Cholesterol, Disability, NDIS Behaviour Support and Counselling Clinical Reviews
While the NDIS does not pay for mainstream health and medical reviews, from our holistic perspective as senior specialists in behaviour support and counselling therapies, we take the larger-view on how health issues overlap and create, make worse, or improve disability related issues.
In the disability realm, when you are living with chronic life-long conditions that hinder your quality of life, in relation to broader lifestyle health behaviours, an ounce of prevention is worth a ton of cure.
– Dr Joseph, Senior Specialist Behaviour and Lifestyle Health Counselling Psychotherapy.
This article does not provide direct health advice, rather simply explores a topic for consideration by you and your treating physician. For all health related matters and decisions, you should always seek the direct advice of your GP or primary health practitioner.
An Ounce of Prevention.
If we can prevent, manage, or hold off future chronic health conditions like mobility concerns, metabolic disorders, gut-brain dysfunction, and larger health issues like inflammatory conditions such as diabetes, heart failure, asthma, etc… who would not feel this is worth a bit of learning and effort?
In the midst of meeting participant’s NDIS goals and therapy reviews, we usually provide some level of lifestyle health discussion to encourage and motivate individuals to take care of themselves and/or to help carers or staff to encourage healthy lifestyle options. This approach is central to an active participation in daily lifestyle choices and control.
What is Cholesterol?
Cholesterol is a complex topic these days. In all truth, medical science is divided on the nature of cholesterol and its purpose, function, utility, and its dangers in the human body.
Sadly for people with disability, studies show that over medication is often the case. In the current model, most GPs and specialists see cholesterol as a nasty substance that needs to be controlled by pharma, most often statins. But most drugs have a lengthly list of side effects. This is also true for statins.
Put really simply, cholesterol is a fatty substance that is essential for the body’s many functions and for brain health. In my professional view, there are many ways to holistically treat high cholesterol before ever considering statins.
The Crux of Statin Prescription: A Restrictive Practice?
As a behaviour specialist, we always attempt to address medication for behaviours of concern as a last resort. In fact, medications for behaviours of concern is considered a Restrictive Practice, meaning that the practice needs to be understood as a last resort and to work toward reducing and eliminating the practice where possible. This means that, in all truth, people with restrictive practices in medications should have comprehensive clinical reviews to look at other less restrictive options to treat the issues.
In our clinical view, and for many people, statins and other drugs to reduce cholesterol falls in this “could be prevented” category. However, the culture of medicine at the moment suggests that this preventative and lifestyle medicine approach is sadly extremely rare. It is therefore unlikely that most GPs will actively engage the range of lifestyle and diet considerations that could prevent, reduce, and eliminate medication by statins.
To take this rationale one step further, by seeing correctly that high cholesterol is at base and most certainly a lifestyle and behavioural issue, and by medicating this issue prior to, or by default exclusion of, behaviour support analysis and lifestyle review, under the NDIS definitions for Restrictive Practices it is plausible to argue that medication of people with disabilities in Australia with statin drugs may constitute a Restrictive Practice under legislation. As such, specialist behaviour support and lifestyle review is necessary to assist the individual to prevent, reduce, or eliminate use of statins or other medications to reduce cholesterol.
Clinical Factors.
Cholesterol is made up of two primary types of lipids, LDL and HDL. The LDL kind is the main focus of medicalised lipid reduction and statin prescription. We posit that the problem here is that avoiding the treatment of predominant behavioural and lifestyle factors ignores the bulk of contextual factors that lead to not just lipid elevation but also to more troubling health crisis.
Lipids are only one part of a larger story in the human body. But medical intervention tends to target very specific measures to the exclusion of non-specific outcomes from medications. In other words, a person’s lipids might be reduced but they may also deal with chronic side effects they are not aware of until these result in symptoms. By the time symptoms appear, it may be too late as the side effects have disrupted the homeostasis or balance in the body.
There are a range of other factors that are quite significant that ought to gain attention prior to or alongside statin medication, such as inflammatory markers, gut dysfunction, muscle and joint issues, mobility and fitness markers, use of alcohol, smoking, diet and nutrition… These constitute a range of lifestyle medicine factors that are increasingly shown to make significant differences in all cause mortality.
The Outdated Lipid Hypothesis.
Studies in lipid reduction show questionable outcomes and cannot be correlated with absolute reduction in death or in production of a longer lifespan. For example, one quite major study shows that statin use is by far not associated with adequate outcomes in comparison to the risks associated with statin use.
Byrne et al (2022) conducted a study that provided a “meta-analysis of 21 randomized clinical trials in primary and secondary prevention that examined the efficacy of statins in reducing total mortality and cardiovascular outcomes.”
They found that “there was significant heterogeneity but also reductions in the absolute risk of 0.8% for all-cause mortality, 1.3% for myocardial infarction, and 0.4% for stroke in those randomized to treatment with statins compared with control, with relative risk reductions of 9%, 29%, and 14%, respectively.” Most significantly, they showed that “A meta-regression was inconclusive regarding the association between the magnitude of statin-induced LDL-C reduction and all-cause mortality, myocardial infarction, or stroke.”
They concluded that “The results of this meta-analysis suggest that the absolute risk reductions of treatment with statins in terms of all-cause mortality, myocardial infarction, and stroke are modest compared with the relative risk reductions, and the presence of significant heterogeneity reduces the certainty of the evidence. A conclusive association between absolute reductions in LDL-C levels and individual clinical outcomes was not established, and these findings underscore the importance of discussing absolute risk reductions when making informed clinical decisions with individual patients.”
Statins and Risks.
Other known risk profiles for statin use are well documented. There are two categories of risks that we have found. One is absolute risk, which we define as dependent on the nature of biosynthesis of the drug in the body – i.e. these risks are of low level but chronic concern and are likely ongoing in all patients even where bloodwork does not register a problem due to the thresholds associated with testing for various concerns.
The second category of risk we observe in the literature are systemic risks that evolve from the above endogenous functions of the chemical pathways in the body – i.e. key concerning risk profiles that suggest the danger of taking a statin does not correlate to benefit. This analysis holds even more true considering the questionable efficacy of statins overall to do what they in fact claim to do.
The first category of absolute risks do not appear to only rely on percentages of cases but are prevalent within the biological functions of the chemical in the body. To make this easier for those who listen to this article, we copy the table below at the end of the paper with its links.
For example, statins are known to,
- lower Vitamin K2 production in kidney.
- to lower testosterone.
- to lower CoQ-10.
- to increase liver enzymes.
- to lower DHEA.
What is most concerning about these factors is that they represent a chronic underlying dysregulation that diminishes bioavailability of key elements the body needs to function, or that conversely promote unhealthy levels of elements that make it harder for the liver or other organs to function. Each of these elemental-changes from statin use relate to possible longer term chronic and acute inflammatory disease presentations. In other words, while focusing exclusively on lowering one type of lipid profile and ignoring the more holistic utility and function of lipids in the body, the non-specific outcomes of statin use leading to dysfunctional biological and systemic factors far outweigh the marginal gains that lipid reduction entails.
For example, studies have shown that statins,
- increase the risk of type two diabetes.
- Statins are shown to result in chronic lower energy levels and may be associated with chronic fatigue syndrome.
- Statins appear to worsen memory and may be associated with the onset of dementia.
- They increase the risk of getting shingles.
- Statins increase erectile dysfunction.
Furthermore, recent studies show that statins double the risk of dementia. In a study on “Lipophilic Statins in Subjects with Early Mild Cognitive Impairment” Padmanabham et al (2021) showed the “Associations with Conversion to Dementia and Decline in Posterior Cingulate Brain Metabolism” by engaging “in a Long-term Prospective Longitudinal Multi-Center Study.” We note that the lipophilic statins include atorvastatin, simvastatin, lovastatin, fluvastatin, cerivastatin, and pitavastatin. These appear to more than double the risk of developing dementia compared with those who do not take statins.
The authors conclude that, among subjects with early mild cognitive impairment and low to moderate serum cholesterol levels at baseline, lipophilic statin use was associated with more than double the risk of converting to dementia over eight years of follow-up compared with statin non-use, and with highly significant decline in metabolism of posterior cingulate cortex — the region of the brain known to decline the most significantly in the earliest stages of Alzheimer’s disease. In contrast, no such clinical or metabolic decline was found for users of other statins, nor statin users having higher baseline serum cholesterol levels.
Regarding loss of energy and chronic fatigue, Golomb BA, Evans MA, Dimsdale JE, White HL. did a study on the “Effects of Statins on Energy and Fatigue With Exertion: Results From a Randomized Controlled Trial.” The authors suggest they had “the first randomized evidence affirming unfavourable statin effects on energy and exertional fatigue.” They registered “effects seen in a generally healthy sample given modest statin doses” that “contributed to the significant adverse effect of statins on energy and fatigue with exertion.”
Tolerability of the statins was questioned as they found that symptoms tend to show up over longer periods of time on the drug. “There was a significant relation between EnergyFatigEx and actual activity: reduced activity and exertional tolerance (irrespective of activity) in turn predict hard adverse outcomes. Effects may take time to manifest, as may benefits of statin use.” And they conclude that, “physicians should be alert to patients’ reports of exertional fatigue or diminished energy during statin use.”
We found several studies that show a direct link between statin use and sleep disturbances and more concerning, how insomnia is associated with increased risk of heart disease. We will not go into these studies as this paper is already long enough. Suffice to say, that the issues of risk do not appear hypothetical but are endemic to the ways that statins function in the body.
Which is to say, the drug does not simply target LDL but impacts the metabolic processes underlying several functions in the body which is why there is such a wide range of non-specific outcomes (side effects). By not understanding the function of the drug, medical intervention ostensibly does not account for nor take adequate responsibility for the non-specific outcomes and risk profiles that are well documented in the literature.
Inflammation, not Cholesterol.
Tsoupras et al (2018) makes an important contribution to understanding that the focus of contemporary medicine on attacking cholesterol is based on false assumptions. They suggest that, “Since the Seven Countries Study, dietary cholesterol and the levels of serum cholesterol in relation to the development of chronic diseases have been somewhat demonised.” At the same time, the focus on what really counts has been lost in the west.
The authors say that, “the principles of the Mediterranean diet and relevant data… demonstrate that the key to longevity and the prevention of chronic disease development is not the reduction of dietary or serum cholesterol but the control of systemic inflammation.”
They show how inflammatory conditions in the body lead to arterial proliferation of serum cholesterol what moves to the inflamed tissues to address the inflammatory cycle. Cholesterol is more correctly understood as the helper. The problem arises when too much cholesterol collects in the region of inflamed tissue and tends to ossify, to become more densely packed. When these dense bits break off and enter the blood stream they can cause heart attack, clotting of the lungs, or stroke.
The authors suggest that, “it is inflammation induced by several factors, such as platelet-activating factor, that leads to the onset of cardiovascular diseases (CVD) rather than serum cholesterol.” This information sets the stage for reconsidering the causal factors that lead to the very diseases and risks for mortality that are the underlying rationale for statin prescription. As we saw above, the absolute reduction of risk by long term statin use is so low when compared to risks, we have to wonder why the medication is used in so many cases where lifestyle and behavioural interventions would suffice.
The authors conclude that “The key to reducing the incidence of Cardiovascular Disease is to control the activities of platelet-activating factor and other inflammatory mediators via diet, exercise, and healthy lifestyle choices.”
They further explain that “cholesterol is an essential biomolecule for the normal function of all our cells. So, how much do we really need to lower cholesterol? The authors take this question and reply that because, “cholesterol plays a crucial role in several of our cellular and tissue mechanisms, it is not surprising that there are several consequences due to the aggressive reduction of cholesterol levels in the body.”
Fascinating as well, that by reducing healthy fats in the diet, the body does not benefit. The authors say that “targeting cholesterol and fat intake” through low-fat diets “can lead to less absorption and lower bioavailability of other lipids containing high value nutrients.” They include lipid soluble vitamins and minerals, and especially vitamin D. They explain that these lipid functions and the lipids themselves provide numerous bioavailable benefits and anti-inflammatory functions while “reducing the risk of chronic diseases.”
They conclude that, “lower cholesterol levels do not equate to better health, or to lower risk of chronic diseases such as Cardiovascular Disease. Homeostasis must be maintained, even with regard to cholesterol, both HDL and LDL.”
We have by far not addressed many issues in this topic, not the least of which are healthy options to reduce and control cholesterol as a healthy lifestyle approach. We therefore include a few additional and helpful references below that did not find space in the article above.
Bibliography.
Altura B, Altura B, “Magnesium: the forgotten mineral in cardiovascular health and disease.” A Gem Lecture at SUNY Downstate. Alumni Today, pp. 11–22, spring 2001.
Byrne P, Demasi M, Jones M, Smith SM, O’Brien KK, DuBroff R. 2022, Evaluating the Association Between Low-Density Lipoprotein Cholesterol Reduction and Relative and Absolute Effects of Statin Treatment: A Systematic Review and Meta-analysis. JAMA Intern Med. 2022;182(5):474–481. doi:10.1001/jamainternmed.2022.0134 https://jnm.snmjournals.org/content/6…
Golomb BA, Evans MA, Dimsdale JE, White HL., 2021, Effects of Statins on Energy and Fatigue With Exertion: Results From a Randomized Controlled Trial. Arch Intern Med. 2012;172(15):1180–1182. doi:10.1001/archinternmed.2012.2171.
Harvard Medical School, 2019, (https://www.health.harvard.edu/heart-health/new-insights-about-inflammation).
Leritz, E.C., McGlinchey, R.E., Salat, D.H. et al. 2016, Elevated levels of serum cholesterol are associated with better performance on tasks of episodic memory. Metab Brain Dis 31, 465–473 (2016). https://doi.org/10.1007/s11011-016-9797-y
Li W et al., 1999, Extracellular magnesium regulates effects of vitamin B6, B12 and folate on homocysteinemia-induced depletion of intracellular free magnesium ions in canine cerebral vascular smooth muscle cells: possible relationship to [Ca2+]i, atherogenesis and stroke. Neurosci Lett, vol. 274, no. 2, pp. 83–86, 1999.
Olatunji LA, Soladoye AO. 2007, Effect of increased magnesium intake on plasma cholesterol, triglyceride and oxidative stress in alloxan-diabetic rats. Afr J Med Med Sci. 2007 Jun;36(2):155-61. PMID: 19205579.
Prasanna Padmanabham, Stephen Liu, Daniel Silverman, 2021, Lipophilic Statins in Subjects with Early Mild Cognitive Impairment: Associations with Conversion to Dementia and Decline in Posterior Cingulate Brain Metabolism in a Long-term Prospective Longitudinal Multi-Center Study, Journal of Nuclear Medicine May 2021, 62 (supplement 1) 102 (https://jnm.snmjournals.org/content/62/supplement_1/102).
Rosanoff A, Seelig MS. 2004, Comparison of mechanism and functional effects of magnesium and statin pharmaceuticals. J Am Coll Nutr. 2004 Oct;23(5):501S-505S. doi: 10.1080/07315724.2004.10719389. PMID: 15466951
Tsoupras A, Lordan R, Zabetakis I. 2018, Inflammation, not Cholesterol, Is a Cause of Chronic Disease. Nutrients. 2018;10(5):604. Published May 12. doi:10.3390/nu10050604.
Yvan-Charvet L, Bonacina F, Guinamard RR, Norata GD. 2019, Immunometabolic function of cholesterol in cardiovascular disease and beyond. Cardiovasc Res. Jul 1;115(9):1393-1407. doi: 10.1093/cvr/cvz127. PMID: 31095280.
This article does not provide direct health advice, rather simply explores a topic for consideration by you and your treating physician. For all health related matters and decisions, you should always seek the direct advice of your GP or primary health practitioner.
Links from tables in article
- lower Vitamin K2 production in kidney https://academic.oup.com/jn/article/1… ,
- to lower testosterone https://care.diabetesjournals.org/con… https://www.ncbi.nlm.nih.gov/pubmed/2… ,
- to lower CoQ-10, https://www.ncbi.nlm.nih.gov/pubmed/2… https://www.ncbi.nlm.nih.gov/pmc/arti…,
- to increase liver enzymes https://www.ncbi.nlm.nih.gov/pmc/arti…,
- to lower DHEA https://www.ncbi.nlm.nih.gov/pmc/arti…
- increase the risk of type two diabetes https://www.ncbi.nlm.nih.gov/pubmed/2… https://onlinelibrary.wiley.com/doi/f…
- Statins are shown to result in chronic lower energy levels and may be associated with chronic fatigue syndrome https://jamanetwork.com/journals/jama… https://www.ncbi.nlm.nih.gov/pubmed/2…
- Statins appear to worsen memory and may be associated with the onset of dementia https://jamanetwork.com/journals/jama…
- They increase the risk of getting shingles https://journals.plos.org/plosone/art… https://academic.oup.com/cid/article/…
- Statins increase erectile dysfunction https://www.ncbi.nlm.nih.gov/pubmed/1… https://www.ncbi.nlm.nih.gov/pubmed/1…
Featured image by Cats Coming.
