Showing posts with label lipid - blood test. Show all posts
Showing posts with label lipid - blood test. Show all posts

26.6.11

HDL and Immunity - Perfect Health Diet

HDL and Immunity | Perfect Health Diet

HDL – high-density lipoprotein – particles are good for you: High HDL levels are associated with lower mortality overall and lower mortality from many diseases – not only cardiovascular disease but also cancer and infection.

People with high HDL are only one-sixth as likely to develop pneumonia [1], and in the Leiden 85-Plus study, those with high HDL experienced 35% lower mortality from infection [2].
Each rise of 16.6 mg/dl in HDL reduced the risk of bowel cancer by 22% in the EPIC study. [3]
In terms of overall mortality, in the VA Normative Aging Study, “Each 10-mg/dl increment in HDL cholesterol was associated with a 14% [decrease] in risk of mortality before 85 years of age.” [4]
This must be surprising to those who think HDL is only a carrier of cholesterol. The lipid hypothesis presumed that the function of HDL is to clear toxic cholesterol from arteries, cholesterol having evolved for the purpose of giving us heart attacks. HDL then brings cholesterol to the liver which disposes of it returns it to the blood via LDL (which evolved for the purpose of poisoning arteries with cholesterol, and giving HDL something to do). (Hat tip to Peter for this formulation of the lipid hypothesis.)

But there is an alternative hypothesis: that infections cause disease, and that HDL has an immune function. This hypothesis would explain why HDL protects against infections and against all diseases of aging.

Conclusion

HDL particles are “Trojan Horses” that attack pathogens and neutralize their toxins.
If you want to remain free from infectious diseases – which is to say, all diseases – to a ripe old age, it’s important to make your HDL particles numerous.

On Thursday, I’ll discuss ways to do that.

References

[1] Gruber M et al. Prognostic impact of plasma lipids in patients with lower respiratory tract infections – an observational study. Swiss Med Wkly. 2009 Mar 21;139(11-12):166-72. http://pmid.us/19330560.
[2] Berbée JF et al. Plasma apolipoprotein CI protects against mortality from infection in old age. J Gerontol A Biol Sci Med Sci. 2008 Feb;63(2):122-6. http://pmid.us/18314445
[3] van Duijnhoven FJ et al. Blood lipid and lipoprotein concentrations and colorectal cancer risk in the European Prospective Investigation into Cancer and Nutrition. Gut. 2011 Mar 7. [Epub ahead of print] http://pmid.us/21383385.
[4] Rahilly-Tierney CR et al. Relation Between High-Density Lipoprotein Cholesterol and Survival to Age 85 Years in Men (from the VA Normative Aging Study). Am J Cardiol. 2011 Apr 15;107(8):1173-7. http://pmid.us/21296318.
[5] Kieft R et al. Mechanism of Trypanosoma brucei gambiense (group 1) resistance to human trypanosome lytic factor. Proc Natl Acad Sci U S A. 2010 Sep 14;107(37):16137-16141. http://pmid.us/20805508.
[6] Cheung MC et al. Phospholipid transfer protein in human plasma associates with proteins linked to immunity and inflammation. Biochemistry. 2010 Aug 31;49(34):7314-22. http://pmid.us/20666409.
[7] Genovese G et al. Association of trypanolytic ApoL1 variants with kidney disease in African Americans. Science. 2010 Aug 13;329(5993):841-5. http://pmid.us/20647424.
[8] Henning MF et al. Contribution of the C-terminal end of apolipoprotein AI to neutralization of lipopolysaccharide endotoxic effect. Innate Immun. 2010 May 25. [Epub ahead of print] http://pmid.us/20501516.
[9] El Harchaoui K et al. High-density lipoprotein particle size and concentration and coronary risk. Ann Intern Med. 2009 Jan 20;150(2):84-93. http://pmid.us/19153411.

How to Raise HDL | Perfect Health Diet

How to Raise HDL | Perfect Health Diet

Conclusion

HDL can be raised in destructive ways – such as ingestion of toxins or pathogens – but there are healthy ways to raise HDL.

I believe the following four ways are healthiest, and are sufficient to optimize HDL levels:

  • Eat a nourishing diet rich in saturated and monounsaturated fat, especially dairy fat, but low in omega-6 fats, fructose, and other toxins. In short: eat the Perfect Health Diet.
  • Be physically active. Be on your feet as much as possible; favor a standing desk over sitting. Do resistance exercise or other intense exercise occasionally.
  • Engage in intermittent fasting, and consume a lot of coconut oil, coconut milk, or MCTs to stimulate the ketone receptor.
  • Drink alcoholic beverages – but only when consuming meals low in polyunsaturated fats. Drink up when you eat beef, but be cautious when the entrée is salmon.

Niacin, the most effective pharmaceutical for raising HDL, has some toxicity and is probably inferior to coconut oil and intermittent fasting except in people with protozoal or fungal infections.

Our best wishes for high HDL!

Related posts:

References

[1] Navab M et al. HDL and cardiovascular disease: atherogenic and atheroprotective mechanisms. Nat Rev Cardiol. 2011 Apr;8(4):222-32. http://pmid.us/21304474.

[2] Ahmed K et al. GPR109A, GPR109B and GPR81, a family of hydroxy-carboxylic acid receptors. Trends Pharmacol Sci. 2009 Nov;30(11):557-62. http://pmid.us/19837462.

[3] Spate-Douglas T, Keyser RE. Exercise intensity: its effect on the high-density lipoprotein profile. Arch Phys Med Rehabil. 1999 Jun;80(6):691-5. http://pmid.us/10378497.

[4] Bey L, Hamilton MT. Suppression of skeletal muscle lipoprotein lipase activity during physical inactivity: a molecular reason to maintain daily low-intensity activity. J Physiol. 2003 Sep 1;551(Pt 2):673-82. http://pmid.us/12815182.

[5] Yanagibori R et al. The effects of 20 days bed rest on serum lipids and lipoprotein concentrations in healthy young subjects. J Gravit Physiol. 1997 Jan;4(1):S82-90. http://pmid.us/11541183.

[6] Costa RR et al. Effects of resistance training on the lipid profile in obese women. J Sports Med Phys Fitness. 2011 Mar;51(1):169-77. http://pmid.us/21297577.

[7] Hamilton MT et al. Role of low energy expenditure and sitting in obesity, metabolic syndrome, type 2 diabetes, and cardiovascular disease. Diabetes. 2007 Nov;56(11):2655-67. http://pmid.us/17827399.

[8] Tall AR et al. Metabolic fate of chylomicron phospholipids and apoproteins in the rat. J Clin Invest. 1979 Oct;64(4):977-89. http://pmid.us/225354.

[9] Rice BH et al. Ruminant-produced trans-fatty acids raise plasma total and small HDL particle concentrations in male Hartley guinea pigs. J Nutr. 2010 Dec;140(12):2173-9. http://pmid.us/20980644.

[9b] Mozaffarian D et al. Trans-palmitoleic acid, metabolic risk factors, and new-onset diabetes in U.S. adults: a cohort study. Ann Intern Med. 2010 Dec 21;153(12):790-9. http://pmid.us/21173413.

[10] Lakshman R et al. Is alcohol beneficial or harmful for cardioprotection? Genes Nutr. [Epub ahead of print] http://pmid.us/20012900.

[11] Thornton J et al. Moderate alcohol intake reduces bile cholesterol saturation and raises HDL cholesterol. Lancet. 1983 Oct 8;2(8354):819-22. http://pmid.us/6137650.

[12] McConnell MV et al. Effects of a single, daily alcoholic beverage on lipid and hemostatic markers of cardiovascular risk. Am J Cardiol. 1997 Nov 1;80(9):1226-8. http://pmid.us/9359559.

[13] Brien SE et al. Effect of alcohol consumption on biological markers associated with risk of coronary heart disease: systematic review and meta-analysis of interventional studies. BMJ. 2011 Feb 22;342:d636. http://pmid.us/21343206.

[14] Suh I et al. Alcohol use and mortality from coronary heart disease: the role of high-density lipoprotein cholesterol. The Multiple Risk Factor Intervention Trial Research Group. Ann Intern Med. 1992 Jun 1;116(11):881-7. http://pmid.us/1580443.

[15] Carlson LA, Hamsten A, Asplund A. Pronounced lowering of serum levels of lipoprotein Lp(a) in hyperlipidaemic subjects treated with nicotinic acid. J Intern Med 1989; 226: 271–6.

[16] Carlson LA. Nicotinic acid: the broad-spectrum lipid drug. A 50th anniversary review. J Intern Med. 2005 Aug;258(2):94-114. http://pmid.us/16018787.

[17] Dunbar RL, Gelfand JM. Seeing red: flushing out instigators of niacin-associated skin toxicity. J Clin Invest. 2010 Aug 2;120(8):2651-5. http://pmid.us/20664168.

[18] Bassan M. A case for immediate-release niacin. Heart Lung. 2011 Mar 15. [Epub ahead of print] http://pmid.us/21414665.

[19] Lukasova M et al. Nicotinic acid inhibits progression of atherosclerosis in mice through its receptor GPR109A expressed by immune cells. J Clin Invest. 2011 Mar 1;121(3):1163-73. http://pmid.us/21317532.

[20] Li Y et al. Effects of multivitamin and mineral supplementation on adiposity, energy expenditure and lipid profiles in obese Chinese women. Int J Obes (Lond). 2010 Jun;34(6):1070-7. http://pmid.us/20142823.

[21] Yanai H, Morimoto M. Effect of ascorbate on serum lipids and urate metabolism during exhaustive training. Clin Sci (Lond). 2004 Jan;106(1):107-9. http://pmid.us/12927020.

[22] Choi MJ. Effects of dietary taurine supplementation on plasma and liver lipids in OVX rats fed calcium-deficient diet. Nutr Res Pract. 2008 Spring;2(1):13-6. http://pmid.us/20126359.

[23] Elvevoll EO et al. Seafood diets: hypolipidemic and antiatherogenic effects of taurine and n-3 fatty acids. Atherosclerosis. 2008 Oct;200(2):396-402. http://pmid.us/18242615.

[24] Ruiz-Roso B et al. Insoluble carob fiber rich in polyphenols lowers total and LDL cholesterol in hypercholesterolemic sujects. Plant Foods Hum Nutr. 2010 Mar;65(1):50-6. http://pmid.us/20094802.

[25] Giacosa A, Rondanelli M. The right fiber for the right disease: an update on the psyllium seed husk and the metabolic syndrome. J Clin Gastroenterol. 2010 Sep;44 Suppl 1:S58-60. http://pmid.us/20616745.

[26] Ishikawa M et al. Taurine’s health influence on Japanese high school girls. J Biomed Sci. 2010 Aug 24;17 Suppl 1:S47. http://pmid.us/20804624.

[27] Hata Y, Nakajima K. Life-style and serum lipids and lipoproteins. J Atheroscler Thromb. 2000;7(4):177-97. http://pmid.us/11521681.

HDL: Higher is Good, But is Highest Best? | Perfect Health Diet

HDL: Higher is Good, But is Highest Best? | Perfect Health Diet

Conclusion

There’s little data to evaluate the healthfulness of very high HDL levels, but what data we have suggests that more is better.

There’s also a plausible (to me) evolutionary story for why our optimal HDL levels may be far higher than the ones selected by evolution.

For most biomarkers I would trust evolutionary selection and let my body do whatever it wants; but for HDL I will make an exception. I think we will benefit from dietary tactics that raise HDL levels above the evolutionary norm. And this is especially true for those with infectious diseases.

So my judgment is: let’s be like Richard Nikoley and aim for high HDL. I’ll discuss how on Tuesday.

References

[1] Pirillo A et al. Modification of HDL3 by mild oxidative stress increases ATP-binding cassette transporter 1-mediated cholesterol efflux. Cardiovasc Res. 2007 Aug 1;75(3):566-74. http://pmid.us/17524375.
[2] Berrougui H, Khalil A. Age-associated decrease of high-density lipoprotein-mediated reverse cholesterol transport activity. Rejuvenation Res. 2009 Apr;12(2):117-26. http://pmid.us/19405812.
[3] Feingold KR, Grunfeld C. The acute phase response inhibits reverse cholesterol transport. J Lipid Res. 2010 Apr;51(4):682-4. http://pmid.us/20071695.
[4] Undurti A et al. Modification of high density lipoprotein by myeloperoxidase generates a pro-inflammatory particle. J Biol Chem. 2009 Nov 6;284(45):30825-35. http://pmid.us/19726691.
[5] Smith JD. Myeloperoxidase, inflammation, and dysfunctional high-density lipoprotein. J Clin Lipidol. 2010 Sep-Oct;4(5):382-8. http://pmid.us/21076633.
[6] Lindeberg S et al. Determinants of serum triglycerides and high-density lipoprotein cholesterol in traditional Trobriand Islanders: the Kitava Study. Scand J Clin Lab Invest. 2003;63(3):175-80. http://pmid.us/12817903.
[7] Wang S et al. Prevalence and associated factors of dyslipidemia in the adult chinese population. PLoS One. 2011 Mar 10;6(3):e17326. http://pmid.us/21423741.
[8] He J et al. Serum total and lipoprotein cholesterol levels and awareness, treatment, and control of hypercholesterolemia in China. Circulation. 2004 Jul 27;110(4):405-11. http://pmid.us/15238453.
[9] Rahilly-Tierney CR et al. Relation Between High-Density Lipoprotein Cholesterol and Survival to Age 85 Years in Men (from the VA Normative Aging Study). Am J Cardiol. 2011 Apr 15;107(8):1173-7. http://pmid.us/21296318.

What Do You Know About LDL bloood cholesterol?

Part 1 of 2: What Do You Think You Know About LDL Cholesterol? (Part One) | Free The Animal

Extract:

So, you want to reduce your LDL like a good soldier? Then increase your triglycerides dramatically. All else remaining equal, each 5-point increase in Trigs gets you a point off your LDL. Increase Trigs by 100 (easy to do with grains, sugar, and other refined carbs) and you can lower your LDL by 20.


So what are triglycerides? Most simply, fat circulating in your blood. Government recommendations are for a level of 150 and below. Mine are 47, and what you might not know about high-fat (and consequently low-carb) dieters is that they all have pretty low triglycerides (in the 50-80 area). Those who eat lots of grains and sugars in the form of bread, pasta, rice, processed foods, sweetened sodas, and, yes, fruit juices: you'll see triglyceride (fat circulating in blood) levels of 200 and on up, sometimes way up. 300-400 and above are not uncommon. Alright, so, eat lots of natural fat (from animals, coconut, and olives) in order to reduce your sugar intake (carbohydrate) and you'll dramatically reduce your triglycerides; eat low fat with lots of sugar (carbohydrate — yes; bread and pasta is, essentially: sugar), raise the fat levels in your blood, and potentially lower your LDL.


Part 2 of 2:  What Do You Think You Know About LDL Cholesterol? (Pt 2 of 2) | Free The Animal

Extract:
So, what's your LDL? Unless you've actually had it measured, you do not know. Neither does your doctor. Are you on medications or dietary prescriptions as a result of the fiction that you believe is your LDL? And how about particle size? Large & fluffy are actually good, while small and dense are very bad. You might have a low LDL, but with a high percentage of small and dense particles, and you could be at 6 or 10 times the risk as someone with an LDL of 250, but 99% large & fluffy. Don't be fooled by your doctor, HMO, hospital, or the drug companies.


And guess what will reduce your small and dense LDL every time? You guessed it: get off the grains, (particularly wheat), sugar, processed foods, processed vegetable oils; and take omega 3s and vitamin d to get your levels above 60.

How do you find out what your LDL actually is? Dr Davis says, "Our preferred method is NMR (LipoScience) LDL particle number, probably the most accurate of all. Second best: apoprotein B, direct measured LDL, and non-HDL.

Low carb/paleo - high Cholesterol, Doug McGuff MD

Is Cholesterol a Problem to Be Managed? | Free The Animal
comments by Dr Doug McGuff MD:
dougmcguffmd
Richard,
Remember, cholesterol measurements are really what I call “a downstream measurement of upstream phenomenon”. In John's case, he is naturally lean, which means his insulin sensitivity on his fat cells is relatively low. Also, his hormone sensitive lipase (the enzyme that mobilizes triacylglycerol from the fat cells) is probably more active than your average person. As a result of these two facts, he is going to have more circulating fat in his blood. He is less likely to store fat in the adipocytes and is more likely to mobilize them for utilization as energy. As a result, his total cholesterol and in particular his triglycerides will measure high. However, his LDL is lower because his systemic inflammation is lower and thus has a decreased need for a low-density protein to carry cholesterol to these sites of inflammation for patching.
This situation will occur in the very lean (below 9-10% bodyfat) and those making the transition to becoming a fat-burner. The cholesterol and triglycerides are not higher because of increased production in the liver (due to overconsumption of refined carbs in the face of full glycogen stores which requires fat conversion to protect against dangerous elevations of serum glucose). In the case of the fat-burner the numbers are higher because fat is slow to be stored and is easily released for use as fuel.
The triglycerides, rather than being stored in the fat cells where they stimulate inflammatory mediators, are dumped into the circulation where they go to the mitochondria of your cells for beta-oxidation to produce energy. The numbers by themselves are meaningless, the context in which they were collected means everything….which is why I don't measure.
To those that are actively losing weight while on a H-G diet, remember you are on a high fat diet (your own fat) which has to be in circulation to be used as energy. If you plunge a needle into a vein and take a sample of what is going on during this transition, the numbers are going to look funky and will absolutely freak out the average MD.
For a good explanation of what I am talking about, see the youtube clip of my lecture in Salt Lake City at http://www.bodybyscience.net. Go to clip #5 and the discussion of the above starts at about 4:50.

Low carb - but triglycerides go. . . up?"

"I lost 30 lbs and my triglycerides went . . . up?"

Article from the Heart Scan Blog - of  Wr William Davis

Low carb - but triglycerides go. . . up?"
“How could that happen? You said losing weight would make my HDL go up and my triglycerides go down!”
Yes, I had said that. But I was oversimplifying.

The truth is that, when there is weight loss, especially profound weight loss like Brad experienced eliminating wheat and cornstarch products, there is mobilization of fat stores. Fat is stored energy. Energy is stored as . . . triglycerides.
So when there is substantial weight loss, there is a flood of triglycerides in the blood, and triglyceride levels in the midst of weight loss can commonly jump up, not uncommonly to the 200-300+ mg/dl range. When triglycerides go up, there is also a drop in HDL (triglycerides interact with HDL particles, modify their structure and make them more readily destroyed, thereby dropping blood levels). Occasionally, substantial weight loss like Brad experienced will drop HDL really low, as low as the 20′s.
Once weight stabilizes, this effect can last up to 2 months before correcting. Only then will triglycerides drop and HDL rise. The rise in HDL occurs even more slowly, requiring several more months to plateau.
In other words, weight loss like Brad’s causes triglycerides to increase and HDL to decrease, to be followed later by a drop in triglycerides and a rise in HDL.
I know of no way to block this phenomenon.

And perhaps we shouldn’t, since this is how fat stores are mobilized and “burned off.”

Peter August 16, 2008 at 1:33 am
Hi Dr Davis,While fat is stored as triglycerides, it is released from adipose stores as non esterified fatty acids, and these will be predominantly palmitic acid in humans. Non esterified palmitic acid appears to be an excellent inducer of insulin resistance, and insulin resistance has been hypothesised by several authors to be a completely normal physiological adaption to fasting or seasonal carbohydrate absence. While weight loss is on going, the circulation is flooded with NEFA and “physiological” insulin resistance should predominate. If the person continues to consume “good” carbohydrate at above acute metabolic needs, the excess will get shipped out of the liver as VLDLs. Under insulin resistance lipoprotein lipase, routinely under the control of insulin, won’t be doing much lipolysis and so VLDLs can hang around in the circulation… Muscle can happily accept NEFA as a prime source of energy without lipoprotein lipase having to split the lipids from VLDLs, so leave the VLDLs there to show up as fasting trigs….Once weight is stable the NEFA release from adipose tissue will be much better matched to metabolic needs. With the improved insulin sensitivity due to loss of visceral fat, control of both adipose hormone sensitive lipase and endothelial lipoprotein lipase activity should normalise and allow VLDLs and HDL to settle in to more cardiologically acceptable numbers.Just an idea. The prediction it makes is for a reduced HbA1c due to the reduction in bulk carbohydrate (this must happen to allow lipolysis for weight loss), coupled with no drop or an increase in fasting blood glucose due to the NEFA induced insulin resistance. Very curious as to whether this happened…Idea is open for kicking.Peter

High LDL on Low-Carb Paleo - causes and cures

Low Carb Paleo, and LDL is Soaring – Help! | Perfect Health Diet

(pre-article to: Answer Day: What Causes High LDL on Low-Carb Paleo? | Perfect Health Diet)

Here’s the puzzle. Someone adopts a low-carb Paleo diet. Very healthy diet, right? But their LDL cholesterol level starts to rise. And rise. And rise.
Larry Eshelman emailed me last December with this problem. His LDL history:
  • 103 mg/dl (1990-2002, eating a low fat diet)
  • 115 mg/dl (2002-2007, eating a low carb diet)
  • 195 mg/dl (2007-2009, after reading Gary Taubes and adding saturated fat)
  • 254 mg/dl (Dec 2009, very low-carb Paleo for 5 weeks)
  • 295 mg/dl (Jun 2010, very low-carb Paleo for 7 months)
(SI system readers, convert to mmol/l by dividing by 38.67.)

A common problem

This is not a terribly uncommon problem in the Paleo community; it afflicts famous and brilliant bloggers as well as ordinary folks. It’s been discussed by Richard Nikoley in several posts:

Cholesterol - high cholesterol need not be bad

Reader Feedback – Doctors and Cholesterol | Free The Animal
  • Let's not forget that Dr. Ravnskov has pointed out that people with higher cholesterol live the longest.
    http://westonaprice.org/moderndiseases/benefits_cholest.html
    And as Mary Enig says, a total blood lipoprotein count between 200 and 240 is normal, not a disease process.
    http://westonaprice.org/knowyourfats/fats_phony.html
    In any population, all measurable characteristics vary within a normal range in a Bell Curve fashion. Just as some people are shorter than average and some taller than average, some have smaller and some have larger feet, and some have lower and some have higher total lipoproteins. Thus, "high" cholesterol is not by itself indicative of a disease process any more than above average height indicates a disease process.
    I have read that taller people have, in general, a lower life expectancy than shorter people (don't have the reference). Assuming this is true, it would not give warrant for height reduction surgery for taller than average people. Similarly, even if it could be demonstrated that people with lower total lipoprotein counts did live longer, that would not give warrant to subject individuals with "above average" total lipoprotein counts to artificial cholesterol reduction.
    This gets back to the whole issue of reductionism. Tim's doctor thinks a blood cholesterol of 226 is a disease process. He completely ignores the context (patient) in which this occurs. Rather than evaluating the patient, he reduces the patient to a lab number. He wants to treat the cholesterol, not the patient.
    Don
Cholesterol - high cholesterol