Dietary Fiber Reduces Effects of Second Hand Smoke

fiber and secondhand smoke

By Case Adams, Naturopath

Researchers from Colorado State University have confirmed that increased intake of fiber doesn’t just help colon health. It also reduces the toxic effects of secondhand smoke.

The researchers studied data collected from 29,579 non-smokers. They analyzed their dietary intake of fiber along with consumption of omega-3s, soy isoflavones, lutein and beta-cryptoxanthin. They measured the relationship between their intake of these nutrients together with their secondhand smoke exposure and its resulting effects of coronary heart disease.

Their secondhand smoke exposure was measured by whether they lived with one person who smoked or multiple people who smoked.

The researchers found that those who had the highest quartile of dietary fiber intake had a 62% reduced risk of suffering from the cardiovascular effects of secondhand smoke compared to those with a low intake of dietary fiber.

The researchers concluded:

“We provide evidence that a diet high in fiber may ameliorate the harmful effects of secondhand smoke exposure on risk for coronary heart disease.”

Secondhand smoke and heart disease

The relationship between secondhand smoke and heart disease has been established in a multitude of other research. In a recent study from Scotland, researchers found that secondhand smoke exposure for more than 40 hours per week had more than five-and-a-half times increased risk of peripheral arterial disease.

And discontinuing the exposure can dramatically improve ones risk. In a recent analysis by Harvard Medical School researchers, quitting smoking reducing the risk of a heart attack by 36% at two years after quitting.

How does fiber reduce the risk of heart disease?

As far as the mechanisms relating to how dietary fiber reduces the risk of heart disease in general, this has been established some time ago, as fiber will bind to and reduce low-density lipoproteins within the intestines — reducing their absorption into the bloodstream.

Low-density lipoproteins have a greater aptitude towards oxidation. This means they are degraded by oxygen into lipid peroxides. In this form, these lipid radicals will damage the walls of blood vessels — causing atherosclerosis and heart disease.

Now it so happens that the toxins in cigarettes and other tobacco smoke also produces oxidative radicals that also damage blood vessel walls, as these toxins are released from the lungs into the bloodstream. This is why secondhand smoke produces more heart disease.

So — increased fiber intake reduces lipid peroxides and thus reduces artery damage. This means that the artery damage caused by secondhand smoke for a person on a fiber-rich diet will be less.

As in any wound — say we get wounded on the skin — the body begins to heal the wound. The body will do a good job repairing it unless the wounding continues. If the wounding continues, the body’s immune system can only repair it so far. Just imagine a scrape on the skin that keeps getting scraped. It won’t heal very well.

The bottom line is that the more we do to remove the wounding of the walls of the blood vessels — with a good diet and smart environmental moves — the better shape our arteries will be in. They will thus be more elastic, and more able to repair themselves when they do become damaged now and again.

Learn the diet of our healthiest ancestors.

REFERENCES:

Clark ML, Butler LM, Koh WP, Wang R, Yuan JM. Dietary fiber intake modifies the association between secondhand smoke exposure and coronary heart disease mortality among Chinese non-smokers in Singapore. Nutrition. 2013 Nov-Dec;29(11-12):1304-9. doi: 10.1016/j.nut.2013.04.003.

Lu L, Mackay DF, Pell JP. Association between level of exposure to secondhand smoke and peripheral arterial disease: cross-sectional study of 5,686 never smokers. Atherosclerosis. 2013 Aug;229(2):273-6. doi: 10.1016/j.atherosclerosis.2013.05.015.

Rigotti NA, Clair C. Managing tobacco use: the neglected cardiovascular disease risk factor. Eur Heart J. 2013 Nov;34(42):3259-67. doi: 10.1093/eurheartj/eht352.