Don’t Worry About Cholesterol

A comment by Dr. Charlie, biochemist.

~~~

Sorry for delay in getting back to you re TC/ apoB and Gabriella’s concern over a patient who had a blip in her LDL readings. In a way I’m glad that I did because just by chance I watched again the Wisdom of Clouds speech by Tom Naughton and the lecture by Prof Tim Noakes on YouTube, entitled “The Great Diet Controversy: UCT taught me to Challenge Beliefs”.

Although we could discuss the size and shape of the cholesterol bearing particles and whether it’s the number or total quantity that should be considered, I think that it is more important to consider whether the whole concept of the cholesterol hypothesis is correct. In the early days of the hypothesis many trials attempted but failed to establish a clear link between cholesterol and CHD – yet the medical profession were eventually persuaded that there was a very positive relationship.

I would agree with Noakes’ response to a question concerning cholesterol levels and say that women should not pay any attention to them – no work has shown any link for them and for men over 50, high cholesterol levels have been shown to be protective. For example, many studies, including the famous Framingham study begun in 1948, have shown that in people over 50/60, higher levels of cholesterol are protective (ie the death rate comes down with higher cholesterol). I just happen to have to hand the results of a recent Scandinavian study. This study published in the Scandinavian Journal of Health Care [I think that's the one - Ed] looked at the levels of cholesterol and risk of death in almost 120,000 adults living in Denmark.

The researchers found that having higher than recommended levels of total cholesterol was associated with a reduced risk of death. So they looked at the death rates amongst men who had a total cholesterol level of less than 5 mmol/l and compared that figure with the death rates of men who had total cholesterol levels between 5 and 5.99, and those between 6 and 7.99, and those with levels of 8 and above.

  • They found that in men aged 60-70 when compared to those who had a total cholesterol level of less than 5...
  • those with levels of 5.00-5.99 had a 32% reduced risk of death; and
  • those with levels 6.0-7.99 had a 33% reduced risk of death.

Even in individuals with levels of 8.00 mmol/l and above, the risk of death was no higher than it was for those with levels less than 5.0 mmol/l.

The results were similar for women too. In women aged 60-70, levels of 5.0-5.99 and 6.0-7.99 were associated with a 43 and 41 per cent reduced risk of death respectively.

In individuals aged 70 and over, the results were similar, except here, levels of total cholesterol of 8.00 mmol/l or more were associated with a reduced risk of death too (in both men and women).

Together, these findings suggest that the current total cholesterol recommended by medics and other health professionals are way off beam. And the authors of this study suggested –rather meekly that - these associations indicate that high lipoprotein levels do not seem to be harmful to the general population.

So I hope you appreciate that for me the minutiae of particles may be of academic interest but not of medical interest – apart from the fact that higher levels are protective!

~~~

It has been 2007 since I have blogged on this topic, saying essentially the same thing, and nothing seems to change.

Thanks, Dr. Charlie!

Comments

  1. Well I do think cholesterol levels can be useful; very high levels of cholesterol can be indicative of some kind of systemic infection. Very low levels of cholesterol could indicate statinitis, a very serious ailment indeed :)

    • Nils, you wouldn’t be British by any chance?

      That was pithy, sir, and I’m embarrassed that no one has yet to extend you a proper golf clap. [clap]

    • Richard, I’m Dutch actually. I’m glad someone got a chuckle out of it at least. Sad truth being that statins are being prescribed to virtually anyone nowadays, won’t be long before doctors will start suggesting liver removal surgery to curb that pesky cholesterol synthesis.

  2. sootedninjas says:

    heads-up. Ameer just posted your podcast with him.

    • Ameer mentioned “Gaia hypothesis” in the podcast. Unfortunately this one looks like it has been debunked – the best shot at Gaia is a book by Peter Ward “Medea hypothesis”. Peter Ward is a specialist in mass extinctions, especially the largest one – Permian extinction (a separate book “Under the green sky” covers this one).

      A sample:
      http://www.youtube.com/watch?v=3lYN_lXU9PA

  3. My mother – who will be 95 this April – has cholesterol levels well above the recommended levels (that is if she’s not taking a statin…which I discontinued a few years ago, much to her doctors objection and consternation and much to the improvement of her overall health).

    An added note: Her primary physician has retired and her new, much younger female doctor, has not requested that her cholesterol be checked in over a year of care and has never mentioned statins.

  4. gabriella kadar says:

    For sure, I’d never agree to taking a statin and neither do any of the intelligent medical specialists of my acquaintance, but what I noticed is this study was all about LDL and did not mention HDL.

    Denmark is also the country that temporarily and misguidedly instituted a tax on butter and other saturated fat……..for a while. http://www.washingtonpost.com/blogs/wonkblog/wp/2012/11/13/denmark-scraps-worlds-first-fat-tax/
    http://www.economist.com/news/europe/21566664-danish-government-rescinds-its-unwieldy-fat-tax-fat-chance

  5. if cholesterol is an indicator (direct or indirect) of overall inflammation then I’d like to know and work on keeping it low but if there are other markers CRP, homocysteine, fasting BG, etc that are better then I’d rather focus on that and forget being so paranoid about the marker. I am intrigued how Robb Wolf’s LDP-P went from 1400 to 800 after using PS and how thrilled he was with that so it must mean something if Robb is gettin’ giddy.

  6. Hey Bill,

    Would you mind linking to where Robb Wolf discusses the change in his LDL-P? Thanks

  7. Moreorless says:

    Cholesterol after 50 or 60 loses it’s correlation mainly because the sick and elderly can have falling cholesterol.
    I assume the big trials that failed he was referring to were covered in this video
    http://www.youtube.com/watch?v=z-8k1gAog40

  8. It was on Kiefers new podcast called body IO. I think about 20-30 min in. You have to listen to it on soundcloud not apple podcasts.

  9. What does anyone think of this? is it a positive, a negative, or it doesn’t mean anything? is it good the cholesterol is going down.

    http://www.ncbi.nlm.nih.gov/pubmed/14598916
    Resistant starches of beans reduce the serum cholesterol concentration in rats.
    Abstract

    We examined the effects of the resistant starches of adzuki (Vigna angularis), kintoki (Phaseolus vulgaris, variety), and tebou (P. vulgaris, variety) beans on the lipid metabolism in rats. Rats were fed a cholesterol-free diet with 25 g of cornstarch (CS)/100 g diet, 25 g of adzuki starch (AS)/100 g diet, 25 g of kintoki starch (KS)/100 g diet, or 25 g of tebou starch (TS)/100 g diet for 4 wk. The cecal contents in the TS group were significantly higher than those in the CS and KS groups. There were no significant differences in body weight or food intake among the groups. The relative liver weight in the CS group was significantly greater than that of the AS, KS, and TS groups. The serum total cholesterol, VLDL+IDL+LDL-cholesterol, and triglyceride concentrations in the AS, KS, and TS groups were significantly lower than those in the CS group throughout the feeding period. Though the total hepatic cholesterol concentration in the TS group was significantly higher than that in the KS group, there were no significant differences between the CS and other starch groups. The cecal pH value in the CS group was significantly higher than that of the bean starch groups. The cecal butyric acid concentrations in the AS, KS, and TS groups were significantly higher than that in the CS group, and the cecal total short-chain fatty acid (SCFA) concentrations in the AS and TS groups were significantly higher than those of the CS group. The fecal cholesterol excretion of the AS, KS, and TS groups were significantly higher than that in the CS group. The fecal coprostanol excretion in the AS group was significantly higher than that in the CS group. There was a negative correlation between the serum VLDL+IDL+LDL-cholesterol concentration and fecal neutral steroid excretion (r = -0.664, p < 0.001) in the present experiment. Furthermore, the cecal total SCFA concentration was negatively correlated with the serum VLDL+IDL+LDL-cholesterol concentration (r = -0.665, p < 0.001) and positively correlated with fecal neutral steroid excretion (r = 0.481, p < 0.05). The cecal butyric acid level was also negatively correlated with the serum VLDL+IDL+LDL-cholesterol concentration (r = -0.609, p < 0.01) and positively correlated with fecal neutral steroid excretion (r = 0.658, p < 0.001). The results suggest that AS, KS, and TS elevate cecal SCFA concentration, in particular butyric acid concentration, and fecal neutral sterol excretion, and lower the serum total cholesterol level.

    • Spanish Caravan says:

      This is a pretty straight forward. Once you wake up from the propaganda that low-carbing unilaterally lowers cholesterol, then this is fairly easy to accept. I’ve seen hundreds of cholesterol patterns to realize that for most people, high-carb Paleo is what will lower their cholesterol, not the low-carb version. That’s assuming that high-carb Paleo includes some RS and that is probably the case, even if you don’t eat PS.

      The cholesterol-lowering pattern of low-carbing parallels weight loss and metabolic improvements. That’s for about 50-70% of such people. But what people don’t realize is that most successful low carbers started from a very high baseline to begin with. So lowering TC isn’t really that significant. What’s more significant is how it will stabilize.

      The problem, however, is that when compared to those who eat higher carbs, such people generally have higher TC. If, at this point, they embark on a higher carb Paleo, their TC would generally fall. This is the case with hundreds of people that I’ve seen and you generally see two other correlates: your BUN starts going down as you consume less protein and fat, your Cr may also go down due to protein restriction. By looking at just high BUN, low trigs, low WBCs and low FT3/T3, I can generally tell how much carbs they’re eating.

      Now, since LDL is a crapshoot, I wouldn’t exactly embrace the merits of lowering cholesterol. However, people don’t realize is that low-carbing does not really lower TC that much. It seems to because of the confounding factor introduced from the very beginning: those who low carb are metabolic disasters to begin with. The remainder, 30-50%, will always have elevated LDL on a low-carb diet and no matter what they try, they’ll not be able to lower their TC. Two reasons: (1) ApoE4, which is about 1 in 4; and (2) low FT3/T3, which will increase LDL. For some, this will be approach hypercholesterolemia at 350+, which usually translates to high LDL-P. For those, you have no option but to do high-carb Paleo.

    • Thansk,

      what I find intersting is that for so many people their cholesterol numbers get lower when they get in better health, lose weight, work out, etc.

      So even though I don’t agree with so many people taking statins. and I don’t obsess about cholesterol. I find it hard to dismiss cholesterol as a marker all together.

    • Spanish Caravan says:

      Well, the cholesterol components do matter. They rank in the order of importance as follows: HDL, Trigs, LDL. But total cholesterol does not correlate well with health problems except when they’re above say, 300-350. That’s hypercholesterolemia and you’d probably have high LDL-P and some atherosclerosis, although everyone does. Even then, your overall artery health is affected by other factors like ferritin, homocysteine, LP(a), etc.

      But your metabolic status is indicated by your TC/HDL and HDL/Trigs. Those are important numbers, but it’s easy to be confounded by these numbers still. For example, very high HDL due to genetics doesn’t help you as much as HDL “earned” though exercise and proper dieting. Trigs that are too low could indicate immune problems. You watch out for those caveats, you can tell a lot about what people are eating, what their arterial and metabolic health is like. Except for LDL — that is really an X factor. It’s determined by HDL, Trigs, CRP, liver enzymes, WBCs and other markers. LDL >70 but under 200 by itself defies interpretation. That’s what people fail to understand.

  10. Hello,
    I was advised to use a low dose water soluble statin to lower LDL-P. No other risk factors. Any dietary insight would be appreciated.

    December 2013 numbers
    Total Cholesterol 307, down from 525 two years ago when I was eating higher fat and lower carb.
    LDL-C 225
    HDL 71
    LDL-P 2259
    Trigs 56
    Age = 48

    Perfect Health/WAPF style diet
    Started introducing RS a few weeks ago
    Started low dose water soluble statin a few weeks ago
    Compete and train in powerlifting

    • You *might* suffer from hypothyroidism, do you ingest enough iodine? Otherwise you could be suffering from systemic Candida maybe. I don’t think your numbers seem particularily out of whack. I’d ditch the statins, but at least you’re on water soluble statins, which are the least harmful.

    • Spanish Caravan says:

      You may no longer be doing high fat/low carb but you might not be high carb enough. I’m just basing that on your trigs. How many grams of carbs are you eating and how high is your BUN? Safe starches every meal and RS supplementation should lower both your LDL-C and LDL-P. If they don’t go down, it could be due to low T3 and/or ApoE4. If ApoE4 and you’re not doing high carb Paleo, then there’s your explanation. If low T/Ft3, then you could try to increase your T3 via RS; based on symptom improvements, it seems possible.

    • charles grashow says:

      What is your current diet like? What do you eat in an average day?

    • My first meal is usually post workout around 1PM
      3 eggs
      16 oz. raw milk
      banana
      1C blueberries
      50g grass fed whey protein powder
      Small handful of almonds or macadamia nuts

      4PM
      12 oz grass fed beef or lamb (6oz liver once a week)
      8 oz bone broth reduction
      1/2 # non starchy vegetable cooked with butter or coconut oil

      9PM
      6-8 oz seafood (wild salmon, mackerel, shrimp, scallops, mussels, etc)
      1/4-1/2 pound non starchy vegetables cooked with butter or coconut oil
      3-4C of sweet potato mash or white mashed potatoes or white rice or beans

      11PM
      2T Potato starch

    • That was one of Chris Kresser’s recommendations after working with him for the past year and a half and not making any more progress.

    • charles grashow says:

      1) It looks like you’re getting way too much protein

      2) Have you been tested for FH

      3) Have you considered a test like this

      http://www.bostonheartdiagnostics.com/science_portfolio_cholesterol_balance_test.php

      “All individuals differ when it comes to the balance between cholesterol production and absorption. Some people synthesize cholesterol more than they absorb, while others absorb more than they synthesize.

      Knowing how an individual produces and absorbs cholesterol can help determine the most effective LDL-C lowering therapy. Understanding in advance which therapy will have the greatest efficacy allows for a more successful and cost-effective CVD treatment strategy.”

      4) Have you gotten a complete thyroid panel?

    • My BUN was 19 a year and a half ago. I don’t have a recent number.
      I am back at 150-200g of carbs per day as of a couple weeks ago.
      Safe starches with all meals makes me a bit drowsy and slow at work so I usually save them for my last meal of the day and I sleep much better.

    • Thank you for the information. I will read the link.
      I haven’t been tested for FH. I don’t know what the test is.
      I had a thyroid panel done a year and a half ago and my Total T3 was low (62). My Free T3 was (2.7)
      What would you suggest for protein intake? I am 200# and power-lifting 2-3 days a week and conditioning 2 days a week.

    • Spanish Caravan says:

      Well, your T3 is low and FT3 is low-normal. If your TSH is under 3.5-5, it’s what we call the low T3 syndrome driven by carb restriction. But you may or may not have symptoms: have symtoms like cold fingers/toes, low body temp, dry skin, fatigue, constipation driven by slow transit?

      Let’s forget about your LCL-C, as it is meaningless; only LDL-P is somewhat meaningful but then that doesn’t close the book on CVD risk altogether.

      So there’re 3 possibilities: (1) you increase T3 and LDL-P goes down (along with LDL-C). You can do RS2 supplementation or take cytomel or compound T3 medication. But if you have no euthyroid symptoms, there’s no sense in taking it. Test after 2 months of RS supplementation at least 2-3 tbsps at night before going to bed.

      (2) You could be ApoE4 and respond genetically to SaFA. In that case, your only option is to increase carbs even more; reduce red meat, heavy cream, even egg yolks. Eat more monos and legumes in place of SaFA.

      (3) Both your LDL-C and LDL-P might not correlate with dangerous atherosclerosis. We’re told that LDL-P is the “gradient-testing” of atherosclerotic particles, but I don’t think that’s always the case. In this case, I rely on other inflammation markers like liver enzymes, WBCs, ferritin, HS CRP, ESR, etc.

      - ALT/AST between 8-17 or so are ideal: it’s a marker of leanness and being “metabolically thrifty”. Start getting over 25 or so and it tacks onto your CVD risk
      - WBCs above 7.5-8.0 correlate well with arterial inflammation and thrombosis. I bet you’re very low given your low trigs and TC/HDL < 3.5x.
      - You need an iron panel for Ferritin but you're probably ok and <90.
      - How's your ApoB? If your ApoB is under 90 or better yet under 80, you basically have a "split verdict" and I wouldn't worry about LDL-P.
      - How's your Small LDL-P? Under 250 and you're probably fine. You should have all these numbers if you did NMR testing.
      - Your homocysteine could also go up if your T3 is low. But if that's under8-9ish, nothing is "sticking" to the arterial wall even though your LDL-P is high.
      - Get your fibrinogen and Lp(a) measured. These days you can only get Lp(a) if you do VAP testing, which is being shunted aside in favor of NMR. Under 12, A OK. You could have low trigs, Tc/HDL < 3.5x, and low LDL-P and still drop dead from a stroke or heart attack if your Lp(a) is out of line. It's the single most important risk factor but docs will only test if all your relatives dropped dead at say 40.

      See what I mean. CVD risk is not really measured by cholesterol. It's an incomplete picture. You capture only about 40% of the total CVD risk with the 3 cholesterol components and the sum total, which is meaningless in many cases since LDL-C is a crapshoot.

    • charles grashow says:
    • Wow, thanks for all of the information and your time. Looks like I have more homework to do.
      I do have some of the mentioned numbers.

      TSH is 1.91. I do have cold hands and feet. also some fatigue but a lot of that comes with a 60 hour work week.
      I tried iodine supplementation for the better part of a year under Chris Kresser’s supervision but didn’t get the desired effect.
      I will increase the RS to 3T at night and retest in a couple months.

      ALT/AST numbers as a marker of leanness I don’t know what they are.
      I stay fairly lean at 6′ and 198#. Body fat runs close to 12% year round. I put on fat very easy in the midsection when I take carbs up too high for me or fail to make dietary adjustments to compensate for higher carbs ( still trying to figure out what those adjustments are). Although the strength gains in the gym are pretty nice from the extra carbs. I feel best when I fast during the morning and into the afternoon, one or two small afternoon meals and have a large carby meal at night after I finish work (10-11PM).

      WBC is now 4.9 which is the highest it has been in a few years

      HS CRP = .68

      Ferratin is now 125
      That is down from 478 in 2011
      I donate blood every other month but started to get anemic so now just 4 times a year

      Hepatic Function Panel was all good

      I did an NMR but didn’t see an ApoB score

      LDL-P = 150

      LPa = 16.0
      My Father died at 41 from a heart attack but had a very different lifestyle.

      Its funny that I never would have been aware of any of these numbers if I hadn’t been turned down for life insurance as part of life event planning with my business partner. Most folks think I am 10-15 years younger than my actual age and I have never had much cause to see doctors. Overall I feel good and have plenty of Go in the tank. My testosterone is naturally high and I set 4 state records for masters (45-49) in my last power-lifting meet at 198#. I now have a one year old daughter and the insurance question beckons again. Sometimes I think the ignorance was bliss and things were less complicated when the only worries were family, business, getting stronger, reading good books and thinking about food for the joy that it can be.

      I weighs on the mind of a working man having to argue with doctors who think you are an unnecessary accident waiting to happen and if you don’t take the statin will question if your Daughter has a fool for a Daddy.

      If you can’t get life insurance due to high cholesterol numbers it makes you wonder because don’t insurance companies and Vegas always win in the end?

    • charles grashow says:

      You said

      December 2013 numbers
      Total Cholesterol 307, down from 525 two years ago when I was eating higher fat and lower carb.
      LDL-C 225
      HDL 71
      LDL-P 2259
      Trigs 56

      1) So – I don’t understand what you mean by LDL-P = 150.

      2) By a complete thyroid panel I mean something like this
      TSH
      Total T4 (TT4)
      Total T3 (TT3)
      Reverse T3 (rT3)
      T3U
      Free T4 Index (FTI)
      TPO and Anti-TG antibodies
      Free T4
      Free T3

      3) As to Lp(a) this might prove helpful
      http://www.bhlinc.com/clinicians/clinical-references/reference-manual/chapter16

      4) High WBC
      Did you get your blood work done relatively soon after a heavy workout?
      Were you under a great deal of stress when you got tested?

      5) These are the scary numbers
      December 2013 numbers
      Total Cholesterol 307, down from 525 two years ago when I was eating higher fat and lower carb.
      LDL-C 225

      Since the numbers are going down I might wait and get retested in a few months – see if the numbers continue to go down or not

    • Spanish Caravan says:

      Sean, you’re euthyroid. If you contracted it while VLCing, join the club; it would almost be an exception if you didn’t have cold fingers and toes. It’s primary Raynaud’s, which about 10% of the population have. As I’ve posted elswhere, however, the diceyness of Raynaud’s multiplies when you’re immune compromised or genetically vulnerable: autoimmunity is a distinct possibility for such people, in which case your Raynaud’s becomes secondary, with a full-blown autoimmune disease like RA in tow.

      However, it’s so common that you need not worry. And that’s why you don’t need a full thyroid panel like the other guy is suggesting. You’re euthyroid and it’s not Hashimoto’s; no need for antibodies and the only number that will correlate with symptoms is FT3 (in its absence, T3), as long as your TSH is normal. The condition can be addressed by T3 meds but I would take advantage of RS and see if that ups your T3 first. Your high TC is correlated with low T3 and FT3; the free portion is higher so you’re low-normal but your T3 is quite low. That’s enough to push your LDL high. And the reason why your WBCs are lowish normal is also related to T3 and Raynaud’s.

      However, I forgot to read that your TC used to be 525. Check and see if T3/Ft3 was low at that time. If so, that strengthens that correlation but TC that high could be driven by FH / ApoE4. Get your genes mapped by 23andme and it will tell you. If so, then you will benefit from even higher carb Paleo. I’d personally increase my safe starch portions significantly; you’re eating some every meal but you’re also eating considerable SaFA; just do an experiment for 1-2 months where you ease up on all dairy/butter, heavy cream, steak, eggs, and go heavy legumes, fish and poultry. Just try that and
      I’m willing to bet, your TC, especially LDL will plummet to what it was during your SAD days. Concurrently, that should also increase your T3; so that increased carb intake should work whether your high LDL is due to low T3 or ApoE4. Kill 2 birds with one stone. Up the carbs.

      But if your small LDL-P is only 150, while your LDL-P is 2259, that’s terrific. That’s at the top 25%ile. I’d think that significantly lowers the risk of your high overall LDL-P; you’re kind of similar to Jimmy Moore, who has very high LDL-P but his small LDL-P is only like 30, at the top 1-2%. He’s still kicking. Ferritin that high may have been an acute phase reaction if your CRP was around 0.7 when tested. So scratch beneath the surface of high LDL-P and your numbers aren’t as bad. But if you want that to be better, up the carbs and cut the fat, saturated fat, that is.

    • Spanish, can you email me? Address on the about page.

    • charles grashow says:

      @Spanish

      Jimmy Moore’s small LDL-P was 448 per his last blood work

      Also – IMHO it’s very dangerous to tell someone what they have – unless you examine all of the blood work and do a physical exam as well

    • Spanish Caravan says:

      You’re right. His LDL-P is in the 35-40%ile.

      http://livinlavidalowcarb.com/blog/tag/ldl-p/feed

      But I recall him saying that it was 30 during his Thomas Dayspring interview and I became astonished and jotted it down. I suspect he may have gotten that mixed up with his Trigs, which is in fact 38. Listen to it and tell me if doesn’t say it. Dayspring was on twice and I dont’ remember where he says it exactly.

      http://livinlavidalowcarb.com/blog/atlcx-episode-29-dr-thomas-dayspring-cholesterol-testing-what-matters-most/16019

      As for being dangerous, it is alarming to have TC > 350; 525 is definitely alarming. Which is why he’s on a chase to lower it by upping his T3 and lowering his SaFA if he’s ApoE4. But that concern is entirely based on atherosclerosis, which requires a few more things to really worsen and become a CVD threat. Those things are inflammation-related and present themselves as high trigs, low HDL, high WBCs, and other markers indicated above. Atherosclerosis is a precondition; you need thrombosis in most cases to have a coronary or a stroke.

      I do agree that he needs to get his TC down. The reason for that is because if he ever lapses and his trigs go up and HDL go down and other inflammation markers go up, then he does become a sitting duck. However you cut it, the answer is higher carb Paleo.

    • Thanks Spanish for all of the input. I think more of a Mediterranean – paleo approach for a couple months would be worth a try. At that point I will have the RS, a lower SaFA diet that is higher in carbs and the low dose water soluble statin in place to see where the numbers go. If things are better I can ease off the statin and see if the LDL-P numbers stay in line.

    • charles grashow says:

      If you want to try some alternatives to statins you might research these

      http://www.nutritionaloutlook.com/article/cholesterol-control-3-13607
      Cholesterol Control: Bergamot, Berberine, and Amla May Help

      http://www.lef.org/magazine/mag2000/oct2000_itn.htm
      Artichoke extract lowers cholesterol safely

    • charles grashow says:

      Shouldn’t Sean take a test to see if he’s ApoE4?

    • charles grashow says:

      Sean also said

      WBC is now 4.9 which is the highest it has been in a few years.

    • Thanks Charles

    • If someone was ApoE4 than a low SaFA higher carb paleo diet would help control cholesterol. However isn’t ApoE4 a much higher risk for Alzheimer disease which would require a VLC diet or do I have that wrong as well?

    • FYI

      December 6 2013: Pending an FDA decision, 23andMe no longer offers new customers access to health reports.

    • Spanish Caravan says:

      ApoE4, especially if you’re homozygous, is a major factor in Alzheimer’s. However, it is not unilaterally determining. You can get Alzheimer’s with other Apo types. Not all E4s, hor or hetero, get it. But the fear that Alzheimer’s is Type 3 diabetes and the only way to control BG is through severe carb restriction is forcing these people to VLC. That is tragic. You can stave off BG dysregulation by eating 70-150 grams of safe starch carbs. For most people with no insulin secretion problem, that is really the sweet spot for BG control. If you VLC at 30 grams, you might end up with physiological insulin resistance, which offsets any gain you might have. So it ends up being a wash and plus you end up with VLC side effects plus lack of food choices to lower your LDL; try eating only MUFA and PUFA on a VLC diet.

    • Spanish Caravan says:

      That tells me Sean might have been VLCing. WBCs under 3.5, Trigs under 30, FT3 under 2.3. That’s a witch’s brew for kickstarting immune problems.

    • Hello Spanish,

      My latest scheduled lab results came back.
      Changes I have made during the past 60 days between tests:

      2-3 T RS daily – 60 days. Cut back to 2T most days after I started dreaming myself awake several times a night due to David Lynch style vividness during dream state. At 2T sleep is good and dreams are manageable.

      Minimum 150 g safe carbs daily – 60 days. 150 – 200g per day on non active days and 250g or more on heavier training days. Most carbs with last meal of the day.

      Fasting – 6 months. Fasting for 12-16 hours per day and training in a fasted state with the addition of BCAA’s. I only do this because I feel much more energetic and productive in the morning and I don’t have an appetite in the morning. Occasionally I am hungry in the mornings, if so I eat breakfast.

      Seafood at least once a day (twice a day 3-4 days per week) – 60 days. Mostly wild salmon, Spanish mackerel, oysters, mussels, scallops, shrimp, sardines. Also pastured chicken twice a week. The other meal is grass fed beef, lamb, pastured eggs and raw milk (16 oz after heavy training sessions).

      40 mg Pravastatin Sodium daily – 30 days

      Still training for power-lifting 4 days per week and walking 3-4 miles with a weighted vest 2-3 days per week. Plus a few miles a week walking back and forth from work.

      Results:

      LDL-P = 2357 (+98)
      HDL = 65 (no change)
      LDL = 148 (-100)
      LDL size = 22
      LP IR Score <25 (-2)
      Total cholesterol = 226 (-81)
      Trigs = 67 (+12)
      BUN = 29
      Ferratin = 149 (+24)

  11. charles grashow says:

    http://jama.jamanetwork.com/article.aspx?articleid=192897
    Relationship of Baseline Serum Cholesterol Levels in 3 Large Cohorts of Younger Men to Long-term Coronary, Cardiovascular, and All-Cause Mortality and to Longevity

    RESULTS:

    Death due to CHD accounted for 26%, 34%, and 28% of all deaths in the CHA, PG, and MRFIT cohorts, respectively; and CVD death for 34%, 42%, and 39% of deaths in the same cohorts, respectively. Men in all 3 cohorts with unfavorable serum cholesterol levels (200-239 mg/dL [5.17-6.18 mmol/L] and >/=240 mg/dL [>/=6.21 mmol/L]) had strong gradients of relative mortality risk. For men with serum cholesterol levels of 240 mg/dL or greater (>/=6.21 mmol/L) vs favorable levels (<200 mg/dL [<5.17 mmol/L]), CHD mortality risk was 2.15 to 3.63 times greater; CVD disease mortality risk was 2.10 to 2.87 times greater; and all-cause mortality was 1.31 to 1.49 times greater. Hypercholesterolemic men had age-adjusted absolute risk of CHD death of 59 per 1000 men in 25 years (CHA cohort), 90 per 1000 men in 34 years (PG cohort), and 15 per 1000 men in 16 years (MRFIT cohort). Absolute excess risk was 43.6 per 1000 men (CHA), 81.4 per 1000 men (PG), and 12.1 per 1000 men (MRFIT). Men with favorable baseline serum cholesterol levels had an estimated greater life expectancy of 3.8 to 8.7 years.
    CONCLUSIONS:

    These results demonstrate a continuous, graded relationship of serum cholesterol level to long-term risk of CHD, CVD, and all-cause mortality, substantial absolute risk and absolute excess risk of CHD and CVD death for younger men with elevated serum cholesterol levels, and longer estimated life expectancy for younger men with favorable serum cholesterol levels.

  12. charles grashow says:

    http://circ.ahajournals.org/content/103/22/2705.full
    High Prevalence of Coronary Atherosclerosis in Asymptomatic Teenagers and Young Adults
    Evidence From Intravascular Ultrasound

    “Methods and Results—Intravascular ultrasound was performed in 262 heart transplant recipients 30.9±13.2 days after transplantation to investigate coronary arteries in young asymptomatic subjects. The donor population consisted of 146 men and 116 women (mean age of 33.4±13.2 years). Extensive imaging of all possible (including distal) coronary segments was performed. Sites with the greatest and least intimal thickness in each CASS segment were measured in multiple coronary arteries. Sites with intimal thickness ≥0.5 mm were defined as atherosclerotic. A total of 2014 sites within 1477 segments in 574 coronary arteries (2.2 arteries per person) were analyzed. An atherosclerotic lesion was present in 136 patients, or 51.9%. The prevalence of atherosclerosis varied from 17% in individuals 0.5 mm). In these 136 subjects, the intimal thickness at the lesion was 1.08±0.48 mm, and percent stenosis averaged 32.7±15.9%. Figure 3⇓ shows the frequency distribution of greatest intimal thickness in each patient for different age groups, demonstrating that intimal thickness increases progressively with advancing age. In all age groups, a portion of the cohort had ≥1 site with intimal thickness exceeding the 0.3-mm or 0.5-mm thresholds used for the definition of atherosclerosis. Strikingly, when the more stringent definition of >0.5 mm was used, even the 12- to 19-year-old age group showed atherosclerosis in 17% of subjects. By age 40 years, >70% of individuals showed ≥1 coronary site with an intimal thickness >0.5 mm. With a less conservative threshold of 0.3 mm, 21% of teenagers and 91% of individuals >40 years old had ≥1 atherosclerotic lesion.

    Atherosclerotic coronary disease is the leading cause of death and a major source of morbidity in developed countries, resulting in nearly 1 million deaths and $100 billion in annual costs in the United States alone.16 Necropsy studies have demonstrated that atherosclerosis begins at a very early stage in life. The present study provides unequivocal in vivo evidence of atherosclerosis in young asymptomatic individuals with no evidence of clinical coronary artery disease (Figure 3⇑). This study is unique because it provides detailed, clinically relevant, quantitative, in vivo information on early atherosclerosis from an asymptomatic young population.”

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