Tag Archives: lipids

Cholesterol  – under attack again – by vaccine!

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With yet another misguided attempt to remove cholesterol from humans let me explain their stupidity:

The lipid nutrition cycle has large low-density lipids (LDL)
out-bound from the liver, taking fatty nutrition to all organs in the body.
Smaller high-density lipoproteins (HDL) form on the return side, taking excess
or damaged lipids back to the liver. In a healthy person there is a ratio of
about 5:1 (LDL/HDL) when the cycle is working correctly.

The unscientific characterisation this lipid nutrition cycle
ratio as ‘good cholesterol’ and ‘bad cholesterol’ has created an extremely poor
understanding, and consequently inappropriate treatment, of total serum
cholesterol.

The bitly link to my conference presentation (notes &
references) gives the detailed explanation.

In summary it is the failure of the lipid receptor mechanism that allows LDL to build up and that damage is often glycation (AGE) caused by reactive blood sugars (glucose and more recently fructose).

Professionals who talk about good cholesterol and bad cholesterol are simply displaying total ignorance of their field.

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Link

Low-carbohydrate
high-fat (LCHF) diets are at least as effective as other dietary
strategies for reducing body weight, with the additional advantage of
increased satiety and spontaneous reduction in energy intake.

LCHF
diets are an effective dietary strategy to improve glycaemic control
and reduce hyperinsulinaemia in type 2 diabetes mellitus and in
otherwise healthy patients with insulin resistance.

LCHF
diets have unique effects on blood lipid concentrations and
cardiovascular risk factors, characterised by decreased blood TG, ApoB
and saturated fat concentrations, reduced small LDL particle numbers and
increased HDL-C concentrations. The effect on LDL-C concentrations is
variable.

Evidence that supports the prescription of low-carbohydrate high-fat diets: a narrative review — Noakes and Windt 51 (2):
133 — British Journal of Sports Medicine

Low-Cholesterol – A Leading Cause of Failing Health

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Diabetes

In 2008 Dr Luca Mascitelli sent me a paper by Xia et al. [1] which showed how lowering cholesterol could stop insulin production in the human pancreatic beta-cells – a leading cause of diabetes. Here we had a biochemical explanation of the rise in diabetes associated with statin use and the science was excellent.

Adverse-Effects of Cholesterol Lowering

Could low-cholesterol affect other organs of the body?  After a review of published papers in the professional medical journals we had the answer. Yes! Lowering the cholesterol level in the bodies organs (cell membranes) by as little as 10% (molecular ratio) stopped the exchange of nutrients and other products with the blood stream. The organs’ cells shut down and the implications are devastating to health [2].

Muscles – Wastage, Aches, Mobility Issues and Kidney Failure

In muscles the cell walls, becoming deficient in cholesterol, will eventually leak causing muscle loss, mobility problems, ‘cola-coloured urine’ and ultimately kidney failure (muscle waste damaging kidney tubules – rhabdomyolysis).  These effects are warned about in the leaflets that come with statins medications. The connection between the nervous system and the muscles also begins to fail because there is not enough cholesterol, used to wrap the chemical messengers (neurotransmitters Lrp-4 and Agrin) between nerve and muscle causing aches and mobility issues. The heart is the most important muscle and so we could now understand why low cholesterol is associated with progressive heart failure.
See [2] for review details and references.

Central Nervous System

The published work of F W Pfrieger, shows how copious quantities of cholesterol  are used making memories and thought processes. The nerves (neurons) and  connections (synapses) depend on cholesterol for formation and function. The nerve fibres (axons) are protected by myelin (50% cholesterol) which needs constant supply for repair. In our review we discuss a range of problems from Dementias through behavioural change and aggression which are associated with cholesterol depletion and adverse side-effects of statin.
See [2] for review details and references.

Other problems now associated with Low-Cholesterol levels in organs are:
• Raised risk of MRSA and skin infections
• Failure of Bone maintenance (fracture risks)
• Increased Cancer risks
• Increased risk of death associated with falling cholesterol

Cholesterol is vital and the events leading up to this health crisis and contradictory advice from authorities is discussed further in my conference paper report “The High Cholesterol Paradox”

Low-Cholesterol + Elevated Blood Sugars + Statins = Very Poor Health Outcomes

1. 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.
2. 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).

Specific links to papers and blogs are highlighted in throughout

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Link

Thank you for the challenge of putting it simply. We get caught in a
triple jeopardy – Sugar, Low-Fat and Statins. Our Organs are starved of
fatty nutrients. Our cells become leaky and fail. This eventually
progresses via Muscles, Nerves, Central Nervous System to all organs and
tissues. The best way to avoid or mitigate this is to get good Sugar
Control (HbA1c), increase fat nutrition (animal/fish sourced to match
your own fats) and bin the statins. Link to the presentation .pdf – The High-Cholesterol Paradox

Triple Jeopardy – Sugar, Low-Fat & Statins

Sugar-Damage & Heart Disease

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Heart disease is
often associated with undiagnosed diabetes. The secret of managing
this is to request an HbA1c blood test that measures your
sugar-damage. The results in UK are given as a number (mmols/mol)
which counts damaged blood molecules per 1000. That number should
always be less than your age – ideally under 49 for healthy folks
and under 59 for type 2 diabetics controlling it with lifestyle and
metformin. Sugar damage accumulates slowly so as we get older we can
relax the figure a little to avoid low blood sugar from medication.

If you feel hungry
2hrs after a sugary snack (biscuits) you are spiking you blood sugar
and after 2hrs your natural insulin has mopped up the blood sugar
turning it into visceral (belly) fat. The low sugar level / raised
insulin produces a hunger. Another sugar snack cycle begins. Break it
with a low sugar high fat snack and start to lose weight around the
middle (Nuts – check label to avoid added sugar/honey)!

Make your own food
and get to know its composition. Keep a food diary and weigh all
foods you eat to work out how much carbohydrate (sugar generating
food) you eat every day. There is a lot of helpful information on the
package. The per 100g column give you the percentage carbohydrates
and sugar. Don’t count the sugar twice as it is included in the
carbohydrate figure. (of which…)

Everyone is
different so start with 100g carbs per day and find out what you can
process using quarterly HbA1c blood tests from your GP. My personal
target is 80g per day. All foods contain a small amount of
carbohydrate but just worry about the explicit carbs like rice,
pasta, flour, starchy foods (like potato) and sugars.

You’ll need to get the balance of your 2,000
daily calories from fats. You will rarely feel hungry this way as no
excess insulin is produced because you have fewer smaller blood sugar
spikes to deal with. High cocoa-fat chocolate (low sugar) is a guilt
free treat! Try a double cream ganache chocolate for desserts.

Fructose is 7 times
more reactive (dangerous) than glucose so avoid all high fructose corn syrup
(HFCS) as over time they are very damaging to our proteins.

Check the weight of
dry starchy foods (pasta etc.) typically 60% Carbs and an egg sized
portion of potato is 10g carb. You’ll soon get become expert at
assessing portions.

http://bit.ly/1lNab2C has more information

Link

Why cholesterol drugs might affect memory
Dr Duane Graveline has agreed to share his comments on the article in Scientific American with you:  
“When  I saw Melinda Moyers’  first mistake I was amused  for my morning walk
took place in Island Pond, Vermont not Merritt Island  Island, Florida where
I currently reside. It was then I spotted the title  “Why cholesterol
drugs  might affect memory’ and began to get angry. I had spent 15 years
documenting  the cognitive side effects of statin drugs and our FDA’s
Medwatch had recently  reported over 7500 statin associated transient
global amnesia and memory loss  reports received during the time period
2004-2014. A reasonably accurate title  would not read cholesterol
lowering drugs might affect memory. The proper title  would read
cholesterol lowering drugs affect memory. If Ms Moyer has done her  job
she would know these facts just as I know them so why not use them.
Then
 when my name came up again in the article I was surprised to read I
had been  “following a healthy diet to keep my cholesterol low.” Never
since  my research on the subject have I been even remotely concerned
about my  cholesterol. It is irrelevant to heart attack and stroke.
Inflammation is the  underlying cause. Many times in my writing I have
told my readers how ashamed I  was to have raised my family on no eggs,
skim milk and margarine for 17 years so  conned I had been as a much
younger doctor. Had Ms. Moyer but asked me I would  have told her this.
And then she topped it off by saying “he says he has never felt better.”
Now  I am really angry for she has never in the past decade asked me
and since  the year 2000 I have almost completely lost the ability to
walk. I barely make  it with cane and walker and am but a moment away
from wheelchair existence.  Peripheral neuropathy says my neurologist
with my muscle biopsy showing  denervation atrophy (no nerve, no
muscle). Ms Moyer conjured up this entire  thing. If she had only called
me.
Duane Graveline MD  MPH”

It’s Not Dementia, It’s Your Heart Medication: Cholesterol Drugs and Memory

Good or Bad Lipid Profiles

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The 2013 Nobel Prize for Medicine raised expectations of a parallel discussion of extra-cellular lipid circulation in The Lipid Cycle. A better understanding of the health problems caused by disruption to The Lipid Cycle has been blocked for over 40 years by incorrect use of the chemical term ‘cholesterol’ as an inaccurate surrogate when referring to Lipid profiles. This singular error has caused decades of misunderstanding and inappropriate treatments in medicine.

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The Lipid Cycle

The build up of damage to the LDL class of lipids is on the supply side of lipid circulation in the blood has erroneously been referred to as ‘Bad Cholesterol’.

Understand this means it should have better been called ‘Bad-LDL’.

Undamaged or healthy ‘Good-LDL’ on the supply side delivers fatty nutrients to organs and tissue in a controlled manner (receptor-mediated endocytosis). Bad-LDL remains in the blood until scavenged into adipose tissue.

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The HDL lipid class operate on the return side of the lipid cycle and is depleted when LDL is damaged.

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The High Cholesterol Paradox

This summary of my conference presentation explains Lipid Cycle Damage. In my essay, linked from here, there is a relatively easy to read account. It contains supporting academic references for professionals to follow.

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)

The ‘High Cholesterol’ Paradox

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For some people, being told they have ‘high cholesterol’ suggests a decline, for others it is a sign of healthy longevity. What is really going on?

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The real story is the way in which high dietary levels of refined sugars such as Fructose can adversely modify our lipid-protein-labels and break the fatty nutrition cycle supplying all our organs.

Normally high lipid levels with good ratios of LDL (larger nutrient packages) and HDL (returning ’empty’ packages for recycling) are seen in people with healthy long life prospects. 

When the LDL package address (protein marker) is sugar-damaged (glycated) LDL backs up in the blood and less HDL is recycled. The blood lipids are up but the organs can’t use it. e.g The brain is starved of vital fat-soluble nutrients. Taking medication to block cholesterol production will lower blood lipids BUT…. the brain, muscles etc. are  still starved of vital fat-soluble nutrition and the outcome worsens.

The HbA1c test for sugar-damage in the blood protein hemoglobin looks likely to be a great indicator for sugar damage in general so..

‘High Cholesterol’ with good HbA1c levels is a healthy sign.

‘High Cholesterol’ with poor HbA1c levels is a very unhealthy sign.

THE REAL STORY IS SUGAR-DAMAGE

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’