What actually happens is that the cholesterol laden LDL ship gets torpedoed by either too much sugar or too many oxidants (think lack of fruit, veg and antioxidants or smoking). This damaged ship doesn’t look right and, consequently, the immune system’s macrophages, patrol cells which act like vacuum cleaners, gobble up the damaged cholesterol particles. The resultant vacuum cleaner bag, full of damaged cholesterol, is called a ‘foam’ cell and that’s what you find in atheromas, the fatty laden blockages in arteries.
That’s why this study found that the level of sugar-damaged or ‘glycosylated’ LDL and blood levels of glucose or the long-term measure of sugar damage called HbA1c (glycosylated red blood cells) were the best predictors of heart attack risk. The study described these as of ‘high importance’ in the development of heart disease2. Other studies have found that oxidised LDL is also a good predictor3 but this wasn’t measured in this study.
But atheromas, that is dumping points for foam cells full of damaged cholesterol, don't just happen anywhere in the artery wall. They are more likely to occur in weak spots damaged by too much homocysteine. In the absence of sufficient B vitamins blood homocysteine levels rise and the homocysteine damages arteries. Two thirds of deaths from heart attacks in older people are predicted, not by their cholesterol level but by their homocysteine level.4
Whether or not a bulging atheroma is going to lead to a total blockage, which triggers a heart attack, depends on two other factors. How thick the blood is and how narrow the arteries are. Blood thickness depends on two things: omega-3 fats and the B vitamin niacin.
Omega-3 fish oils are so effective blood thinners that, when Sir Hugh Sinclair from Cambridge University tested the effects of eating nothing but seal meat he found that cuts took longer to stop bleeding. That is one of the main reasons why omega-3 fats reduce heart disease much better than statins and always win in head-to-head trials. However, recently the power of omega-3 has been cleverly downgraded. Statins interfere with the function of omega-3 so recent studies giving omega-3 or placebo to people already on statins have shown much less benefit than earlier trials giving them to people not on statins.
The other way to get better flow through the arteries is to relax the arterial muscle. This happens when there’s more magnesium in the surrounding muscle cells and less calcium. Supplementing magnesium, rich in greens, seeds and nuts, is one of the most direct ways to lower blood pressure.5 But it’s not patentable and hence profitable. Instead, patentable ‘calcium channel blocker’ drugs achieve the same goal, but with more profit and more side-effects. Another arterial relaxant is nitrate, rich in beetroot and greens.
So there you have it. The real cause of most heart attacks is a combination of too much sugar and/or not enough antioxidants such as vitamin C, coupled with a lack of magnesium, nitrates and omega-3, and a raised homocysteine level. Eat a whole, low GL diet with seafood and plenty of vegetables, and supplement B vitamins (often older people need a lot more B12 due to poor absorption) and you’re not going to get a heart attack.
Even if you do have high LDL cholesterol the best drug to lower it is niacin6 (vitamin B3), which also stops blood platelets sticking together, thus ‘thinning’ the blood. It also raises HDL levels.7 Having a high cholesterol in the blood is a marker for heart disease, not a cause. The more damaged it becomes the more it accumulates, but it is the damage by sugar and oxidants, not the cholesterol itself, that indicates you’re on the road to a heart attack.
1. A. Sachdeva, et al., ‘Lipid levels in patients hospitalized with coronary artery disease: An analysis of 136,905 hospitalizations in Get With The Guidelines’ American Heart Journal, 2009 Jan;157(1):111–117.e2
2. W. Luo et al., ‘Study on the levels of glycosylated lipoprotein in patients with coronary artery atherosclerosis’, Journal of Clinical Laboratory Analysis (2018), vol 12:e22650.
3. J.Watt ‘The relationship between oxidised LDL, endothelial progenitor cells and coronary endothelial function in patients with CHD.’ Open Heart. 2016 Jan 28;3(1):e000342. doi: 10.1136/openhrt-2015-000342. eCollection 2016 ; see also M. Linna et al., ‘Circulating oxidised LDL lipids, when proportioned to HDL-c, emerged as a risk factor of all-cause mortality in a population-based survival study’ Age Ageing. 2013 Jan;42(1):110-3. doi: 10.1093/ageing/afs074.
4. W. De Ruijter, et al., ‘Use of Framingham risk score and new biomarkersto predict cardiovascular mortality in older people: population basedobservational cohort study’, British Medical Journal, 2009 Jan 8;338:a3083
5. B. Altura and B. Altura, ‘Magnesium in cardiovascular biology’, Scientific
American, 1995 May/June;28–36
6. M. Chapman et al., ‘Niacin and fibrates in atherogenic dyslipidemia: pharmacotherapy to reduce cardiovascular risk.’ Pharmacol Ther. 2010 Jun;126(3):314-45. doi: 10.1016/j.pharmthera.2010.01.008.