Tag Archives: 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

Cholesterol – look after it!

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All
cholesterol molecules throughout the known universe are identical
in every respect. There
is no such thing as ‘good’
or ‘bad’ cholesterol. This
erroneous idea was ruthlessly exploited to market statins. The ‘good’
and ‘bad’ labels actually describe two classes of blood fats (lipids)
also known as HDL and LDL both of which are vital to our lipid
circulation of fatty nutrients.

We
now know that LDL supplies essential fatty nutrients to all organs of
the body. The HDL is in effect the smaller ’empties’ returning the
waste fats to the liver for disposal or recycling.

Excess
dietary sugars can damage the Lipid LDL marker making it unusable.
That damage can be measured (HbA1c is a useful surrogate test for
sugar-damage). When LDL is damaged it builds up in the blood and less
HDL is returned from the organs of the body. The organs are starved
of vital fatty nutrition.

Statins
reduce the symptom of LDL build up but do nothing to fix the problem
of organs not getting fat soluble nutrition. Ultimately statins will
just add to the harm caused by sugar-damage.

Low-Cholesterol and Violent Behaviours

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image

References
58.Lester D. Serum cholesterol levels and suicide: a meta-
analysis. Suicide Life Threat Behav 2002; 32: 333-46.
59. Edgar PF, Hooper AJ, Poa NR, Burnett JR. Violent behavior
associated with hypocholesterolemia due to a novel APOB
gene mutation. Mol Psychiatry 2007; 12: 258-63.
60. Lalovic A, Levy E, Luheshi G, et al. Cholesterol content in
brains of suicide completers. Int J Neuropsychopharmacol
2007; 10: 159-66.
61. Muldoon MF, Manuck SB, Mendelsohn AB, Kaplan JR, Belle
SH. Cholesterol reduction and non-illness mortality: meta-
analysis of randomised clinical trials. BMJ 2001; 322: 11-5.
62. Baigent C, Keech A, Kearney PM, et al.; Cholesterol
Treatment Trialists’ (CTT) Collaborators. Efficacy and safety
of cholesterol-lowering treatment: prospective meta-
analysis of data from 90,056 participants in 14
randomised trials of statins. Lancet 2005; 366: 1267-78.
63. Golomb BA, Kane T, Dimsdale JE. Severe irritability
associated with statin cholesterol-lowering drugs. QJM

2004; 97: 229-35

Cholesterol & Insulin

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diabetes [9]. The underlying mechanisms of the
potential adverse effects of statins on carbohydrate
homeostasis are complex [10] and might be related
to the lipophilicity of the statin [11]. Indeed,
retrospective analysis of the West of Scotland
Coronary Prevention Study (WOSCOPS) revealed
that 5 years of treatment with pravastatin reduced
diabetes incidence by 30% [12]. The authors
suggested that although lowering of trigliceride
levels could have influenced diabetes incidence,
other mechanisms such as anti-inflammatory action
might have been involved; however, in the
multivariate Cox model, baseline total cholesterol
did not predict the development of diabetes [12].
Furthermore, pravastatin did not decrease diabetes
incidence in the LIPID trial which included glucose-
intolerant patients [13]. On the other hand, in the
JUPITER trial (Justification for the Use of Statins in
Prevention: an Intervention Trial Evaluating
Rosuvastatin), which studied apparently healthy
persons without hyperlipidemia but with elevated
high-sensitivity C-reactive protein levels [14], the
risk of diabetes was increased by a factor of 1.25
[95% confidence interval (CI), 1.05 to 1.51] among
individuals receiving rosuvastatin 20 mg daily with
respect to placebo. Strikingly, among persons
assigned to rosuvastatin, the median low density
lipoprotein (LDL) cholesterol level at 12 months was

55 mg per deciliter [interquartile range, 44 to 72
(1.1 to 1.9)].
It is intriguing that salutary lifestyle measures,
which might exert their beneficial action through
an anti-inflammatory mechanism without a strong
cholesterol-lowering effect, beyond reducing
cardiovascular events and total mortality, reduce
also the risk of diabetes and other chronic
degenerative diseases. This fact may represent
a ‘justification’ not to use a drug in low-risk primary
prevention populations: lowering cholesterol at the
expense of increasing diabetes might be counter-

productive over the long-term.

References
9. Sukhija R, Prayaga S, Marashdeh M, et al. Effect of statins
on fasting plasma glucose in diabetic and nondiabetic
patients. J Investig Med 2009; 57: 495-9.
10. Szendroedi J, Anderwald C, Krssak M, et al. Effects of high-
dose simvastatin therapy on glucose metabolism and
ectopic lipid deposition in nonobese type 2 diabetic
patients. Diabetes Care 2009; 32: 209-14.
11. Ishikawa M, Okajima F, Inoue N, et al. Distinct effects of
pravastatin, atorvastatin, and simvastatin on insulin
secretion from a beta-cell line, MIN6 cells. J Atheroscler
Thromb 2006; 13: 329-35.
12. Freeman DJ, Norrie J, Sattar N, et al. Pravastatin and the
development of diabetes mellitus: evidence for
a protective treatment effect in the West of Scotland
Coronary Prevention Study. Circulation 2001; 103: 357-62.
13. K
eech A, Colquhoun D, Best J, et al.; LIPID Study Group.
Secondary prevention of cardiovascular events with long-
term pravastatin in patients with diabetes or impaired
fasting glucose: results from the LIPID trial. Diabetes Care
2003; 26: 2713-21.
14. Ridker PM, Danielson E, Fonseca FA, et al.; JUPITER Study
Group. Rosuvastatin to prevent vascular events in men
and women with elevated C-reactive protein. N Engl J Med
2008; 359: 2195-207.

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.

image

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

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Thank you Dr Verner Wheelock for the extensive critique of the reports . The Cochrane reports analysis was heroic and well structured. We had a huge debate about them at the time on THINCS (www.thincs.org).

For my part I shy away from statistical analysis which doesn’t include ‘All Cause Mortality’ figures. The reason being that failure to look at all the non-cardio deaths and drop-outs from trials cleans and amplifies the apparent benefits of Statins. This means we can never know the Numbers Needed to Harm NNH side of the medication.

My first ever review paper (G Wainwright et al., 2009) looking at the clinical impact of cholesterol lowering in all non-cardiovascular organs, was seminal in that it pointed up a fundamental flaw in the whole statin concept i.e. Cholesterol is vital and inhibiting its production is destined to create a wide and varied set of Adverse Events in statin users in the longer term.  That is why ‘all cause mortality’ data is not made available (caveat emptor).

In our second review paper(Seneff et al., 2011)  we became aware of the fact that LDL/HDL ratios were associated with LDL consumption by organs and not production by the liver. The whole LDL argument had been inverted.  If LDL is damaged by glycation,  LDL goes up and HDL falls.  The liver’s glycated-LDL is unused and the corresponding HDL return to the liver does not happen.

LDL HDL Cycles

How such a fundamental part of the lipid nutrition cycle could be missed is hard to understand. Obsession with statins and statin finance has done immense harm to cardio-medicine and I believe we are seeing the start of a major NICE scandal as the BMA object to the guidance.

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

Seneff, S., Wainwright, G., and Mascitelli, L. (2011). Is the metabolic syndrome caused by a high fructose, and relatively low fat, low cholesterol diet? Arch Med Sci 7, 8–20.

109. Cochrane Collaboration Evaluates Statins for Primary Prevention of Heart Disease | Verner’s Views

Link

Current guidelines encourage ambitious long term cholesterol lowering with statins, in order to decrease cardiovascular disease events. However, by regulating the biosynthesis of cholesterol we potentially change the form and function of every cell membrane from the head to the toe. As research…

Nowhere is the impact of cholesterol depletion more keenly studied than in the neurologic arena.   

The work of Pfrieger et al. described the functional role of cholesterol in memory through synaptogenesis [24]. Mauch et al. [25] reported evidence that cholesterol is vital to the formation and correct operation of neurons to such an extent that neurons require additional sources of cholesterol to be secreted by glial cells. A recent mini-review by Jang et al. describes the synaptic vesicle secretion in neurons and its dependence upon cholesterol-rich membrane areas of the synaptic membrane [26]. Furthermore, working on rat brain synaptosomes, Waseem [23] demonstrated that a mere 9.3% decrease in the cholesterol level of the synaptosomal plasma membrane could inhibit exocytosis. These data might be particularly worrisome for lovastatin and simvastatin which are known to cross the blood brain barrier [27].

In fact, the proposed use of statins as a therapeutic agent in Alzheimer’s Disease (AD) [28] counters Pfrieger’s evidence [24]. Indeed, a reduction in cholesterol synthesis leads to depletion of cholesterol in the lipid rafts – i.e. the de-novo cholesterol is required in the neurons for synaptic function and also in the neuronal membrane fusion pores [29].

Cognitive problems are the second most frequent type of adverse events, after muscle complaints, to be reported with statin therapy [30] and this has speculatively been attributed to mitochondrial effects. The central nervous sytem (CNS) cholesterol is synthesised in situ and CNS neurons only produce enough cholesterol to survive. The substantial amounts needed for synaptogenesis have to be supplemented by the glia cells. Having previously shown that in rat retinal ganglion cells without glia cells fewer and less efficient synapses could form, Göritz et al. [31] indicate that limiting cholesterol availability from glia directly affects the ability of CNS neurons to create synapses. They note that synthesis, uptake and transport of cholesterol directly impacts the development and plasticity of the synaptic circuitry. We note their very strong implication that local de-novo cholesterol synthesis in situ is essential in the creation and maintenance of memory..  

There should be further consideration of cholesterol depletion on synaptogenesis, behaviours and memory loss for patients undergoing long-term statin therapy. This is particularly important with lipophilic statins which easily cross the blood brain barrier [32].

The effects of statins on cognitive function and the therapeutic potential of statins in Alzheimer´s disease are not clearly understood [28]. Two randomised trials of statins versus placebo in relatively younger healthier samples (lovastatin in one, simvastatin in other) showed significant worsening of cognitive indices relative to placebo [33, 34]. On the other hand, two trials in Alzheimer samples (with atorvastatin and simvastatin respectively) suggested possible trends to cognitive benefit, although these appeared to dissipate at 1 year [35, 36]. A recent Cochrane review concluded that there is good evidence from randomised trials that statins given in late life to individuals at risk of vascular disease have no effect in preventing Alzheimer´s disease or dementia [37]. However, case reports and case series from clinical practice in the real world reported cognitive loss on statins that resolved with discontinuation and recurred with rechallenge [30].

Evidence from observational data and prestatin hypolipidemic randomised trials showed higher hemorrhagic stroke risk with low cholesterol [30]. In fact, in the Stroke Prevention with Aggressive Reductions in Cholesterol Levels (SPARCL) trial as compared with placebo, the use of high-dose atorvastatin was associated with a 66% increase in the relative risk of hemorrhagic stroke among the patients receiving the statin drug [38]. In addition to treatment with atorvastatin, an exploratory analysis of the SPARCL trial found that having hemorrhagic stroke as an entry event, male sex, and advancing age at baseline accounted for the great majority of the increased risk of hemorrhagic strokes [39]. However, a sensitivity analysis excluding all patients with a hemorrhagic stroke as an entry event in the SPARCL trial found that statin treatment was still associated with an increased risk of hemorrhagic stroke [40]. Furthermore, in a subgroup of patients with a history of cerebrovascular disease enrolled in the Heart Protection Study [41] which did not include patients with hemorrhagic stroke, a similar increased risk of hemorrhagic stroke during follow-up was demonstrated [40].

References:

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[24] Pfrieger FW. Role of cholesterol in synapse formation and function Biochim Biophys Acta 2003; 1610: 271-80.

[25] Mauch DH, Nägler K, Schumacher S, et al. CNS synaptogenesis promoted by glia-derived cholesterol Science 2001; 294: 1354-7.

[26] Jang D, Park S, Kaang B. The role of lipid binding for the targeting of synaptic proteins into synaptic vesicles BMB Rep 2009; 42: 1-5.

[27] Saheki A, Terasaki T, Tamai I, Tsuji A. In vivo and in vitro blood-brain barrier transport of 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitors Pharm Res 1994; 11: 305-11.

[28] Kandiah N, Feldman HH. Therapeutic potential of statins in Alzheimer’s disease. J Neurol Sci. 2009 Mar 23. [Epub ahead of print].

[29] Jeremic A, Jin Cho W, Jena BP. Cholesterol is critical to the integrity of neuronal porosome/fusion pore Ultramicroscopy 2006; 106: 674-7.

[30] Golomb BA, Evans MA. Statin adverse effects: a review of the literature and evidence for a mitochondrial mechanism Am J Cardiovasc Drugs 2008; 8: 373-418.

[31] Göritz C, Mauch DH, Nägler K, Pfrieger FW. Role of glia-derived cholesterol in synaptogenesis: new revelations in the synapse-glia affair J Physiol Paris 2002; 96: 257-63.

[32] Vuletic S, Riekse RG, Marcovina SM, Peskind ER, Hazzard WR, Albers JJ. Statins of different brain penetrability differentially affect CSF PLTP activity. Dement Geriatr Cogn Disord 2006; 22: 392-8.

[33] Muldoon MF, Barger SD, Ryan CM. et al. Effects of lovastatin on cognitive function and psychological well-being. Am J Med 2000; 108: 538-46.

[34] Muldoon MF, Ryan CM, Sereika SM, Flory JD, Manuck SB. Randomized trial of the effects of simvastatin on cognitive functioning in hypercholesterolemic adults. Am J Med 2004; 117: 823-9.

[35] Sparks DL, Sabbagh M, Connor D, et al. Statin therapy in Alzheimer’s disease. Acta Neurol Scand Suppl 2006; 185: 78-86.

[36] Simons M, Schwärzler F, Lütjohann D, et al. Treatment with simvastatin in normocholesterolemic patients with Alzheimer’s disease: A 26-week randomized, placebo-controlled, double-blind trial. Ann Neurol 2002; 52: 346-50.

[37] McGuinness B, Craig D, Bullock R, Passmore P. Statins for the prevention of dementia. Cochrane Database Syst Rev 2009 Apr 15; (2): CD003160.

[38] Amarenco P, Bogousslavsky J, Callahan A 3rd, et al.; Stroke Prevention by Aggressive Reduction in Cholesterol Levels (SPARCL) Investigators. High-dose atorvastatin after stroke or transient ischemic attack. N Engl J Med 2006; 355: 549-59.

[39] Goldstein LB, Amarenco P, Szarek M, et al.; SPARCL Investigators. Hemorrhagic stroke in the Stroke Prevention by Aggressive Reduction in Cholesterol Levels study. Neurology 2008; 70:2364-70.

[40] Vergouwen MD, de Haan RJ, Vermeulen M, Roos YB. Statin treatment and the occurrence of hemorrhagic stroke in patients with a history of cerebrovascular disease. Stroke 2008;39:497-502.

[41] Collins R, Armitage J, Parish S, Sleight P, Peto R; Heart Protection Study Collaborative Group. Effects of cholesterol-lowering with simvastatin on stroke and other major vascular events in 20 536 people with cerebrovascular disease or other high-risk conditions. Lancet 2004; 363: 757–67.

Synaptogenesis and Neural Cholesterol

Link

The impact of statin drugs goes far beyond those declared by the advisory leaflet in the packet. It is really time that the professions got to grips with the fundamental biochemistry of mevalonate inhibitions. More about the book ‘The Dark Side of Statins’ later in the year!

I hope this video will encourage people to consider the wider implications of the biochemical action of statins as they target the important pathway affecting much more than cardiovascular outcomes.

Statin drugs will continue to devastate the quality of life of its users. ‘All cause mortality data’ is not fully released. Failure to appreciate mevalonate pathway effects is allowing this devastating avalanche of adverse impacts to continue, with the blessing of professionals who should know better.

Dark Effects of statins are listed on in adverts and on the leaflet supplied with the medication. more info at: http://www.spacedoc.net .

Statins – The Dark Side – Video Link