harvey LJ, McArdle HJ. Biomarkers of copper status: a brief update. Br J Nutr. 2008 Jun;99 Suppl 3:S10-3. http://pmid.us/18598583.
[6] Aliabadi H. A deleterious interaction between copper deficiency and sugar ingestion may be the missing link in heart disease. Med Hypotheses. 2008;70(6):1163-6. http://pmid.us/18178013.
[7] Das UN. Long-chain polyunsaturated fatty acids, endothelial lipase and atherosclerosis. Prostaglandins Leukot Essent Fatty Acids. 2005 Mar;72(3):173-9. http://pmid.us/15664301.
via this link:
Hi Paul,
Thank you. I’m a little confused here. In your book, you recommend taking a multi-vitamin and then some other supplements. My multi-vitamin already supplies a good amount of some of the other micronutrietns.
Selenium – 200 mcg recommended. 110 mcg on multi-vit.
Copper – 2 mg recommended. 2 mg on multi-vit.
Chromium – 200 mcg recommended. 120 mcg on multi-vit.
Should I take only 90 mcg of selenium, 80 mcg of chromium and no extra copper?
I already take ~5,000 IUs of vit D and 300-400mg of magnesium. I will take the other supplements (Vit K2, Iodine and Vit C) per your advice and track my lipids. I will definitely keep you posted on my how things pan out.
Thank you for all the awesome information Paul! Greatly appreciate it!
– Raj
Hi Paul, –thanks for your reaction.
(a) Liver issues: I never come across a post saying one had significant PALS after starting paleo, but then it gradually normalized. On Chris M’s hypothesis these should be common. Do you know of (m)any cases naturally attributable to fatty liver?
The tipical commenter with PALS has it after starting paleo and then it just gets more pronounced.
(b) So there are quite a few of us on this thread too, who seem to think (probably sometimes, but perhaps not invariably, mistakenly) that they are well nourished, take no standard toxins and have no inflammation. It’s clear, you think that most cases of PALS are due to malnutrition, –and the other two members (toxins, pathogens) of the fearful triad. Is your position that a genetically determined PALS reaction to SaFATs unrelated to the triad factors (perhaps downregulating LDL receptors or whatever) (i)cannot exist (ii) is more rare than people imagine (iii) makes no sense (iv)can be refuted…?
Notice that on the further hypothesis that triad unrelated PALS is harmless, this configuration would not challenge your reasonable view that the body does not tend to try to harm itself for no reason. Neither would it challenge your triad hypothesis. It would only be contrary to the idea that PALS is *invariably* vascular damage mediated. None of this entails of course that the hypothesis is correct, and triad-unrelated (TU-)PALS exists. But does anything suggest strongly that it doesn’t?
All of this reminded me of a resource that I had almost forgotten. MIT offers Open Courseware at no cost. The listing of Biology topics is at http://ocw.mit.edu/courses/#biology
Hi Billy,
I know Larry has one of those devices, perhaps he has advice.
Hi KC,
A combination zinc/copper supplement is perhaps the best way, as long as the zinc doesn’t get too high.
I think on top of diet I would try to stop at 25 mg zinc / 3 mg copper. Multis are usually 15 mg / 1 mg. That leaves 10 mg / 2 mg. If you can find a pill with 15 mg / 1 mg that would be close enough.
Hi Raj,
Your multi is pretty potent. You have to look at the book discussion and do subtraction:
Selenium plateau range is 200 mcg to 400 mcg. Typical food intake may be 100 mcg. With 110 mcg in a multi, that’s probably sufficient. I’d probably supplement with 100 mcg more just to be safe, since selenium is so important, unless you eat selenium-rich foods.
Copper plateau range about 2 to 5 g. Diet about 1 g. If your multi has 2 mg that should be sufficient.
Chromium we couldn’t estimate a plateau range for lack of data: it’s basically non-toxic and food intake is thought to be negligible, but the minimum amount to is unknown. Your multi amount is probably sufficient, but it would be safe to add up to another 200 mcg on top if you wanted.
So your multi is sufficient but if you had clinical evidence of some kind of malnutrition like high LDL then you might consider a little extra.
Hi donat,
(a) I think equilibration of liver fat will be fairly rapid – weeks at most. Most people get their lipids tested once a year, so I don’t think this explanation really works.
(b) I think toxins and pathogens cause inflammation, malnutrition does not. But malnutrition can cause high LDL. So high LDL with low inflammation markers does indicate malnutrition specifically.
Your genetic question is an open issue in my mind. I think infections can do most of the things people attribute to genetics. I may blog about that soon — in mice, LDL changes in response to diet are much larger in infected mice.
I don’t say that PALS is invariably vascular damage mediated, but I think vascular damage probably is the explanation in 90% of PALS cases.
Of course there is familial hypercholesterolemia, so we know that genetic changes alone can produce high LDL. But these don’t bear on PALS directly, since they have low LDL before going Paleo. Genetic sensitivity of LDL to macronutrient consumption hasn’t really been explored as far as I know.
Thank you Paul. I do have high LDL.
What I’m discovering though is that my body temp is low… super low. I run anywhere from 95 F to 96.5 F in the AM. Since I’m getting at least some amount of copper, selenium and chromium from the multi (+ my varied diet) I think it makes sense that my LDL is high due to… Iodine deficiency (and hence hypothyroidism). I haven’t eaten seaweed in a looong time and I don’t supplement with Iodine and the fact that my body temp is running low proves that my thyroid is not functioning as well as it should.
From reading your book, another possibility is Vit C deficiency.
I’m planning on getting my thyroids checked this week during which I’ll also have my blood lipids and C-reactive protein measured. I’ll use that as bench mark and start the supplements after that. I will report back in 4 weeks when I recheck all these.
This is great thread and will be of great use to others reading it if those of us who have high LDL can try out the various options and report back in a few weeks. Thanks all!
Raj, I eat seaweed that I think is the densest natural source of iodine on Earth (Laminaria digitata) and my TSH is .86 but my temperature is always 97.* unless I’m sick. There’s a lot of variation with body temperature, so it may not be hypothyroidism.
From the posts here, it seems we have high LDL people who are exceptions to every possible deficiency listed, but we have a few examples of people who have lowered LDL-C via increases in minerals, though not the same ones. It’s somewhat strange that a copper deficiency would cause the same symptom as an iodine deficiency. I could see selenium and iodine deficiencies causing the same symptoms though. Perhaps the liver consumption corrected a selenium deficiency for Larry, and Derek has sufficient selenium from the liver he’s eaten for so long but low iodine. Perhaps high LDL like we have is only possible on an ancestral diet, and it makes known a deficiency in one of these minerals via elevated lipids.
As for me, I’m going to be eating liver from now on whether or not it corrects this because it’s so nutrient dense in general and I think I may actually be developing a taste for it. I did a half pound over the weekend and I may do a half pound this week before switching to 1/4 lb weekly. It seems dangerous to try to hit all micronutrient targets listed here via liver consumption due to the high preformed vitamin A content, though our healthy vitamin D levels should afford us some protection.
Hi Paul,
You wrote: “… my sense is the main effect of vitamin C is to reduce the oxidation of LDL to oxLDL”.
I wonder about that. I remember at least two studies that seem to suggest no significant influence of vitamin C on oxLDL [1,2]. This is somewhat speculative though, because in those studies vitamin C level was certainly not the only variable that changed. And the levels in those studies did not go as low to suggest a deficiency.
Still, given the limitations, a rise in plasma vitamin C did not coincide with a drop in oxLDL [1] and neither did a drop in C with a rise in oxLDL [2].
My understanding is that the role of vitamin C in atherosclerosis/heart attack is not in oxLDL reduction, but mainly in collagen production. Vitamin C deficiency lowers collagen production, which weakens the fibrous cap covering the atherosclerotic lesion. So it is more likely to rupture [3].
This is also suggested as the reason why rabbits can get atherosclerosis without having heart attacks: they produce their own vitamin C, so their fibrous caps don’t rupture [3].
Based on this and the information of your post, my guess would be:
Vitamin C ↓ ⇒ Collagen ↓ ⇒ Vacular damage ↑ ⇒ Local LDL production ↑
John
References:
[1] Silaste M.L., et al. Changes in dietary fat intake alter plasma levels of oxidized low-density lipoprotein and lipoprotein(a). Arterioscler Thromb Vasc Biol. 2004 Mar;24(3):498-503. http://pmid.us/14739118
[2] Young J.F., et al. Green tea extract only affects markers of oxidative status postprandially: lasting antioxidant effect of flavonoid-free diet. Br J Nutr. 2002 Apr;87(4):343-55. http://pmid.us/12064344
[3] Masterjohn C. High Cholesterol And Heart Disease – Myth or Truth? http://www.cholesterol-and-health.com/Does-Cholesterol-Cause-Heart-Disease-Myth.html
Hat tip Peter Dobromylskyj for [1,2]: http://high-fat-nutrition.blogspot.com/2007/12/fruit-and-vegetables-re-post.html
Hi Raj,
Fixing the thyroid is very important. Be sure to go slowly with iodine – that will minimize problems.
Hi Travis,
Copper deficiency can actually cause hypothyroidism. I blogged about that here: http://perfecthealthdiet.com/?p=1272.
I like your plan, it’s basically what I do — liver for copper, not too much out of concern for vitamin A. I do supplement iodine though.
Laminaria is kelp, correct?
Hi John,
The first study [1] shows that if you lower fat intake and replace it with fruits and vegetables, oxLDL goes up. It’s true C intake was slightly higher in the +fruit+vegetable-fat (but higher PUFA fat) diet, but I think the other changes were much more significant. Just the increased omega-6 consumption I think would overwhelm the vitamin C effect.
The other diet [2] also suggests that fruits and vegetables oxidize LDL. This is consistent with some studies showing a pro-oxidant effect.
Definitely collagen is the most important benefit of vitamin C. But in terms of effect on LDL specifically, I think C is likely to help by reducing oxidation.
Thanks for the intriguing thoughts!
Best, Paul
Masterjohn has also written about the affects of vitamin E interfering with the oxidation of LDL cholesterol, but only the natural form of tocopherols, like that found in unrefined red palm oil. This is one of the main reasons why I still cling to hope that I can one day adjust to the ‘interesting’ flavor of red palm oil. The protective affects of the natural E seem to be quite noteworthy.
http://blog.cholesterol-and-health.com/2010/11/i-warned-them-this-drug-might-kill.html#comments
Laminaria is indeed kelp. I get mine from seaveg.com. They have the nutritional information listed here: http://www.seaveg.com/shop/index.php?main_page=page&id=15&chapter=1
The kelp they list there isn’t the exact species, but it’s roughly the same. 3mg for 7g of it is really, really dense. With that kind of iodine level, I can only assume that selenium is quite high as well. I take a gram or less of it a day.
Billy,
I have a CardioCheck machine which checks total cholesterol, HDL and triglycerides. I’ve compared my results with lab tested results, and CardioCheck seems to be about as reliable as a glucose meter. Typically, the difference is about 10%, but I’ve seen differences as large as 24% (CardioCheck measured my HDL as 72 whereas the lab result came back as 89.) I find the CardioCheck to be somewhat useful to see how my lipids are trending, but it is no replacement for a professional lab test.
On the other hand, I once used it to do a postprandial test of my triglycerides, testing every hour for 7 hours after eating a high fat meal. This would be fairly expensive if done under the supervision of a doctor.
However, keep in mind that the test strips are not cheap, about $4.50 per strip, and you need different strips for the three lipid values that it tests.
I don’t regret buying mine, but one should be aware of its limitations before buying.
–Larry
My typical diet – well up until recently, quite LC or even VLC; but I recently started adding potatoes back in order to improve sprint performance (for five-a-side soccer games).
Lets see…
Breakfast (0730 / 0800)
Yoghurt and and small handful of berries (usually blueberries, occasionally raspberries).
A couple of brazil nuts.
Meat (Fried beef steak (preferably ribeye) / lamb chops / mutton / slow cooked stew)
Veg (Brassica – generally lightly boiled) – but had some asparagus this week.
Sometimes ice-cream.
Lunch (1330):
Varies – often one of:
2 rashers of bacon + 2 eggs. (the bacon usually being ayrshire, streaky or occasionally back). Fried in lard.
An omelett (plain, chess or cheese + onion) cooked in ghee.
Light snack : Cheese, cold meat (couple of slices of tongue), boiled egg, picked onion
Liver + onions (once a week)
Haddock – poached or fried, with sweated leeks, and fresh lemon
Mackerel – steamed with ginger, sliced onion, sliced lemon, ginger
Random other fish as takes my fancy.
Currently beef hash after football game
Supper (1800 – 1930):
Variable can be any of
nothing (if not hungry),
a light snack – as above – if not had it earlier
maybe a almond meal + cheese + egg ‘pancake’
A couple of boiled eggs (soft or hard).
At weekends I may have a roast (beef/lamb, occasionally chicken/duck), with roast parsnips, roast potatoes, carrots.
The stews will be something like diced beef, lamb shanks, lamb heart, with stock (home made), carrots, onion, peppers, mushrooms, occasionally marrow fat, spices. Extra fat may be added to stews. Since I usually don’t thicken them, they can also yield a soup starter.
The yoghurt and ice-cream are home made, the latter to Peter’s recipe (a pint double cream, 6 egg yolks, a little glucose, a little honey).
I’ve been off grains for a couple of years, but may re-consider polished rice.
I’ve started scattering potatoes in to more meals, but not settled on a pattern yet.
For example I just had about 150g of boiled new potatoes drizzled with lemon juice for supper tonight, I’ll have the same for breakfast tomorrow (plus the fruit/yoghurt) followed by beef hash + cabbage for lunch.
I also tend to consume a lot of double cream – say 5/6 pints a week. Usually in cups of tea, and/or in the above ice-cream.
I eat about 100g of dark (70 – 85% cocoa) chocolate a week.
Frying is usually in dripping, ghee, butter or occasionally lard – depending upon the dish.
So I’d expect to have the selenium covered (brazil nuts), K2 (cheddar cheese), C from fresh fruit/veg/liver (but don’t know how much is lost in cooking veg), D3 from supplement (currently ~ 7500 IU/day). I’ve not had any thyroid checks.
I don’t take much alcohol, may 2/4 glasses every 2-3 weeks.
Thanks for taking the time, Derek. It looks like iodine would be fairly sparse in there, especially if your salt isn’t iodized. Other than that, looks like a nutritious and highly satisfying diet.
One thing I wonder about with regard to selenium and brazil nuts is if anyone is alarmed by the barium and radium content: http://www.orau.org/ptp/collection/consumer%20products/brazilnuts.htm
Hi Paul,
I have a follow-up question to my earlier question about the pervasiveness of atherosclerosis among people eating a SAD or even a so-called “healthy” low-fat diet.
Is there evidence that switching to a paleo style diet like the one you recommend can reverse atherosclerosis? I ask because before I discovered your book and the whole paleo diet movement, I read Caldwell Esselstyn’s book on reversing heart disease with a super low-fat vegan diet. He appears to have compelling clinical evidence that his vegan diet does actually decrease arterial plaque, decrease symptoms of heart disease, and decrease the incidence coronary events. And folks like Dean Ornish and Joel Fuhrman claim similar results with similar low- or no animal protein/fat diets.
And, whether or not such evidence exists for a paleo diet, I am wondering what your thoughts are regarding how and why Esselstyn (and Ornish and Fuhman) are able to achieve the impressive results they seem to obtain using a super low fat diet. And does their success suggest that a paleo diet might do even better? I look forward to your response.
-Alex
Hi Alex,
First let me say that low-fat vegan diets are far from optimal for atherosclerosis and heart disease. They have some advantages over SAD, but only because the Standard American Diet gets 66% of calories from toxic sources — grains, sugars, soybean oil. Obviously a low-fat diet reduces omega-6 intake, and these diets also reduce sugar and usually diversify grain intake. So the Esselstyn/Ornish/Fuhrman diets may have some advantages compared to SAD, but they are not healthy diets.
The evidence that they have benefited people is mostly anecdotal and the anecdotes run negative as well as positive. Similar diets haven’t fared that well in clinical trials against low-carb and Paleo alternatives.
Good diets can reverse atherosclerosis. Dr. William Davis has a lot of clinical experience with this, and his principal recommendations — give up wheat, optimize vitamin D, optimize omega-6 to omega-3 ratio, supplement iodine (http://www.heartscanblog.org/2011/01/five-most-powerful-heart-disease.html) — are all tenets of our diet. See his blog for stories of people reversing atherosclerosis, seeing regression in calcium scores, etc.
There have also been short-term clinical trials of Paleo type diets. E.g. this one: http://pmid.us/17583796. People with heart disease had big improvements in various health markers on the Paleo diet.
The Perfect Health Diet specifically doesn’t have a clinical history, but I would expect that our diet will prove best of all for reversing atherosclerosis. However it takes years to gather clinical data.
Hope this helps!
Best, Paul
Hey Paul, I got some more tests back and I wonder if they may have some relevance to the issue of high cholesterol, in my case 391. My 25(OH)D was 85 ng/ml and total testosterone was listed as 374 (300-1080) with free test as 1.8% (1.6-2.9). The latter is waaay lower than I expected as I exhibit none of the symptoms of low testosterone, but assuming that it’s what I have day to day, perhaps one of these nutrient deficiencies causes the excess cholesterol that we consume/produce with this diet to sit idly by instead of being converted into testosterone. We’ll see if 3 months of liver consumption makes the LDL drop and/or the testosterone rise.
Since LDL is seldom measured directly, I’m not all that sure that what we’re seeing is a real effect rather than an artifact. At low TGs, the formulas tend to give whacky results for LDL.
That wouldn’t explain everything, but it might explain a lot.
Suppose for a minute that David is correct. What if Paleo lowers everyone’s trigs so significantly that it really does throw the LDL calc off enough to send us all into a needless frenzy. lol.
That may be true, but even with the Iranian equation, my LDL is strikingly high. I’ve seen lipid panel results posted by people where their TGs were 20 points lower than mine, but their LDL was much lower. Most of those people also had a significantly higher HDL, due most likely to myristic acid consumption from coconut. It’s possible that having such a high HDL is sending cholesterol back to the liver at a rate high enough that LDL-C doesn’t become elevated I suppose.
Poisonguy had this intruiguing remark a while back:
“whether copper’s lowering of LDL is therapeutic or from a toxic mechanism”
Presumably meaning to raise the possibility that copper like PUFAs decrease LDL perhaps by oxidizing it and oxLDL is cleared faster?…?
Just speculating based on Wilson’s disease and a bit of the literature. Copper is actively secreted, so it’s difficult to accumulate. So, supplementation could still keep the levels inside Paul’s safe plateau range. I worked as a toxicologist for 12 years (still do a bit of it for Big Pharma), and metals have always been a concern to me. You can’t change one without affecting another, because they all compete fom absorption with one another or enhance one’s absorption. Increase copper, and you can get increased iron and/or decrease zinc. I’m still on the bubble about this copper thing. Since the bioavailability of copper in non-paleo diets is next to zero (phytic acid is a strong binder of cations), I just can’t get my head around paleos being copper deficient (by Paleos, I mean PHD dieters too).
Thanks Poisonguy. (reassuring about the nick)
Paul,–Thanks for the clarification. So we agree that probably not *all* PALS (paleo-lipid syndrome: high LDL and HDL/TG ratio) cases are due to vascular damage. As for genetically determined variation/individual susceptibility to PALS on a high fat diet this looks quite relevant:
Endogenous and diet-induced hypercholesterolemia in nonhuman primates: effects of age, adiposity, and diabetes on lipoprotein profiles. Metabolism. 2011 Mar 2. PMID: 21376354
“In response to the HFHC [high fat high cholesterol] diet, some monkeys were more sensitive to the dietary cholesterol and showed greater increases in serum cholesterol (by >13 mmol/L) compared with
others who showed only a relatively modest increase in serum cholesterol (~2.5-mmol/L increase). Baseline cholesterol level played no role in this wide range of hypercholesterolemia in response to the HFHC diet”
Without going into the details, the effects are PALS-like as far as can be made out: “shift in the total LDL-C subclass from pattern A/B to
pattern A” (Lack of relevant data and diet confounders prevent an even stronger statement about PALS-likeness.)
“The environmental conditions were identical for all monkeys.” “The monkeys were fed, ad libitum, an LFLC monkey grainbased chow diet (Lab Diet 5038, PMI NutritionInternational, Richmond, IN) throughout their lives.”
So either the strong responders had vascular damage or they just reacted strongly to high (saturated) fat diet. In either case, on the face of it, the difference appears to be not primarily due to variation in the (external) environment.
Stephan did a very well written piece on copper last year.
http://wholehealthsource.blogspot.com/2010/04/copper-and-cardiovascular-disease.html
So if you supp copper, shouldn’t you also supp some zinc, or do they aggrevate each other?
Hi Jack,
Yes, Stephan’s post is excellent. I linked to it in the post, just below the “Copper Deficiency and LDL” heading.
You do need both zinc and copper. We estimate the optimum for zinc around 30-40 mg/day. Food provides around 15 mg for most people and a multivitamin typically 15 mg. Most supplements are more than 10 mg. So there’s not much room to take supplemental zinc in addition to a multi. You could do it occasionally, not every day. A 50 mg zinc tablet once a week in addition to the multi would be fine.
The trouble with high doses of zinc is that they inhibit copper absorption.
That’s funny. I had read your entire article too. I just didn’t realize that was the same essay by Stephan. I don’t take a multi, so a bit of zinc might work for me if I add copper. Honestly I’m nervous about all these minerals. I know they are important. I just wish the optimal levels were more concretely known. The risks toying around supps like this make me hesistant.
Thanks Paul
“I agree, a diet survey would be very informative. Probably very few of the high LDL people eat beef liver.”
I have been low-carb/paleo for almost 7 years. For what it’s worth, here’s my cholesterol data:
1999 Total C 202, HDL 62. This was pre-paleo. Before that my cholesterol was always unremarkable except for a time when my HDL was low enough that my doctor recommended drinking red wine. Exercise brought it back up.
2004 Total C 221, Tri 62, HDL 63, LDL 146 The year I started paleo.
2005 Total C 219, Tri 53, HDL 74, LDL 134
2007 Total C 310, Tri 98, HDL 80, LDL 210. Blood work done in the middle of a bad GERD episode when I was taking PPIs and/or Zantac.
2009 Total C 285, Tri 59, HDL 86, LDL 187
2010 Total C 284, Tri 56, HDL 90, VLDL 11, LDL 183
2010 VAP test, Total C 298, Tri 62, HDL 88, VLDL 13, LDL 196 all Pattern A.
I solved the GERD problem with Chris Kresser’s advice and now take HCL with meals. Also, your tip to eat cranberries was a big help. I had a yeast infection after taking a lot of antibiotics last year. I have also started adding back some “safe starches,” mostly yams, per your recommendation for better mucous production.
I have known about the need for a zinc/copper balance since 2006 when Dr. Eades blogged about it.
http://www.proteinpower.com/drmike/uncategorized/low-carb-diets-and-copper/
I used to eat a lot of nuts (almonds esp.) but now my craving for them has subsided. I eat calves liver once a week and have done so for a very long time. My water is usually mineral water with a high magnesium content, or filtered water with a pinch of sea salt in it (the gray stuff). I eat grass-fed beef that I get direct from the rancher, all kinds of meat, fish, eggs, raw butter or ghee, coconut oil, red palm oil. My produce and eggs come from a farmer’s market here in So. Cal. (probably one of the best in the country). So I just can’t believe I am “malnourished” and need to supplement with copper.
Hi Grandma,
Welcome! It sounds like you have your diet and health well under control.
I may do another post on causes of high LDL, just to explore a few other possible causes. But your numbers are good, it would just be refinement. Glad to hear your GERD/yeast are better.
Thanks for the link to Dr. Eades, I’m glad he brought copper up too.
I agree, it doesn’t seem likely you have a copper deficiency.
Best, Paul
Concerning the apoE allele effects to diet vs lipids, there is this old study:
http://www.jlr.org/content/36/4/653
What happens to your lipids when eating SAFA seems to be determined by your apo phenotype.
Those with apoE4 allele see rising LDL, while those with apoE2 see falling LDL.
This seems to explain nicely the sometimes contradicting diet vs lipids results.
Thank you, Morty, that’s a nice study!
Hi Paul,
My cholesterol has risen some since eating LC/VLC. I’m going to supplement as per your suggestions. I just took a blood test to establish a baseline. How long should I wait before I test again to see the effect of the supplements? Thanks! Billy
Hi Billy,
It could easily take months to fix a copper deficiency. 2 months should be enough time to see an effect. That’s how long it’s been for Larry. But improvement might continue for a year or even more. If there’s a thyroid dependency that may take some time.
Best, Paul
Paul,
What do you think of Dr Davis’ post from today about “Claudia’s LDL”?
http://www.heartscanblog.org/2011/03/letter-from-insurance-company.html
Claudia’s lipid panel showed 196 LDL, but then her measured LDL was actually 89.
What do you make of this?
Hi Jack,
It wasn’t her measured LDL that was 89, but her LDL particle number is consistent with an LDL mass of 89 mg/dl if she had the same particle size distribution as the general population.
I think further research is needed to elucidate exactly what this means – moderate LDL particle number and big LDL sizes leading to above average LDL mass. It’s a pretty healthy pattern, but maybe not the optimal pattern. It might have diagnostic value for certain conditions.
If I were her doctor I’d make sure the insurer got the directly measured LDL, which is surely lower. Also, I’d advise her to go on our supplement regimen and see if her LDL number comes down.
Dr Davis is being a little cagy here. Since he has a size distribution he must have a directly measured LDL mass, but he doesn’t give it to us.
At some point I’ll look more deeply into VLDL/IDL/ApoE/CETP biology and then maybe I’ll have more to say about what low particle number / large size means. But for now, I’d just agree that her insurance company is grossly over-reacting, without necessarily thinking that her lipids are completely fine. She is probably healthier than most Americans in the lowest insurance risk pool.
Why are paleo people ignoring the “elephant in the room” explanation here? It’s well known that dietary palmitic acid down-regulates the LDL receptor, and raises LDL levels. All of the people quoted in the previous article with high LDL are intentionally eating as much palmitic acid as possible!
There really is no paleolithic or hunter-gatherer precedent for this kind of palmitic acid consumption, at least outside of the inuits. Hunter gatherers do not as a rule have access to large amounts of dairy fat, or feed-lot marbled steaks, but get fat directly from nearly whole wild animals which are considerably lower in palmitic acid overall. Hunter gatherer diets also tend to not be “very low carb” but contain on average about ~45% of energy from “safe carbohydrate sources” compared to the nearly zero-carb of many low carb dieters.
We know that (1) hunter gatherers eat much less palmitic acid than many modern day “paleo dieters” and (2) they tend to have low, rather than high LDL cholesterol. I’d say it’s extremely likely that palmitic acid is playing a role here, even if nutrient deficiency *also* is.
It may very well be true that the unusual lipid profile of a low-carb dieter (high HDL, high LDL, low trigs, LDL pattern A) presents a very low risk of cardiovascular disease, but it’s not “paleo” and isn’t an experiment I want to test with my own life/body. There’s simply no evolutionary precedent for extremely high LDL levels.
Keep in mind that familial hypercholesterolemia is also a disease of deficient LDL endocytosis not entirely unlike the down-regulation of LDL seen with high palmitic acid consumption. FH is of course, highly associated with cardiovascular disease at a young age.
I should also probably clarify what I mean by “high” vs “low” LDL. I really doubt there’s any cause for concern over levels like Chris Kessler’s “high” 138mg/dl, but I think the people in the 300-600mg/dl range should probably be a bit more concerned than they are.
Thanks, Tyler. It’s a great point. I’m planning to continue the LDL series and maybe I’ll have something to say about the palmitate issue.
I also agree, LDL of 300 is vastly more worrisome than LDL of 130.
Sorry, that was a typo- should be “Chris Kresser”
I also raised the LDL downregulation issue above (7 March), in the context of individual variability. However for those people for whom higher carbs are not a good option, Tyler’s suggestion is not going to work. And the problem is really that quite possibly (though of course we don’t know for sure) the higher carbs (even if safe) to replace palmitic acid are a worse option for (almost?) everybody. Equally for other potential replacements.
Alas we all have to test this ‘experiment’ with our life, we can only choose which arm we are in.
(I don’t think we know for sure which is more ‘paleo’ whether the question makes sense (eg. maybe there was more than one kind) or even whether it matters (paleo was not optimalized for health(span). But there are strong views out there that high palmitic diet IS in fact ‘paleo’.)
I guess I’m filling the time here, while waiting for Paul’s next post on this.
(sorry, it was 6 March)
Following up from my post about 2 months ago, here are the changes in my lipid profile from a draw a couple days ago:
TC: 391 to 323
HDL: 55 to 67
TGs: 54 to 37
LDL (Iranian): 269 to 192
The changes I made were cutting most of the butter out of my diet, increasing carbs from 50-75g a day to 150-350g and adding .25-.75lb of lamb liver per week.
Can’t say for sure what it was that caused the change, but given how many people commented that they’ve eaten a lot of liver for a long time and still have elevated LDL, I suspect that it was the removal of butter. I was eating close to a pound a week before and now I use a very small amount just to get lamb steaks to not stick to the pan.
I’m still unsure about the medical significance of aberrant LDL values, but because hominins have a fairly limited history of dairy fat consumption, I’m going to play it safe and rely on grass-fed lamb tallow and pastured egg yolks for dietary fat.
Hi Travis,
I also don’t know the medical significance, but this looks like an improvement.
I don’t think butter is harmful directly, but the extra fat and reduced carbs may have added to oxidative stress. I would look at antioxidant status, especially the minerals, for further improvements.
Best, Paul