Health

Update 22.7.26: Article on Statins added - see below

Update 3.6.26: New lifetime calculator  available from downloads page - why not try it.....?

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Our health is, arguably, our most valuable possession - and we all need to look after it. 

Our GPs are our first line of defence when things do go wrong,  but there's no substitute for active prevention of illness, and only we can do this effectively. This means adopting a sensible and healthy lifestyle, and making frequent checks on our health, many of which we can perform ourselves.

Having experienced routine GP health checks myself in the recent past, and having spent several years working in the NHS as a Clinical Biochemist, it occurred to me that it might be useful to produce an easy-to-use health checker, designed to advise others how to  carry out their own health-related tests, and then interpret the results. 

Many of the tests described can be done at home with inexpensive equipment. Other more complex tests, such as blood tests normally done at clinics or GP surgeries, should be available to you (although you my need to ask for access to them at your GP surgery; once your access has been authorised, you can normally get access to all your test results and medical records via the NHS app, or if your device is not able to run this, via the SystmOnline platform on a Windows pc). 

Why not check them out and see if you're really  as healthy as you think....

Read on for more details.

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First, here's some background on health issues to put things in context. 

Heart disease and stroke are two of the major causes of death in the UK population. 

Maintaining healthy blood pressure, cholesterol and lipid levels, and a healthy Body  Mass Index (BMI),  is crucial to avoiding these modern-day scourges, particularly later in life. Controlling your blood glucose levels is also important  - Type 2 Diabetes has increased alarmingly in recent years. This complaint increases the likelihood of strokes and coronaries and other circulation-related conditions,  and is often linked to obesity. Our highly-processed modern Western diet, which is designed to be high in fat and carbohydrate to satisfy our palates and appetites, and our increasingly sedentary and exercise-poor lifestyles, both serve to increase the risk to health. Why  ?

Millions of years of evolution has optimised our physiology and metabolism for a low fat, high roughage diet and an active lifestyle. This is because our ancestors were faced with a restricted  diet at best, with recurrent bouts of starvation when times were really lean. Those who could hunt and make best use of what little food was available were the ones who survived to reproduce - the others simply didn't. 

Hence evolution favoured those who were best able to chase their prey, were able to survive the frequent 'lean' times, and who had the appetite to consume as much as possible when their hunts  were successful. It was also vital for them to be able to escape any predators themselves, so fleetness of foot was essential. This has left many of us us with a legacy of a strong appetite, a low  resting metabolic rate, and a need to exercise regularly - all of which are completely out of tune with the way modern society and its commercialism now encourage us to live.

As a result, our largely sedentary 21st century existence, lack of the incentive to exercise, and a high intake of heavily-processed and calorie-rich food, all conspire to set up an imbalance between energy input and output. It can also compromise our gut health through lack of 'roughage' in the diet. Our busy lifestyle also often mitigates against getting enough exercise to burn off the excess calories we all consume. GLP-1 agonists have started to make inroads in the worst cases, but can only reduce appetitie temporarily, and have undesirable side-effects.

Why can't we just adopt a 'healthier ' diet, and eat less ? ,  you may ask. 

Sadly, such a diet, rich in fresh  fruit and vegetables, is usually a more expensive option and is now simply beyond the means of some of the poorest in our society, where the UK's obesity epidemic is the most prevalent. The food industry has hitherto promoted 'fast' foods high in carbohydrate & fat and these tend to be cheaper and more readily available than healthier alternatives. Although there are some signs of change, this is a slow process, and hasn't been helped by the cost of living crisis.

Another problem  is that hypertension, atherosclerosis and obesity are 'silent' killers, since they are often asymptomatic until a life-threatening problem occurs. And they affect all levels of society - no one is immune. Even if you do notice you're starting to feel 'a bit less healthy', the temptation is to carry on and adjust. The male of the species  is particularly resistant to consulting its GP, and often uses the chronic problem of getting an appointment, and the desire 'not to bother them' as an excuse to stay away. I know - I've been there...

There's no doubt that early diagnosis of any abnormalities that do appear will pay dividends in later life. Continued monitoring will help ensure the advantage is maintained in later years, and is likely to prolong 'good quality' life. 

This does mean putting some effort into the monitoring process, of course, but a lot can be done by the individual to assess and improve their own health. 

This 'self-assessment' process is particularly important at a time when the UK health service is under severe strain, with both GP and dental appointments now 'like gold dust' and often only available many months after you really need them. The NHS is now actively promoting 'self help' and GP practices are introducing more 'holistic' medical strategies to encourage this, in an attempt to reduce GP workloads and improve outcomes. Recent attempts to compel GPs to offer urgent appointments online to eliminate the '8.30 phone scramble' have had limited excess - the sad truth of it is that we haven't trained enough doctors over the past 2 decades, and those still working in the NHS are either retiring early, emigrating  or defecting to the private sector for better salaries.

What can I do myself ?

You can help maintain good health by generating your own blood pressure, heart rate and BMI readings at home. You can do this easily and with a minimum of equipment.

Cholesterol and blood glucose testing is widely available in pharmacies. It's often included in routine GP health screens, particularly in the older age groups. By monitoring all these key health parameters, and acting on them where necessary, you can do much to reduce your risk of poor-quality life with chronic illness in old age and prevent a premature death.

Childhood obesity is also a particular worry just now, since it has already reached near epidemic proportions in UK, and spells real trouble ahead for tomorrow's teenagers and adults. Bad dietary habits are most easily established (and broken!)  in early childhood. If you are a parent, check out your child's status now - it may save them (and you !) from much angst in later life.

Download the Health Checker app (Health_Check.xlsx) to find out how  best to generate and interpret your data. The assessments and recommendations are based on current NHS guidelines, and links to these and a BMI calculator designed specifically for children are provided within the app. Apart from the links I've provided  to NHS web pages, the calculator is entirely offline and your data is therefore kept confidential.

Always consult your GP if you have concerns about any of the results, and before considering any self-treatment.

Statins – The Good, the Bad and the Ugly

Many of us find ourselves prescribed one or other of the Statins by our GPs nowadays, often as a result of a routine health check.

But are they really necessary, and what are the risks of taking them ?

In this article, we’ll try to explain exactly what the statins are, how they work, and why the medical profession are so keen on prescribing them for us ‘en masse’.

I’ll start with the ‘why’, to try to put the need for these drugs into context….

Our modern diet is rich in carbohydrates and fats, and often takes the form of highly processed ready meals, which also contain a lot of salt. The problem is that this type of ‘challenge’ to our digestive systems on a continuous basis is an issue – our guts, brains and metabolism simply weren’t designed for it.

The explanation for this mismatch is relatively simple. For the vast majority of our evolutionary history, food was scarce, and whatever came along had to be pounced upon and used to the full…otherwise we simply starved. Our digestive systems and metabolism evolved to cope with this ‘boom and bust’ cycle, such that those with the biggest appetites and the best hunting skills got the most food, were best able to make good use of it to keep them and their offspring alive, and were therefore the most likely to survive and reproduce.

The profusion of cheap and calorie-rich food that is now available to us is a very recent event in evolutionary terms (effectively only the last 75 years since the end of WW2). We were never designed to live with a continuous surplus of this sort, and our sedentary existence, increasingly spent peering at computer screens for long periods nowadays, merely compounds the problem by not allowing us to ‘burn off’ the excess calories it delivers (neither has it helped our eyesight, with myopia already at epidemic proportions).

One of the most noticeable direct consequences of this is another ‘epidemic’… of obesity. This is particularly worrying in that it has also spread to our kids, thus affecting their health prospects. The increasing demand for the new GLP-1 therapies shows that we all want to get thinner, but in many cases our appetites are preventing us from doing so without medical help.

Both government and our healthcare professionals are becoming increasingly worried about the problem, not least because of the huge drain on NHS resources obesity and type 2 diabetes and their consequences present.  The increasing number of affected individuals who are signed-off as permanently unfit for work as a result of obesity- and diet-related  health conditions also contribute yet more to the benefits bill, which is adversely affecting our economic prospects…..and their mental health.

But there is a less obvious, but more direct threat to our health from our ‘bad’ dietary habits and lifestyles in the form of excess blood lipids.

To explain how this happens, let’s first take a look at some basic biochemistry. We all carry fats around in our blood circulation in various different forms. This is to allow these important energy-rich ‘fuels’ to be moved between the our gut where the food is absorbed to the sites where they are either processed and stored, or used to ‘power’ our life processes.

Fats, along with carbohydrates are the principal fuels we all need to stay alive. If we have too much of them in our blood, however, we run the risk of our blood vessels ‘furring up’ with so-called ‘plaques’ of lipid related material. This process is similar to what happens to water pipes and the inside of our kettles in hard water areas, where calcium and other insoluble salts in the water precipitate out and coat the inside of our pipes and our heating elements.

If this is allowed to continue, eventually one or more of our key arteries or veins will become partially or even completely blocked, cutting off the flow of glucose and oxygen to the tissue it supplies. If this happens in the coronary arteries, part of the heart muscle will die, and our heart may stop altogether. If it happens in the brain, it can cause a stroke, with loss of function to the area affected. Both of these events are potentially fatal, and may occur without warning.

Modern diets, unfortunately for us, are rich in the very agents that encourage high lipid and glucose levels in the blood, and therefore drive the furring-up process. There is a known strong correlation between high lipid levels and risk of heart attack or stroke; Type 2 diabetes is associated with high glucose levels, and the condition produces blunted responses to a carbohydrate-rich meal, with higher than ideal peak blood glucose levels as a result. Diabetes has many unpleasant consequences, and can result in poor circulation and even blindness if not treated.

Hence the desire on the part of our clinicians to screen for high blood lipid levels, and recommend therapies to reduce them if they are deemed to be too high. Many  of us do have raised lipid levels (the UK population mean for Total Cholesterol is around 6.7 mmol/l, whereas the ideal range is below 5.0 mmol/l), so most patients registering with a new GP practice are offered a blood test at which time a lipid profile sample is usually taken. This test may also include HbA1C, which is form of haemoglobin known to give an indication of our ‘exposure’ to glucose over time, and assess the risk of our developing Type 2 diabetes.

What do we mean by a lipid ‘profile’, and what is its significance ?

As already mentioned, fats are carried around the bloodstream in various different forms – usually associated with more soluble molecules such as proteins to ensure they don’t clump together and block our blood vessels. Cholesterol is an important endogenous precursor of the bile acids involved in digestion, and of steroid hormones such as oestradiol and testosterone. The ‘standard’ lipid profile will measure ‘Total’ Cholesterol, as well as Triglycerides and High- and Low-Density Lipoproteins (HDL and LDL). HDL and LDL are large soluble fat-protein complexes, and LDL in particular has a tendency to drive plaque formation and has thus acquired the moniker of ‘Bad’ cholesterol.

If you’ve recently had a lipid profile done, you should be able to access your results through the NHS smartphone app or via SystmOnline – you can check out the data and what it means using the Health.xlsm Excel app, which you can download here. The Excel app also provides interpretation and advice on BMI and blood pressure, and explains what we can all do at home with minimal equipment to monitor our own health. All the figures used are based on NHS recommended values.

If, as is quite likely, you have a total cholesterol value above the idealised threshold of 5.0 mmol/l, and /or a LDL value much above 3.0 mmol/l, you may be recommended to start on one or other of the statins. This is particularly likely to happen if you are deemed to be ‘at high risk’ of cardiac ill-health for other reasons.

What are Statins ?

Statins are a class of drug designed to reduce lipid levels, in particular the ‘bad’ form of blood cholesterol (i.e. LDL). Contrary to what you might expect from their class name, they are not just designed keep them static. They achieve a reduction by altering cholesterol metabolism such that less of it is produced by the liver. To understand this fully, we need to delve into a bit more biochemistry and look at how lipids in our food are absorbed and transported, and how this ties up with how they are used by the body, and ultimately, disposed of.

Human Lipid Metabolism

As discussed, lipids are key to our existence, and serve many functions, not simply acting as fuels to provide us with energy. Lipid metabolism encompasses the digestion, absorption, transport, synthesis, and breakdown of fats to provide energy, and produce structural components for our cells and tissues, and important signalling molecules.

Lipid metabolism involves a complex set of biochemical processes that allow the body to utilize fats from dietary intake or stored fat reserves. Lipids, including triglycerides, cholesterol, fatty acids, and phospholipids (see figure 3 for structures), serve as energy sources, components of cell membranes and precursors for steroid hormones. The body regulates lipid metabolism tightly so as to maintain energy balance and prevent disorders such as dyslipidemia, fatty liver disease, and cardiovascular disease.

Digestion and Absorption

The process begins in the digestive tract, where dietary fats are emulsified by bile salts from the liver, increasing the surface area for enzymatic action. Pancreatic lipase hydrolyzes triglycerides into monoglycerides and free fatty acids, while cholesterol esters are de-esterified into free cholesterol. These digestive products form micelles, which transport the lipid products to the intestinal epithelial cells (enterocytes) for absorption into the circulation. Inside enterocytes, fatty acids and monoglycerides are re-esterified into triglycerides and packaged with cholesterol and proteins into chylomicrons, which enter the lymphatic system before reaching the bloodstream.

Transport and Storage

Because lipids are hydrophobic (i.e. don’t mix with water on their own), they require combination with proteins for effective and safe transport in the blood. Chylomicrons are the ‘first line’ lipoproteins, which facilitate absorption of dietary lipids in the gut, while very-low-density lipoproteins (VLDL) and low-density lipoproteins (LDL) are effectively circulating transporters, which move endogenous triglycerides and cholesterol from the liver to peripheral tissues.

High-density lipoproteins (HDL) mediate reverse cholesterol transport back to the liver for reprocessing. Triglycerides are stored in adipocytes, and in muscle cells as an energy reserve, while cholesterol is incorporated into cell membranes or used for steroid hormone synthesis. As discussed, LDL is the ‘villain of the piece’ when it comes to blood vessel plaque formation, and is therefore the primary target of statin therapy.

Lipid Breakdown

Stored triglycerides are broken down through lipolysis, releasing free fatty acids and glycerol when energy is needed. Fatty acids undergo beta-oxidation in mitochondria and peroxisomes, producing acetyl-CoA, which enters the citric acid cycle to generate ATP, which is the universal ‘energy currency’ of our cells. During prolonged fasting or carbohydrate restriction, acetyl-CoA can also be converted into ketone bodies in the liver, providing an alternative energy source for the brain, heart  and muscles.

Lipid Biosynthesis

Lipogenesis is the synthesis of fatty acids and triglycerides from excess carbohydrates or proteins. This process occurs primarily in the liver and adipose tissue. Cholesterol is synthesized via the mevalonate pathway (Figure 2) and is essential for membrane structure, bile acids, and steroid hormones. Phospholipids are produced for cell membranes and signalling functions.

Regulation and Clinical Significance

Lipid metabolism is regulated by hormones such as insulin, glucagon, and epinephrine, which control lipogenesis, lipolysis, and beta-oxidation. Poor metabolic control can lead to so-called dyslipidemia, characterized by elevated LDL, low HDL, and high triglycerides, and this contributes to atherosclerosis and cardiovascular disorders. Non-alcoholic fatty liver disease (NAFLD) and metabolic syndrome are also linked to impaired lipid handling and insulin resistance.

Where do the statins fit in ?

Now we’ve looked in more detail at general biochemistry  surrounding the way we handle the fats in our diet, we can focus on how statins work. The statins as a drug class are inhibitors of one of the key enzymes in the lipid biosynthesis pathway, HMG CoA reductase. Figure 1 shows a schematic diagram of the various different lipoprotein forms and the way in which their synthesis is achieved in the liver. By inhibiting this key biosynthetic pathway early on, it is possible to reduce the amount of cholesterol produced, and hence the amount circulating in the blood, without causing harmful accumulations of other precursors, or affecting other life processes. Provided removal of the lipid products that are produced downstream of the blockage, or via other pathways, continues as normal, the overall level of cholesterol in the blood should decrease as a result of statin therapy.

Therapy, Side Effects and Treatment Programs

Statins, once prescribed, are generally taken long-term or until treatment is discontinued for a specific reason. To maintain lower blood levels of Total cholesterol and LDL, a steady state level of the drug is needed to keep the restriction in place; if we stop taking it, there is a risk that lipid levels will rise again.

All drugs produce side effects if taken in sufficient quantities. The objective of therapy for any drug is to minimise the side effects while maximising the benefits of the drug. The statins, by interfering with a key step in lipid metabolism, do have significant side effects, ranging from common mild and transient ones such as headache and effects on the gut to (fortunately) much rarer ones such as severe allergic reactions and muscle damage. You’ll find a full list of side effects and reactions in the product leaflet supplied with each pack. With statins, side effects or often transitory, and disappear as the body adapts to the new challenge.

 Pharmacokinetics and drug dosing

One important feature of a drug’s behaviour we need to consider when deciding what dose to take is its pharmacokinetics (PK). This describes to the level of the active drug we find in the circulation after a dose, and will depend on how quickly it’s absorbed, and how rapidly it’s removed.           .

PK can be a complex subject, so I won’t bore the reader with details of that at present, but it’s useful to take a quick look at how a frequently prescribed ‘first line’ statin, Atorvastatin, is likely to behave after multiple dosing daily at the lowest dose of 10 mg; we’ll also see how this relates to its functional role in inhibiting HMG CoA Reductase in liver cells.

How often do we need to take Atorvastatin ? Using a simple one-compartment model, the blood concentration profile expected for the standard daily dosing regime at 10 mg is shown in Figure 5. Comparing this with the profile with 12 hourly dosing with 5mg, and we get a much less ragged profile with lower peaks and comparable trough values (Figure 6). Why then isn’t a 12 hourly regime recommended ?

The answer is 2-fold: 1) a 24 hourly dose is more convenient for the patient  and 2) What’s important here is the therapeutic ‘end point’ i.e the inhibition of the enzyme, rather than the blood level of the drug itself. Before the enzyme can be inhibited, the drug has to get from the bloodstream into the liver and find its way to the cells where cholesterol biosynthesis is going on. This takes time, as does the binding of the inhibitor to the enzyme, and by the same token, the dissociation from it. This will happen as circulating levels of the drug fall, since binding is reversible.

In practice the lags involved in drug distribution mean that a 24hourly dosing regime is adequate to keep the enzyme sufficiently inhibited to reduce blood levels of Cholesterol, triglycerides and LDL effectively without producing side effects at the peak concentrations.

Clinicians will normally start patients on a low dose (typically 10 mg for Atorvastatin) and work upwards, while monitoring for any side effects early on in the treatment program and testing for changes in lipid profiles over time (usually at 1 month and 3 months post first dose) to ensure the medication is  actually doing the job (and the patient is remembering to take the tablets!). The side effect profiles for different statins do vary, so in the event of Atorvastatin presenting with tolerability issues early on, there is also scope for switching to other statins. When starting a statin for the first time, it’s wise to start with the lowest possible dose and work upwards, to ensure any serious side effects are picked up early. If you do encounter problems when starting treatment, always report them to a pharmacy or your GP, and if necessary stop taking the medication while seeking advice if the side effects are severe.

Some other benefits of Statin therapy 

Apart from reducing the risk of blood vessel occlusion, the statins also have other beneficial effects, in particular on the heart. There is good evidence that they reduce cardiac excitability - anyone with a raised ventricular ectopic burden (i.e. more frequent 'missed' or 'extra' beats) may well find this is reduced or even disappears after they start statin therapy. Thus they can be a valuable adjunct to antiarrythmic therapy with cardioselective beta-blockers such as bisoprolol. They can also reduce the likelihood of further myocardial infarcts in patients already diagnosed with an MI.

The Importance of Dietary Control

One of the problems that emerges when a patient is prescribed statins after a sustained period spent attempting lipid lowering via dietary restrictions alone is the ‘relaxation effect’. Once on statin therapy, there is a temptation to resume one’s old ‘bad’ dietary habits, which were probably at least partly responsible for the high lipid burden once one has started taking statins. The reasoning is typically “..the statins will keep my cholesterol low whatever I eat, won't they, so I can have what I want now..”.

This is, unfortunately, a common misunderstanding of the power of statins to ‘cure all dietary ills’. They can’t, and we shouldn’t expect them to. They will only work properly if we maintain a ‘sensible’ balanced diet with minimal exposure to highly processed foods and plenty of fruit, vegetables and other roughage-containing foods. We should treat them as a valuable tool in reducing cholesterol exposure when we fail to do so by dietary restriction alone, not as a 'cure-all' for our dietary 'sins'.

This admittedly rather disappointing reality does generate other benefits, though. A balanced diet won’t just improve our heart and circulatory health by preventing the effects of atherosclerosis, but will help control obesity and blood sugar levels, both of which contribute to development of type 2 diabetes and all its associated ills. The harsh reality is that if you want a longer life with minimal ill-health, particularly in your final years, a sensible diet and control over blood glucose and lipid levels is a must.

Non-dietary alternatives to statins

If for some reason you’re unable to tolerate effective doses of one or other of the statins, and find it impossible to reduce your lipid levels by dietary control alone (as unfortunately do many people who try it) all is not lost. Here is a brief list of the alternative options:

* Ezetimibe (Zetia) – Reduces cholesterol absorption in the small intestine, lowering LDL by about 20% and can be combined with other therapies for greater effect

* Bempedoic Acid (Nexletol) – Works in the liver to reduce cholesterol production, lowering LDL by 20–25% with fewer muscle-related side effects than statins.

 *   Combination Pills – Ezetimibe with bempedoic acid (Nexlizet) or with simvastatin (Vytorin) can reduce LDL by 40–60%.

  *  PCSK9 Inhibitors – Injectable drugs like alirocumab (Praluent), evolocumab (Repatha), and inclisiran (Leqvio) enhance liver clearance of LDL cholesterol, offering substantial reductions, especially for familial hypercholesterolemia.

   * Bile Acid Sequestrants – Medications such as cholestyramine bind bile acids in the gut, prompting the liver to convert more cholesterol into bile acids, lowering LDL levels that way.

* Fibrates – Drugs like gemfibrozil primarily lower triglycerides but can modestly affect LDL and HDL cholesterol.

Please note that most if not all of these are prescription medicines in UK, so will need to be discussed with your GP before you can obtain them.

Final Thoughts

In this brief review of the statins, we’ve tried to explain how statins can be used as a ‘therapeutic management tool’ to keep our lipid profiles healthy and prevent serious damage to our blood vessels, with all that implies. We’ve also looked at some basic biochemistry, to provide the background for explaining how the statins actually work, and considered briefly how the drug is handled by the body and how this relates to dosing.

We’re all living longer, sadly without making much impression on the ageing process, and this is placing ever increasing pressure on the NHS. We really need to be more proactive in managing our own health – the lack of availability of GP appointments isn’t likely to be remedied soon, so the more we can do to prevent chronic illness, and the need to see our GPs, the better. There’s a lot we can do to monitor our own health – take a look at the Excel app, which you can download using the link above, to find out more about what you can do at home, and how to interpret your GP test results.

First published: 22.7.26

Figure 1:  Chemical Structures of Key Lipids 

Figure 2:Structure of Atorvastatin 

Figure 3:Mevalonate pathway and the effect of Statins 

Figure 4: Statins and Lipoprotein Production in the Liver 

Figure 6: Atorvatstatin blood PK multi-dose 12h 5mg