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Wednesday, April 12, 2017

How much longer will you live if you take a statin?


"Looking at the Heart Protection Study (HPS) done in the UK, we used a technique for analysing survival time called RMST (restricted mean survival time). I won’t go into the details. The HPS study lasted for five years, and we calculated that the average increase in survival time was 15.6 days. This was at the end of five years of treatment (with a confidence interval of 5 days either side). For 4S, the figure was 17 days."

"Framing this slightly differently, what this meant was that taking a statin for one year, in the highest risk group possible, would increase your life expectancy by around three days."

"However, more recently the BMJ did decided to publish another paper entitled: ‘The effect of statins on average survival in randomised trials, an analysis of end point postponement.

Results: 6 studies for primary prevention and 5 for secondary prevention with a follow-up between 2.0 and 6.1 years were identified. Death was postponed between −5 and 19 days in primary prevention trials and between −10 and 27 days in secondary prevention trials. The median postponement of death for primary and secondary prevention trials were 3.2 and 4.1 days, respectively."

Conclusions: Statin treatment results in a surprisingly small average gain in overall survival within the trials’ running time. For patients whose life expectancy is limited or who have adverse effects of treatment, withholding statin therapy should be considered
Overall their findings were far less impressive, even, than ours. They calculated, approximately, a single day of increase in life expectancy for each year of taking a statin. Slightly more in secondary prevention, slightly less in primary (people who have not previously had a heart attack or a stroke).
The main take away message I believe, is the following. Statins do not prevent fatal heart attacks and strokes. They can only delay them. They delay them by about one or two days per year of treatment. For those who have read my books you will know that I have regularly suggested we get rid of the concept of ‘preventative medicine’. We need to replace it with the concept of ‘delayative medicine’.


Read Dr. Kendrick's complete article here.
The effect of statins on average survival in randomised trials, an analysis of end point postponement
  1. Malene Lopez Kristensen
  2. Palle Mark Christensen
  3. Jesper Hallas
  4. Objective To estimate the average postponement of death in statin trials.
  5. Primary outcome measures The average postponement of death as represented by the area between the survival curves.
    Results 6 studies for primary prevention and 5 for secondary prevention with a follow-up between 2.0 and 6.1 years were identified. Death was postponed between −5 and 19 days in primary prevention trials and between −10 and 27 days in secondary prevention trials. The median postponement of death for primary and secondary prevention trials were 3.2 and 4.1 days, respectively.
  6. Conclusions Statin treatment results in a surprisingly small average gain in overall survival within the trials’ running time. For patients whose life expectancy is limited or who have adverse effects of treatment, withholding statin therapy should be considered.

Strengths and limitations of this study

  • This is the first study ever to systematically evaluate statin trials using average postponement of death as the primary outcome.
  • We have only estimated the survival gain achieved within the trials’ running time, whereas in real life, treatment is often continued much longer.
  • We have only focused on all-cause mortality. Other outcomes may also be relevant, for example, non-fatal cardiovascular end points.
Read the complete article here.

Wednesday, March 29, 2017

Cholesterol Paradox: A Correlate Does Not a Surrogate Make


Abstract

The global campaign to lower cholesterol by diet and drugs has failed to thwart the developing pandemic of coronary heart disease around the world. Some experts believe this failure is due to the explosive rise in obesity and diabetes, but it is equally plausible that the cholesterol hypothesis, which posits that lowering cholesterol prevents cardiovascular disease, is incorrect. The recently presented ACCELERATE trial dumbfounded many experts by failing to demonstrate any cardiovascular benefit of evacetrapib despite dramatically lowering low-density lipoprotein cholesterol and raising high-density lipoprotein cholesterol in high-risk patients with coronary disease. This clinical trial adds to a growing volume of knowledge that challenges the validity of the cholesterol hypothesis and the utility of cholesterol as a surrogate end point. Inadvertently, the cholesterol hypothesis may have even contributed to this pandemic. This perspective critically reviews this evidence and our reluctance to acknowledge contradictory information.


Read the complete article here.

Friday, February 3, 2017

The Functional Medicine Approach to High Cholesterol

"The message that “cholesterol is bad and if you have high cholesterol you should take a statin to lower it” is out of date and not in sync with the most recent scientific evidence. Unfortunately, the latest findings have not trickled down to the average primary care doctor—or even the average cardiologist. Today I discuss the six underlying causes of high cholesterol and how addressing those issues can often alleviate the need to take statins."

The Functional Medicine Approach to High Cholesterol

Tuesday, January 10, 2017

Study says there's no link between cholesterol and heart disease

Mon, 13 Jun 2016 12:33:00 EST
"Controversial report claims there's no link between 'bad cholesterol' and heart disease," the Daily Mail reports, while The Times states: "Bad cholesterol 'helps you live longer',".
The headlines are based on a new review which aimed to gather evidence from previous observational studies on whether LDL cholesterol (so-called "bad cholesterol") was linked with mortality in older adults aged over 60. The conventional view is that having high LDL cholesterol levels increases your risk of dying of cardiovascular diseases, such as heart disease.
Researchers chose 30 studies in total to analyse. 28 studies looked at the link with death from any cause. Twelve found no link between LDL and mortality, but 16 actually found that lower LDL was linked with higher mortality risk – the opposite to what was expected.
Only nine studies looked at cardiovascular mortality link specifically – seven found no link and two found the opposite link to what was expected.
However, there are many important limitations to this review. This includes the possibility that the search methods may have missed relevant studies, not looking at levels of other blood fats (e.g. total and HDL cholesterol), and the possibility that other health and lifestyle factors are influencing the link.
Most importantly, as the researchers acknowledge, these findings do not take account of statin use, which lowers cholesterol. People found to have high LDL cholesterol at the study's start may have subsequently been started on statins, which could have prevented deaths. 

Where did the story come from?

The study was carried out by researchers from the University of South Florida, the Japan Institute of Pharmacovigilance and various other international institutions in Japan, Sweden, UK, Ireland, US and Italy.
Funding was provided by the Western Vascular Institute. The study was published in the peer-reviewed BMJ Open and, as the journal name suggests, the article is open-access, so can be read for free.
Four of the study authors have previously written book(s) criticising "the cholesterol hypothesis". It should also be noted that nine of the authors are members of THINCS – The International Network of Cholesterol Skeptics. This is described as a group of scientists who "oppose…that animal fat and high cholesterol play a role [in heart disease]".
If you were playing Devil's Advocate, you could argue that this represents a preconceived view of the authors regarding the role of cholesterol, rather than the open, unbiased mind you would hope for in the spirit of scientific enquiry. That said, many important scientific breakthroughs happened due to the efforts of individuals who challenged a prevailing orthodoxy of thinking.
In general, the UK media provided fairly balanced reporting, presenting both sides of the argument – supporting the findings, but with critical views from other experts.



Read the complete article here.

Thursday, March 10, 2016

Thursday, 10 March 2016

Congenital abnormalities in baby born to mother using lovastatin

This study was published in the Lancet 1992 Jun 6;339(8806):1416-7

Study title and authors:
Congenital abnormalities (VATER) in baby born to mother using lovastatin.
Ghidini A, Sicherer S, Willner J.

This paper can be accessed at: http://www.ncbi.nlm.nih.gov/pubmed/1350826

This paper reports the case of an infant born with many malformations after the mother used a statin during pregnancy.

(i) A woman was treated for five weeks with lovastatin, starting approximately six weeks from her last menstrual period.
(ii) The statin was discontinued when her pregnancy was diagnosed at 11 weeks' gestation.
(iii) A female infant was delivered by cesarean section at 39 weeks' gestation. The infant had a constellation of malformations termed the VATER association (vertebral anomalies, anus not developed properly, an abnormal connection between the oesophagus and the trachea with part of the oesophagus missing, and kidney, forearm and wrist abnormalities).
(iv) Her anomalies included a deformed chest, spinal deformity, absent left thumb, foreshortened left forearm, shortened left elbow, fusion of the ribs on the left, anomalies in the spine, deformed left forearm, and a narrow lower oesophagus.

Friday, March 4, 2016

Sugar Consumption Plays Greater Role in Heart Disease than Saturated Fat

Science News
from research organizations

Sugar consumption plays greater role in heart disease than saturated fat

Date:
January 13, 2016
Source:
Elsevier
Summary:
Atherosclerotic Coronary Heart Disease (CHD) is responsible for one in every six deaths in the United States as well as being the leading cause of death throughout the developed world. Healthcare professionals have for many years sought to limit and control CHD by focusing on prevention and, from a dietary perspective, on limiting saturated fats.
 

Atherosclerotic Coronary Heart Disease (CHD) is responsible for one in every six deaths in the United States as well as being the leading cause of death throughout the developed world. Healthcare professionals have for many years sought to limit and control CHD by focusing on prevention and, from a dietary perspective, on limiting saturated fats.
 
In an article published in the journal Progress in Cardiovascular Diseases, Saint Luke's Mid America Heart Institute cardiovascular research scientist and James J.. DiNicolantonio, PharmD, and James H. O'Keefe, MD, examined the question of whether that focus may be misplaced and ask does sugar have a greater impact on coronary heart disease than saturated fat?

The theory of dietary saturated fats as the principal promoter of elevated serum cholesterol and heart disease stems from research beginning in the 1950's by an American scientist Ancel Keys. It was this theory which was embraced by the American Heart Association and the US federal government in the 1960s and 70s. However, at the same time of Keys research, a British physiologist John Yudkin argued that sugar intake was more closely related to incidence of and mortality from CHD.

Both Yudkin and Keys were able to support their theories through observational studies in large part because people eat foods, not isolated food constituents. Dietary sources of saturated fat are also often dietary sources of sugar and people who eat lots of sugar often also eat lots of saturated fat.
Along with co-author, Sean C. Lucan, MD, MPH, MS, from the Albert Einstein College of Medicine, DiNicolantonio and O'Keefe evaluated the evidence to date linking saturated fats and sugars to CHD, considering basic science, epidemiology, and clinical trial data related to CHD risk, CHD events, and CHD mortality. The authors concluded that sugar consumption, particularly in the form of refined added sugars, are a greater contributor to CHD than saturated fats.

"While the original studies upon which the longstanding guidelines were based were largely observational," said DiNicolantonio, "We now have more than a half century of data as well as increased understanding of how nutrition impacts the body and specifically coronary heart disease."
The metabolic aspects of saturated fatty acids (SFAs) are complex but existing research suggests that certain SFAs may actually confer measurable benefits for lipid profiles and CHD risk. For instance, some SFAs increase high-density lipoprotein cholesterol (HDL), which is often referred to as the "good cholesterol" as this lipoprotein is associated with a reduced risk of CHD
Replacing saturated fats, or any other component, from one's diet almost inevitably means replacing it with something else. When carbohydrates, particularly refined carbohydrates like sugar, replace saturated fats, which can have a negative impact on lipid profiles (HDL tends to fall and triglycerides tend to rise).

As stated earlier, people don't eat isolated fatty acids -- they eat foods that are a mix of various fatty acids and other food constituents. While high intakes from processed meats may increase risk of CHD, higher intakes from dairy sources of saturated fat may not only pose no risk but actually decrease risk.

Consuming a diet high in sugar for just a few weeks has been shown to cause numerous abnormalities found in patients with CHD, such as high total cholesterol, triglycerides, LDL, oxidized LDL, uric acid, insulin resistance and abnormal glucose tolerance, low HDL, and altered platelet function. The overall effect of consuming a diet high in sugar on these numerous health markers is likely more detrimental to overall health compared to increased consumption of saturated fat, which can increase LDL but at the same time raise HDL.

Added fructose -- generally in the form of sucrose (table sugar) or high fructose corn syrup (HFCS) in processed foods and beverages seems especially potent for producing harm. Consuming these sugars can lead to resistance in leptin, which is a key hormone in the maintenance of normal body weight. The overconsumption of added fructose undoubtedly increases the risk for obesity, which is also a risk factor for CHD.

Excess fructose also markedly increases the risk for non-alcoholic fatty liver disease (NAFLD) -- the most common liver disease in the US and a strong independent risk factor for CHD. The association between NAFLD and CHD is stronger than the link between CHD and smoking, hypertension, diabetes, male gender, high cholesterol or metabolic syndrome.

Sugars occurring naturally in fruits and vegetables pose no increased risk for CHD. The problem is refined sugars -- with ultraprocessed foods being of greatest concern. Products with added sugars represent 75% of all packaged foods and beverages in the US and most commonly contain sucrose or HFCS, which seem to raise CHD risk even more than other sugars such as glucose.

A diet high in sugar has also been found to promote prediabetes and diabetes. And patients with both of these conditions have a much greater risk for CHD compared to normal healthy patients, particularly a severe narrowing of the left main coronary artery.

Ultra-processed foods also tend to be sources of saturated fats but the harms associated with eating these products may have nothing to do with the fat and everything to do with processed foods themselves. Therefore, best advice is to avoid processed foods rather than to simply avoid SFAs as avoiding SFAs might direct people away from foods that are not only completely benign but actually beneficial (such as dairy foods) but also steer people towards foods that may be harmful -- i.e. low-fat, ultra-processed, with huge amounts of hidden added sugars.

"After a thorough analysis of the evidence it seems appropriate to recommend dietary guidelines shift focus away from recommendations to reduce saturated fat and towards recommendations to avoid added sugars," said Dr DiNicolantonio. "Most importantly recommendations should support the eating of whole foods whenever possible and the avoidance of ultra-processed food."
 

Journal Reference:
  1. James J. DiNicolantonio, Sean C. Lucan, James H. O’Keefe. The Evidence for Saturated Fat and for Sugar Related to Coronary Heart Disease. Progress in Cardiovascular Diseases, 2015; DOI: 10.1016/j.pcad.2015.11.006
Read the complete article here.

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:

Sugar,
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

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
 
 




  



 
http://paleozonenutrition.com/2015/10/09/why-i-wont-take-statins-for-my-high-cholesterol/