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Question If You No Longer Take Statins.


@Bluetit1802 yes same thing happened to my FIL in the 80s had it happen when virually walking past the hospital but did not make it.


@Indy51 I can understand your ambivilance to it but that was a failure in after care and as such unforgivable.

When I had my op the surgical team where brilliant but the after care did leave a lot to be desired. Though one thing was good was that a couple of days after the the op I was given an ultra sound scan to check that the graft had not moved I am still waiting for my follow up appointment but have had an angio cat scan, again to check that all is in order. So maybe things have changed for the better hopefully.

Normally it takes about six weeks for the graft to become fully embedded.
 
@DavidGrahamJones
I was prescribed statins on being diagnosed T2 in June 2016 despite low levels of cholesterol. The rationale was the higher risk of cvd for T2 patients. A recent blood test revealed I had low nos of platelets a side effect of statins. I've stopped taking them as I'm not convinced the benefits outweigh side effects. I'm having a cholesterol test next week so I'll compare results with and w/o statins.
 

It is a very personal decision, my total cholesterol, as of just before christmas is 4, despite eating more cheese, yoghurt and nuts during last year (gained 11 kgs, so a bad piece of advice being told I didn't eat enough because I obviously did). I hope your test results are favourable.
 
@DavidGrahamJones
Thanks David. I understand that nuts in moderation are nutritional and I eat them instead of biscuit snacks.
I think statin prescribing has become routine for type2s as a tick box reaction. The research I've seen shows some protection in small numbers of patients. They do not offer guaranteed protection from cvd or strokes per se and there are risks when cholesterol levels are too low! There is psychological pressure to follow Drs advice so it's often a hard call.
 

What are the risks from low cholesterol?
 
douglas99 said:
No causal relationship in any though.
Is there any proof that low cholesterol is the risk, and that leads to any fatality?
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Gosh you read those reports quickly !

Having proven to myself that the statistics they used to justify the need, efficacy, and safety for statins, I say that their science is also flawed, and that there is also no cause / effect from taking their pills, especially for women and older foks.

Given that the trials were run entirely by drug companies with NO independent oversight, and that these same companies refuse to publish the data, then I personally refuse to take statins Full Stop,
 
JohnEGreen said:
Are you serious cholesterol is vital to life one risk of seriously low cholesterol is death.
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I don't think that's ever been actually achieved to be honest.
Unless 'low cholesterol' has been recorded a a cause of death somewhere?
But even that would be a bit woolly with no number.
 

Many I have seen before, but yes, I do.

I don't approach with the view that anything said by a HCP must be automatically rubbished, as they know nothing, haven't got diabetes, are obese themselves, are paid for by drug companies etc, so, starting from the viewpoint the statistics are just that, simply what is written down, and not what hasn't been.

- People die from high cholesterol, and they die from low cholesterol.
They don't, they die from something else, just cholesterol can be measured at the time

There is a bathtub curve knocking around somewhere, (I'm surprised it hasn't appeared yet), which has the classic, low cholesterol high deaths, high cholesterol high deaths. Middle, lower deaths.

No one ever mentions the low cholesterol content is mainly from poorer countries, with poorer quality diets, and the high cholesterol is from richer countries, with processed diets.
I can drive my cholesterol down significantly, simply by a very low calorie diet.
I can drive mine up excessively by a high saturated fat diet.

I work very well with my HCP's and I can ask for cholesterol tests at random, which I did when I was getting to grips with reversing diabetes. Their help was invaluable.
We didn't just concentrate with a blinkered view view purely on BG, we looked at everything, including cholesterol, obesity, and exercise.

But, basically, if I starve, I will die, and my cholesterol will be low. If i overeat, who knows, maybe I'll die, maybe I won't, but I know my cholesterol will be high.

But, it won't be recorded as cholesterol on my death certificate, as cholesterol is merely a marker on my diet.

For what it's worth, my cholesterol was 'normal' by NHS definition last checkup, and my DN suggested I stop the statins, and get re-tested in about 3 months.
So, there goes her kickback if we believe the conspiracy theorists.
 
douglas99 said:
Unless 'low cholesterol' has been recorded a a cause of death somewhere?
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They may not use the word cause, but there is some association. Not that I really care, I'm more concerned about low cholesterol and what happens in the brain.

https://www.ncbi.nlm.nih.gov/pubmed/21160131
http://circ.ahajournals.org/content/92/9/2396 (a paper by Carlos Iribarren, Dwayne M. Reed, Randi Chen, Katsuhiko Yano, James H. Dwyer
There is also the graph from the British Heart Foundation which shows Cardio Vascular Events increasing as people's total cholesterol goes above 5.4 and worryingly below 5.4 as well. That graph is here somewhere on this forum. I might look for it if I have time.
 
Consequences of hypolipidemia
1- Effects on plasma membrane
Since about 44% of the human cell membrane is composed of lipids, they serve as a major structural component. Cell membranes are absolutely essential for the cell survival as well as for biological functions [68]. It is not known how very low plasma cholesterol levels would affect membrane composition and function but some indirect evidence might shed some light on this issue. Acanthocytes are dense, contracted red blood cells with several irregularly spaced thorny projections on the surface due to abnormal membrane fluidity. Acanthocytosis is a known clinical feature of abetalipoproteinemia and was also reported to be associated with hypolipidemia in celiac disease. In the later case acanthocytes disappeared two weeks after initiation of gluten free diet [69]. Acanthocytosis was also reported with hypobetalipoproteinemia in advanced chronic liver disease [63]. The exact mechanism of formation of acanthocytes is unclear, but reversal of the usual phosphatidylcholine-sphingomyelin ratio is considered to be a possible mechanism [70]. In a recent animal study, the hypolipidemic agent Atorvastatin caused significantly lower cholesterol and higher phospholipid content of red blood cell membrane, thus decreasing the cholesterol to phospholipid ratio. Although these structural changes were not associated with any obvious adverse rheological alterations, but they show that hypolipidemia may be associated with cell membrane lipid changes [71].

2- Intracerebral hemorrhage (ICH)
Intracranial hemorrhage accounts for approximately 10% of all strokes, and carries a significantly high morbidity and mortality as the 30-day fatality rate reaches up to 50% [72]. Several studies have demonstrated that low cholesterol is a risk factor for ICH [73–75]. Others have reported that hypercholesterolemia is protective against ICH [76–78]. Iribarren et al [74] described the association between low serum cholesterol level and cerebral hemorrhage in elderly men. In another study of young patients hypocholesterolemia (</=160mg/dl) was found in 35% of the patients with ICH compared to only 13% having hypertension [7].

Hypocholesterolemia was more common in ICH patients aged <20 years and in those with cryptogenic ICH [7]. Other authors have mentioned hypocholesterolemia <160mg/dl (4.14 mmol/l) as a contributing risk factor for Hypolipidemia intracerebral hemorrhage in previously healthy people [75]. The causal relationship is unclear; however, some investigators have proposed that the interaction of high diastolic blood pressure and low cholesterol levels weakens the endothelium of the intracerebral arteries [75], while another study reported platelet hypoactivity is associated with hypocholesterolemia [79], therefore affected patients may be more prone to bleeding.

3- Adrenal failure
Cholesterol molecules are the precursors for adrenal steroid hormones. The adrenal gland requires a continuous supplement of cholesterol for the biosynthesis of adrenal corticosteroids, which can be supplied by LDL receptor-mediated uptake or through local synthesis [80]. Thus, at least theoretically; hypocholesterolemia will be associated with hypocortisolemia, and during stress cortisol production may not be high enough to protect against the cell damage. Hence critically ill patients will be predisposed to adrenal failure [23, 30, 81]. Although few human and animal studies support this hypothesis [30, 81], several authors have shown that in reality this does not happen [80, 82, 83]. Animal studies of the hypolipidemic drug Nafenopin have shown that despite significant lowering of serum cholesterol levels, this failed to alter blood corticosterone [82] and aldosterone [83] concentrations. This is probably because of the increased endogenous cholesterol synthesis as a result of compensatory smooth endoplasmic reticulum hypertrophy [82, 83]. Furthermore, one study of adult patients receiving 80 mg of the potent HMG CoA reductase inhibitor Simvastatin for two months showed that despite a 36%, reduction in total cholesterol level, there was no adverse effect on ACTH-stimulated adrenal corticosteroid production [80]. In summary; the available evidence is insufficient to support or refute the hypothesis that hypocholesterolemia can lead to adrenal failure.

4- Sepsis
Hypocholesterolemia in healthy men is reported to be associated with significantly fewer circulating lymphocytes, total T cells, and CD8+ cells [84], thus the host immunity will be altered and the patient may be prone to infection. Harris et al reported that lipoproteins bind to and neutralize bacterial endotoxin lipopolysaccharide (LPS) [85]. LPS binds to LPS binding protein [86], activating the cell surface CD14 receptor [87] which stimulates the release of several proinflammatory cytokines, including TNF, IL-1, and IL-6 [88]. If LPS binds to lipoproteins, then cytokine release is decreased [89]. It is assumed that hypolipidemia impairs the LPS neutralization, hence predisposing to more severe inflammation. Recently Kitchens et al [90] demonstrated that despite hypocholesterolemia, circulating lipoproteins maintain their ability to bind and neutralize LPS. However in spite of this recent contradiction this issue remains unsolved as evidence remains inconclusive. Several authors report that hypocholesterolemia may be a predisposing factor to sepsis in the critically ill patient [23, 30]. A significant relationship has been observed between preoperative hypocholesterolemia and incidence of postoperative septic complications. Leardi et al reported that the highest incidence of postoperative septic complications is seen in patients with cholesterol levels below 105 mg/dl [10]. Moreover, a very low level of cholesterol is also considered to be a prognostic factor during infection, predicting an unfavorable outcome in elderly patients [52]. Hypocholesterolemia is the most frequently observed laboratory finding in fatal cases of pneumonia in the elderly [91], in a study conducted at a nursing home; hypocholesterolemia was the only admission feature associated with death due to bacteremia [2]. Pacelli et al reported hypocholesterolemia as an independent predictor of death in patients with intra-abdominal infection [92]. In neutropenic patients with fever, non-survivors had significantly lower serum cholesterol levels compared to survivors [93]. From these whole data one can conclude that hypocholesterolemia is a risk factor for infection in certain conditions as well as a prognostic indicator during sepsis.

5- Disease mortality
Studies suggest that lipoproteins play a role in the binding and neutralization of endotoxins [85]. Epidemiologic studies have identified a relationship between hypocholesterolemia (<130 mg/dL) and increased mortality from all causes [14]. Crook et al stated that, in hospitalized patients the lower the plasma cholesterol the higher the mortality, and they demonstrated an increase in the mortality rate from 39% to 71% as plasma cholesterol dropped from <77.2mg/dl (2mmol/dl) to <58mg/dl (1.5 mmol/l) [11]. A low baseline serum cholesterol level is associated with higher mortality rates in patients with liver cirrhosis. There is a significant relationship and increased risk of mortality in patients with HIV and HCV co-infections [62]. Hypocholesterolemia is also associated with increased mortality in patients with tuberculosis [94]. Several epidemiological studies suggest an inverse relationship between serum cholesterol levels and cancer mortality [34]. Following a severe trauma, dying patients appear to have progressive hypocholesterolemia [24]. In conclusion, hypocholesterolemia has a statistically significant relationship to mortality in the critically ill patient and is an independent predictor of mortality in this group.

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3074286/
 
You seem to have missed off the conclusion there.

'Hypolipidemia is a common disorder affecting about 2–3% of apparently healthy individuals and up to 6% of hospitalized patients. It might be a marker for an underlying, serious problem. '

Marker being the key word, not 'cause'

Each to his own though, I've always gone for mainstream health care, and my body seems to work accordingly,
I'll keep my cholesterol healthy for me, and eat to suit.
if others prefer to choose a different option and actively drive cholesterol up, maybe they'll be proved right one day.
 
The following is a recent study published in the British Medical Journal (BMJ) which carries some weight.
http://bmjopen.bmj.com/content/6/6/e010401.full

There have been several similar studies released in 2016 that also show that much of what was understood previously about our endocrine system has been based on dubious science, and that there is very little correlation between TC and mortality,

Edit to add: The following is a blog, but it is well written, and provides a full list of reference material at the end I have read several of the referenced reports from their archive, so this blogger seems to have done his research well (and recently too)
http://www.second-opinions.co.uk/low-chol.html#.WHJftFy0Vf4
 
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I have taken statins for the last 10 years but it was never suggested that I took CoQ10. I have never suffered from any leg pains though but I do think they could have been the cause of my having T2 as I was not typical for it as I was never overweight and I did not eat a high starchy or processed food diet
 
If I had gone for main stream health care I would be dead now!
The main stream changes and some medical advice is not clear cut, unless one lives in a black and white universe.

This simple assessment using the amount of Cholesterol one has is a gross over simplification. LCHF causes high HDL and low Trigs, so much so someone with a total of 4.0 could have more metabolic disease than someone with a total of 6.0!
D.
 
My surgery always does fasting, with a full breakdown, so no issues there.

Oddly enough, it was high saturated fats that gave me the highest LDL I've ever had, the Mediterranean diet that gave me the best.

Possibly LCHF works differently for each individual, rather than a one size fits all approach to it?
 

Maybe everyone with high LDL died before they were 60, or 80?
And is 'all cause mortality' particularly relevant?

Either way, until I get to 60, I think I'll go along with the studies that show increasing risk is associated with increasing LDL, which even this review doesn't disagree with.
 
Pinkorchid said:
I have never suffered from any leg pains though but I do think they could have been the cause of my having T2
Click to expand...

I'm genuinely pleased that it doesn't affect everyone in exactly the same way, sorry it may very well have helped you develop type II. You're probably aware that in the U.S. of A. there is a class action against the manufacturer, not sure what stage they're at. The upper leg pain is quite bad and in my case still present. I also know that I have low levels of CoQ10 which could be attributed to old age but how much and why doesn't every old person feel the same leg pain no one can tell me.
 
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