Friday, February 12, 2016

The Damage Triad: Sugar, Low-Fat and Statins - glynthincs

"Many statin victims find themselves caught up in a triad of life-style damage:

Low-Fat  and
Statin Damage

The three effects combine to cause a devastating set of circumstances which left unrecognised will lead to kidney failure, dementia and neuro-muscular damage - Life threatening, painful and debilitating conditions.  General practitioners are briefed by the statin manufacturers to see these effects as part of the original reason for prescribing statins.  They are encouraged to prescribe for the side-effects rather than think about their cause. Eventually it is too late to fix the damage. Then what? Pre-mortem or post-mortem?

The cruel irony is that statin related deaths from dementia, kidney disease and organ failure are rarely attributed. They cannot be used in off-set against the relatively insignificant statistical claim that statins may prevent heart attacks!

I have published reviews in medical journals, and made a conference presentation with references supporting this summary. You can read more in “The High-Cholesterol Paradox” which has references to key journal papers.

Download it free on this link: http://bit.ly/1fkGYgb  Following the link will result in the .pdf being downloaded to your download folder to save or view.

Read the complete article here.

Saturday, October 10, 2015

The High-Cholesterol Paradox - Wainwright


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 
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



Monday, September 28, 2015

Why women should not take statin drugs!

Several articles written by very credible doctors and researchers conclude that the risk far out weighs the benefit.

Read more here - Statins and women.

Do Statins Speed up Aging… Or Slow It? - Eenfeldt

Do Statins Speed up Aging… Or Slow It?

"What the researchers showed was that statin drugs make stem cells – that rejuvenate the body – divide more slowly in a test tube. This could be expected, as statins slow access to the cholesterol building blocks needed for cell division.

However, slowing the division of stem cells is not necessarily speeding up the aging process (even if it might feel that way). As stem cells have a limited number of divisions it could actually preserve stem cells. It could be argued to likely slow the aging process."

Read the complete article here.

Tuesday, February 10, 2015

Coronary Calcium Imaging Improves on Framingham Score Regardless of Symptoms in Analysis - Medscape

Coronary Calcium Imaging Improves on Framingham Score Regardless of Symptoms in Analysis

HOUSTON, TX — In asymptomatic and symptomatic patients at low risk for coronary artery disease, the use of coronary artery calcium (CAC) imaging improves long-term prediction of risk beyond that established by the Framingham Risk Score (FRS) and exercise-treadmill and stress-perfusion testing, according to the results of a new study[1]. The same findings were observed even among individuals who met the appropriate-use criteria for functional testing, report investigators.
"What we were able to show was that across all Framingham Risk Scores, calcium scoring significantly added in terms of predicting outcome and reclassifying risk in these individuals," senior investigator Dr John Mahmarian (Houston Methodist DeBakey Heart and Vascular Center, TX) told heartwire . "There have been several studies looking at low Framingham Risk Score patients, and this study bolsters the argument that calcium scoring adds tremendously in that [low-risk] group."
Furthermore, the researchers also looked at several treadmill variables—peak-exercise capacity, exercise-tolerance test (ETT) ischemia, and the Duke treadmill score—and found the addition of the calcium score to any of the variables significantly improved the reclassification of risk beyond that achieved with the clinical-data and functional-test results.
The results of the study, which was led by Dr Su Min Chang (Houston Methodist DeBakey Heart and Vascular Center), are published February 9, 2015 in JACC: Cardiovascular Imaging.

Read the complete article here.