The High-Cholesterol Paradox - Wainwright

http://www.lizscript.co.uk/glyn/paradox.pdf

The High-Cholesterol Paradox

 
  

Based upon European WAPF Conference 2014 presentation accredited by:

 

The Naturopathic Nutrition Association,

Federation of Nutritional Practitioners (FNTP)

British Association of Applied Nutrition (BAAN),

British Association of Nutritional Therapy (BANT)

  

Glyn Wainwright MSc MBCS CITP CEng - Independent Researcher, Leeds UK

 

 

The Paradox

   

Being told you have ‘high cholesterol’ is commonly taken as a sign of an unhealthy destiny. Research suggests that for many elderly people the news that they have ‘high cholesterol’ is more often

associated with good health and longevity1.

For over 50 years this has been a paradox, the ‘High-Cholesterol Paradox’. What is really going on?


  

Hypothesis becomes Dogma

   

In the 1950s the prestigious American MD, Dr Ancel Keys2, supported a popular theory that heart disease was caused by dietary Fats and Cholesterol (Lipids) circulating in the blood. In 1972 a British Professor, Dr John Yudkin3, published a book called ‘Pure, White and Deadly’ which proposed over-consumption of refined sugar as the leading cause of diabetes and heart disease. The science

 

 

 

 

 
Until the 1970s there had been a small but consistent percentage of overweight and obese people in the population. By the 1980s obesity rates had begun to climb significantly. This sudden

acceleration of obesity is very closely associated with the adoption of new high-sugar, low-fat

formulations in processed foods - the consequences of the McGovern report recommendations being

adopted around the world. Advice to reduce our intake of saturated fats, obtained from meat and dairy, caused a rise in the use of plant based oils and so-called ‘vegetable fats’. This was misleadingly promoted as healthy. The biochemical destiny of dietary ‘Saturated Fat’ is not the same as that of excess ‘Carbohydrates and Sugars’.

 

Fats do not cause obesity or disease. It is the excess sugars (glucose and fructose - High Fructose Corn Syrup HFCS) which create abdominal 

obesity4.

The erroneous idea, and fear, of artery blocking fats was exploited to market fat substitutes. Invite anyone talking about ‘artery blocking fats’ to hold a pat of butter in a closed fist. As the butter melts and runs out between their fingers, ask ‘How do fats, which are evolved to be fluids at body temperature, block the vascular ‘pipes’ in our bodies?’

Plant oils are not the natural lipids for maintaining healthy human or animal cell membranes. Animal sourced fats, and essential fatty acids (EFA), are identical to those we require for the maintenance of the healthy human body.

Let us explore some more big anomalies in the last 40 years of dietary health guidance.

 

Good Cholesterol? Bad Cholesterol? Spot the Difference?

All biochemists can confirm that all cholesterol molecules throughout the known universe are
identical in every respect. So how can there be ‘good’ or ‘bad’ cholesterol. It is now possible to
frighten people with unscientific descriptions like ‘Good’ and ‘Bad’ when talking about cholesterol.
This single misleading description may have prevented a whole generation from knowing the true causes of the very real disturbance in the levels of fatty nutrients 

(Lipids) circulating in our blood4.

Healthy Lipids
   

If the total blood serum cholesterol (TBSC) is high and the organs are getting enough lipids, the blood lipid circulation is healthy. The large parcels of fatty nutrients (LDL lipids) sent by the liver are consumed by our organs (receptor-mediated endocytosis) and the smaller fatty wrappers and left-over lipids (HDL Lipids) return to the liver. The Fatty Nutrients (LDL) and the recycled lipids (HDL) are in balance. Such a healthy-lipid ‘High-Cholesterol’ person is well nourished and likely to have a long and healthy life.

 

Damaged Lipids

  

If the total blood serum cholesterol is high but the fatty nutrient droplets (LDLs) have sugar-damaged labels, the organs are unable to recognise and feed on them. The supply of fatty nutrients to organs is broken. The liver continues to supply fatty nutrients (albeit with damaged LDL labels), but the organs’ receptors are unable to recognise them. The organs thus become starved of their fatty

nutrients. Like badly labelled parcels in a postal service, the sugar-damaged lipids build up in the blood (raised LDL) and fewer empty wrappers are returned to the liver (low HDL). LDL (erroneously called ‘bad’ cholesterol) is raised in the blood, awaiting clearance by the liver. There is less HDL (erroneously called ‘good’ cholesterol) being returned by the organs. High Cholesterol (high levels of total blood serum cholesterol TBSC) when caused by damage to the LDL lipid parcels is a sign that lipid circulation is broken. These fats (LDL) will be scavenged to become visceral fats, deposited around the abdomen. This type of damage is associated with poor health. So it really doesn’t matter how high your total blood serum cholesterol (TBSC) is. What really counts is the damaged condition of the blood’s fatty nutrient parcels  

(LDL lipids). In our research review of metabolic syndromes4 (e.g. diabetes, heart

disease, obesity, arthritis and dementia) we explained that the major cause of lipid damage was sugar-related.

 

Sugar Damage (AGEs)

 

The abbreviation AGE (Advanced Glycation End-product) is used to describe any 

sugar-damaged protein. As we age, excessive amounts of free sugars in the 

blood5 may eventually cause damage quicker than the body can repair it. The

sugars attach by a chemical reaction and the sugar called fructose is known to

be 10 times more reactive, and therefore more dangerous than our normal blood
sugar (glucose). Since the 1970s we have been using increasing quantities of
refined fructose (from high-fructose corn syrup). Its appealing sweetness, and

ability to suppress the ‘no longer hungry’ receptor6 (ghrelin receptor) is driving

excessive food intake. Its ability to damage our fatty nutrients and lipid  

circulation is also driving waist-line obesity and its associated health problems4,7.

Checking for Damage in our Lipids  There is a ‘simple to administer’ commonly available blood test used to check for
sugar-damage. It is used to check the proteins in the blood of people who are
diabetic or at risk of becoming diabetic. It tests for Glycated Haemoglobin
(HbA1c) by counting the proportion of damaged molecules (per 1000) of
Haemoglobin protein in the blood (mmol/mol). Researchers looking at ways of
testing for damage to lipids, have found that sugar-damaged blood protein test
(HbA1c), presents a very reasonable approximation of the state of sugar-damage
in the blood lipids. Until there is a good general test for sugar-damage in blood
lipids, this test (HbA1c) could be a sensible surrogate. This is a better way of
assessing health than a simple cholesterol test (TBSC).
Improved sugar-damaged blood protein (HbA1c) scores in diabetic patients is
accompanied by improvements in their lipid profiles. This could be very useful to
anyone wanting to improve health outcomes by managing lifestyle and nutrition.
 

Clinical Consequences of Lowering Cholesterol

    

In 2008 Dr Luca Mascitelli asked me to examine a paper by Xia et al8. It was very

interesting to note that lowering cholesterol by as little as 10% (molecular in cell

walls) in the pancreas (pancreatic beta-cells) prevented the release of insulin
(cholesterol-mediated exocytosis). This paper described a mechanism by which
‘cholesterol lowering drugs’ directly cause diabetes. It was known that in statin
drug trials which looked at glucose (blood sugar) control there was poor bloodsugar
control in the statin user groups. Since 2011 the USA government (FDA)  

required statins to carry a warning about the risk of causing diabetes9.

 

 

 

Memories are made of this – Cholesterol
  

The healthy human brain may only be 5% of body weight but it requires over

25% of the body’s cholesterol. The nervous system uses huge quantities of  

cholesterol for insulation, protection and structure (myelin). F W Pfrieger et al.10

have shown that the formation of the memory (synapses) is dependent on good
supplies of cholesterol. Post-mortem studies show that depleted cholesterol levels in the cerebrospinal
fluids are a key feature of dementias. It was also reported that behavioural
changes and personality changes are associated with low levels of cerebrospinal
cholesterol. In another review paper on Dementia we commented extensively on the damage

done by fructose and the depletion of cholesterol availability. Low cholesterol

levels in the nervous system are not conducive to good mental health.

 

Consequences of Lowering Cholesterol

.
.
.
.
.
.
Read the complete article here  



  


 

Triglycerides: Mother of Meddlesome Particles - Davis

Triglycerides: Mother of Meddlesome Particles



Triglycerides are a crucial risk factor for coronary plaque growth, even at levels previously thought to be normal. Dr. Davis discusses why and how this oft-neglected factor can be harnessed to strengthen your program.

While the world obsesses over cholesterol, a potent stimulator of plaque growth is frequently ignored—triglycerides. A subject of controversy in past, the data are now clear: triglycerides spawn unwanted lipoprotein particles that trigger plaque growth. Track Your Plaque members are advised that control of triglycerides is essential to everyone’s plaque control program.

Triglyceride control is crucial if you are interested in gaining control over coronary plaque. Triglycerides should be brought under control at the start of your program. If you are experiencing plaque growth (increasing heart scan scores), seriously reining in triglycerides should be considered.

How important are triglycerides?

 

For years, the relationship between coronary heart disease and triglycerides remained muddled by the confounding effects of low HDL. In other words, increased triglycerides tend to occur alongside low HDL. This caused many to dismiss the importance of triglycerides. To make matters even murkier, high triglycerides in some situations generated high risk for heart disease, while in others it appeared unrelated to heart disease, even when markedly elevated (in the thousands!).

Thanks to the evolving science of lipoproteins, the issues are crystallizing. One important fact has emerged: triglycerides are a critical risk factor for coronary plaque growth, even at levels previously thought to be normal. Yes, high triglycerides frequently occur with low HDL, but they also behave independently. High triglycerides are a common cause of heart disease, even in people with low or normal cholesterol values. It is crucial that you (and your doctor) pay close attention to triglycerides if you are to succeed in controlling your plaque. We urge Members to make triglyceride control a priority in their program.

 

Where do triglycerides come from?

 

The liver produces a particle called “very low-density lipoprotein”, or VLDL, packed full of triglycerides. The higher your triglycerides, the more VLDL you will have. Sometimes triglycerides are increased due to genetic factors. More commonly, triglycerides are high due to excess weight, indulging in processed carbohydrates, and resistance to insulin (metabolic syndrome).

VLDL is like that bad kid on the block you want your kids to avoid. VLDL particles in the blood come into contact with LDL and HDL particles and they’re never quite the same. When a LDL or HDL particle meet VLDL, the triglycerides of VLDL are passed on. The result: LDL and HDL become bloated with triglycerides. Triglyceride-loaded LDL and HDL are a ready target for a set of enzymes in the blood and liver that reconfigure these particles into smaller versions, small LDL and small HDL. Recall that both small LDL and HDL are highly undesirable particles that stimulate plaque growth.

Although “official” (ATP-III) guidelines suggest that triglycerides over 150 mg are undesirable, we regard any value over 60 mg as high. An ideal level for an intensive Track Your Plaque approach is <45 font="font" mg.="mg.">

 

How will I know if I have this pattern?

 

On a conventional cholesterol panel, increased triglycerides and low HDL are tip-offs that excess VLDL are available to contribute to coronary plaque growth. At what triglyceride level does this cascade begin to take effect and create this collection of particles? Levels of 45 mg/dl or greater. In the Track Your Plaque program, we aim for zero plaque growth or reduction, and so we target triglyceride levels of 60 mg/dl or less.

You’ll notice that low HDL and increased triglycerides are also patterns that characterize the metabolic syndrome. In our experience, over 50% of adults show at least some of the characteristics of the metabolic syndrome. In our society of inactive, sedentary lifestyles and packaged, processed foods, metabolic syndrome is rampant. That means increased triglycerides from VLDL are also running rampant. The result: a 3 to 7-fold increase in risk for heart attack. Eliminating the metabolic syndrome is another battle we need to fight to conquer plaque. (See Shutting Off the Metabolic Syndrome.)

 

How can triglycerides be reduced?

 

Our triglyceride target of 60 mg or less dramatically reduces triglyceride availability. Without triglycerides, LDL and HDL can’t be processed into undesirable small particles. Among the strategies we use to reach our triglyceride target of 60 mg or less:

• Fish oil—The omega-3 fatty acids in fish oil are our number one choice for substantially reducing triglycerides. Fish oil, 4000 mg per day, is a good starting dose (providing 1200 mg EPA+DHA); higher doses should be discussed with your physician, though we commonly use 6000–10,000 mg per day without ill-effect. Flaxseed oil, while beneficial for health, does not correct lipoprotein patterns. Consider a concentrated fish oil preparation (e.g., Omacor™, a prescription preparation, or “pharmaceutical grade” preparations from the health food store) if you and your doctor decide a high dose is necessary.
• Weight loss to ideal weight or ideal BMI (25). If achieved with a reduction in processed carbohydrates, the effect will be especially significant. Exercise will compound the benefits of weight loss, triggering an even larger drop in triglycerides.
• Reduction in processed carbohydrates—especially snacks; wheat-flour containing foods like breads, pasta, pretzels, chips, bagels, and breakfast cereals; white and brown rice; white potatoes. The reduction of high- and moderate-glycemic index foods is the factor that reduces triglycerides. High triglycerides are therefore a pattern that develops when someone follows a low-fat diet. For this reason, we do not advocate low-fat diets like the Ornish program. Reducing your exposure to wheat-containing snacks and processed foods is an especially useful and easy-to-remember strategy that dramatically reduces triglycerides.
• Elimination of high-fructose corn syrup—This ubiquitous sweetener is found in everything from beer to bread. High-fructose corn syrup causes triglycerides to skyrocket 30% or more.
• Niacin in doses of 500–1500 mg is an effective method of reducing triglycerides. Niacin also raises HDL, increases large HDL, reduces the number of small LDL particles, reduces VLDL, and modestly reduces total LDL. The preferred forms are over-the-counter Slo-Niacin® and prescription Niaspan®, the safest and best tolerated. Immediate-release niacin (just called niacin or nicotinic acid on the label) can also be taken safely, provided it is taken no more frequently than twice per day. Total daily doses of >500 mg should only be taken under medical supervision. Avoid nicotinamide and “no-flush niacin” (inositol hexaniacinate), neither of which have any effect whatsoever.
• Green tea—The catechins (flavonoids) in green tea can reduce triglycerides by 20%. Approximately 600–700 mg of green tea catechins are required for this effect, the equivalent of 6–12 servings of brewed tea. (Tea varies widely in catechin content.) Nutritional supplements are also available that provide green tea catechins at this dose. The weight loss accelerating effect of green tea may add to its triglyceride-reducing power.
• The thiazolidinediones (Actos®, or pioglitazone, and Avandia®, or rosiglitazone), usually prescribed for pre-diabetes or diabetes, can reduce triglycerides by 30%; Actos may be more effective than Avandia in this regard. However, these agents are accompanied by weight gain.
• The fibrate class of prescription drugs (fenofibrate, or Tricor®, and gemfibrozil®, or Lopid) reduce triglycerides 30–40%, i.e., almost as effectively as fish oil.

The evil influences of VLDL and triglycerides are therefore erased from your risk profile by achieving the Track Your Plaque target of triglycerides 60 mg/dl or less. One or more of these strategies are usually required to bring your triglycerides to target. 

        William Davis, MD


Selected references:

Packard CJ. Understanding coronary heart disease as a consequence of defective regulation of apolipoprotein B metabolism. Curr Opin Lipidol 1999; 10:237–244.

Otvos J. Measurement of triglyceride-rich lipoproteins by nuclear magnetic resonance spectroscopy Clin Cardiol 1999;22 (Suppl II) II-21–II-27.

Grundy SM. Hypertriglyceridemia, atherogenic dyslipidemia, and the metabolic syndrome. Am J Cardiol 1998;81(4A):18B–25B.

Zilversmit DB. Atherogenic nature of triglycerides, postprandial lipidemia, and triglyceride-rich remnant lipoproteins. Clin Chem 1995;41(1):153–158.