Hacker News new | ask | show | jobs
by HamSession 2849 days ago
There are a lot of factors that can go into heart disease. Some of these factors are:

1. Under/over working out, especially for white men over working out can lead to increased shear stress on the arteries

2. Genetic familia hypercholesterolemia aka high cholesterol. This is caught by a blood test and fixed with statins.

3. High Blood Pressure again exams and medication

4. Size of ldl particles, this one is new

5. Genetic markers especially 9p21.3, sadly about a third of people have this marker. How it works we don't entirely know, but the best guess I've come up with is it has to do with interlukin

6 signaling which signals inflammation. Solution to this might be taking curcumin, lower weight, Mediterranean diet.

7. Low HDL again mostly genetic, niacin may help some as may exercise

From my research into the matter it seems that the initial damage is done via HBP, shear stress, or cell repair failure. Then inflammatory markers attach to site causing white blood cells and ldl to infiltrate between the inner and outer walls. Eventually the plaque grows and the inner wall continues to thin until one of two scenarios occur 1) hard cap forms (calcification) and the plaque grows until it restricts enough blood that it causes heart attack or 2) The much more dangerous scenario of the inner wall thinning and breaking causing a clot and instant heart attack. The bad part about 2) is that its undetectable except for angiograph or nuclear stress (treadmill can if the heart rate goes high enough and the doctor skilled at interpretation). Some hope for 2) is that statins seem to encourage calcification of those thin walls thus preventing the heart attacks.

This is just what causes the heart attack and the actual fix (stenting and balloon angioplasty) has its own issues. Where the only surefire fix after a heart attack is a bypass, but if more than 2 plaques are found you need to harvest veins which don't last as long. What the entrepreneur world needs to focus on in my opinion is easier at home detection of coronary plaques (sound, radar, electrical, magnetic, etc.). If the government got involved nanorobotics and bio compatible hearts could be explored along with angiogensis via external stimulation, but each of those would be a moonshot program.

1 comments

There is a faulty assumption that higher cholesterol leads to higher risk of heart disease, but the fact the opposite is true.

http://www.zoeharcombe.com/2016/11/familial-hypercholesterol...

A few of the other facts/assumptions you make are outdated. Statins do very little to improve mortality. Inflammation can be reduced by cutting out carbs and sugar. Eating more saturated fats and omega 3 also reduces your risk of heart disease.

In fact the whole dietary advice given over the last 60 years is responsible for the epidemic we now have with obesity, diabetes and heart attacks. But they can't come out and say they are wrong, but they are slowly changing it a bit at a time.

I wouldn't put much faith into the non ldl hypothesis we have extensive studies that show that lower cholesterol (total and ldl) cause less myocardial infarctions.

[1] https://www.nejm.org/doi/pdf/10.1056/NEJMoa1405386 People with a gene that naturally produces lower ldl levels lead to less Hard CD events.

[2] https://www.thelancet.com/journals/lancet/article/PIIS0140-6... Statins cause less heart disease and strokes even more than originally thought.

[3] https://www.thelancet.com/journals/lancet/article/PIIS0140-6... Even if people with low risk factors cutting LDL with stains causes lower number of events

[1] This study makes the assumption that lower ldl is less risk and then looks for mutations in genes that lower ldl. It's putting the cart before the horse.

> e. In each study, we estimated the odds ratio for disease among carriers of any NPC1L1 inactivating mutation, as compared with noncarriers. We then calculated the summary odds ratios and 95% confidence intervals for coronary heart disease among carriers, using a Mantel–Haenszel fixed-effects meta-analysis without continuity correction

[2] This starts off by saying that if we gave statins to 10000 people who are at risk that it would help 1000 and 500 people only. In addition 100 people might have adverse effects. If you ask me, an expensive drug that barely helps and only increases mortality by 5 days on average isn't worth it, and it comes with chances of adverse affects. If we just eat foods high in saturated fats and raise our HDL that is far better.

[3] a meta analysis of randomized trials. Says 11 out of 1000 patients had a reduction of major vascular events. So that is saying out of 90 or so people who take statins, only 1 of them will see any benefits.

Basically statins are poison that give hardly any benefit and treat an assumption that lower ldl leads to less heart attacks.

Try this one https://bmjopen.bmj.com/content/5/9/e007118.full

> The median postponement of death for primary and secondary prevention trials were 3.2 and 4.1 days, respectively.

The average life increase of taking statins is 4 days!