Statin use associated with a 340% increased risk of acute memory loss

This study was published in JAMA Internal Medicine 2015 Jun 8

 

Study title and authors:

Statin Therapy and Risk of Acute Memory Impairment.

Strom BL, Schinnar R, Karlawish J, Hennessy S, Teal V, Bilker WB.

Rutgers Biomedical and Health Sciences, Rutgers University, Newark, New Jersey

 

This study can b accessed at: http://www.ncbi.nlm.nih.gov/pubmed/26054031

The objective of the study was to assess whether statin users and users of other cholesterol lowering drugs show acute decline in memory compared with nonusers. The study lasted 26 years and included 482,543 statin users, 482,543 matched non users of any cholesterol lowering drugs and 26,484 users of non statin cholesterol lowering drugs.

The study found:
(a) Statin users had a 340% increased risk of acute memory loss within 30 days immediately following exposure compared to non users.
(b) Non statin cholesterol lowering drug users had a 260% increased risk of acute memory loss within 30 days immediately following exposure compared to non users.

Strom concluded: "Both statin and nonstatin lipid lowering drugs were strongly associated with acute memory loss in the first 30 days following exposure in users compared with nonusers".

Statins related to memory dysfunction

This paper was published in Current Drug Safety 2012 Feb;7(1):33-4

Study title and authors:
Statin related memory dysfunction in a Nigerian woman: a case report.

Okeahialam BN, Isiguzoro I.
Department of Medicine, Jos University Teaching Hospital, Jos, Plateau State, Nigeria. basokeam@yahoo.com

This paper can be accessed at: http://www.ncbi.nlm.nih.gov/pubmed/22663955

This paper describes the case of a woman who with Simvastatin developed memory deficits which adversely affected activities of her daily living.

(i) The woman was first observed in 2005 at 41 years of age for sensation of weight in the chest.
(ii) She was put on atorvastatin (Lipitor) 10 mg daily.
(iii) Levels of her high density lipoprotein (HDL) cholesterol fell and since low HDL cholesterol increases heart disease risk, the drug was withheld.
(iv) In 2008 she restarted statin treatment, this time she took Simvastatin (Simvor) 10 mg daily.
(v) While on this, she complained of feeling ill and cramped up each morning.
(vi) She stopped taking Simvastatin.
(vii) In time Simvastatin was re-introduced at 20mg daily.
(viii) She started to experience muscle cramps, incoherence in thought and speech as well as memory impairment.
(ix) She reduced the dose to 10 mg daily with some respite in the short term.
(x) With time and still on 10mg nocte of simvastatin she once again started to have rising muscle pains. Lapses in memory were also observed. She was not remembering things and to her embarrassment, kept repeating instructions which she had earlier given. The urge to read vanished and if she forced herself to read, she could not absorb.
(xi) She totally discontinued Simvastatin which led to recovery.

Okeahialam also notes that low levels of cholesterol and low levels of low density lipoprotein (LDL) cholesterol may be associated with cognitive dysfunction and concludes: "It is suggested that patients on statins be monitored for side effects especially memory deficits which can adversely effect quality of life... It may also be unwise to reduce the lipid (cholesterol) sub fractions to very low levels".

Statin therapy causes memory complaints and mood changes

This paper was published in Pharmacotherapy 2010;30(6):236e–240e

Study title and authors:

Changes in Memory Function and Neuronal Activation Associated with Atorvastatin Therapy
Beth A. Parker, Ph.D., Donna M. Polk, M.D., Vimal Rabdiya, M.D., Shashwath A. Meda, M.S., Karen Anderson, R.N., Keith A. Hawkins, Psy.D., Godfrey D. Pearlson, M.D., and Paul D. Thompson, M.D.

This paper can be accessed at: http://www.pharmacotherapy.org/Case_Reports/Pharm3006e_Parker-CR.pdf

This paper, headed by Dr Beth Parker from the Hartford Hospital, describes a 65-year-old man who reported cognitive complaints (memory complaints and mood changes) after taking atorvastatin 10 mg/day for one year. He had no history of alcohol consumption, major head trauma, psychiatric problems, or memory impairment.

(i) After one year of taking the statin the patient described his complaints as “fuzzy thinking” and “brain fog.” His wife also noted that the patient demonstrated a progressive decline in cognitive function and memory accompanied by increasing mood changes.

(ii) Cognitive testing and assessment of neuronal activation using functional magnetic resonance imaging (fMRI) (procedure that measures brain activity) were performed during a working memory task while he was receiving atorvastatin therapy.
(iii) The patient demonstrated altered neuronal activation and reduced performance on the cognitive tests, which was consistent with his cognitive symptoms.
(iv) He stopped taking atorvastatin. The cognitive tests were repeated two months after discontinuation of the drug and the patient exhibited improved cognitive test performance and fMRI patterns similar to those expected in a healthy individual.
(v) The patient also reported subjective improvement of his cognitive complaints within days of cessation of atorvastatin.

Dr Parker concludes that a: "growing number of reports suggest that statins evoke adverse cognitive effects".

Clinicians should be aware of possible adverse cognitive reactions during statin therapy

This paper was published in Pharmacotherapy 2006 Aug;26(8):1190-2

 

Study title and authors:

Short-term memory loss associated with rosuvastatin.

Galatti L, Polimeni G, Salvo F, Romani M, Sessa A, Spina E.

Department of Clinical and Experimental Medicine and Pharmacology, Section of Pharmacology, University of Messina, Messina, Italy. lgalatti@unime.it

 

This paper can be accessed at: http://www.ncbi.nlm.nih.gov/pubmed/16863497

This paper reports the case of rosuvastatin-related short-term memory loss.

(i) A 53-year-old man experienced memory loss after being treated with rosuvastatin at 10 mg per day.
(ii) After discontinuation of rosuvastatin, the neuropsychiatric adverse reaction resolved gradually, suggesting a probable drug association.
(iii) During the following year, the patient remained free from neuropsychiatric disturbances.

The lead researcher of the paper, Dr Laura Galatti, concludes that clinicians should be aware of possible adverse cognitive reactions during statin therapy.

Statins may be implicated in neurodegenerative diseases

This post includes a summary of a paper published in Neurobiology of Aging 2010 Sep;31(9):1543-53

Study title and authors:
Mevastatin accelerates loss of synaptic proteins and neurite degeneration in aging cortical neurons in a heme-independent manner.

Kannan M, Steinert JR, Forsythe ID, Smith AG, Chernova T.

Books:

MRC Toxicology Unit, University of Leicester, Leicester, United Kingdom.

This paper can be accessed at: http://www.ncbi.nlm.nih.gov/pubmed/18951667

Kannan investigated the effectes of statins on cultured neurons.

The study found:
(a) Statins impaired synaptic proteins.
(b) Statins reduced N-methyl-d-aspartate receptor currents (N-methyl-d-aspartate receptor currents help in memory funcion).
(c) Statins accelerated neurodegeneration associated with aging.

To conclude: Statins exert a neurotoxic effect in cultured neurons and may be implicated in neurodegenerative diseases such as Parkinson’s, Alzheimer’s, Amyothrophic Lateral Sclerosis, Multiple Sclerosis and Huntington’s.

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Statin side effects

This post includes a summary of a study published in Biofactors 2005;25(1-4):147-52

Study title and authors:
Treatment of statin adverse effects with supplemental Coenzyme Q10 and statin drug discontinuation.

Books:

Langsjoen PH, Langsjoen JO, Langsjoen AM, Lucas LA.

East Texas Medical Center and Trinity Mother Francis Hospital, Tyler, 75701, USA. langsjoen@compuserve.com

This paper can be accessed at: http://www.ncbi.nlm.nih.gov/pubmed/16873939

This study investigated the effects of discontinuing statin drugs and beginning Coenzyme Q10 supplementation in cardiology (heart disorder) clinic patients. The study included  The study included fifty new cardiology clinic patients who were on statin drug therapy (for an average of 28 months), who on their initial visit were evaluated for possible adverse statin effects (muscle pain, fatigue, shortness of breath, memory loss, and peripheral neuropathy). All patients discontinued statin therapy due to side effects and began supplemental Coenzyme Q10. The patients were followed for an average of 22 months.

The study found that after stopping statins and starting Coenzyme Q10:
(a) Fatigue decreased from 84% to 16%.
(b) Muscle pain decreased from 64% to 6%.
(c) Shortness of breath decreased 58% to 12%.
(d) Memory loss decreased from 8% to 4%.
(e) Peripheral neuropathy decreased from 10% to 2%.
(f) Measurements of heart function either improved or remained stable in the majority of patients.
(g) There was no adverse consequences from statin discontinuation.

The researchers conclude that: "Statin-related side effects, including statin cardiomyopathy, are far more common than previously published and are reversible with the combination of statin discontinuation and supplemental Coenzyme Q10".

*Dietary sources of Coenzyme Q10 include all animal products, particularly heart meat.

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Learning, Your Memory, and Cholesterol

This post features an article by Chris Masterjohn and a recipe for buffalo-zucchini fritatta.

Learning, Your Memory, and Cholesterol
July, 2005 by Chris Masterjohn

One of the many important roles cholesterol plays in the body is in our nervous system, enabling learning and memory to take place. In fact, one of the reasons that sleep is beneficial to our learning and memory is because it enables our brain to make more cholesterol!

Books:

While the war on cholesterol is waged full-speed ahead, and many web sites are now touting low-fat, low-cholesterol diets as "brain-healthy" due to unfortunate misinterpretations about the role of a cholesterol byproduct in Alzheimer's disease, science is continually showing that cholesterol is one of the most important parts of our brains.

Sleep, Memory, Learning, and Cholesterol

Evidence to date strongly supports the concept that sleep plays an important role in increasing performance of newly learned activities, consolidating memories, and increasing brain plasticity-- which is the ability to form new, as well as break, connections between neurons called synapses.

These benefits of sleep are not simply the absence of stress from sleep-deprivation, but an independent, critical role, in the actual process of learning and memory-formation.1

But why?

Exciting research was published in the pages of Neuron last year (2004),2 identified about 100 genes that increase their activity during sleep. They found about as many that increased their activity during wake, and others whose activity varied with circadian rhythm, independent of sleep or wakefulness.

While there are many important cellular and molecular events that happen during sleep, and we are only cracking the surface in our understanding of them, one of the things this study showed is that cholesterol synthesis increases during sleep-- which, given the research described below, undoubtedly is part of the reason sleep is beneficial to mental functioning.

Cholesterol is abundant in the tissue of the brain and nervous system. Myelin, which covers nerve axons to help conduct the electrical impulses that make movement, sensation, thinking, learning, and remembering possible, is over one fifth cholesterol by weight.3

Even though the brain only makes up 2% of the body's weight, it contains 25% of its cholesterol.4

One of the groups of genes that the above study found to be upregulated during sleep were genes important for the synthesis and maintenance of myelin, including myelin structural proteins and genes relating to the synthesis and transport of cholesterol.

But the benefits of cholesterol extend beyond both sleep and myelin. In fact, in 2001, cholesterol was found to be the most important factor in the formation of synapses, the basis of our learning and memory.

Memories and Learning are Directly Dependent on Cholesterol

In the late 1990s and early 2000s, research was pointing to an unknown compound made by glial cells that was responsible for the ability of neurons to form synapses, or connections between each other.

Thoughts, memories, learning, and all mental function is dependent on the formation of synapses, so the ability to form them will directly impact mental functioning and health.

In the absence of this-- as yet unknown-- "glial factor," neurons formed few synapses, and the synapses they formed were inefficient and poorly functioning. In the presence of glial cells, which secrete the unknown factor, neurons formed many, highly efficient synapses.

So what is this "glial factor"?

Research in 2001, by Mauch, et al., published in volume 294 of Science magazine, determined that the unknown glial factor is cholesterol, which is released by the glial cells in a carrier called "apolipoprotein E."5

Initially, the researchers thought that the apolipoprotein E (apoE) may have been the glial factor itself. But it turned out that when neurons were treated with apoE, the beneficial effects on synapse formation were not observed.

The researchers then reasoned that, since apoE fit the bill in some ways, but did not have the desired effect, some of the lipids it carried may have been the elusive glial factor.

As it turned out, treating the neurons with a 10 mcg/mL solution of cholesterol increased synapse formation by 12 times! Other lipids, carried by apoE, such as phosphatidylcholine and sphingomyelin, did not have a significant effect, and were even toxic to the neurons at very high doses.

On the other hand, when low-cholesterol glial secretions were produced by using the cholesterol-lowering drug, mevastatin, the effect of the glial secretion on synapse formation was strongly diminished. When cholesterol was added back to the low-cholesterol secretion, the positive effect on synapse formation was fully restored.

The authors identified cholesterol as a limiting factor of synpase formation. In other words, the need for cholesterol in the brain is large enough relative to the supply of cholesterol that the availability of cholesterol can directly limit the ability to form synapses.

Neurites Lose Their Way Without Cholesterol

"Neurites" refer to the extensions from the cell of a neuron that connect with other neurons or muscles. The type of neurite that sends impulses away from the cell is an axon, and the type of neurite that receives impulses is a dendrite.

Connections between neurons, called synapses, are contantly being formed and broken in our brains, where dendrites and axons meet.

But they can't just grow randomly. Neurites grow in response to a stimulus given by a signaling protein in the membranes of neurons.

These signaling proteins rely on lipid rafts, which are beds of cholesterol and phospholipids made from long-chain saturated fatty acids that secure some proteins.

A 2004 study found that disrupting lipid rafts by extracting some of the cholesterol from the membrane of a neuron completely destroyed the ability of neurons to find the signaling proteins attracting them!6

Statins Could Kill Your Memory — Eggs Could Cure It

We now know that the formation of synapses, or connections between neurons, is directly dependent on the availability of cholesterol.

The formation of these synapses are what give us the ability to remember and learn. The benefits of sleep for memory formation and learning are in part a result of increased cholesterol synthesis during sleep.

The implications are important and powerful. In our society's quest to lower cholesterol at all costs and without second thought, could some of the methods we use, such as taking cholesterol-lowering drugs, or eating low-fat, low-cholesterol diets, be limiting the availability of cholesterol to our nervous system?

The authors of the 2001 Science study described above concluded that the "results imply that genetic or age-related defects in the synthesis, transport, or uptake of cholesterol in the CNS may directly impair the development and plasticity of the synaptic circuitry."

But the authors left out one thing: in addition to genetic or age-related defects, there is currently a booming industry founded upon the deliberate inhibition of the synthesis of cholesterol using pharmaceutical drugs. Some statins cross the blood-brain barrier (BBB); others may affect cholesterol levels in the brain without necessarily crossing the BBB; still, without crossing the BBB, the peripheral nervous system could likewise be damaged.

In fact, amnesia and cognitive dysfunction are reported as side-effects in some statin users. Dr. Duane Graveline, MD, former NASA scientist and astronaut, describes his bout of statin-induced memory loss, in which his wife caught him wandering aimlessly in his yard while he failed to recognize her.

In an article on the side-effects of cholesterol-lowering drugs, the Geriatric Times cites two randomized trials, several case reports, and one large case series pointing to memory loss as a result of statin drugs.

Conversely, dietary cholesterol can help reverse the effects of declining memory with age.

Mary Enig, PhD, cites a study in her book, Know Your Fats, that found that the cholesterol in eggs can help improve memory in the elderly.5

Remember...

One of the basic parts of ourselves that defines us as humans is our mind. We imagine, think, study, learn, remember, come up with new ideas, remember old faces, and form friendships and familial relationships that are based, in large part, on our memories of those people.

Cholesterol is a central building block of the connections within our brain that hold these memories and learning processes together. Remember that... thanks to cholesterol, you can!

This article can be accessed at: http://www.cholesterol-and-health.com/Memory-And-Cholesterol.html

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Recipe of the day

Buffalo-Zucchini Fritatta

Makes 2 Servings

Ingredients:

Food Mall: Ground Buffalo

5 Eggs

4oz Ground Buffalo
1 Large Zucchini, grated

Instructions:
Preheat oven to 350F.

In a bowl, whisk the eggs with a splash of water. Set aside.

In an omelet or saute pan over medium-high heat, cook the buffalo until browned and cooked through. Add the zucchini and stir.

Add the egg mixture.

Place pan in preheated oven and continue to cook until set, about 5-10 minutes (depending on pan).

Gently shake the pan to loosen the frittata and slide it onto a serving plate.