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Sugar-Damage in the Lipid Nutrition Cycle

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Maybe raised total blood serum cholesterol (TBSC) was trying to tell us something about health, but it was not the message we have been fed for the last 60 years.

Cholesterol has been misrepresented since the 1950s as a cause of heart disease. In reality an excess of dietary sugar that created an unhealthy lipid profiles in our blood stream.  Attempts to fix the problem by a drug called a statin added to our health woes because it targets the wrong issue.

When LDL nutrition is sugar-damaged (Glycated LDL) is raised in the blood. Unrecognised by our fat starved organs it is eventually scavenged by less discriminating visceral fat stores. 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.

Preventing the liver from producing new undamaged LDL by using a statin fails to address the problem of getting fatty nutrients to fat starved organs. The action of statins adds to the patients musculo-skeletal and neurological woes by depleting vital supplies of CoQ10 and dolichol.

The problem is fixed by reducing sugar-damage – as measured by an HbA1c test on sugar damage to a blood protein called haemoglobin. Several diabetes clinicians have observed this key connection between sugar damage and poor lipid profiles.

A Healthy Lipid Nutrition Cycle

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.

Sugar-Damage in a Broken Lipid Cycle

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).

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.

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For the full essay with references read follow this ‘bitly link’: http://bit.ly/1fkGYgb

Link

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 was contested by ‘interested parties’, and the matter was resolved by ‘government decree’ in a US Senate report. On Friday January 14th 1977, Senator George McGovern’s Senate Select Committee on Nutrition and Human Needs published ‘Dietary Goals for the United States’.

This document sided heavily with Dr Keys’ lipid theory. Thus ‘hypothesis became dogma’, without the benefit of scientific proof. The McGovern report recommended that we consume more carbohydrates (sugar generating foods) with more limited amounts of fats, meat and dairy. Since the 1970s there has been a rise in the use of High-Fructose Corn Syrups in processed food, and the introduction of low-fat foods which tend to have added sugar to make them attractive to eat. 

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 blood-sugar 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

Drug treatments which lower cholesterol are acknowledged to cause adverse side-effects (ADRs) in at least 10% of Statin users11. This figure may be as high as 30%.

Conservative estimates indicate that in at least 1% of patients the side-effects are serious enough to be life threatening (e.g. Rhabdomyelitis, Dementia, Behavioural Disorders and Violence).

Our review12 found that cholesterol lowering therapies were implicated in:

·         Damage to muscles (including the heart) and exercise intolerance13

·         Increased risk of Dementias (Impaired Synaptogenesis and Neuro-transmission)14

·         Failure of Myelin Maintenance (Multiple Sclerosis  Risks)15

·         Neuro-muscular problems, aches and pains (Amyotrophic Lateral Sclerosis)16

·         Diabetes  (Insulin release inhibited)8

·         Poor Maintenance of Bones and Joints

·         Suppression of protective skin secretions (Apo-B)  and  increased MRSA infection17

Why would anyone want to lower cholesterol?

What is needed is a lowering of damage to lipids  – caused by sugar.

References

1.            Weiss, A., Beloosesky, Y., Schmilovitz-Weiss, H., Grossman, E. & Boaz, M. Serum total cholesterol: A mortality predictor in elderly hospitalized patients. Clin. Nutr. Edinb. Scotl. 32, 533–537 (2013).

2.            Mancini, M. & Stamler, J. Diet for preventing cardiovascular diseases: light from Ancel Keys, distinguished centenarian scientist. Nutr Metab Cardiovasc Dis 14, 52–7 (2004).

3.            Yudkin, J. Pure, white and deadly: how sugar is killing us and what we can do to stop it. (2012).

4.            Seneff, S., Wainwright, G. & Mascitelli, L. Is the metabolic syndrome caused by a high fructose, and relatively low fat, low  cholesterol diet? Arch. Med. Sci. AMS 7, (2011).

5.            Bierhaus, A., Hofmann, M. A., Ziegler, R. & Nawroth, P. P. AGEs and their interaction with AGE-receptors in vascular disease and diabetes mellitus. I. The AGE concept. Cardiovasc Res 37, 586–600 (1998).

6.            Lindqvist, A., Baelemans, A. & Erlanson-Albertsson, C. Effects of sucrose, glucose and fructose on peripheral and central appetite signals. Regul. Pept. 150, (2008).

7.            Seneff, S., Wainwright, G. & Mascitelli, L. Nutrition and Alzheimer’s disease: the detrimental role of a high carbohydrate diet. Eur. J. Intern. Med. 22, 134–140 (2011).

8.            Xia, F. et al. Inhibition of cholesterol biosynthesis impairs insulin secretion and voltage-gated calcium channel function in pancreatic beta-cells. Endocrinology 149, 5136–45 (2008).

9.            FDA publication. FDA Expands Advice on STATIN RISKS. (2014). at <http://www.fda.gov/downloads/ForConsumers/ConsumerUpdates/UCM293705.pdf>

10.          Pfrieger, F. W. Role of cholesterol in synapse formation and function. Biochim Biophys Acta 1610, 271–80 (2003).

11.          Roger Vadon (Producer). BBC File on 4 Statins. (2008).

12.          G Wainwright, L Mascitelli & M Goldstein. Cholesterol-lowering therapy and cell membranes. Stable plaque at the expense of unstable membranes? Arch. Med. Sci. 5, 289–295 (2009).

13.          Hall, J. B. Principles of Critical Care  – Rhabdomyolysis and Myoglobinuria. (McGraw Hill 1992, 1992).

14.          Mauch, D. H. et al. CNS synaptogenesis promoted by glia-derived cholesterol. Science 294, 1354–7 (2001).

15.          Klopfleisch, S. et al. Negative impact of statins on oligodendrocytes and myelin formation in vitro and in vivo. J Neurosci 28, 13609–14 (2008).

16.          Goldstein, M. R., Mascitelli, L. & Pezzetta, F. Dyslipidemia is a protective factor in amyotrophic lateral sclerosis. Neurology 71, 956; author reply 956–7 (2008).

17.          Goldstein, M. R., Mascitelli, L. & Pezzetta, F. Methicillin-resistant Staphylococcus aureus: a link to statin therapy? Cleve Clin J Med 75, 328–9; author reply 329 (2008).

The High- Cholesterol Paradox (full essay)

Link

The Bio-chemical Science pages of Glyn Wainwright, Publisher, Independent Reader of Research and Honorary Recording Engineer for Leeds Symphony Orchestra<

Anecdote: A  diabetic clinician told me she had noticed that when patients had good control of their hba1c (an indicator of sugar-damage in blood ) their ‘cholesterol’ score also improved.

Every molecule of cholesterol in the body is known to be identical to every other. 

The Good/Bad labeling of cholesterol is extremely unscientific and unhelpful, and that is a matter of scientific fact.

How were  intelligent, well educated, medical professionals  persuaded to popularise this ‘Good ‘ cholesterol versus  ’Bad’ cholesterol idea?

The unscientific phrase ‘Bad Cholesterol’ is a misleading description of damage to the ’lipid transport system ‘, whose basic function was described by the Nobel Prize winners James E. Rothman, Randy W. Schekman and Thomas C. Südhof.  (Awarded “for their discoveries of machinery regulating vesicle traffic, a major transport system in our cells”.

The lipid transport system is used by the body to deliver essential supplies of fat, cholesterol, and other fat-soluble nutrients.

The lipid transport system is able to repair and recycle, but can be progressively overwhelmed by the damage accumulated over several decades.

This  damage to the lipid system is caused by oxidation and glycation: the result of excessive consumption of refined sugars (in particular High Fructose syrups).

It is not ‘bad cholesterol’ but sugar-damage to the proteins that make the lipids available to the organs of our body.

Unconsumed ‘damaged’ ldl  in the blood is an indicator of trouble because the organs are being starved  of vital fats cholesterol and fat-soluble nutrients.

‘Bad Medicine’ prevents the liver and all other organs from making essential cholesterol   indirectly stop the supply of lipids to the blood.

Cholesterol lowering medications have a variety of very broad variety of adverse-effects, all attributable to organs being starved of fat, cholesterol and fat-soluble nutrients.

The ‘bad medicine’s do not tackle the cause of damage to the ldl –  lipids supply.

The primary cause of this ldl damage is the oxidation and glycation of the  ldl’s components.

The main dietary and lifestyle causes of ldl damage are over-consumption of refined sugars and inactivity.

The reactive sugars like fructose, found in manufactured corn syrups are particularly troublesome, because they directly attach to ldl-protein mechanisms causing a mal-function which starves the organs.

Important protective and anti-oxidant functions rely on Cholesterol and CoQ10 –  both of which  are reduced  anti-cholesterol medications. 

The unscientific use of the incorrect description ‘Bad Cholesterol’ has held back medicine for over 40 years and it is time to look at the evidence in more detail:-

“Cholesterol Lowering Therapies and Membrane Cholesterol”   Wainwright G Mascitelli L  &  Goldstein M R, Archives of Medical Science, Vol. 5 Issue 3 p289-295 2009

“Is the metabolic syndrome caused by a high fructose, and relatively low fat, low cholesterol diet?”   Seneff S, Wainwright G, and Mascitelli L Archives of Medical Science  Vol. 7 Issue 1 p8-20 2011 doi: 10.5114/aoms.2011.20598

 "Nutrition and Alzheimer’s disease: the detrimental role of a high carbohydrate diet"   Seneff S., Wainwright G., and Mascitelli L. European Journal of Internal Medicine 2011, doi:10.1016/j.ejim.2010.12.0172011

‘Good/Bad Cholesterol ‘ and ‘Bad Medicine’

Link

MHRA Drug Safety Update Summary
Statin use may be associated with a level of hyperglycaemia in some patients where formal diabetes care is appropriate. The risk appears to be mainly in patients already at increased risk of developing diabetes. However, the overall benefits of statins strongly outweigh any risks, including in those at risk of developing diabetes or those with pre-existing diabetes

The explanation for this is probably the fact that a 10% depletion in cell-membrane cholesterol will cause pancreatic beta cell to stop all insulin release

Xia F, Xie L, Mihic A, et al. Inhibition of cholesterol biosynthesis impairs insulin secretion and voltage-gated calcium channel function in pancreatic beta-cells. Endocrinology 2008; 149: 5136-45.

Statins: risk of hyperglycaemia and diabetes

Link

MHRA Drug Safety Update Summary

In August 2012 we published advice that simvastatin is now contraindicated with concomitant use of certain medicines, such as ciclosporin, danazol, and gemfibrozil. In addition, the recommendations for the maximum dose of simvastatin have changed when used with a number of other medicines, including amlodipine and diltiazem. These changes were driven primarily by concerns about an increased risk of myopathy and/or rhabdomyolysis at higher plasma concentrations of simvastatin, which may result from such drug interactions.

Following further consideration by the Pharmacovigilance Expert Advisory Group of the Commission on Human Medicines, this article summarises the evidence underlying the new advice that the maximum recommended dose for simvastatin in conjunction with amlodipine and diltiazem is now 20 mg/day. The prescribed doses of amlodipine and diltiazem need not be changed.

MHRA Drug Safety Update – Statin

Link

Myopathy is a known side effect of all statins, including simvastatin, and the risk increases with higher doses. However, its most serious form, rhabdomyolysis, is a very rare side effect. The risk of myopathy is greater in: elderly patients (>65 years); women; patients with renal impairment or hypothyroidism; patients who consume large quantities of alcohol; those with a history of previous muscle problems during treatment with statins or other lipid-lowering drugs; or those with family history of muscle disorders. Concomitant use of some medicines may also increase the risk of muscle damage.

Statins MHRA warning

UK GPs warned over muscle risk with Statin