Combating my Lp(a) levels

You can read more about what Lp(a) is and why it is a concern for me in: Big10 #4 Monitor Your Heart Health

In summary, Lipoprotein(a) is a dangerous type of LDL which is controlled by genetics and does not respond to dietary changes or medications. I tested positive (moderate risk) for this. In this journal post I summarise my findings and conclusion from looking in this topic in more detail.

Strategies to reduce Lp(a) directly

From some reading I identified the following possible approaches to reduce my Lp(a) levels:

• High dose Niacin (B3) supplementation.
• Statins.
• PCSK9 inhibitors.
• Novel treatments that are currently going through approval.
• Apheresis (a technique to remove LP(a) from blood) which I quickly discounted due to high cost and invasive nature, making it only appropriate for high-risk patients).

Strategies for additional heart health to offset the extra risk from Lp(a)

From some reading I identified the following approaches to try and minimise the impact of the Lp(a) risk without actually reducing its level:

• Aspirin.
• Statins.
• Boosting my Omega-6:Omega-3 ratio.
• Try to drive LDL (apoB) and Triglycerides down even further by doubling down hard on healthy eating, sleep, low sugar, anti-inflammatory diet.
• A CTCA (CT Coronary Angiogram) scan to look for any evidence of soft plaque which would provide confidence if clear and further motivation if not (my prior coronary calcium scan was clear for hard plaque).

Statins research

What are statins:

Statins work by slowing down the production of LDL-cholesterol in the liver, where it’s made. Because the liver isn’t making so much cholesterol, it then takes cholesterol out of your blood to make bile with, so your blood cholesterol levels fall. Statins slow down LDL-cholesterol production by blocking an enzyme called HMG-CoA-Reductase – the medical name for statins is HMG-CoA Reductase inhibitors. Enzymes are proteins in the body which speed up normal processes. In this case, LDL production. The following statins are available in the UK:

• Atorvastatin
• Rosuvastatin
• Pravastatin
• Simvastatin
• Fluvastatin

Their utility for Lp(a):

It seems that Lp(a) is not responsive to statins, e.g. as illustrated in this meta study. In fact, Lp(a) may show a slight increase with statins e.g. as illustrated in this meta study

Suitability for me:

There may thus be a risk in using statins to assist driving down my LDL (which are good and could maybe be brought lower by natural means) since they may increase my Lp(a) which is my specific risk.

PCSK9 inhibitors research

What are PCSK9 inhibitors:

They are injected medications which are known as monoclonal antibodies, a type of laboratory-made protein that inhibits a protein called PCSK9, which is made in the liver. Research has shown that people with high levels of this protein tend to have high cholesterol throughout their lives and develop heart disease early, but people with low levels tend to have low cholesterol and a lower risk of heart disease. This discovery led to the development of PCSK9 inhibitors to lower cholesterol

Their utility for Lp(a):

PCSK9 inhibitors have been shown to reduce Lp(a) levels by roughly 20–30%, though they are not explicitly approved for high Lp(a)

Suitability for me:

I suspect this is too dramatic and intervention given my Lp(a) level, current good LDL etc. It’s an injectable treatment used for high risk patients or those who cannot tolerate statins.

Aspirin research

Aspirin’s utility for Lp(a) control:

Aspirin acts as an antiplatelet agent, making blood less “sticky” and inhibiting the platelet aggregation that Lp(a) accelerates. It thus reduces the risk of heart attack and stroke. Research, including studies using data from the Multi-Ethnic Study of Atherosclerosis (MESA), found that aspirin use was associated with a 46% reduced risk of coronary heart disease (CHD) events in individuals with elevated Lp(a) (>50 mg/dL or >125 nmol/L — depending on the unit used).

Studies suggest that for individuals with elevated Lp(a), the risk/benefit profile often favours the use of daily low-dose aspirin The risk here is stomach ulcers/bleeding which must be balanced against the benefit of daily low-dose aspirin.

Suitability for me:

Nothing in my blood pressure readings, calcium scan, or other LDL levels suggests any near-term risk of a cardiac incident. Given my healthy blood pressure, weight and diet, I would not be a candidate for long-term, low-dose aspirin due to the associated risk. The question is (like statins) is it worth the associated risk for the benefit?. I think not, but, if I had Lp(a) in combination with high blood pressure and/or elevated LDL (apoB) levels, this would be worth it.

High dose Niacin research

Niacin’s utility for Lp(a):

Niacin is one of the few agents known to significantly lower Lp(a) levels, which are generally resistant to statin therapy, with research indicating reductions by 20–30% and sometimes higher in specific cases. While effective for lowering Lp(a), niacin does not always improve cardiovascular outcomes and can cause significant side effects, including flushing, liver inflammation, and increased insulin resistance. I already take a high-quality source of Niacin (via the product Tru Niagen) as a stable, safe, tested precursor to NAD+ (for cellular energy and anti-aging). Specifically, what I take is Nicotinamide Riboside at the dose of 300mg/day (single tablet).

Suitability for me:

The cost of increasing the Niacin product I take by threefold would be too high, especially given the side effects (especially insulin resistance) and the lack of evidence that despite Lp(a) reductions, there is any reduction in CVD. Taking a cheaper product is likely to come with discomfort like flushing.

New treatments research

Two interesting treatments which aim to stop Lp(a) at the source rather than remove it from the blood are in the pipeline:

• Olpasiran
• Pelacarsen

Given that treatments to effectively silence my genetic risk are probably only a few years out, rather than making dramatic interventions, it seems smarter to try and further reduce my LDL (apoB test score) – via a scrupulous diet audit - and correct my ‘OK but not great’ Omega-6:Omega-3 ratio.

Omega-3 supplementation adjustment

My current Omega-6:Omega-3 ratio is 13.5:1, and a level of at least 4:1 would be the ideal. Despite switching from a generic vegetarian Omega-3 supplement to a high-quality algae-based one, I was only able to get my ratio down from 17.7 to the current score of 13.5.

Rather than doubling my current Omega-3 vegan algae oil supplement dose, I have decided to switch to a high-quality, high strength fish-based supplement and compare the effect: Bare Biology Omega-3 Fish Oil Capsules. One thing to be careful of with fish oils is that they can be high in vitamin A and D (when the fish liver is used). As vitamin A and vitamin D are both are fat soluble and can be damaging in excess, I’ve asked the supplier, and they confirmed they use only the flesh and not the liver, and there is no vitamin A or vitamin D in their products. At my last blood tests my vitamin D was right at the top of optimal, so I don’t want to go much higher. I’ve never had vitamin A tested, as Thriva doesn’t offer it, but at my next vitamin tests I’ll use a different supplier to check vitamin A as well as my other normal vitamin tests (just to be sure!). It is worth noting that different products have different mixtures of DHA (better for brain health) and EPA (better for heart health). Both are important, but in this context the EPA is crucial:

• My previous one a day (vegan algae oil) was: 300 mg DHA and 150 mg EPA
• This product (fish oil) is two a day giving: 500 mg DHA and 1,100 mg EPA (I would have had to take 7 a day of my previous supplement to get that much EPA!)

Why not tackle the other side of the ratio (Omega-6)? An audit of my diet shows that the sources of Omega-6 in my diet are all coming from healthy foods that I actively don’t want to reduce (e.g. nuts, seeds, tofu, avocado) and not from bad seed oils or processed food. Rather than trying to drive down Omega-6 by excluding foods that have a range of other benefits, I think it is better to ramp up on Omega-3. I’m not happy to be compromising on my ethical principles with this change to use a fish product – but it’s required in this case, and I’ve gone for a sustainably fished product to minimise the environmental impact of this change.

Food audit

If I don’t ’treat’ my Lp(a), I need to get my LDL down to even lower than the normal healthy range to make ‘headroom’ for the elevated Lp(a).

I already have a very healthy diet that is mostly free of processed foods and sugar and is high in gut-healthy, anti-inflammatory, anti-oxidant ingredients. But I already found a few culprits:

• Cheddar cheese (high in saturated fats) – sometimes (perhaps once a fortnight) I eat this as part of family meals. Removed this from my diet
• Vegetarian ‘brown food’ like sausages – rarely but sometimes as part of family meals
• I found palm oil in the ‘healthy’ microwave popcorn I like. Removed this from my diet
• 85% dark chocolate brand - I’ve been thinking of this as a healthy part of my diet but a bit of reading shows in reality it is high in saturated fat, is a source of sugar and adds little to the polyohenols I already get. Removed this from my diet
• The kefir I take is a full-fat version (contains saturated fat). I take enough pro-biotics and pre-biotics to skip this.
• I eat about two eggs a week – but the yolk is a source of saturated fats and I get plenty of high-quality protein elsewhere – so I can skip these.
• Occasionally I have coconut milk (high in saturated fat) - as part of family dinners. Skip the sauce for those meals.

Label ingredients to carry on looking out for:

• Partially hydrogenated oils
• Coconut oil, palm oil, and palm kernel oil
• Saturated fat
• Sugar

There’s more to do here – based on close ongoing monitoring of what I eat and what I cook with – but that’s a good start!

I guess that makes me a vegan who takes fish oil supplements!! Whatever that is!