Tag Archives: cholesterol

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

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.

Conflicting Evidence – A Statin Paradox

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We know that all cells (all tissues) cease their exocytosis and endocytosis  activity, if the membrane cholesterol content drops by
around 10%.  This is easily achieved on statin therapy. Everything slows down.

In the case of bone remodelling both osteoclasts (cutters) and osteoblasts (builders) will reduce their repair activity in bone remodelling.
Calcium loss from bones will be reduced but micro-fracture repairs will not be repaired on statin therapy. Bone density is maintained on statin therapy but the developing micro-fractures weaken the skeleton.

It’s all about what is measured and how long you follow through.
Statin trials can be designed to prove both benefit and detriment to bones.
This is why experimental osteoporosis treatment by statins  to maintain bone density ultimately gives way to increased fracture risk.
Two competing bone remodelling processes are failing and conflicting measures can be used to conflict statin safety.

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You will find this pattern repeats in damage and  repair of myelin in MS studies.

To summarise: Short-term gain- long-term pain on statins

Dr Luca Mascitelli and myself went into this in our review paper 2009 at http://bit.ly/Ob9wKM

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Low-Cholesterol and Violent Behaviours

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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.

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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 treatment and placebo groups’ mortality lines should be independent: a trend in one should have no consequential influence on the other. However:

  • All 4 lines are essentially identical for 1.6 years.
  • Then there is a departure — by both lines at the same time.

The fact that both lines — treatment and placebo — depart at the same time is important. Why should the treatment suddenly become beneficial at exactly the same time as non-treatment becomes detrimental?

The average line of both treatment and non-treatment groups follows a ‘natural’ mortality curve; any natural survival curve would have its slope increasing downward. (i.e. becoming more negative.)

Both treatment and placebo lines follow this natural curve for 1.6 years. Then both diverge. The placebo group shows this slope change increasing (negative) at a faster rate than all other lines. But, surely, it should follow the natural mortality curve. Why doesn’t it?

The slope of the treatment group is nearly constant from 1.8 years onward. It’s not a curve at all, but an almost straight line — and it shouldn’t be. What it says is that old people die at the same rate as younger ones. And life isn’t like that.

Is this evidence that the data of the 4S trial were not handled in an honest manner? Were deaths occurring in the treatment group assigned to the placebo group? Is this why the two curves, which should be independent, are apparently related? Or is there a mistake somewhere? Is there an error in logic?

Statins: Saviours of Mankind or Expensive Scam?