There are a lot of misconceptions and debates about heart disease, its outcome and risk factors. But one thing that experts seem to agree on is that people with metabolic disorders, like obesity and type 2 diabetes, are far more predisposed to cardiovascular complications than the average population.

To put this into perspective, a patient with type 2 diabetes in the UK is 56% more likely to die from a severe heart attack called ST elevation myocardial infarction. There is also a strong relationship between obesity and coronary heart disease risk factors.

However, risk tolerance varies from one person to the next and, as we will discuss later in this article, managing certain modifiable risk factors can help reduce the risk of bad outcomes.

Looking at the most nuanced scientific literature on cardiovascular disease, we have examined a number of recent compelling studies looking at the main drivers of atherosclerosis – one of the most common diabetes-related heart disease complication – and found that the atherosclerotic process is much more complex than it appears.

The development and progression of atherosclerosis leading to plaque accumulation in arteries is multi-faceted and involves many biological processes, hence a multitude of arguments put forth by physicians for how it all begins and the ways to address it.

When it comes to hypotheses for atherosclerosis, most of the research is also based on correlational data, so not all of them constitute valid actionable root causes per se.

Atherosclerosis is an obstructive disease leading to plaque accumulation prompting gradual narrowing of the artery, with the eventual impaired control of flow, plaque rupture and thrombosis.

There are multiple coincident factors that are implicated in the development and progression of metabolic syndrome-mediated heart disease. Atherosclerosis is a disease of compounding injuries involving multiple causative agents, so it’s important to understand the interaction and synergy between multiple factors.

A widely discussed theory, now refuted by most prominent scientists, is that heart disease is caused by too much “bad” LDL cholesterol and should therefore be the only target of therapy we need to worry about. But, recent lipidology papers argue that atherosclerosis is not a cholesterol-mediated disease, it is a lipoprotein-mediated disease.

One explanation given by researchers is that because atherosclerosis is caused by an inflammatory response to sterols in artery walls, and sterol delivery relies on lipoproteins – the vessels that carry cholesterol molecules – it is much better predicted by the number of lipoprotein particles than by the concentration of cholesterol they carry, which is what clinicians currently measure in a standard metabolic blood panel.

Available information on cholesterol and the root causes of atherosclerosis at large is so conflicting for patients who really want to understand this topic but are not familiar with the scientific terminology and/or who don’t have time to dig into the huge number of new studies published each week.

Atherosclerosis is a disease of (sometimes inevitable) compounding injuries involving multiple causative agents, but managing certain modifiable risk factors can help delay the onset of bad outcomes.

From a problem-solving perspective, and to paraphrase the Irish chemical engineer, Ivor Cummings, the best way to accurately measure heart disease risk factors, is to consider the interplay between the most direct modifiable driver of the issue and the most addressable factorto achieve acceptable solution.

The atherosclerotic process is believed to involve plaque accumulation that prompts the gradual narrowing of blood vessels, but it is important to understand that by the time that happens, many other probable pathologic processes have already happened. These other processes include apolipoprotein B particles-derived insulin resistance, and new research suggests that low vitamin D-induced inflammation may play a role.

Fortunately, we can prevent this cascade of events from occurring and increase the odds in our favour by focusing on modifiable risk factors.

Common prescriptive strategies (depending on the specific situation at hand and management of other comorbidities) involve modifications of hormones and lots of statin drugs, which possess effects doctors are still unsure about.

Last week, however, we looked at primary prevention of cardiovascular disease with a mediterranean diet, which received a considerable amount of attention from the scientific community as a promising dietary intervention for patients with pre-existing heart disease risks.

Atherosclerosis takes a long time to evolve, and involves many steps. The jugular question is when do we need to start treating patients and what this tells us about prevention?

It is up to each person and their doctor to determine how aggressively they want to confront cardiovascular disease risks but adopting a more health promoting diet, such as a low carb, plant-based diet, may be to some extent less risky than signing up for treatments we don’t fully understand the complexities of yet.

Not to mention that eating a more healthy diet can, if and when successful, (modestly but still) help reduce the NHS’s annual financial burden of over £100 million associated with the prescription (not limited to diabetes patients) of statins drugs.

Whilst the medical community still has more to learn about heart disease within people with diabetes, research is showing that it is possible for many of us to reduce the risk through healthy dietary methods which, if started soon enough, could reduce the need to take heart medications and the side effects that come with the drugs.

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