Medication use is very common, with many people taking multiple regular prescription medications on a daily basis. For those not regularly involved with medications, it can be an overwhelming and scary topic! It’s also a question present on many client screening questionnaires.



The purpose of this article is to give you an introduction to some of the most common medications you will come across with your clients, and discuss the implications (if any) on body transformation/composition, nutrition, and physical performance.

This is by no means intended to replace the advice from your clients’ doctor/s and or pharmacist; it is simply an introduction and guide. Throughout the article we will discuss six basic ‘classes’ of medications, sticking to a basic formula which will cover the following.
  • What is it called?
  • What does it do?
  • How does it do it (in broad terms)
  • Implications

1. Medications used to treat high blood pressure and heart disease.

Within this class we will cover a few common medications, namely the so-called ACE inhibitors, calcium channel blockers, and beta blockers. These are some of the most common medications you will come across – ACE inhibitors are the first line pharmacological treatment for high blood pressure in Australia.

Angiotensin converting enzyme (ACE) inhibitors block the actions of so-called angiotensin converting enzyme, with the end result being lower blood pressure with slightly lowered salt and fluid retention. Common examples include ramipril, perindopril and captopril. Common trade names include Coversyl® and Tritace®. ACE inhibitors are common, safe, and effective. They are also used in patients with diabetes, as they help protect the kidneys from diabetes induced kidney damage.

Calcium channel blockers (CCB’s) are another rather common medication used to treat high blood pressure and some other cardiovascular diseases. They reduce the amount of calcium that can enter the muscle cells of the heart and blood vessels. This ultimately relaxes blood vessels, which reduces blood pressure and therefore the workload on the heart. There are different types of CCB’s, however this is beyond the scope of this article. Examples of common CCB’s include amlopidine, nifedipine and verapamil.

ACE inhibitors are available as stand alone medications, with some also available in combination with calcium channel blockers. Coveram® is an example of the latter – perindopril and amlodipine. They are often used in combination to treat high blood pressure that is not responding to a single medication.

Beta-blockers

Beta-blockers are an older class of medication, but still very common and very effective in some conditions. There are multiple types with various modes of action. Beta-blockers can be used to slow heart rates, reduce blood pressure, and reduce tremors in some cases. Metoprolol, bisporlol, carvedilol and atenolol are a few examples of beta-blocking medications. They achieve their results by ‘blocking’ the actions of so-called beta receptors – receptors located in various regions of the body that are responsive to adrenaline.




Implications of ACE-I’s, CCB’s, and beta-blockers.

ACE inhibitors and CCB’s will generally have no discernable effect on transformation, nutrition or performance. Some beta-blockers may potentially reduce exercise performance by reducing heart rate and therefore cardiac output – the amount of blood pumped by the heart. Many patients also complain of fatigue and lethargy due to beta-blockers, however this is a side effect that many become accustomed to.

Essentially all patients are vulnerable to fat gain and impaired fat loss when taking beta-blockers. There have been numerous studies supporting this, with a variety of mechanisms proposed (see below). Ensuring your clients nutrition is based on their metabolic classification can go a long way to counteracting these mechanisms. Keep in mind however, that even with nutrition and exercise that are matched ideally to the client, they may still experience increased difficulty in achieving their goals.

Potential Mechanisms of β-Blocker–Associated Weight Gain
  • Reduction in resting energy expenditure
  • Reduction in the thermic effect of food
  • Reduction in exercise tolerance
  • Increase in tiredness
  • Reduction in nonexercise thermogenesis
  • Inhibition of lipolysis
  • Exacerbation of insulin resistance

Proton pump inhibitors (PPI’s).

These are another very common class of medication, and they are sued to prevent and treat heart burn/gastric reflux, and to allow gastric ulcers to heal. In 2006, global expenditure on PPI’s was estimated to be around $USD 26 Billion! PPI’s essentially turn down gastric acid production. Losec® and Nexium® are common examples; omeprazole and esomeprazole.

There continues to be much debate in the medical community about the long term impact of PPI’s on nutrition. On one hand there is a suggestion that long term treatment can lead to deficiencies in Vitamin B12, iron, calcium and magnesium due to impaired absorption.

Certain vitamins, minerals and nutrients are absorbed more readily in an acidic environment, and with PPI’s reducing acidity this has been proposed as the mechanism. However there are an almost equal number of studies that did not support these claims. At this stage, PPI’s appear to be a safe and effective way to manage reflux and ulcers.

Regardless of whether they are at an increased risk of B12, iron, calcium and magnesium absorption clients on these agents should be ensuring adequate intake of all of their FEON’s.

PPI’s do not have any effect on exercise or sport performance.

The ‘statins’

The ‘statins’ as they are known are used to treat elevated cholesterol levels. Technically, they inhibit an enzyme called 3-hydroxy-3-methyl-glutaryl-CoA reductase, commonly abbreviated to HMG-CoA reductase. HMG-CoA is an important enzyme in the synthesis of cholesterol; statins block its activity.

Statin use is common, with an estimated 2 million patients in Australia taking them regularly. Common examples include Crestor® (rosuvastatin), Lipitor® (atorvastatin), and Pravachol® (pravastatin). There are other classes of medications also used in the management of cholesterol, however the statins are by far the most common.




In terms of their effects on body composition/transformation, nutrition and exercise performance, statins are a bit of a mixed bag.

Let me explain.

There are mountains of research on the topic of ‘statin induced myopathy’. There is a suggestion that up-to 20% of patients taking statins will develop muscle pains and/or weakness. This can vary from minor ‘niggles’ all the way through to potentially life threatening rhabdomyolysis – the destruction of muscle fibres that leads to myoglobin being released into the bloodstream.

Regardless of the severity, statin myopathy is common and is the reason many people stop taking statins, or are changed to a different type of medication. Even for those on the less severe end of the spectrum, muscle fatigue and weakness may be minor, but enough to have noticeable effects on exercise performance. Keeping this in mind during exercise programming and execution can be very helpful.

From a metabolic perspective, adhering to the principles of MP may actually decrease the need for statin therapy for some clients. In particular, optimising the omega-3 levels and omega-3 to omega-6 ratio can be a powerful lipid lowering intervention. It is worth keeping in mind however that there is a significant genetic component in deranged cholesterol levels, and for some, despite ‘doing everything right’ they will still require medication to optimise levels.

There is a small risk that statins may contribute to the development of type 2 diabetes, however this seems to be most relevant to patients at high risk of cardiovascular disease. By association, many of the factors placing these patients at risk of heart disease also dramatically increase their chance of developing diabetes. Regardless of associations, the benefits of statins for reducing the occurrence of heart attacks and strokes far outweigh any risk.

Warfarin

Warfarin is not an especially common medication, but at the same time, it’s far from rare. It is a class of medication called an anti-coagulant, meaning it reduces the bloods ability to form clots. Clots that form in the blood can sometimes travel and become lodged in other parts of the body, such as the brain and lungs, causing a stroke or pulmonary embolism respectively.

Atrial fibrillation (AF), a condition in which the top two chambers of the heart beat in a chaotic and irregular condition can increase the risk of clot formation, and is therefore a common reason why some patients are commenced on warfarin. Other reasons include mechanical heart valve replacements, and after deep vein thromboses (DVT’s) or pulmonary embolisms.

Warfarin works by decreasing the amount of Vitamin K that can be fed into metabolic pathways that produce ‘clotting factors’. Clotting factors are substances in the blood that are fed into pathways in specific sequences to help form blood clots. Some of these clotting factors require Vitamin K for their synthesis, and this is where warfarin exerts its action.

Warfarin dosing is tricky and complex – give too much and patients can bleed to death from small wounds or a bump to the head; give too little and you may as well not be using it! Given this, patients require at least a monthly blood test whilst on warfarin therapy.

When it comes to exercise performance, warfarin has no direct effects. However, the underlying reason why a patient is taking warfarin may impact exercise performance. As an example, a patient may have developed left ventricular failure due to a stenotic (partially blocked) aortic valve. After having this replaced, he/she may be on warfarin, and the clients exercise capacity is likely to be limited by pre-existing heart failure.

Nutrition and supplementation for clients taking warfarin

This is an important topic. Patients are often advised to limit their Vitamin K intake. Vitamin K is found in rich supply in many green vegetables. This is perhaps not the greatest advice, and is somewhat opposite to what MP encourages. Never fear, there is a solution!

A generally accepted position is that it's not so much the total daily vitamin K intake that causes issues, but it's more if people are varying their vitamin K intake from day to day that issues come about. If you can manage to keep a relatively constant level of vitamin K in a clients plan, then their dose of warfarin can be adjusted accordingly.

It can mean using a slightly higher dose of warfarin than may have otherwise been required, and once the INR is stable, if the vegetable intake is stable, there shouldn't be any major issues. The concern is that eating 'too many vegetables' can counteract the warfarin through increased vitamin K levels. Whilst this can occur, if levels are kept relatively stable it should be fine.

MP Members: Download Vitamin K content of common foods

There is an extensive list of medications, both prescription and over the counter (OTC) with which warfarin has interactions – some increase its action, others decrease it. Some vitamin/mineral and herbal supplements can also interact significantly with warfarin (see below). The point here is to always check with your clients’ doctor and pharmacist before making any changes to their nutritional or supplementation regimen. Warfarin can be scary, even for professionals – don’t hesitate to ask for professional help, I really can’t over state this enough!



Antidepressants

Another very common class of medications, which reflect how common depressive and anxiety disorders are. Current data suggest that antidepressants are in the top four most commonly prescribed medications in Australia – statins, PPI’s and blood pressure meds making up the other three.

Similarly to cardiovascular medications, there are many classes and variations of antidepressants, however some of the more common agents include.
  • Pristiq® (desvenlafaxine)
  • Zoloft® (sertraline)
  • Avanza® (mirtazapine)
  • Lexapro® (escitalopram)

Regardless of their class, most antidepressants work by helping the brain restore the balance of the chemical messengers serotonin and noradrenaline - these can become out of balance in depressive and anxiety disorders. Some agents work on serotonin, where as others work on both serotonin and noradrenaline.

Many antidepressants disrupt glucose metabolism to varying extents, and this is both interesting and highly complex. There is significant overlap and interplay between the pharmacological effects of antidepressants and the metabolic effects of depression. Either way, weight gain is not uncommon.

Some antidepressants contribute to hyperglycaemia (high blood sugar levels), whilst also worsening insulin function and impairing nutrient partitioning. Antidepressants are also capable of inducing states of carbohydrate craving and increased appetite, via their effects on dopamine, serotonin and histamine receptors in the brain.

With newer antidepressants however, weight gain and appetite stimulation is less of an issue. The exception to this is Avanza® (mirtazapine), which is a moderately potent appetite stimulant, and often prescribed for this purpose alone in some patients. There continues to be a complex interplay between psychobehavioural and physiological factors in patients undergoing treatment with antidepressants. There is no solid research available that has detected the exact mechanism by which antidepressants alter glucose and lipid metabolism.



Whether or not a client is taking antidepressants, adhering to MP nutrient timing rules will ensure optimal glucose metabolism and insulin function. Many patients complain of stomach upset, cramps, bloating and diarrhoea due to their antidepressants, however this is generally in the first week or so of treatment so is unlikely to be a long term issue.

When it comes to exercise performance, some clients may experience a degree of lethargy and tiredness due to their medication. Again, many adapt to this and it ceases to be an issue. Exercise has been clearly shown to improve neurotransmission and neurological function, and in itself forms a vital aspect of the management of mental illness. See my article Exercise, Nutrition and mental health – is there a link?

Summing up

A short message to those undertaking their MP Transformation whist on any of these medications. Yes, obviously, the medications we’ve discussed here can affect physiology, metabolism and possibly results from exercise.

However, for the next 12 weeks here’s what I’d like you to do…

Instead of worrying about limitations, commit to your trainer and the MP program. In my experience, when people commit totally, they always exceed their best expectations.

Keep in mind that adhering to the principles of MP over time will not only lessen the metabolic effects of common medications, but can also reduce the requirement for some clients. Don’t forget, Success is a process, a journey; not a destination.

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Dr Doug Blomeley is our resident medical practitioner. He lives the MP lifestyle read more from Doug here.

References

Ali, T., Roberts, D. N., Tierney, W. M. (2009). Long-tem safety concerns with proton pump inhibitors. The American Journal of Medicine, 122, 896-903.
Das, U. N. (2002). Estrogen, statins, and polyunsaturated fatty acids: similarities in their actions and benefits—is there a common link? Nutrition, 18(2), 178-88.

Durrington, P. M. (2010). The effects of statins on skeletal muscle strength and exercise performance. Current Opinion in Lipidology, 21(4), 324-28.

Gullestad, L., Birkeland, K., Nordby, G., Larsen, S., & Kjekshus, J. (1991). Effects of selective 2-adrenoceptor blockade on serum potassium and exercise performance in normal men. British Journal of Clinical Pharmacology, 32, 201-7.

Lainscak, M., Keber, I., & Anker, S. D. (2006). Body composition changes in patients with systolic heart failure treated with beta blockers: A pilot study. International Journal of Cardiology, 106(3), 319-322.

Lee, P., Kengue, A. P., Greenfield, J. R., Day, R. O., Chalmers, J., & Ho, K. K. Y. (2011). Metabolic sequelae of β-blocker therapy: weighing in on the obesity epidemic? International Journal of Obesity, 35, 1395-1403.


McIntyre, R. S., Soczynska, J. K., Konarski, J. Z., & Kennedy, S. H. (2006). The effect of antidepressants on glucose homeostasis and insulin sensitivity: synthesis and
mechanisms. Expert Opinions on Drug Safety, 5(1), 157-168.


Sataar, N., Preiss, D., Murray, H. M., Buckley, B. M., de Craen, A. J. M., Seshasai, S. R. K., et al. (2010). Statins and risk of incident diabetes: a collaborative meta-analysis of randomised statin trials. The Lancet, 375(9716), 735-42.

Sharma, A. M., Pischon, T., Hardt, S., Kunz, I., & Luft, F. C. (2001). Hypothesis: β-Adrenergic Receptor Blockers and Weight Gain, A Systematic Analysis. Hypertension, 37, 250-54.





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