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

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Read the complete article here  



  


 

Does Red Meat Cause Inflammation? - Kresser

    Does Red Meat Cause Inflammation?

 

By Chris Kresser on April 5, 2013  

So far in my series on red meat, I’ve discussed why red meat is good for you and why grass fed is a better choice than grain fed. We now know that red meat is a healthy choice, due to its high nutritive value and superior fatty acid profile among other reasons. In the comments on these posts, however, I’ve noticed a few readers have mentioned other components in red meat that are concerning, due to evidence for the potential for inflammation or carcinogenesis.

Yet is this evidence strong enough to advise a reduction in red meat, or is this yet another false alarm creating unnecessary fear of eating meat?

Red meat and inflammation: another myth bites the dust.

Two different controlled trials have measured inflammation markers in response to increased red meat intake, and both have found that red meat does not elevate these markers. The first study concludes that increasing red meat consumption by replacing carbohydrates in the diet of non-anemic individuals actually reduces markers of inflammation. (1) The other study showed that in anemic women, inflammation markers on a diet high in red meat were not significantly different from those on a diet high in oily fish. (2) This evidence suggests that red meat is not more inflammatory than other meats for most people, and is potentially less inflammatory than dietary carbohydrates.

However, I’d like to discuss a couple of other specific mechanisms that are often blamed for inflammation.

Neu5Gc

Despite the lack of controlled trials demonstrating that red meat is inflammatory, there has been recent concern over a compound in red meat called Neu5Gc. (3) Neu5Gc is a monosaccharide that acts as a type of signaling molecule in mammalian cells, and one of its functions is to help the immune system distinguish between ‘self’ cells and ‘foreign’ cells. (4) Humans lost the ability to produce Neu5Gc millions of years ago through a genetic mutation, although we still produce the closely related compound Neu5Ac. (5) Humans are unique in this respect, because most other mammals still produce Neu5Gc, which is why that compound is found in mammalian meat.

When humans consume red meat and milk products, we incorporate some of this compound into our own tissues, especially tissues that grow at a fast pace such as fetuses, epithelial and endothelial tissue, and tumors. (6) The concern is that most of us also have anti-Neu5Gc antibodies circulating in our blood, and some researchers have suggested that these antibodies react with the Neu5Gc in our tissues to create chronic inflammation, leading to chronic diseases such as cancer.

The problem is that researchers are nowhere near proving that hypothesis. Research is in the very earliest stages, and while some fascinating hypotheses involving this molecule are being generated, the studies needed to confirm or refute these hypotheses are nonexistent. Most of the studies done on the topic acknowledge that at this point, any role in chronic inflammation is speculative, but many who have cited their research neglect to acknowledge that limitation. Thus begins a new round of fear mongering at the expense of red meat.

In the absence of conclusive evidence one way or another, it can be helpful to remember that red meat has been part of the human diet for much of our history, and remains an important dietary element of many healthy cultures. For example, the traditional diet of the Masai was composed almost entirely of red meat, blood, and milk – all high in Neu5Gc – yet they were free from modern inflammatory diseases. (7) If Neu5Gc really caused significant inflammation, the Masai should’ve been the first to know, because they probably couldn’t have designed a diet higher in Neu5Gc if they tried.

Arachidonic Acid

Arachidonic acid (AA) is often cited as a source of inflammation, and because AA is found primarily in eggs and meat, this concern could contribute to the view that red meat is inflammatory. AA is an essential omega-6 fatty acid that is a vital component of cell membranes and plays an important role in the inflammatory response. (8) It’s especially necessary during periods of bodily growth or repair, and is thus a natural and important component of breast milk. (9) AA is sometimes portrayed as something to be avoided entirely simply because it is ‘inflammatory,’ but as usual, that view drastically oversimplifies what actually happens in the body.

It’s true that AA plays a role in inflammation, but that’s a good thing! It ensures that our body responds properly to a physical insult or pathogen, and it also helps ensure that the inflammatory response is turned off when it’s no longer needed. AA interacts with other omega-3 and omega-6 fatty acids in intricate and subtle ways, and an imbalance in any of those fats has undesirable effects. For example, low doses of EPA tend to increase tissue levels of AA, while high doses decrease levels of AA, which probably explains why the benefits of fish oil supplementation are lost at higher doses. (10) In epidemiological studies, higher plasma levels of both AA and the long-chain omega-3 PUFA were associated with the lowest levels of inflammatory markers. (11, 12) And clinical studies have found that adding up to 1,200 mg of AA per day—which is 12 times higher than the average intake of AA in the U.S.— to the diet has no discernible effect on the production of inflammatory cytokines. (13, 14) What’s more, our Paleolithic ancestors (who were largely free of chronic, inflammatory disease) consumed at least twice the amount of AA that the average American does today. (15)
Finally, it’s important to note that red meat actually has a lower concentration of AA than other meats because of its lower overall PUFA content. (16)(17) Additionally, red meat has been shown to increase tissue concentrations of both AA and the long chain omega-3s DHA and EPA, preserving the all-important balance of omega-3 and omega-6. (18)

Charred meat and cancer

The final concern I want to address involves compounds that are produced when meat is cooked, including advanced glycation end products (AGEs), heterocyclic amines (HAs), and polycyclic aromatic hydrocarbons (PAHs). Again, this applies to all meat, not just red meat, but it can still contribute to the perception that red meat is unhealthy.

HAs and PAHs have both been shown to cause cancer in animal models, and although these results can’t necessarily be extrapolated to humans, it’s probably wise to limit exposure to these two compounds. (19)(20) HAs and PAHs are formed when meat is cooked using high-heat or dry cooking methods such as frying, grilling, or smoking. But while cooked meat is the only significant source of HAs, PAHs are a ubiquitous environmental contaminant, and the bulk of dietary PAHs actually come from vegetables and grains. (21) In fact, levels of PAH in leafy vegetables are comparable to levels in smoked meat! However, the highest food levels of PAH are found in charred meats that have been cooked over an open flame.

AGEs are different from the other compounds in that they can be formed both endogenously and exogenously. (22) Like HAs and PAHs, AGEs are formed when foods – particularly meat – are cooked, although they are also naturally present even in uncooked meat. However, dietary AGEs do not tell the whole story, because they can also form through various metabolic pathways in the body.

One study showed that while omnivores generally have higher dietary intakes of AGEs than vegetarians, vegetarians actually end up with higher concentrations of AGEs in their plasma. (23) The authors hypothesized that their results were due to the increased fructose intake of vegetarians, although another plausible mechanism appears to be the inhibition of AGE formation by carnosine, an amino acid found in meat. (24)(25) Either way, I wouldn’t be terribly concerned about AGEs in meat, although I still recommend favoring lower-heat cooking methods to avoid HAs and PAHs.

If you do want to grill or fry your meats, you can significantly reduce the formation of all of these compounds by using an acidic marinade, which has the added bonus of tasting great! Marinating beef for one hour reduced AGE formation by over half, and marinades can cut HA formation in meat by up to 90%. (26)

Overall, there’s no good evidence that red meat is more inflammatory than other meats, and some evidence indicating that it’s less inflammatory. Just like any other food, it’s certainly possible for people to have individual intolerances to red meat that might induce inflammation, but there’s no reason for most people to restrict red meat on the basis of inflammation. Additionally, AGEs from meat are probably not a concern, and meat eaters might even be better off when it comes to plasma levels of AGEs. Any concerns about other compounds produced by cooking meat can be minimized simply by favoring wet or low-heat cooking methods, or using a marinade when high-heat methods are desired.

I hope I’ve addressed all the remaining health concerns with eating red meat, but I’d like to hear your thoughts in the comments below.
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