What Causes Elevated LDL Particle Number? - Kresser

What Causes Elevated LDL Particle Number?

By Chris Kresser on May 3, 2013

 

In the last article in this series, I explained that LDL particle number (LDL-P) is a much more accurate predictor of cardiovascular disease risk than either LDL or total cholesterol. In this article, I’m going to briefly outline the five primary causes of elevated LDL-P.

Conventional medicine is primarily focused on suppressing symptoms. If your blood pressure is high, you take a medication to lower it. If your blood sugar is high, you take a medication to lower it. If your cholesterol is high, you take a medication to lower it. In most cases there is rarely any investigation into why these markers are high in the first place, with the possible exception of some basic (but often incorrect) counseling on diet and exercise.

On the other hand, functional medicine—which is what I practice—focuses on treating the underlying cause of health problems instead of just suppressing symptoms. If your blood sugar, blood pressure or cholesterol are high, the first question a functional medicine practitioner will ask is “why?” If we can identify the root cause of the problem, and address it at that level, medication is often unnecessary.

To use a simple analogy, if you have weeds in your garden, what happens if you just cut the weeds from the top? They grow right back—and sometimes faster than before! If you really want to get rid of them once and for all, you have to pull them up by their roots.

With this in mind, let’s look at some of the potential causes of elevated LDL particle number. If your LDL-P is high, it makes sense to test for and treat any of the conditions below (with the exception of the last, which is genetic and thus can’t be treated) before—or at least along with—taking pharmaceutical drugs.

Insulin resistance and metabolic syndrome

LDL particles don’t just carry cholesterol; they also carry triglycerides, fat-soluble vitamins and antioxidants. You can think of LDL as a taxi service that delivers important nutrients to the cells and tissues of the body.

As you might expect, there’s a limit to how much “stuff” that each LDL particle can carry. Each LDL particle has a certain number of cholesterol molecules and a certain number of triglycerides. As the number of triglycerides increases, the amount of cholesterol it can carry decreases, and the liver will have to make more LDL particles to carry a given amount of cholesterol around the body. This person will end up with a higher number of LDL particles.

Consider two hypothetical people. Both have an LDL cholesterol level of 130 mg/dL, but one has high triglycerides and the other has low triglycerides. The one with the high triglyceride level will need more LDL particles to transport that same amount of cholesterol around the body than the one with a low triglyceride level.

Numerous studies have found an association between increased LDL particle number, and metabolic syndrome. One study measured ApoB, a marker for LDL particle number, in a group of 1,400 young Finns with no established disease. The participants with the highest LDL particle number were 2.8 times more likely to have metabolic syndrome than those with the lowest levels of LDL-P. (1) A much larger study of over 300,000 men also found a strong association between LDL-P and metabolic syndrome and its components (i.e. insulin resistance, abdominal obesity, high blood pressure, etc.). (2)

Poor thyroid function

Poor thyroid function is another potential cause of elevated particle number. Thyroid hormone has multiple effects on the regulation of lipid production, absorption, and metabolism. It stimulates the expression of HMG-CoA reductase, which is an enzyme in the liver involved in the production of cholesterol. (As a side note, one way that statins work is by inhibiting the HMG-CoA reductase enzyme.) Thyroid hormone also increases the expression of LDL receptors on the surface of cells in the liver and in other tissues. In hypothyroidism, the number of receptors for LDL on cells will be decreased. This leads to reduced clearance of LDL from the blood and thus higher LDL levels. Hypothyroidism may also lead to higher cholesterol by acting on Niemann-Pick C1-like 1 protein, which plays a critical role in the intestinal absorption of cholesterol. (3, 4)

Studies show that LDL particle number is higher even in subclinical hypothyroidism (high TSH with normal T4 and T3), and that LDL particle number will decrease after treatment with thyroid hormone. (5)

Infections

Another cause of high cholesterol profile is infection. Multiple studies have shown associations between bacterial infections like Chlamydia pneumoniae and H. pylori, which is the bacterium causes duodenal ulcers, and viral infections like herpes and cytomegalovirus and elevated lipids. (6) For example, H. pylori leads to elevated levels of total cholesterol, LDL cholesterol, lipoprotein (a), ApoB or LDL particle number, and triglyceride concentrations as well as decreased levels of HDL. (7)

Several mechanisms have been proposed to explain the association between infections and elevated blood lipids. Some evidence suggests that viral and bacterial infections directly alter the lipid metabolism of infected cells, and other evidence suggests that lipids increase as a result of the body’s attempt to fight off infection. Other evidence suggests that LDL has antimicrobial properties and is directly involved in inactivating microbial pathogens. This has been confirmed by studies showing that mice with defective LDL receptors—and thus very high levels of LDL—are protected against infection by gram-negative bacteria like H. pylori. (8)

Leaky gut

One of the primary functions of the intestinal barrier is to make sure that stuff that belongs in the gut stays in the gut. When this barrier fails, endotoxins such as lipopolysaccharide (LPS) produced by certain species of gut bacteria can enter the bloodstream and provoke an immune response. Part of that immune response involves LDL particles, which as I mentioned above, have an anti-microbial effect. A protein called LPS-binding protein, which circulates with LDL particles, has been shown to reduce the toxic properties of LPS by directly binding to it and removing it from the circulation. (9) Studies have also shown significant increases in LPS-binding protein (and thus LDL particles) in cases of endotoxemia—a condition caused by large amounts of circulating endotoxins. (10)

Though more research is needed in this area, the studies above suggest that a leaky gut could increase the level of LPS and other endotoxins in the blood, and thus increase LDL particle number as a result. I have seen this in my practice. I recently had a patient with high LDL-P and no other risk factors. I tested his gut and discovered H. pylori and small intestine bacterial overgrowth (SIBO). After treating his gut, his LDL-P came down to normal levels.

Genetics

The final cause of elevated LDL-P is genetics. Familial hypercholesterolemia, or FH, involves a mutation of a gene that codes for the LDL receptor or the gene that codes for apolipoprotein B (ApoB). The LDL receptor sits on the outside of cells; the LDL particle has to attach to the LDL receptor in order to deliver the nutrients it’s carrying and be removed from the circulation. ApoB is the part of the LDL particle that binds to the receptor. If we use a door lock as an analogy, apolipoprotein B would be the key, and the LDL receptor is the lock. They both need to be working properly for LDL to deliver its cargo and to be removed from the bloodstream.

Homozygous carriers of FH have two copies of the mutated gene. This condition is very rare. It affects approximately 1 in a million people. And people that are homozygous for this mutation have extremely high total cholesterol levels, often as high as 1000 mg/dL. And unfortunately they usually die from severe atherosclerosis and heart disease before the age of 25.

Heterozygous carriers, however, only have a single copy of the mutated gene, and the other copy is functioning normally. This is much more common. The prevalence is between 1 in 300 to 1 in 500 people, depending on which study you look at. These heterozygous carriers of FH have total cholesterol levels that often range between 350 and 550 mg/dL, along with very high LDL particle number. They have about three times higher risk of death from heart disease than people without FH if it goes untreated.

It’s important to note that people with FH have primarily large, buoyant LDL particles, and yet are still at much higher risk for cardiovascular disease. While it’s true that small, dense, oxidized LDL particles are more likely to cause atherosclerosis, large, buoyant particles can also be harmful when their concentration is high enough. This is one reason why LDL particle number is a superior marker to LDL particle size.

In the next article in this series, I will debunk the myth that statins extend lifespan in healthy people with no pre-existing heart disease.
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Important safety label changes to cholesterol-lowering statin drugs

FDA Drug Safety Communication: Important safety label changes to cholesterol-lowering statin drugs

Facts about statins

A class of prescription drugs used together with diet and exercise to reduce blood levels of low-density lipoprotein (LDL) cholesterol (“bad cholesterol”) Marketed as single-ingredient products, including Lipitor (atorvastatin), Lescol (fluvastatin), Mevacor (lovastatin), Altoprev (lovastatin extended-release), Livalo (pitavastatin), Pravachol (pravastatin), Crestor (rosuvastatin), and Zocor (simvastatin) Also marketed as combination products, including Advicor (lovastatin/niacin extended-release), Simcor (simvastatin/niacin extended-release), and Vytorin (simvastatin/ezetimibe)

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

Safety Announcement

[2-28-2012] The U.S. Food and Drug Administration (FDA) has approved important safety label changes for the class of cholesterol-lowering drugs known as statins. These changes were made to provide the public with more information for the safe and effective use of statins and are based on FDA’s comprehensive review of the statin class of drugs (see Data Summary below). The changes include the following:

Infographic About Cholesterol and Statins1 2

Monitoring Liver Enzymes
Labels have been revised to remove the need for routine periodic monitoring of liver enzymes in patients taking statins. The labels now recommend that liver enzyme tests should be performed before starting statin therapy and as clinically indicated thereafter. FDA has concluded that serious liver injury with statins is rare and unpredictable in individual patients, and that routine periodic monitoring of liver enzymes does not appear to be effective in detecting or preventing serious liver injury.

Adverse Event Information
Information about the potential for generally non-serious and reversible cognitive side effects (memory loss, confusion, etc.) and reports of increased blood sugar and glycosylated hemoglobin (HbA1c) levels has been added to the statin labels. FDA continues to believe that the cardiovascular benefits of statins outweigh these small increased risks.

Drug Interactions
The lovastatin label has been extensively updated with new contraindications (situations when the drug should not be used) and dose limitations when it is taken with certain medicines that can increase the risk for muscle injury (see Lovastatin Dose Limitations below).

Healthcare professionals should refer to the drug labels for the latest recommendations for prescribing statins (also see Additional Information for Healthcare Professionals below). Patients should contact their healthcare professional if they have any questions or concerns about statins.

Additional Information for Patients

• The statin drug labels have been revised to provide patients with more information on the safe and effective use of statins. Patients should be aware of the following information:
  • There have been rare reports of serious liver problems in patients taking statins. Patients should notify their healthcare professional right away if they have the following symptoms: unusual fatigue or weakness; loss of appetite; upper belly pain; dark-colored urine; or yellowing of the skin or the whites of the eyes.
  • Memory loss and confusion have been reported with statin use. These reported events were generally not serious and went away once the drug was no longer being taken.
  • Increases in blood sugar levels have been reported with statin use.
  • Certain medicines should never be taken (are contraindicated) with lovastatin (Mevacor) (see Lovastatin Dose Limitations below).
• Patients should contact their healthcare professional if they have any questions or concerns about statins.
• Patients should report side effects from the use of statins to the FDA MedWatch program, using the information in the "Contact FDA" box at the bottom of the page.
  

Additional Information for Healthcare Professionals

• Healthcare professionals should perform liver enzyme tests before initiating statin therapy in patients and as clinically indicated thereafter. If serious liver injury with clinical symptoms and/or hyperbilirubinemia or jaundice occurs during treatment, therapy should be interrupted. If an alternate etiology is not found, the statin should not be restarted.
• There have been rare post-marketing reports of cognitive impairment (e.g., memory loss, forgetfulness, amnesia, memory impairment, confusion) associated with statin use. These reported symptoms are generally not serious and reversible upon statin discontinuation, with variable times to symptom onset (1 day to years) and symptom resolution (median of 3 weeks).
• Increases in glycosylated hemoglobin (HbA1c) and fasting serum glucose levels have been reported with statin use.
• Healthcare professionals should follow the recommendations in the lovastatin label regarding drugs that may increase the risk of myopathy/rhabdomyolysis when used with lovastatin (see Lovastatin Dose Limitations below).
• Healthcare professionals should report adverse events involving statins to the FDA MedWatch program using the information in the "Contact FDA" box at the bottom of this page.
  

Data Summary

Removal of routine monitoring of liver enzymes from drug labels

FDA reviewed current monitoring guidelines, including the National Lipid Association’s Liver Expert Panel and Statin Safety Task Force recommendations.^{1, 2} The Liver Expert Panel stated that the available scientific evidence does not support the routine monitoring of liver biochemistries in asymptomatic patients receiving statins. The Panel made this recommendation because (1) irreversible liver damage resulting from statins is exceptionally rare and is likely idiosyncratic in nature, and (2) no data exist to show that routine periodic monitoring of liver biochemistries is effective in identifying the very rare individual who may develop significant liver injury from ongoing statin therapy. The Panel believed that routine periodic monitoring will instead identify patients with isolated increased aminotransferase levels, which could motivate physicians to alter or discontinue statin therapy, thereby placing patients at increased risk for cardiovascular events.¹ The National Lipid Association’s Statin Task Force also stated that routine monitoring of liver function tests is not supported by the available evidence.²

FDA reviewed post-marketing data to evaluate the risk of clinically serious hepatotoxicity associated with statins. FDA had conducted several post-marketing reviews of statins and hepatotoxicity between years 2000 and 2009 by searching the Agency’s Adverse Event Reporting System (AERS) database. Those reviews consistently noted that reporting of statin-associated serious liver injury to the AERS database was extremely low (reporting rate of ≤2 per one million patient-years). FDA’s updated review focused on cases of severe liver injury, defined as a 4 (severe liver injury) or a 5 (death or liver transplant) using the Drug Induced Liver Injury Network (DILIN) liver injury severity scale, which were reported to AERS from marketing of each statin through 2009. Cases meeting those criteria were further assessed for causality. Seventy-five cases (27 cases with a severity score of 4, and 48 cases with a severity score of 5 (37 deaths and 11 liver transplants) were assessed for causality. Thirty of the 75 cases (14 deaths, 7 liver transplantations, and 9 severe liver injury) were assessed as possibly or probably associated with statin therapy. No cases were assessed as highly likely or definitely associated with statin therapy. FDA concluded that, despite a rising use of statins as a class since the late 1990s, there has not been a detectable increase in the annual rates of fatal or severe liver injury cases possibly or probably causally associated with statin use.

FDA also reviewed cases from the DILIN and Acute Liver Failure Study Group (ALFSG), organizations that have been submitting reports to FDA of drug-associated liver injury in their liver injury outcome studies. As of January 1, 2011, DILIN had submitted 25 reports of statin-associated liver injury to FDA, 12 of which gave hospitalization as an outcome. A 2010 article from ALFSG included 133 prospectively identified cases of idiopathic drug-induced liver injury resulting in acute liver failure.³ Of these 133 patients, 15 were taking statins, and in six of these 15 individuals a statin was identified as the only potential drug to cause drug-induced liver injury.

Based on all available data, FDA has determined that all currently marketed statins appear to be associated with a very low risk of serious liver injury and that routine periodic monitoring of serum alanine aminotransferase (ALT) does not appear to detect or prevent serious liver injury in association with statins.

Cognitive adverse events

FDA reviewed the AERS database, the published medical literature (case reports and observational studies),^4-13 and randomized clinical trials to evaluate the effect of statins on cognition.^14-17

The post-marketing adverse event reports generally described individuals over the age of 50 years who experienced notable, but ill-defined memory loss or impairment that was reversible upon discontinuation of statin therapy. Time to onset of the event was highly variable, ranging from one day to years after statin exposure. The cases did not appear to be associated with fixed or progressive dementia, such as Alzheimer’s disease. The review did not reveal an association between the adverse event and the specific statin, the age of the individual, the statin dose, or concomitant medication use.

Data from the observational studies and clinical trials did not suggest that cognitive changes associated with statin use are common or lead to clinically significant cognitive decline.

Increases in glycosylated hemoglobin (HbA1c) and fasting plasma glucose

FDA’s review of the results from the Justification for the Use of Statins in Primary Prevention: an Intervention Trial Evaluating Rosuvastatin (JUPITER) reported a 27% increase in investigator-reported diabetes mellitus in rosuvastatin-treated patients compared to placebo-treated patients. High-dose atorvastatin had also been associated with worsening glycemic control in the Pravastatin or Atorvastatin Evaluation and Infection Therapy – Thrombolysis In Myocardial Infarction 22 (PROVE-IT TIMI 22) substudy.¹⁸

FDA also reviewed the published medical literature.^19-26 A meta-analysis by Sattar et al.,19 which included 13 statin trials with 91,140 participants, reported that statin therapy was associated with a 9% increased risk for incident diabetes (odds ratio [OR] 1.09; 95% confidence interval [CI] 1.02-1.17), with little heterogeneity (I2=11%) between trials. A meta-analysis by Rajpathak et al.,²⁰ which included 6 statin trials with 57,593 participants, also reported a small increase in diabetes risk (relative risk [RR] 1.13; 95% CI 1.03-1.23), with no evidence of heterogeneity across trials. A recent study by Culver et al.,²⁶ using data from the Women’s Health Initiative, reported that statin use conveys an increased risk of new-onset diabetes in postmenopausal women, and noted that the effect appears to be a medication class effect, unrelated to potency or to individual statin.

Based on clinical trial meta-analyses and epidemiological data from the published literature, information concerning an effect of statins on incident diabetes and increases in HbA1c and/or fasting plasma glucose was added to statin labels.

Lovastatin drug-drug interactions

Information regarding drug-drug interactions and contraindications and dose limitations has been added to the lovastatin label. Subsequent to the June 2011 label revisions to the simvastatin-containing products, which were based largely on the Study of the Effectiveness of Additional Reductions in Cholesterol and Homocysteine (SEARCH) trial,²⁷ a review of drug-drug interactions with lovastatin was conducted because the physicochemical and pharmacokinetic properties of lovastatin are comparable to those of simvastatin.

Lovastatin is a sensitive in vivo cytochrome P450 3A4 (CYP3A4) substrate. Strong CYP3A4 inhibitors are predicted to significantly increase lovastatin exposure. A literature review indicates that itraconazole, a strong CYP3A4 inhibitor, increases lovastatin exposure up to 20-fold and the drug interaction appears to result in rhabdomyolysis.²⁸ The effect of itraconazole on lovastatin exposure can therefore be extrapolated to other strong CYP3A4 inhibitors, including ketoconazole, posaconazole, erythromycin, clarithromycin, telithromycin, human immunodeficiency virus (HIV) protease inhibitors, boceprevir, telaprevir, and nefazodone.

Lovastatin Dose Limitations

Previous lovastatin label	New lovastatin label
Avoid lovastatin with: Itraconazole Ketoconazole Erythromycin Clarithromycin Telithromycin HIV protease inhibitors Nefazodone	Contraindicated with lovastatin: Itraconazole Ketoconazole Posaconazole Erythromycin Clarithromycin Telithromycin HIV protease inhibitors Boceprevir Telaprevir Nefazodone
Do not exceed 20 mg lovastatin daily with: Gemfibrozil Other fibrates Lipid-lowering doses (≥1 g/day) of niacin Cyclosporine Danazol	Avoid with lovastatin: Cyclosporine Gemfibrozil
	Do not exceed 20 mg lovastatin daily with: Danazol Diltiazem Verapamil
Do not exceed 40 mg lovastatin daily with: Amiodarone Verapamil	Do not exceed 40 mg lovastatin daily with: Amiodarone
Avoid large quantities of grapefruit juice (>1 quart daily)	Avoid large quantities of grapefruit juice (>1 quart daily)

References

1. Cohen DE, Anania FA, Chalasani N; for the National Lipid Association Statin Safety Task Force Liver Expert Panel. An assessment of statin safety by hepatologists. Am J Cardiol. 2006;97(8A):77C-81C.
2. McKenney JM, Davidson MH, Jacobson TA, Guyton JR. Final conclusions and recommendations of the National Lipid Association Statin Safety Assessment Task Force. Am J Cardiol. 2006;97(8A):89C-94C.
3. Reuben A, Koch DG, Lee WM; for the Acute Liver Failure Study Group. Drug-induced acute liver failure: results of a U.S. multicenter, prospective study. Hepatology. 2010;52(6):2065-2076.
4. Orsi A, Sherman O, Woldeselassie Z. Simvastatin-associated memory loss. Pharmacotherapy. 2001;21:767-9.
5. Wagstaff LR, Mitton MW, Arvik BM, Doraiswamy PM. Statin-associated memory loss: analysis of 60 case reports and review of the literature. Pharmacotherapy. 2003;23:871-80.
6. Evans MA, Golomb BA. Statin-associated adverse cognitive effects: survey results from 171 patients. Pharmacotherapy. 2009;29:800-811.
7. Parker BA, Polk DM, Rabdiya V, et al. Changes in memory function and neuronal activation associated with atorvastatin therapy. Pharmacotherapy. 2010;30(6):236e-240e.
8. Zamrini E, McGwin G, Roseman JM. Association between statin use and Alzheimer's disease. Neuroepidemiology. 2004;23:94-98.
9. Zandi PP, Sparks DL, Khachaturian AS, et al. Do statins reduce risk of incident dementia and Alzheimer disease? The Cache County Study. Arch Gen Psychiatry. 2005;62:217-224.
10. Zhou B, Teramukai S, Fukushima M. Prevention and treatment of dementia or Alzheimer's disease by statins: a meta-analysis. Dement Geriatr Cogn Disord. 2007;23:194-201.
11. Beydoun MA, Beason-Held LL, Kitner-Triolo MH, et al. Statins and serum cholesterol's associations with incident dementia and mild cognitive impairment. J Epidemiol Community Health. 2011;65:949-957.
12. Bettermann K, Arnold AM, Williamson J, et al. Statins, risk of dementia, and cognitive function: secondary analysis of the Ginkgo Evaluation of Memory Study. J Stroke Cerebrovasc Dis. http://dx.doi.org/10.1016/j.jstrokecerebrovasdis.2010.11.002³. Accessed January 31, 2012.
13. Benito-León J, Louis ED, Vega S, Bermejo-Pareja F. Statins and cognitive functioning in the elderly: a population-based study. J Alzheimers Dis. 2010;21:95-102.
14. Muldoon MF, Barger SD, Ryan CM, et al. Effects of lovastatin on cognitive function and psychological well-being. Am J Med. 2000;108:538-546.
15. Muldoon MF, Ryan CM, Sereika SM, Flory JD, Manuck SB. Randomized trial of the effects of simvastatin on cognitive functioning in hypercholesterolemic adults. Am J Med. 2004;117:823-829.
16. Trompet S, van Vliet P, de Craen AJ, et al. Pravastatin and cognitive function in the elderly. Results of the PROSPER study. J Neurol. 2010;257:85-90.
17. Feldman HH, Doody RS, Kivipelto M, et al. Randomized controlled trial of atorvastatin in mild to moderate Alzheimer disease: LEADe. Neurology. 2010;74:956-964.
18. Sabatine MS, Wiviott SD, Morrow DA, McCabe CH, Cannon CP. High-dose atorvastatin associated with worse glycemic control: a PROVE-IT TIMI 22 substudy. Circulation. 2004;110(Suppl I):S834.
19. Sattar N, Preiss D, Murray HM, et al. Statins and risk of incident diabetes: a collaborative meta-analysis of randomised statin trials. Lancet. 2010;375(9716):735-742.
20. Rajpathak SN, Kumbhani DJ, Crandall J, Barzilai N, Alderman M, Ridker PM. Statin therapy and risk of developing type 2 diabetes: a meta-analysis. Diabetes Care. 2009;32(10):1924-1929.
21. Sukhija R, Prayaga S, Marashdeh M, et al. Effect of statins on fasting plasma glucose in diabetic and nondiabetic patients. J Investig Med. 2009;57:495-499.
22. Koh KK, Quon MJ, Han SH, Lee Y, Kim SJ, Shin EK. Atorvastatin causes insulin resistance and increases ambient glycemia in hypercholesterolemic patients. J Am Coll Cardiol. 2010;55:1209-1216.
23. Thongtang N, Ai M, Otokozawa S, et al. Effects of maximal atorvastatin and rosuvastatin treatment on markers of glucose homeostasis and inflammation. Am J Cardiol. 2011;107:387-392.
24. Kostapanos MS, Liamis GL, Milionis HJ, Elisaf MS. Do statins beneficially or adversely affect glucose homeostasis? Curr Vasc Pharmacol. 2010;8:612-631.
25. Mills EJ, Wu P, Chong G, et al. Efficacy and safety of statin treatment for cardiovascular disease: a network meta-analysis of 170,255 patients from 76 randomized trials. QJM. 2011;104:109-124.
26. Culver AL, Ockene IS, Balasubramanian R, et al. Statin use and risk of diabetes mellitus in postmenopausal women in the Women's Health Initiative. Arch Intern Med. 2012;172(2):144-152.
27. Armitage J, Bowman L, Wallendszus K; for the Study of the Effectiveness of Additional Reductions in Cholesterol and Homocysteine (SEARCH) Collaborative Group. , et al. Intensive lowering of LDL cholesterol with 80 mg versus 20 mg simvastatin daily in 12,064 survivors of myocardial infarction: a double-blind randomised trial. Lancet. 2010;376:1658-1669.
28. Lees RS, Lees AM. Rhabdomyolysis from the coadministration of lovastatin and the antifungal agent itraconazole. N Engl J Med. 1995;333:664-555.

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Whatever the nutrition authorities have to say… the exact opposite is likely to be the truth!- Kristjan Gunnarsson

How to Win an Argument With a Nutritionist or Registered Dietitian

By: Kris

For reasons I have disclosed before, I prefer not to get in to online arguments with nutritionists.
I used to enjoy it, but ended up becoming frustrated so I gave it up.

But… I often observe these arguments online.

It’s fun. Usually.

There’s an annoying pattern I’ve noticed though.

The people who are arguing with the nutritionists, who seem to have all the facts straight and are trying to make their point, don’t cite any studies.

This is a problem!
I get it…
Not everyone has a ton of studies bookmarked on their computer and it can be quite a hazzle to start looking them up at the time of need.

But citing studies is critical in an argument about science. Nutrition = science!
So, with this article I decided to collect studies for the main arguments against some of the more foolish claims made by nutritionists, vegans and know-it-all low-fat zealots.

All of them are in a copy-paste friendly format. Just highlight the URLs to the studies and Click Ctrl+C (Cmd+C on mac) or right click and select “Copy.”

If you tend to get in to these online arguments a lot, I suggest you bookmark this page!
Remember Kris’s Law:

“Whatever the nutrition authorities have to say… the exact opposite is likely to be the truth!”

(Disclaimer: Many nutritionist are good people and seem to know what they are talking about, but the ones that seem to be the most active in the mainstream media seem to do little other than spreading potentially dangerous misinformation.)

Nutritionist Says: Protein is Bad For Your Bones

Put on: this face.
There are some short-term studies showing that the increased acid load from a high protein intake can lead to increased calcium excretion. That is true, but this is only a short-term phenomenon.

The long-term epidemiological studies on protein intake and bone health shows the exact opposite. Increased protein intake correlates with improved bone health and a lowered risk of fractures.

http://www.ncbi.nlm.nih.gov/pubmed/21102327
http://onlinelibrary.wiley.com/doi/10.1359/jbmr.2000.15.12.2504/full
http://www.ajcn.org/content/69/1/147.short
http://onlinelibrary.wiley.com/doi/10.1359/JBMR.040204/full
http://www.springerlink.com/content/0595572652p658w7/
http://www.jacn.org/content/24/suppl_6/526S.short

Nutritionist Says: Protein is Bad For Your Kidneys

Put on: this face.
There is NO evidence that increased protein is harmful for people with healthy kidneys.
In fact, the studies show that increased protein can lower blood pressure:

http://jama.jamanetwork.com/article.aspx?articleid=201882
http://hyper.ahajournals.org/content/38/4/821.short
http://www.ncbi.nlm.nih.gov/pubmed/20711407
…and improve blood sugar control in type II diabetics:

http://www.ajcn.org/content/78/4/734.short
http://care.diabetesjournals.org/content/25/3/425.short
http://diabetes.diabetesjournals.org/content/53/9/2375.short
High blood pressure and diabetes are the key risk factors for kidney failure. Consequently, eating more protein, not less, should be good for the kidneys.

The advice to restrict protein intake for the bones and kidneys is likely to have the exact opposite effect.

Here are two review articles that show no harmful effect of protein consumption on kidney health:

http://www.jissn.com/content/1/1/45
http://www.nutritionandmetabolism.com/content/2/1/25

Nutritionist Says: Whole Wheat is Good For You

Put on: this face.

Whole wheat raises the blood sugar faster than most other foods and its glycemic index isn’t much lower than refined wheat..

Additionally, gluten is likely to be harmful for people who don’t have celiac disease.

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1954879/
http://www.ncbi.nlm.nih.gov/pubmed/21224837
http://www.ncbi.nlm.nih.gov/pubmed/6111631
Whole wheat raises small, dense LDL, which is extremely atherogenic and can lead to heart disease:

http://www.ajcn.org/content/76/2/351.short

Nutritionist Says: Low-Carb Diets Are Dangerous

Put on: this face.

This is simply not true. There are no documented severe reactions to low-carb diets and they tend to improve all the main biomarkers of disease, including HDL cholesterol, triglycerides, blood sugar, LDL particle size, blood pressure and body fat levels.

Low-carb diets have an outstanding safety profile and appear to be healthier, more effective and easier to follow than low-fat diets:

http://www.ncbi.nlm.nih.gov/pubmed/12679447
http://www.ncbi.nlm.nih.gov/pubmed/17341711
http://www.ncbi.nlm.nih.gov/pubmed/19099589
http://www.ncbi.nlm.nih.gov/pubmed/19439458
A lot more studies on this here.

Nutritionist Says: Eating Fat Makes You Fat

Put on: this face.

This seems logical enough, but doesn’t hold up in practice.

Diets that are high in fat, but low in carbs, and eaten without restricting calories are usually a lot more effective than low-fat, high-carb diets that are calorie restricted.

http://www.ncbi.nlm.nih.gov/pubmed/12761365
http://www.ncbi.nlm.nih.gov/pubmed/12761364
http://www.ncbi.nlm.nih.gov/pubmed/12679447
http://www.ncbi.nlm.nih.gov/pubmed/15148063
Again, more studies here.

Nutritionist Says: Saturated Fat is Unhealthy

Put on: this face.

Not true. Saturated fat raises HDL cholesterol and changes the LDL pattern from small, dense (bad) to large, fluffy (good).

This has been studied extensively and an association of saturated fat with heart disease has never been proven.

http://www.ajcn.org/content/77/5/1146.short
http://www.ncbi.nlm.nih.gov/pubmed/1386252
http://www.ajcn.org/content/67/5/828.short
http://www.ajcn.org/content/early/2010/01/13/ajcn.2009.27725.abstract
http://www.sciencedirect.com/science/article/pii/S0899900711003145

Nutritionist Says: Eggs Are Bad For You

Put on: this face.

Not true at all. Eggs, especially the yolks, are incredibly nutritious and highly satiating. There has never been any proven association between egg consumption and cardiovascular disease.

http://www.ncbi.nlm.nih.gov/pubmed/16340654
http://onlinelibrary.wiley.com/doi/10.1111/j.1467-3010.2006.00543.x/full
http://digitalcommons.uconn.edu/dissertations/AAI3138385/

Nutritionist Says: Diet Soda Can Help You Lose Weight

Put on: this face.

This is true in the context of a controlled diet. However, most people don’t count calories and do not eat a controlled diet.

In the context of a western, ad libidum diet, epidemiological studies show that diet soda consumption is associated with severe weight gain, diabetes and the metabolic syndrome.

http://circ.ahajournals.org/content/117/6/754.full.pdf+html
http://care.diabetesjournals.org/content/32/4/688.short
http://www.nature.com/oby/journal/v16/n8/abs/oby2008284a.html

Nutritionist Says: Sugar is Just Empty Calories

Put on: this face.

It’s true that sugar is empty calories, but that’s just the tip of the iceberg. Sugar can also lead to fatty liver, insulin resistance and may be a significant contributor to the metabolic syndrome.

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2673878/
http://www.sciencedirect.com/science/article/pii/S0168827808001645
http://www.nature.com/nrgastro/journal/v7/n5/full/nrgastro.2010.41.html

Conclusion

Kris’s law still holds.

It doesn’t seem like it is about to change in the next few decades. Modern nutrition keeps on clinging to the old ideas that brought us the obesity epidemic and for some reason they seem completely unwilling to change their minds.

Are there any other myths (lies?) you would like me to cover? Shoot me a comment below and I’ll see if I can add them to the list.

I’d love for this post to become a “weapon” for all of us to change the world, one nutritionist at a time.
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Read the complete article here.

Dr Davis was interviewed by Wellness Mama  recently. The full interview can be seen here. I have shown only the part that specifically addresses heart disease.
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2. How is wheat consumption linked to heart health?

Wheat consumption causes heart disease. It’s not cholesterol, it’s not saturated fat that’s behind the number one killer of Americans; it’s wheat.

The nutrition community has been guilty of following a flawed sequence of logic: If something bad for you (white processed flour) is replaced by something less bad (whole grains) and there is an apparent health benefit, then a whole bunch of the less bad thing is good for you. Let’s apply that to another situation: If something bad for you—unfiltered Camel cigarettes—are replaced by something less bad—filtered Salem Cigarettes—then the conclusion would be to smoke a lot of Salems. The next logical question should have been: What is the health consequence of complete removal? Only then can you observe the effect of whole grains vs. no grains . . . and, from what I witness every day, you see complete transformations in health.

Consumption of wheat, due to its unique carbohydrate, amylopectin A, triggers formation of small, dense LDL particles more than any other common food. Small, dense LDL particles are the number one cause for heart disease in the U.S. The majority of adults now have an abundance of small LDL particles because they’ve been told to cut their fat and “eat plenty of healthy whole grains.” This situation of excessive small LDL particles can appear on a conventional cholesterol panel as higher levels of LDL (“bad”) cholesterol, along with low HDL cholesterol and higher triglycerides that often leads to statin drugs. When more sophisticated lipoprotein testing is obtained, then the explosion of small LDL particles becomes obvious.

Compound this with the increased appetite triggered by the gliadin protein in wheat that acts as an appetite-stimulant, and you gain weight. The weight gained is usually in the abdomen, in the deep visceral fat that triggers inflammation, what I call a “wheat belly.” Wheat belly visceral fat is a hotbed of inflammation, sending out inflammatory signals into the bloodstream and results in higher blood sugar, blood pressure, and triglycerides, all adding up to increased risk for heart disease.
Say goodbye to wheat and small LDL particles plummet, followed by weight loss from the wheat belly visceral fat. Inflammation subsides, blood sugar drops, blood pressure drops. In short, elimination of wheat is among the most powerful means of reducing risk for heart disease.

How to prevent diabetes and heart disease for $16

November 26, 2010   Chris Kresser

In the last article we discovered that the blood sugar targets established by the American Diabetes Association are far too high, and do not protect people from developing heart disease, diabetes or other complications. And we looked at what the scientific literature indicates are safer targets for fasting blood sugar, hemoglobin A1c and either OGTT or post-meal blood sugar.

In this article I’m going to introduce a simple technique that, when used properly, is one of the most effective ways to maintain healthy blood sugar and prevent cardiovascular and metabolic disease – without unnecessary drugs.

I love this technique because it’s:

• Cheap. You can buy the equipment you need for $16 online.
• Convenient. You can perform the tests in the comfort of your home, in your car, or wherever else you might be.
• Personalized. Instead of following some formula for how much carbohydrate you can safely eat, this method will tell you exactly what your carbohydrate tolerance is, and which carbs are “safe” and “unsafe” for you.
• Safe. Unlike the oral glucose tolerance test (OGTT), which can produce dangerous and horribly uncomfortable spikes in blood sugar, this strategy simply involves testing your blood sugar after your normal meals.

The strategy I’m referring to is using a glucometer to test your post-meal blood sugars. It’s simple, accessible and completely bypasses the medical establishment and pharmaceutical companies by putting the power of knowledge in your hands.

It’s one of the most powerful diagnostic tools available, and I use it with nearly all of my patients. Here’s how to do it.

Step one: buy a glucometer and test strips

A glucometer is a device that measures blood sugar. You’ve probably seen them before – they’re commonly used by diabetics. You prick your finger with a sterilized lancet, and then you apply the drop of blood to a “test strip” that has been inserted into the glucometer, and it measures your blood sugar.

There are literally hundreds of glucometers out there, and their accuracy, quality and price varies considerably. The one I recommend to my patients is called the Relion Ultima, which can be purchased with 20 test strips for $16.00 online at Walmart.com. (Note: as a rule I don’t like to support Walmart, but I haven’t been able to find this unit anywhere else at a similar price.) Even better, the test strips, which you’ll need on an ongoing basis to monitor your blood sugar, are relatively cheap for the Relion Ultima. You can get a 100 of them for $39 at Walmart online ($0.39/strip).

I’m sure there are many other choices that work well, but this is the unit I have the most experience with, and in general it is very reliable. Another good choice is the TrueTrack meter drugstores sell under their own brand name (i.e. Walgreens, Sav-on, etc.). Other models to consider are the One Touch Ultra or one of the Accu-Chek meters. The problem with these, however, is that the test strips tend to be more expensive than the Relion Ultima.

Step two: test your blood sugar

1. Test your blood sugar first thing in the morning after fasting for at least 12 hours. Drink a little bit of water just after rising, but don’t eat anything or exercise before the test. This is your fasting blood sugar level.
2. Test your blood sugar again just before lunch.
3. Eat your typical lunch. Do not eat anything for the next three hours.
Test your blood sugar one hour after lunch.
4. Test your blood sugar two hours after lunch.
5. Test your blood sugar three hours after lunch.

Record the results, along with what you ate for lunch. Do this for two days. This will tell you how the foods you normally eat affect your blood sugar levels.

On the third day, you’re going to do it a little differently. On step 3, instead of eating your typical lunch, you’re going to eat 60 – 70 grams of fast acting carbohydrate. A large (8 oz) boiled potato or a cup of cooked white rice will do. For the purposes of this test only, avoid eating any fat with your rice or potato because it will slow down the absorption of glucose.

Then follow steps 4-6 as described above, and record your results.

Step three: interpret your results

If you recall from the last article, healthy targets for blood sugar according to the scientific literature are as follows:

Marker	Ideal*
Fasting blood glucose (mg/dL)	<86
OGGT / post-meal (mg/dL after 1 hour)	<140
OGGT / post-meal (mg/dL after 2 hours)	<120
OGGT / post-meal (mg/dL after 3 hours)	Back to baseline
Hemoglobin A1c (%)	<5.3

*To convert these numbers to mmol/L, use this online calculator.
Hemoglobin A1c doesn’t apply here because you can’t test it using a glucometer. We’re concerned with the fasting blood sugar reading, and more importantly, the 1- and 2-hour post-meal readings.

The goal is to make sure your blood sugar never rises higher than 140 mg/dL an hour after a meal, drops below 120 mg/dL two hours after a meal, and returns to baseline (i.e. what it was before you ate) by three hours after a meal.

There are a few caveats to this kind of testing. First, even reliable glucometers have about a 10% margin of error. You need to take that into account when you interpret your results. A reading of 100 mg/dL could be anything between 90 mg/dL and 110 mg/dL if you had it tested in a lab. This is okay, because what we’re doing here is trying to identify patterns – not nit-pick over specific readings.

Second, if you normally eat low-carb (less than 75g/d), your post-meal readings on the third day following the simple carbohydrate (rice or potato) challenge will be abnormally high. I explained why this occurs in the last article, but in short when you are adapted to burning fat your tolerance for carbohydrates declines. That’s why your doctor would tell you to eat at least 150g/d of carbs for three days before an OGTT if you were having that test done in a lab.

If you’ve been eating low-carb for at least a couple of months before doing the carbohydrate challenge on day three of the test, you can subtract 10 mg/dL from your 1- and 2-hour readings.

This will give you a rough estimate of what your results would be like had you eaten more carbohydrates in the days and weeks leading up to the test. It’s not precise, but it is probably accurate enough for this kind of testing.

Step four: take action (if necessary)

So what if your numbers are higher than the guidelines above? Well, that means you have impaired glucose tolerance. The higher your numbers are, the further along you are on that spectrum. If you are going above 180 mg/dL after one hour, I’d recommend getting some help – especially if you’re already on a carb-restricted diet. It’s possible to bring numbers that high down with dietary changes alone, but other possible causes of such high blood sugar (beta cell destruction, autoimmunity, etc.) should be ruled out.

If your numbers are only moderately elevated, it’s time to make some dietary changes. In particular, eating fewer carbs and more fat. Most people get enough protein and don’t need to adjust that.

And the beauty of the glucometer testing is that you don’t need to rely on someone else’s idea of how much (or what type of) carbohydrate you can eat. The glucometer will tell you. If you eat a bowl of strawberries and it spikes your blood sugar to 160 mg/dL an hour later, sorry to say, no strawberries for you. (Though you should try eating them with full-fat cream before you give up!) Likewise, if you’ve been told you can’t eat sweet potatoes because they have too much carbohydrate, but you eat one with butter and your blood sugar stays below 140 mg/dL after an hour, they’re probably safe for you. Of course if you’re trying to lose weight, you may need to avoid them anyways.

You can continue to periodically test your blood sugar this way to see how you’re progressing. You’ll probably notice that many other factors – like stress, lack of sleep and certain medications – affect your blood sugar. In any case, the glucometer is one of your most powerful tools for preventing degenerative disease and promoting optimal function.

Resources

If you haven’t already, check out Jenny Ruhl’s excellent Blood Sugar 101 site. Jenny won’t tell you this herself, but she’s an authority on blood sugar and probably knows more about it than 99.9% of health care practitioners (she’s an author). In particular, check out the “Painless Blood Sugar Testing”, “Frequently Asked Questions” and “How to Lower Your Blood Sugar” sections. I’d link to them directly, but her site uses frames and doesn’t allow it.
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Read full article here.

FDA Expands Advice on Statin Risks

If you’re one of the millions of Americans who take statins to prevent heart disease, the Food and Drug Administration (FDA) has important new safety information on these cholesterol-lowering medications.

FDA is advising consumers and health care professionals that:

• Routine monitoring of liver enzymes in the blood, once considered standard procedure for statin users, is no longer needed. Such monitoring has not been found to be effective in predicting or preventing the rare occurrences of serious liver injury associated with statin use.
• Cognitive (brain-related) impairment, such as memory loss, forgetfulness and confusion, has been reported by some statin users.
• People being treated with statins may have an increased risk of raised blood sugar levels and the development of Type 2 diabetes.
• Some medications interact with lovastatin (brand names include Mevacor) and can increase the risk of muscle damage.

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Read the rest of the FDA article here.

Is Your Bottled Water Killing You? By William Davis, MD

Health Benefits of Magnesium Replacement What can you expect from supplementing magnesium to optimal levels? Research over the past 20 years suggests that magnesium supplementation will accomplish several critically important goals: Magnesium improves insulin sensitivity. Magnesium helps correct impaired insulin sensitivity, the fundamental defect that characterizes pre-diabetes and metabolic syndrome. An intracellular enzyme called tyrosine kinase requires magnesium to allow insulin to exert its blood-sugar-lowering effects. In several studies, daily oral magnesium supplementation substantially improved insulin sensitivity by 10% and reduced blood sugar by 37%.21-23 Magnesium helps correct abnormal lipoprotein patterns. Improved insulin sensitivity from magnesium replacement can markedly reduce triglyceride levels.23 Reduced triglyceride availability, in turn, reduces triglyceride-rich particles, such as very low-density lipoprotein (VLDL) and small low-density lipoprotein (small LDL), both of which are powerful contributors to heart disease.24 Magnesium supplementation can also raise levels of beneficial high-density lipoprotein (HDL).24 Magnesium suppresses abnormal heart rhythms. Magnesium has gained a foothold in hospital care following coronary bypass surgery, when the abnormal heart rhythm known as atrial fibrillation commonly occurs. Magnesium may help suppress this rhythm outside of the hospital as well,25 suggesting a preventive role in averting abnormal heart rhythms. Magnesium reduces blood pressure. Magnesium regulates blood pressure by modulating vascular tone. Magnesium works in ways similar to the prescription hypertension drugs known as calcium-channel antagonists (such as diltiazem and nifedipine), which block calcium channels that trigger constriction of the arteries. Magnesium stimulates the production of prostacyclins and nitric oxide, which are potent artery-relaxing agents.26 Magnesium exerts a modest effect of reducing blood pressure, reflecting its whole-body artery-relaxing properties.27 Magnesium can block migraine headaches. Magnesium has been explored as a means to prevent or relieve migraine headaches. People suffering migraine headaches tend to have lower magnesium levels.28 A study from the State University of New York showed that intravenous magnesium relieved headache symptoms in 15 minutes in 80% of recipients.29 Other studies have since corroborated magnesium’s beneficial effect on migraine headaches, including a trial in children, in which oral supplementation with magnesium oxide reduced the frequency and severity of migraine.30 Magnesium may improve exercise performance. Extensive research in athletes has found that intensive exercise triggers magnesium loss through urinary excretion and perspiration. When magnesium is low, supplementation enhances exercise performance by reducing lactate blood levels (indicating brief, strength-based anaerobic muscle activity), decreasing oxygen requirements, and increasing muscle strength.31,32 Magnesium may benefit many other conditions. Other conditions in which magnesium is believed to exert positive effects include fibromyalgia,33 asthma (acute episodes have been treated successfully with both intravenous and aerosolized magnesium),34 prevention of osteoporosis,35 and premenstrual syndrome.36 Can you correct metabolic syndrome and its complications—such as insulin resistance and high blood pressure—without replacing magnesium? Of course you can, just as you can operate your car without changing the oil. However, magnesium deficiency will catch up with you, and consuming this basic supplement will help you to more easily achieve your health goals. Strategies for Optimizing Your Magnesium Intake According to the US Department of Health and Human Services, nearly all of us fail to achieve even the modest magnesium RDAs of 420 mg for adult males and 320 mg for adult females. Most American adults ingest about 270 mg of magnesium a day, well below the RDA and enough to generate a substantial cumulative deficiency over months and years.37 The magnesium RDA refers to elemental magnesium, defined as the amount of magnesium regardless of its source or form. Magnesium is generally available as various “salts” (not to be confused with table salt), and the amount of elemental magnesium contained in each varies depending on the salt. For example, the amount of magnesium in magnesium oxide is 60%; in magnesium carbonate, 45%; in magnesium citrate, 16%; and in magnesium chloride, 12%.38 Thus, magnesium oxide supplements tend to contain more elemental magnesium per pill than do magnesium citrate supplements. Magnesium salts differ in absorption. Magnesium oxide, though inexpensive and widely available, is thought to be relatively less absorbed than the citrate and chloride forms.39-41 You can also increase your magnesium intake by choosing foods rich in magnesium, which are listed in the table below.42 Foods rich in magnesium (magnesium content in mg) Almonds (1 oz; 24 nuts) 78 Oatmeal (1 cup, cooked) 56 Artichokes (1 cup) 101 Pumpkin seeds (1 oz; 142 seeds) 151 Barley (1 cup, raw) 158 Rice, brown (1 cup, cooked) 84 Beans, black (1 cup, cooked) 120 Soybeans (1 cup, cooked) 148 Beans, lima (1 cup, cooked) 101 Spinach (1 cup, cooked) 163 Brazil nuts (1 oz; 6-8 nuts) 107 Trail mix (1 cup) 235 Halibut (1/2 filet) 170 Walnuts (1 oz; 14 halves) 45 Filberts, hazelnuts (1 oz) 46 Wheat flour, whole grain (1 cup) 166 Oat bran (1 cup, raw) 221 Source: USDA National Nutrient database for Standard Reference, Release17 Dietary Sources of Magnesium Nuts, pumpkin seeds, spinach, and oat bran are particularly rich and healthy sources of magnesium. Another strategy for boosting magnesium intake is to supplement your diet with the soluble fiber known as inulin. Like other soluble fibers, inulin may exert modest cholesterol- and triglyceride-reducing effects. However, it also enhances magnesium absorption in the intestine.43 Inulin can be taken as a supplement, and is contained in some foods (for example, the Stonyfield Farms brand of yogurt). Inulin can help increase satiety (the sense of fullness you get with eating), resulting in decreased calorie intake throughout the day.44 Inulin thus holds promise in supporting efforts to lose weight.45 One more important way to optimize your magnesium intake is to choose water that is rich in magnesium. Unfortunately, in the US, this is easier said than done. The FDA regulates bottled water and mandates that the only additives permitted are fluoride and antimicrobials to deter bacterial growth. Magnesium cannot therefore be added to water labeled spring water or mineral water. Magnesium Content of Mineral Waters The following waters contain far more than the usual amounts of magnesium. Some, like Apollinaris and Pellegrino, are widely available in American grocery stores, while others are found only in upscale groceries or through websites of the water producers. Mineral Water Magnesium Content Original Fountain of Youth Mineral Water (Florida) 609 mg/L Apollinaris (Germany) (410 mg/L of sodium) 130 mg/L Adobe Springs (California and other western states) 110 mg/L Badoit (France) 85 mg/L Colfax (Iowa) 91 mg/L Deep Rock (Colorado) 60 mg/L Evian 24 mg/L Gerolsteiner (Germany) 108 mg/L Noah’s California Spring Water 110 mg/L Pellegrino Sparkling Mineral Water (Italy) (43.6 mg/L of sodium) 55.9 mg/L Manitou Mineral Water (Colorado) 43 mg/L Rosbacher 93 mg/L St. Gero 109.4 mg/L Both Apollinaris and Pellegrino contain more sodium than most other waters, and therefore should be avoided by those who are limiting their sodium intake due to existing hypertension, fluid retention, or kidney disease. Magnesium-rich mineral waters are not easy to find, but they are out there. By FDA definition, mineral waters must contain at least 250 parts per million (ppm) of total dissolved solids. Not all mineral water contains significant quantities of magnesium. For example, Napa Valley’s Calistoga Springs, labeled as “mineral water,” contains 0.61–0.96 mg/L of magnesium, or virtually none. Magnesium Dosage Guidelines The recommended dietary allowance (RDA) for magnesium is 420 mg a day for adult men and 320 mg a day for adult women.46 Most people fail to achieve the RDA, which may lead to magnesium deficiency.37 The most common adverse reaction from the use of magnesium supplements is diarrhea. Other gastrointestinal symptoms include nausea and abdominal cramping. Diarrhea and other gastrointestinal symptoms are less likely to occur if magnesium supplements are taken with food.46 Magnesium supplements are contraindicated in those with kidney failure. Those with myasthenia gravis (an autoimmune disorder that results in progressive skeletal muscle weakness) should avoid magnesium supplements.46 To determine the amount of magnesium contained in bottled water labeled “mineral water” but not listed above, go to the bottler’s website to determine the water’s composition. With the exception of Florida’s Original Fountain of Youth Mineral Water, drinking an entire liter of many so-called mineral waters provides only a modest amount of magnesium. Thus, for instance, if you are currently ingesting around 250 mg a day of magnesium from your diet, drinking a liter of Gerolsteiner a day (supplying 108 mg/L of magnesium) will increase your magnesium consumption only to about 350 mg per day. However, by adding a magnesium supplement that provides as little as 100 mg of elemental magnesium, you will have more than achieved the RDA for an adult male. Since many mineral waters are expensive (around $2-3 per liter), magnesium supplements are a far less costly way to optimize your magnesium intake. Conclusion The intensification of municipal water treatment has resulted in a growing epidemic of magnesium deficiency, with most Americans failing even to achieve the modest levels set by the government-recommended RDA. Most of us have daily deficiencies in magnesium intake of only 70-200 mg a day. The consequences of magnesium deficiency can be dramatic, including poor insulin response, migraine headaches, high blood pressure, and abnormal and even dangerous heart rhythms. Fortunately, there are plenty of healthy choices—foods rich in magnesium, low-cost magnesium supplements, and waters rich in magnesium—that can you help reach or exceed the magnesium RDA and attain the numerous health benefits conferred by optimal magnesium intake. Dr. William Davis is an author and cardiologist practicing in Milwaukee, WI. He is founder of the Track Your Plaque program, a heart disease prevention and reversal program that shows how CT heart scans can be used to track and control coronary plaque. He can be reached at www.TrackYourPlaque.com. The Basics of Water and Water Purification While the Environmental Protection Agency regulates the quality of tap water, the Food and Drug Administration (FDA) is responsible for regulating bottled water. In 1995, the FDA issued its most recent regulations classifying various waters: Artesian well water is water that naturally flows upward from an underground aquifer to a well, without the need for pumping. Mineral water is water from an underground source that contains at least 250 parts per million (ppm) of dissolved solids consisting of minerals and trace elements. Mineral content of 250-500 ppm is often called “low mineral content” or “light mineral water,” while content of 1500 ppm or greater is “high mineral content.” (In Europe, spring waters with dissolved solids equal to or less than 500 mg/L are considered “mineral with low mineral content” or simply “mineral water.”) Minerals and trace elements cannot be added artificially to water labeled as mineral. Spring water, like artesian well water, comes from an underground source but flows naturally to the earth’s surface. It cannot come from a public or municipal source. Spring water must be collected directly at the spring or through a borehole tapping the underground source. Mineral content is less than 250 ppm and cannot be added after collection. Well water is water from a hole bored or drilled into the ground, which taps into an aquifer and is drawn to the surface using a pump. Many homes in the US that do not have access to municipal water use well water. To make matters even more complicated, any water—regardless of the source—can be treated or filtered. This is usually done to modify its taste or to remove undesirable ingredients. Methods of treatment are defined as: Distillation. Water is vaporized and collected, leaving behind any solid residues, including minerals. Distilled water contains no minerals whatsoever. Reverse osmosis. In this common water-purifying process, water is forced through membranes to remove minerals in the water. Deionization. Also called demineralization or ion exchange, this process uses synthetic resins to remove ions and minerals from water. This is very effective at removing ionized impurities, but does not remove organic, bacterial, pathogenic, or particulate matter efficiently. Deionized water contains no magnesium. Absolute 1 micron filtration. Water is passed through filters that remove particles larger than 1 micron in size, including Cryptosporidium, a parasite that causes intestinal infestation. This process does not affect the water’s mineral content. Ozonation. Many bottled water companies use this process instead of chlorine to rid water of bacteria. Ozonation does not affect the mineral content of water. Many bottled waters are simply tap water processed using one or more of the above processes of distillation, reverse osmosis, deionization, or filtration. This leaves the water virtually devoid of both nutrients and contaminants. Of the 700 or so brands of bottled water available in the US, 80% are processed water. Many experts say that treated water like this is virtually identical to that produced by home water purifiers. The appeal of these waters is therefore a reduction in impurities like lead and pesticide residues, or better taste—but not enhanced mineral content. Bottled processed waters contain little or no magnesium. It should also be noted that unlike tap water, purified waters and water purifiers reduce or eliminate the fluoride that is added by many municipal treatment facilities to promote dental health. Although the FDA permits producers to add it back to purified water, few actually do. Waters derived from natural sources like artesian well water, well water, mineral water, and spring water are generally slightly richer in mineral content than are processed and tap waters. However, the difference is small. Nearly all American bottled waters obtained from natural sources—whether artesian, well, spring, or mineral waters—contain less than 6 ppm of magnesium, a trivial amount.

References

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Magnesium disorders and cardiovascular diseases. Clin Cardiol. 1992 Aug;15(8):556-68. 11. Smetana R, Stuhlinger HG, Kiss K, Glogar DH. Intravenous magnesium sulphate in acute myocardial infarction—is the answer “MAGIC”? Magnes Res. 2003 Mar;16(1):65-9. 12. Kousa A, Havulinna AS, Moltchanova E, et al. Calcium:magnesium ratio in local groundwater and incidence of acute myocardial infarction among males in rural Finland. Environ Health Perspect. 2006 May;114(5):730-4. 13. Anderson TW, Le Riche WH, MacKay JS. Sudden death and ischemic heart disease. Correlation with hardness of local water supply. N Engl J Med. 1969 Apr 10;280(15):805-7. 14. Available at:http://www.nsf.org/international/press_release.asp?p_id=12041. Accessed November 14, 2006. 15. Laires MJ, Monteiro CP, Bicho M. Role of cellular magnesium in health and human disease. Front Biosci. 2004 Jan 1;9:262-76. 16. Berkelhammer C, Bear RA. A clinical approach to common electrolyte problems: 4. Hypomagnesemia. Can Med Assoc J. 1985 Feb 15;132(4):360-8. 17. Roffe C, Sills S, Crome P, Jones P. Randomised, cross-over, placebo controlled trial of magnesium citrate in the treatment of chronic persistent leg cramps. Med Sci Monit. 2002 May;8(5):CR326-30. 18. Bilbey DL, Prabhakaran VM. Muscle cramps and magnesium deficiency: case reports. Can Fam Physician. 1996 Jul;42:1348-51. 19. Bussone G. Pathophysiology of migraine. Neurol Sci. 2004 Oct;25 Suppl 3S239-41. 20. He K, Liu K, Daviglus ML, et al. Magnesium intake and incidence of metabolic syndrome among young adults. Circulation. 2006 Apr 4;113(13):1675-82. 21. Guerrero-Romero F, Tamez-Perez HE, Gonzalez-Gonzalez G et al. Oral magnesium supplementation improves insulin sensitivity in non-diabetic subjects with insulin resistance. A double-blind placebo-controlled randomized trial. Diabetes Metab. 2004 Jun;30(3):253-8. 22. Rodriguez-Moran M and Guerrero-Romero F. Oral magnesium supplementation improves insulin sensitivity and metabolic control in type 2 diabetic subjects: a randomized double-blind controlled trial. Diabetes Care. 2003 Apr;26(4):1147-52. 23. Yokota K, Kato M, Lister F, et al. Clinical efficacy of magnesium supplementation in patients with type 2 diabetes. J Am Coll Nutr. 2004 Oct;23(5):506S-9S. 24. Rasmussen HS, Aurup P, Goldstein K, et al. Influence of magnesium substitution therapy on blood lipid composition in patients with ischemic heart disease. A double-blind, placebo controlled study. Arch Intern Med. 1989 May;149(5):1050-3. 25. Piotrowski AA, Kalus JS. Magnesium for the treatment and prevention of atrial tachyarrhythmias. Pharmacotherapy. 2004 Jul;24(7):879-95. 26. Sontia B, Touyz RM. Role of magnesium in hypertension. Arch Biochem Biophys. 2006 May 24. 27. Jee SH, Miller ER, III, Guallar E, et al. The effect of magnesium supplementation on blood pressure: a meta-analysis of randomized clinical trials. 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Fructose is a stealth poison

From the blog of Dr. William R. Davis
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Restaurant eating: A fructose landmine from Heart Scan Blog by Dr. William Davis


3 people liked thisThere is no remaining question that fructose is among the worst possible things humans can consume.
Followers of the Heart Scan Blog already know this, from conversations like The LDL-Fructose Disconnect, Where do you find fructose?, and Goodbye, fructose.

But fructose, usually as either high-fructose corn syrup (44%, 55%, occasionally higher percentage fructose) or sucrose (50% fructose), is ubiquitous. I've seen it in the most improbable places, including cole slaw, mustard, and dill pickles.

It's reasonably straightforward to avoid or minimize fructose exposure while eating at home, provided you check labels and focus on foods that don't require labels (like green peppers, salmon, and olive oil, i.e., unprocessed foods). But when you choose to eat at a restaurant, then all hell can break loose and fructose exposure can explode.

So what are some common and unsuspected fructose sources when eating at a restaurant?

Salad dressings--Dressings in all stripes and flavors are now made with high-fructose corn syrup and/or sucrose. This is especially true of low-fat, non-fat, or "lite" dressings, meaning oils have been replaced by high-fructose corn syrup. It can also be true of traditional non-low-fat dressings, too, since high-fructose corn syrup is just plain cheap.

Olive oil and vinegar are still your safest bets. I will often use salsa as a dressing, which works well.
Sauces and gravies--Not only can sauces be thickened with cornstarch, many pre-mixed sauces are also made with high-fructose corn syrup or sweetened with sucrose. Barbecue sauce is a particular landmine, since it is now a rare barbecue sauce not made with high-fructose corn syrup as the first or second ingredient. Sauces for dipping are nearly always high-fructose corn syrup-based.
Ketchup--Yup. Good old ketchup even is now made with high-fructose corn syrup. In fact, you should be suspicious of any condiment.
Highball, Bloody Mary, Margarita, Daiquiri, beer--Even the before-dinner or dinner drink can have plenty of fructose, particularly if a mix is used to make it. While Blood Marys seem the most benign of all, adorned with celery, pickle, and olive, just take a look at the ingredient label on the mix used: high-fructose corn syrup.
Fructose is a stealth poison: It doesn't immediately increase blood sugar; it doesn't trigger any perceptible effect like increased energy or sleepiness. But it is responsible for an incredible amount of the health struggles in the U.S., from obesity, to diabetes, to hyperlipidemias and heart disease, to arthritis, to cataracts.